Cardiac Pacing and Device Therapy

David R. Ramsdale • Archana Rao

Cardiac Pacing
and Device Therapy
Authors
David R. Ramsdale, M.B., Ch.B., Archana Rao, M.B., Ch.B.,
FRCP, M.D. MRCP, M.D.
The Liverpool Heart and Chest Hospital The Liverpool Heart and Chest Hospital
Liverpool Liverpool
UK UK

ISBN 978-1-4471-2938-7 ISBN 978-1-4471-2939-4 (eBook)

DOI 10.1007/978-1-4471-2939-4
Springer London Heidelberg New York Dordrecht

Library of Congress Control Number: 2012945913

© Springer-Verlag London 2012

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of translation, reprinting, reuse of illus-
trations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and
transmission or information storage and retrieval, electronic adaptation, computer software, or
by similar or dissimilar methodology now known or hereafter developed. Exempted from this
legal reservation are brief excerpts in connection with reviews or scholarly analysis or material
supplied specifically for the purpose of being entered and executed on a computer system, for
exclusive use by the purchaser of the work. Duplication of this publication or parts thereof is
permitted only under the provisions of the Copyright Law of the Publisher’s location, in its cur-
rent version, and permission for use must always be obtained from Springer. Permissions for use
may be obtained through RightsLink at the Copyright Clearance Center. Violations are liable to
prosecution under the respective Copyright Law.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
While the advice and information in this book are believed to be true and accurate at the date of
publication, neither the authors nor the editors nor the publisher can accept any legal responsibility
for any errors or omissions that may be made. The publisher makes no warranty, express or
implied, with respect to the material contained herein.

Printed on acid-free paper

Springer is part of Springer Science+Business Media (www.springer.com)

To Bernie and Pran for their patience and love.
Foreword

The first 50 years of cardiac pacing have recently been celebrated. Since the
first pacemaker implant in 1958, the continuously unfolding story of cardiac
stimulation has been a dramatic and fascinating one, enhanced by the more
recent entry of the implantable defibrillator and cardiac resynchronization
therapy onto the clinical stage. That these implantable devices have had a
great impact on the management of patients with cardiac arrhythmias, saving
and improving countless lives, is beyond scientific refute.
In keeping pace with the technological wizardry and the burgeoning
scientific evidence base underpinning device medicine, it is sometimes
difficult to appreciate the daily background to providing these benefits to
individual patients. Accurately and safely the diagnosis must be made, the
optimal device chosen and implanted specifically to match the clinical need,
and both patient and device meticulously followed up. In this book, the
authors have sought to throw open the doors of their pacing clinic and operat-
ing theater to reveal, in a plethora of fine and rare images, the ‘nuts and bolts’
of daily care for patients presenting for pacing and device therapy. A formal,
classically structured textbook of device medicine this is not – there are many
such comprehensive texts available – nor is it intended to be. This book is an
invitation to join the authors, who combine long interventional experience
and modern specialism in device therapy, in their daily decision making and
practical application, sharing the many sights they have seen through the lav-
ish illustrations which illuminate their own experience, and which they now
share both to inform and enthrall the reader.
Physicians are only part of a network of health professionals who need
increasing amounts of information about implantable devices in order to pro-
vide top class, modern care. This book can be recommended to all who are
entering, already involved in, or just fascinated by, this absorbing and satisfy-
ing branch of cardiology – especially those who would like to lighten their
learning through turning pages which are so easy on the eye!

Liverpool, UK Richard Charles

vii
Preface

This illustrated book is intended to provide an introduction to all those who

have or who are developing an interest in cardiac pacing and device therapy.
They include senior house officers, trainees, clinical fellows, consultant car-
diologists involved in a pacemaker program, cardiac physiologists and other
allied medical professionals, medical students, and colleagues in the medical
device industry.
There are few well-illustrated publications which provide a practical intro-
duction to the indications for use, technique of implantation, recognition and
treatment of complications, and the organization of follow-up and surveillance
of paced patients. We would have valued such a book when we were training
and we hope that young doctors with an interest and passion for cardiology
might find this a useful introduction to this fantastic subspecialty. Besides the
above topics, we felt it would be remiss of us not to present chapters on tem-
porary and epicardial pacing, elective generator change, explant procedures,
pacing in children, implantable cardioverter defibrillators, cardiac resynchro-
nization therapy, troubleshooting in pacing, and training guidelines/regula-
tions for those intending to make a career in pacing/device implantation.
At a time in the UK when pacing is being devolved from specialist tertiary
cardiac centers to smaller district general hospitals and in the USA where
pacemaker implantation is no longer the responsibility of the surgeon and in
the domain of cardiologists, there is a need for a text which offers a guide to
pacing issues to be used alongside a comprehensive practical training pro-
gram in an experienced pacing center. “A picture is worth a thousand words,”
and this book is intended to be generously illustrated with black and white
and color illustrations to aid understanding in the practical aspects of pacing.
Some line diagrams are used in order to simplify the teaching of technique,
and where appropriate Tables are incorporated as useful aide-mémoires. The
text is hopefully comprehensive enough for an “introduction” to the subject,
but it is not intended to be a pacing reference book nor an exhaustive electro-
physiological guide to the theoretical reasons for pacing in its various modes,
nor a detailed guide to programming. Hopefully it will be a very practical
guide to all those involved in the day-to-day care of paced patients, and par-
ticularly to those cardiologists planning a career in this most interesting and
exciting specialty – the so-called device specialist. The products described
are not intended to be a complete list and equally good alternatives may be
available in the marketplace. However, it is hoped that the text and images

ix
x Preface

will give the reader a greater understanding of the type of technology and
equipment that is currently available from the cardiac device industry.
Perhaps cardiac pacing is one of the best examples where the develop-
ments in technology and the microchip industry have resulted in outstanding
clinical benefits to patients, and it is likely that further innovation and minia-
turization will continue to make this specialty a stimulating and exciting one –
if you will pardon the pun!

Liverpool, UK David R. Ramsdale

Archana Rao
Acknowledgments

We would like to thank many colleagues for their help and cooperation with
the production of illustrations for this book. These include Sue Hughes, Sandra
Belchambers, Barbra Bishop, Tony Bennett, Julie Henderson, Drs. Lindsay
Morrison, Johan Waktare, Derick Todd, Julian Hobbs, Mr. Andy Robinson,
and Mr. Ian Kemp – all from The Liverpool Heart and Chest Hospital. We also
appreciate the assistance of Ian Culshaw, Jill Jenc, Becky Sumner, Elizabeth
McDermott and colleagues from Boston Scientific Ltd.; Carl Hughes, Angela
Reed, David Farrington, Tim Palmer and associates from Medtronic Ltd.;
Jayne Saul, Carmel Breen, and Andrew Rapson from Sorin Group UK; Emma
Hampson-Taylor, Paul Doherty, Tim Montgomery, and Bart Verwer from
Biotronik GmbH & Co.; Danny McGuinness, Denise Coley, and Amy Jo
Meyer from St. Jude Medical Inc.; Philip Needham of Cardionetics Ltd.,
David Grey of Novacor, UK, Patty Muratori from Cameron Health Inc. CA,
USA, Mathias Rosenfeld from Spectranetics Co., CO, USA and Zaida Torres
from Oscor Inc., FL, USA for help in providing technical and device data for
the Tables and some of the illustrations. We thank Dr. Joseph DeRose Jr.,
Professor of Cardiothoracic Surgery, Montefiore-Einstein Heart Center, Albert
Einstein College of Medicine Yeshiva University, New York, USA, for con-
tributing images from DaVinci Robotic surgery for epicardial lead placement
and to Intuitive Surgical®, Inc. for allowing us to publish images of the device
itself. We are grateful to the HRUK Audit Group (formerly the Network
Device Survey Group) for allowing us to use illustrations from the 2010 sur-
vey report. Our special thanks also go to Drs. Victor Grech and Oscar Aqualina
from the Mater Dei Hospital, Malta, for permission to use their images from
the Journal Images in Paediatric Cardiology, to Elizabeth Ihrig, Librarian of
The Bakken for making available to us images from The Collections of The
Bakken Library and Museum and permission to use them in Chapter 1 and to
James E. Fogerty and Ryan Barland from The Minnesota Historical Society
for providing the image of Dr. C. Walton Lillehei. Our thanks also go to The
Heart Rhythm Society and to Dan Zika of eMedicine.com for their permission
to reproduce interesting images in Chapters 15 and 21 respectively.
In particular, we are grateful to Dr. Mark Hall for contributing Chapter 15
and Dr. Adam Fitzpatrick, Dr. Jasveer Mangat, and Dr. Ian Peart for supply-
ing many of the images used in this chapter. We thank Dr. Jay Wright for
Chapter 16, Dr. Khalid Albouaini for his contributions to Chapter 17, Mr.
Aung Oo for providing images for use in Chapter 20, and our good friend, the
Jedi Dr. Simon Modi for help in writing Chapter 21.

xi
xii Acknowledgments

We truly appreciate the help and the expertise of our chapter reviewers
Mrs. Sue Hughes, Mr. Paul Wright, Drs. Richard Charles, Derick Todd,
Johan Waktare, David Bennett, Derek Connelly, and Mr. Aung Oo and repre-
sentatives from the device manufacturers for confirming that the data in the
device Tables were accurate at the time of going to press.
We also thank Mr. Grant Weston, Commissioning Editor, Wendy Vetter,
and all the production staff at Springer for their help and support in producing
this book with so many images.
Contents

1 History and Developments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2 Permanent Pacing: Current Overview . . . . . . . . . . . . . . . . . . . . 43
3 Pathology Associated with Need for Pacing . . . . . . . . . . . . . . . . 51
4 Permanent Pacemaker Implantation for Bradycardias:
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
5 Investigations Prior to Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
6 Permanent Pacemakers and Leads . . . . . . . . . . . . . . . . . . . . . . . 87
7 Implantation Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
8 Predischarge Pacemaker Checks and Advice . . . . . . . . . . . . . . . 183
9 Programmable Functions and Terminology . . . . . . . . . . . . . . . . 193
10 Precautions After Permanent Pacemaker Implantation . . . . . . 215
11 Follow-up After Pacemaker Implantation . . . . . . . . . . . . . . . . . 223
12 Complications of Pacemaker Implantation . . . . . . . . . . . . . . . . 249
13 Temporary Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
14 Pacing in Patients with Structural Cardiac Abnormalities . . . . 315
15 Pacemaker and ICD Implantation in Children . . . . . . . . . . . . . 331
16 Cardiac Resynchronization Therapy. . . . . . . . . . . . . . . . . . . . . . 357
17 Implantable Cardioverter Defibrillators . . . . . . . . . . . . . . . . . . . 403
18 Elective Generator Change. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 441
19 Explant Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455
20 Epicardial/Epimyocardial Pacing . . . . . . . . . . . . . . . . . . . . . . . . 483
21 Troubleshooting After Device Implantation . . . . . . . . . . . . . . . . 501
22 Training in Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 543
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 561

xiii
 History and Developments
Early Developments
In 1882, von Ziemssen reported that an electrical
impulse could activate the exposed human heart!
But it was not until almost 50 years later that two
doctors reported the first cardiac pacing devices.
In 1928, Mark Lidwell, an anesthetist at the Royal
Prince Alfred Hospital in Sydney supported by
physicist Edgar H. Booth of the University of
Sydney, developed a device that delivered an
alternating current via a needle inserted into the
patient’s ventricle. At the Crown Street Women’s
Hospital in Sydney, Lidwell used intermittent
electrical stimulation of the heart and saved the
life of a newborn child suffering cardiac arrest.
He reported his work to the third Congress of the
Australian Medical Society in 1929.
In 1932, an American physiologist, Albert S.
Hyman reported on his invention for reviving the
“stopped heart.” Initially his therapy consisted of
intracardiac injections of stimulating drugs such
as epinephrine, but he soon realized that it was the
needle itself that was responsible for restarting the
heart by setting up an acute current of injury as it
punctured the myocardium. His crude device was
powered by a spring-wound, hand-cranked motor,
and consisted of a timing device and a means for
controlling the duration of the pulse of the current
applied. Hyman called his invention the “artificial
pacemaker” (Fig. 1.1). The clockwork device,
developed in collaboration with his brother,
Charles, in the Electrophysical department of
New York University, drove a DC generator whose
electrical impulses were directed into the patient’s
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_1, © Springer-Verlag London 2012
1
right atrium through a bipolar electrode needle
(Fig. 1.2) introduced via an intercostal space and
used to stimulate the myocardium 30, 60, or
120 ppm. This resuscitation therapy caused much
controversy at the time and Hyman experienced
significant opposition from his peers. Siemens–
Hulske in Germany and their American subsid-
iary Adlanco produced a battery-operated version,
called the Hymanotor (Fig. 1.3). Testing was dis-
appointing and his attempts during World War II
to get the US Navy to use the device for resusci-
tating dying servicemen proved unsuccessful.
Hyman abandoned his work and never published
his human data. A description of Hyman’s pace-
maker with a photograph of Albert’s brother
Charles “resuscitating” a young man appeared in
the 1933 October edition of Popular Science, with
a picture of the device in the background.
At Toronto General Hospital, Canada in 1949,
Wilfred Bigelow (Fig. 1.4) and John Callaghan
started using hypothermia to reduce metabolism
and produce bradycardia and asystole to perform
cardiac surgery. Rewarming did not restart car-
diac contraction sufficiently rapidly and so they
began experiments with sino-atrial node stimula-
tion. In the late 1940s and early 1950s, the prin-
ciple device available to generate electrical
impulses capable of stimulating the heart was a
physiological stimulator by Grass Manufacturing
Company for clinical and physiology laboratory
application. It used a thyratron rectifier tube to
convert AC into DC suitable for stimulating bio-
logical tissue. The stimulation rate, voltage out-
put, and pulse width could be varied (Fig. 1.5).
1
2 1 History and Developments

Fig. 1.1 Hyman’s “artificial G

pacemaker” (Illustration with H
permission from Aquilina [1])
B’
C B˜

E
A

D
I

L K

M’

P K
Fig. 1.2 Glass tubes (P)
holding sterile needles (L) and J
stimulating electrical R
S P
connections (Illustration with
L
permission from Aquilina [1])
Early Developments 3

Fig. 1.3 The Hymanotor

(Illustration with permission
from Aquilina [1])

With the help of electrical engineer John Hopps,

Fig. 1.4 Wilfred Bigelow (1913–2005) – cardiac sur-
geon, Toronto General Hospital (Illustration with permis-
sion from Aquilina [1])
they went on to stimulate the sino-atrial node
endovenously during open-heart surgery using a
mains-powered electronic stimulating device
with vacuum tubes. This was perhaps the first
electronic device specifically built as a cardiac
pacemaker. The electrode was a bipolar intrave-
nous catheter, the predecessor of today’s elec-
trodes, stimulating the endocardium. The devices,
however, were large and only as portable as far as
the mains power cable could extend from the wall
socket!
In 1952, Paul Zoll (Fig. 1.6), a Boston cardi-
ologist, developed a tabletop external pacemaker
that could stimulate a patient with cardiac arrest
transthoracically but the device produced skin
burns, pain, and muscular contractions over the
4 1
Fig. 1.5 Grass physiological cardiac
stimulator (Illustration with permission from
Aquilina [1])
Fig. 1.6 Paul Zoll (1911–1999), seen here on the left was
a Boston cardiologist practicing at the Beth Israel Hospital
(Illustration with permission from Aquilina [1])
History and Developments
whole of the chest. The “Electrodyne pace-
maker-65” comprised an electrocardiograph to
monitor the heart rhythm and an electric pulse
generator to pace the heart (Figs. 1.7 and 1.8). It
delivered electrical pulses with a 2 ms pulse
width and 50–150 V alternating current pulse
amplitude through a pair of 3 cm2 metal elec-
trodes strapped to the patient’s chest directly over
the heart. The mains-powered unit was bulky and
heavy and carried on a cart, and its portability
was also limited. Although this technique dem-
onstrated that pacing could be used to treat com-
plete heart block, it clearly was not practical for
protracted use and being a “fixed-rate” device
could cause “R-on-T” ventricular fibrillation. In
1956, at St. George’s Hospital, London, Aubrey
Leatham and Geoffrey Davies produced the first
“demand” pacemaker which would also pace
Early Developments 5

Fig. 1.7 Transcutaneous

cardiac stimulator
(Illustration with permission
from Aquilina [1])

Fig. 1.8 Electrodyne

pacemaker-65 (Illustration
with permission from
Aquilina [1])
6 1
Fig. 1.9 Earl E. Bakken (1924–present) – founder of
Medtronic (Photograph courtesy of The Institute of
Electrical and Electronic Engineers (IEEE))
through the chest wall. A commercial version
had several modifications, e.g., duration of asys-
tole allowable, sensitivity controls to sense the
ECG, two output ranges, and a battery-operated
version.
In 1957, Drs. W.L. Weirich, V. Gott, and C.W.
Lillehei (surgical investigators at the University
of Minnesota) and Earl Bakken of Medtronic
designed the first battery-powered external/wear-
able pacemaker and demonstrated its efficiency
on 18 patients. This unit was small and made
independent of 110 V power by the use of the
transistors. The foundation had thus been laid for
the use of implanted stimulators in the long-term
treatment of atrioventricular block. The story of
the development of this first battery-powered
pacemaker is an interesting one.
Earl E. Bakken (Fig. 1.9), was an electri-
cal engineer/TV repairman who cofounded
Medtronic Inc. with his brother-in-law Palmer
Hermundslie on 29 April 1949, in a garage in
northeast Minneapolis. The company had led a
precarious existence as a repair service for hos-
pital electrical equipment and regional distribu-
tor for other manufacturers. They would build
new equipment to order or customize standard
instruments for laboratory or clinical researchers
History and Developments
Fig. 1.10 Clarence Walton Lillehei (1918–1999) – car-
diac surgeon, University of Minnesota (Photograph cour-
tesy of The Minnesota Historical Society)
and would hang around hospital surgical suites
setting up equipment, training personnel in its
use, and troubleshooting and repairing it as nec-
essary. Meanwhile they forged working relation-
ships with physicians and their staff.
Clarence Walton Lillehei (Fig. 1.10) was a
leading cardiac surgeon at the University of
Minnesota, Minneapolis, who by 1957 had per-
formed over 300 open-heart operations on young
adults and children. This rapidly evolving field of
surgery was to be a major driving force toward the
development of cardiac pacing. Despite successful
repair of the congenital defect, about 10% of
patients developed postoperative complete heart
block due to damage to the conducting system.
Stimulant drugs such as adrenaline, atropine, or
isoprenaline were only helpful in the short-term
and could not prevent sudden recurrence of heart
block. It was thought that temporary pacing would
keep the patient alive until recovery of the con-
ducting system occurred. The technology devel-
oped by Zoll was clearly inappropriate as the high
voltage pacing stimuli delivered transthoracically
would be far too traumatic for young children. The
physiologist John Johnson proposed the utilization
of the Grass stimulator that was used in the
physiology labs to activate hearts. After several
Early Developments
Fig. 1.11 Lillehei’s Teflon-coated multistranded,
braided, stainless steel pacing wire (Illustration with per-
mission from Aquilina [1])
experiments, Vincent Gott and William Weirich
concluded that a cardiac rhythm could be restored
in animal hearts in which heart block had been sur-
gically created by means of a wire inserted into the
wall of the right ventricle and connected to the
external stimulator using low voltage pulses.
Lillehei and his coworkers developed the myocar-
dial wire: a multistranded, braided stainless steel
wire in a Teflon sleeve (Fig. 1.11). One end of this
was implanted directly into the myocardium and
the other end was exteriorized via a stab incision
and connected to the stimulator. An indifferent
electrode was buried under the skin to complete
the circuit. Effective pacing needed only 1.5 V as
there was direct contact with the myocardium and
the wire could be pulled out once normal conduc-
tion resumed. The first myocardial wire was
implanted on the 30 January 1957 in a 3-year old
girl with heart block following repair of Fallot’s
tetralogy. Pacing was successful and the child soon
7
Fig. 1.12 Bakken’s modified two-transistor circuit
(Illustration with permission from Aquilina [1])
regained sinus rhythm and survived. Myocardial
wires were then implanted electively, ready for
immediate use later should this become necessary.
A technique for their implantation through a hol-
low needle was also developed for nonsurgical
patients who developed Stokes–Adams attacks.
However, the stimulator was large and heavy, of
limited portability and scary for children.
Moreover, the system was totally dependent on its
external mains power supply and on 31 October
1957 a municipal power failure lasting 3 h resulted
in the tragic death of a baby. The hospital had
emergency power generation in its surgical suites
and recovery area but not in its patient rooms. The
next day, Lillehei asked Bakken whether Medtro-
nic could come up with something better.
Bakken recalled seeing a circuit for an elec-
tronic, transistorized metronome in the April 1956
back issue of the journal Popular Electronics.
The blocking oscillator circuit that was utilized
had actually been invented at the MIT Radiation
Laboratory during World War II. He simply
modified the two-transistor circuit (Fig. 1.12)
and placed it into a 4″ square and 1½″ thick alu-
minum box with terminals and switches on the
outside. The circuit was powered by a miniature
9.4 V mercury battery housed within the box.
There was an “on-off” switch and control knobs
for stimulus rate and amplitude (Fig. 1.13).
Bakken demonstrated that the device worked in a
dog in the University’s animal laboratory, but the
8 1
Fig. 1.13 Bakken’s “old
number one” pacemaker and
leads (Photograph courtesy
of The Bakken Museum –
The Collections of The
Bakken Library and
Museum)
Fig. 1.14 One of the “first ten” had handles attached
(Illustration with permission from Aquilina [1])
following day he was surprised to find that
Lillehei had used the prototype on a child with
heart block! After only 4 weeks of experimenta-
tion and work, the first battery-powered, transis-
torized pacemaker was in clinical use. The first
production run of ten or so units were more
refined versions of the original prototype and
went into clinical use soon after at the University.
Two metal handles (borrowed from an old ECG
machine) were added such that a strap could
secure the pacemaker to the body (Fig. 1.14).
The Medtronic Cardiac Pacemaker was not only
portable but wearable (Fig. 1.15)! This pace-
maker became known as the 5800 (because it
History and Developments
Fig. 1.15 A wearable device (1958) (Illustration with
permission from Aquilina [1])
was made in 1958). The product literature
claimed that “the pacemaker was designed for
internal applications with at least one wire
attached directly to the myocardium for tempo-
rary stimulation or with a bipolar patch for pro-
longed stimulation and that its self-contained
miniature power source will operate the instru-
ment for approximately 1,000 h” (Fig. 1.16). The
chosen pacemaker output was a 2 ms square
wave, variable in amplitude from 1 to 20 mA into
a 1,000 W load. The blocking oscillator repetition
rate was variable from 60 to 180 ppm. Lillehei
and Bakken published their early experience in
JAMA in 1960 (Fig. 1.17).
Early Developments
Fig. 1.16 Product literature
of the “first ten” (Illustration
with permission from
Aquilina [1])
Fig. 1.17 Lillehei’s paper in
JAMA 1960
Bakken’s pacemaker was regarded as one of
the first successful applications of transistor tech-
nology to medical devices helping to launch the
new field of “medical electronics.” Prior to 1957,
there had never been a partly or completely
implantable electrical device. It was however
apparent that for long-term pacing a totally
implanted device would have to be designed as
9
ascending infection via the pacing electrodes
occurred frequently even though it could be mini-
mized by tunneling the wire for some distance
before bringing it out through the skin (Fig. 1.18).
Moreover although most patients with postopera-
tive heart block regained sinus rhythm within a
few weeks, one patient required the device for
15 months. Recurrent heart block in patients who
10
Fig. 1.18 Electrodes had to exit through the skin – source of
infection (Illustration with permission from Aquilina [1])
had recovered from their postoperative heart
block caused several deaths. Clearly, these
patients needed indefinite and not temporary pac-
ing in order to survive. In addition, the myocar-
dial wires developed exit block as scar tissue
grew around the site of stimulation increasing
electrical resistance and requiring a progressive
increase in pacing stimulus voltage to maintain
capture. The thoracic muscles began to twitch at
these increased voltages. A totally implantable
system with better designed electrodes was
needed.
Meanwhile elsewhere, on the 16 July 1958,
a transvenous, unipolar Cournand catheter
in which the electrode was at the tip of the
catheter was introduced fluoroscopically by
Seymour Furman, via the basilic vein into
the right ventricular outflow tract, in a patient
with fixed complete heart block who required
colon resection because of a malignancy. Using
a mains-powered stimulator, pacing was con-
tinued for 2 h, during the operative procedure,
and ended with slowing of the stimulation rate
until an unpaced idioventricular rhythm devel-
oped. A 50-ft extension power cord allowed
mobilization with the device being pushed on
a mobile cart (Fig. 1.19). The catheter was
removed without complication and the patient
1 History and Developments
Fig. 1.19 Portability was limited by length of power
cord (Photograph courtesy of The Bakken Museum – The
Collections of The Bakken Library and Museum and The
Heart Rhythm Foundation. This picture first appeared in
Furman and Escher [2])
resumed the idioventricular bradycardia. Two
years later, Furman and colleagues, working
in Montefiore Medical Center in the Bronx,
New York City, reported that they had suc-
cessfully achieved endocardial unipolar ven-
tricular pacing in ambulatory out-patients.
Again a Cournand catheter was used with its
tip sited in the outflow tract of the right ven-
tricle. A transvenous lead was inserted into
the right ventricle via a cephalic vein cutdown
and the lead exteriorized through the skin and
held in place with stainless steel sutures which
required frequent renewal. Superficial infec-
tion was frequent. The pacing device was the
newly available battery operated model 902M
from Atronic Products, PA, USA (Fig. 1.20).
The unit was capable of sensing spontane-
ous cardiac activity and of variation in output
and stimulation rate. A small meter indicated
emission of stimuli or sensed events. Portal
(working with Davies and Leatham in London)
claimed to have been using similar right ven-
tricular endocardial stimulation in patients with
Stokes–Adams attacks from early 1960. They
used a similar Cournand electrode catheter with
a small platinum tip and reported that right ven-
tricular apical pacing provided the most stable
pacing position.
Implantable Devices
Fig. 1.20 (Left) Atronic products Model 902M. (Right)
Mr. HN and his wife seen posing for the New York Daily
News outside of Montefiore Hospital in the Bronx, New
York, on 23 June 1959, holding his external pacemaker.
Fig. 1.21 Ake Senning (1915–2000) – cardiac surgeon,
Karolinska Hospital, Stockholm (Illustration with permis-
sion from Aquilina [1])
Implantable Devices
On 8 October 1958, a major milestone in pacing
was reached when the first pacemaker implanta-
tion was performed in Sweden. The system had
been developed by the surgeon Ake Senning
(Fig. 1.21) and the physician/engineer inventor
Rune Elmqvist (Fig. 1.22) and implanted into a
43-year old engineer called Arne Larsson
11
At 67 years he had 2:1 and third degree AV block and
syncope. The transvenous electrode was inserted via a
cephalic vein cut-down and fastened to the skin with
stainless steel sutures
Fig. 1.22 Rune Elmqvist (1906–1996) – engineer
(Illustration with permission from Aquilina [1])
(Fig. 1.23) at the Karolinska Institute in Solna,
near Stockholm, Sweden. Larsson was in desper-
ate trouble with complete heart block causing
Stokes–Adams attacks 20–30 times per day
requiring resuscitation and his wife hounded
Senning to try their invention. This first experi-
ence with a fully implantable pacemaker system,
the Elema 135 (Elema-Schonander), was reported
at the Second International Conference on
12
Fig. 1.23 Arne Larsson (1915–2001) – first human to
receive an implanted pacemaker on 8 October 1958
(Illustration with permission from Aquilina [1])
Medical electronics in 1959 and published as an
abstract in 1960 (Fig. 1.24). To avoid publicity,
the implantation was done in the evening when
the operating rooms were empty. Via a left-sided
thoracotomy two electrodes were implanted into
the myocardium and tunneled to the pacemaker
box placed in the abdominal wall. The first pace-
maker implanted functioned for only 8 h but the
second one implanted in the same patient lasted
1 week before failing possibly as a result of lead
fracture. The pulse generator delivered impulses
at an amplitude of 2 V and a pulse width of
1.5 ms. The pulse rate was fixed at a constant rate
of 70–80 bpm. The energy utilized was mini-
mized since Elmqvist managed to obtain a few of
the first silicon transistors imported into Sweden
which were more efficient than the older germa-
nium transistors. With them Elmqvist designed a
stable and efficient blocking oscillator with a
small power consumption (Fig. 1.25). Several
types of primary battery cells could have been
used in the pacemaker, but because of the poten-
tial for build-up of hydrogen gas at the zinc anode
in the zinc-mercury cells, nickel-cadmium
rechargeable cells were chosen. Two cells of
1 History and Developments
Fig. 1.24 Elmqvist’s and Senning’s abstract 1960
60 mAh each were sealed, encapsulated, and con-
nected in series. Recharging was accomplished
inductively. A coil antenna with a diameter of
about 50 mm was connected to the cells via a sili-
con diode. This was inductively coupled across
the patient’s skin to a large external flexible coil
25 cm in diameter attached to the patient’s abdo-
men with adhesive tape. Recharging was accom-
plished by a 150 kHz radio-frequency current
generated by an external mains-powered vacuum
tube device connected to the external coil. The
pacemaker required charging once a week for
12 h. The entire unit was handmade and consisted
of the nickel-cadmium batteries, the electronic
circuit, and the coil recharging antenna. These
were encapsulated in a new epoxy resin (Araldite)
produced by Ciba-Geigy, which had excellent
biocompatibility (Fig. 1.26). The approximate
diameter and thickness became 55 mm and
16 mm, respectively, according to the dimensions
of the Kiwi shoe polish can (Fig. 1.27). Elmquist
produced two such units using these cans as
molds (Figs. 1.28 and 1.29). These first units had
two electrode wires, each consisting of a twinned,
stainless steel suture wire with polyethylene
Implantable Devices 13

Fig. 1.25 Elmqvist’s circuit

(Illustration with permission
from Aquilina [1]) OA200
E4-1856 OA 200

200 K 1K
8 µF

DE 0.1 200 turns

−
OC OC
460 460
400 K

8µ F

300K

Fig. 1.27 The Kiwi shoe polish can was an early mold

Fig. 1.26 Pacemaker electronics were encased in Araldite

(Illustration with permission from Aquilina [1])

insulation. The distal ends of the wires were sewn

into the myocardium to act as pacing electrodes.
The proximal ends were hard-wired to the pulse
generator circuit. It was estimated that the elec-
trode had to withstand about 105 bends per day.
Elema pacemakers were implanted in Uruguay
and England in February and March 1960.
Elmqvist constructed the Elema 137 pacemaker
in 1960 using Ruben-Mallory zinc-mercury oxide Fig. 1.28 Internal electronics of pacemaker (Illustration
cells as the power source thus eliminating the with permission from Aquilina [1])
14 1 History and Developments

Fig. 1.29 Early versions

of Elmqvist’s Elema–
Schonander devices

Fig. 1.30 Elema-Schonander model 142

need for periodic recharging of the previous

nickel-cadmium cells. Arne Larsson himself
required five lead systems and 22 pulse genera-
tors of 11 different models until his death on 28
December 2001 aged 86 of a malignancy totally
unrelated to his conduction tissue disease or his
pacemaker system – surviving both the engineer
and surgeon who saved his life. One of these
models is shown in Fig. 1.30.
The first person responsible for the introduc-
tion of an implantable pacemaker which did not
require recharging was an electrical engineer
teaching at the University of Buffalo where he
was working on an oscillator to aid in the record-
ing of tachycardias. His name was Wilson
Greatbach (Fig. 1.31). He discovered the way to
make an implantable pacemaker by accidentally
inserting a 1 MΩ rather than a 10 kΩ resistor into
the oscillator circuit. To his amazement the device
emitted intermittent pulses of energy – just what
Fig. 1.31 Wilson Greatbach (1919–2011) – electrical
engineer (Illustration with permission from Aquilina [1])
a heart pacemaker required. As luck would have
it, the chief of surgery at Buffalo’s Veteran’s
Hospital was Dr. William Chardack who believed
in the viability of an implantable pacemaker. On
7 May 1958, Greatbatch brought what would
become the world’s first implantable pacemaker
to the animal lab at the hospital. There, Chardack
and another surgeon, Dr. Andrew Gage, attached
the two pacing wires to the exposed heart of a
dog. The heart proceeded to beat in synchrony
Implantable Devices
Fig. 1.32 Greatbach’s implantable pacemaker and lead
(Top: Illustration with permission from Aquilina [1]; bot-
tom: Photograph courtesy of The Bakken Museum – The
Collections of The Bakken Library and Museum)
with the device. They were all amazed by what
they saw. Over the first 2 years, experiments were
made with animals, but in 1959, Greatbatch pat-
ented the “implantable pacemaker” (Fig. 1.32),
and William Chardack reported the first success
in a human with this unit on 15 April 1960 in a
77-year old man in complete heart block, Mr.
Henry Hennafield, at Millard Fillmore Hospital
in Buffalo, New York. Chardack first implanted
the lead (a bipolar, Hunter-Roth myocardial lead)
and when the threshold stabilized, implanted the
pulse generator (Figs. 1.33 and 1.34). The batter-
ies were powered by 10 “long-life” mercury cells,
eliminating the need for frequent recharging and
increasing life expectancy of the device to
1–2 years. Chardack also introduced the “early
warning” concept for identifying battery exhaus-
tion by a gradual increase in pacing rate.
Chardack’s patient survived uneventfully for
2 years before his death from natural causes and
the pacemaker worked for 18 months without a
15
Fig. 1.33 The “Bow Tie team” – Greatbach, Chardack,
and Gage (Illustration with permission from Aquilina [1])
Fig. 1.34 Patient having received Greatbach’s pace-
maker (Illustration with permission from Aquilina [1])
problem. This success did not go unnoticed by
Medtronic. On a rainy October evening in 1960,
Hermundslie flew his own plane to Buffalo, met
Chardack and Greatbach in the airport, and
signed a contract for Medtronic to produce the
Chardack–Greatbach implantable pulse genera-
tor. Earl Bakken started producing the Chardack–
Greatbach pacemaker in November, and by the
end of December 1960, Medtronic had received
orders for 50 of the $375 units. Chardack, Gage,
and Greatbatch reported a series of 15 patients
who had pacemakers implanted. Medtronic
developed ever-improving devices and pacing
electrodes over the next decade. Figure 1.35
16
Fig. 1.35 Early Medtronic
bipolar electrodes (circa
1959–1962) and implantable
Pacemaker (circa 1962–
1964) in their cardboard
packaging (Photograph
courtesy of The Bakken
Museum – The Collections
of The Bakken Library and
Museum)
shows a boxed electrode set and a Model 5870
pacemaker (produced 1962–1964) from the
Bakken Artifact Collection. After a time with
Medtronic, Greatbatch founded his own com-
pany in 1970 (Wilson Greatbach Ltd.) and went
on to invent the long-life corrosion-free lithium-
iodine battery to power the device. Inventing was
Greatbatch’s lifelong passion and he held many
patents. He died in September 2011, aged
92 years. Other models of pacemakers were
implanted with similar success in 1960 by Zoll
and colleagues, by Lillehei and colleagues in
1961, and in 1962 by Kantrowitz and his associ-
ates. Shortly after this, other pacemaker manu-
facturers appeared. Vitatron, in Holland produced
1 History and Developments
their first pacemaker in 1962 and Telectronics
Inc. in Australia produced their first devices in
their new manufacturing facility in 1965.
Pacesetter Systems Inc. was founded in 1965 and
through Dr. Robert Fischell – a physicist/inventor
at the Johns Hopkins University Applied Physics
Laboratory – was to produce the first rechargeable
device in the USA which could also be
reprogrammed by using radiowaves. Figures
1.36–1.38 show a fixed-rate (VOO) device from
Vitatron, and the battery cells, circuitry, and tran-
sistors are clearly visible through the transparent
resin. Like its competitors, the devices were large
and had to be placed behind the rectus sheath in
the abdomen. A Medtronic employee, Manuel
Implantable Devices
Fig. 1.36 Vitatron fixed-rate (VOO) device
Fig. 1.37 Vitatron device – batteries and circuitry are
visible through transparent casing
Fig. 1.38 Vitatron device – lead connection point and
device width
Villafana was convinced that lithium batteries
were safe to be used in pacemakers although
Medtronic were resistant to the idea because of
the potentially explosive nature of lithium.
Villafana left Medtronic and formed his own
company Cardiac Pacemakers Inc. (CPI) which
became a world leader in pacing technology in its
own right. The Bakken Artifact Collection in the
17
Bakken Museum (www.thebakken.org) presents
an amazing collection of early pacing devices
and electrodes from many of the prominent man-
ufacturers of the time.
Other investigators pursued a different line of
approach in designing self-contained implantable
pacemakers: inductive coupling. A pair of elec-
trodes were sutured to the epicardium and con-
nected to a coil antenna located subcutaneously.
Minimal or no circuitry was implanted and no
internal batteries were needed – getting around
the problem of unreliable pacemaker circuits and
short battery life. The coil antenna was inductively
coupled to an external coil taped to the patient’s
intact skin. This external coil was connected in
turn to a transistorized pulse generator powered
by an external battery. The electronic compo-
nents, relatively unreliable at this time, were
therefore located entirely outside the body
(Fig. 1.39). Other versions of this system included
triple-helix, silicone-insulated endocardial leads,
and rate-control via an external knob (which the
patient himself could modify at will). Inductively-
coupled pacemakers proved to be very successful
with several hundreds being implanted and sur-
vival rates being over 10 years. These devices
were extensively used in Birmingham, UK, for a
number of years, being produced by the Lucas
factory, more commonly known for its electrical
products intended for use in cars (Fig. 1.40). One
particular disadvantage of this device was that its
removal (e.g., for bathing) could result in brady-
cardia and syncope. They continued to be used
until well into the 1970s and several patients with
later generation pacemakers retained the im-
planted coils from their original devices.
Despite these fantastic developments, faulty
batteries, body fluids leaking into the encasement
through the epoxy resin, and broken leads caused
numerous pacemaker failures that required
emergency surgery. These technical problems
contributed to the delay in the widespread use of
implanted pacemakers for several years but over
the next decade as pacemaker circuitry and power
sources became more reliable and as lead design
improved, reliability and longevity of the systems
18
Fig. 1.39 Inductively-coupled pacing. The system consists
of (a) an external pulse generator; (b) an external trans-
mitting coil; (c) an internal receiving coil; and (d) myocar-
dial electrodes. Both the transmitting and receiving coils
contain an iron-core strip, with which effective electromag-
netic coupling between the coils is achieved, thus inducing
stimulating pulses in the receiving coil without high fre-
quency carrier waves. These devices were implanted in the
University Hospital of Tokyo between 1964 and 1968
(Illustration with permission from Aquilina [1])
Fig. 1.41 Hunter-Roth
electrodes (Illustration with
permission from Aquilina [1])
improved and the totally implantable system
would prove the winner and inductively-coupled
systems would be abandoned forever.
One of the main difficulties, however, was the
electrode. It was soon obvious that the wire sutured
directly to the heart was unsuitable as a long-term
electrode. Stimulation threshold increased after a
few weeks until exit block developed and no
more capture was possible. Moreover, the wire
could not resist the enormous repetitive mechani-
cal stresses of bending. Samuel Hunter (Professor
of surgery at St. Paul) and Norman Roth (Chief
engineer at Medtronic) designed a bipolar stain-
less-steel epicardial electrode with a small defined
1 History and Developments
Fig. 1.40 This Abrams–Lucas inductive-coupled unit
was invented by Leon Abrams in Birmingham and made
by Lucas Industries. Epicardial electrodes were connected
to a coil sutured under the skin of the chest wall while
another coil was secured by adhesive tape onto the skin
over the implanted coil. The surface coil is then connected
by wires to a battery-operated pacing unit kept in a coat
pocket and the pacing delivered with electromagnetic
induction. The patient could easily renew the battery and
adjust the rate
surface area including a silicone rubber base
plate, bearing two spike electrodes which could
be pushed into the myocardium, where it was
then sutured in place (Fig. 1.41). On the 4 April
1959, they implanted such an electrode to pace a
patient suffering from post-myocardial infarction
complete heart block. This type of electrode
improved the reliability of the pacemaker as a
result of a lower chronic pacing threshold and
proved the concept of long-term cardiac pacing.
Another lead was developed in 1959 by Elema
Schonander and the Telecom Company, Ericsson.
This consisted of four thin bands of stainless steel
wound around a core of polyester braid and
Implantable Devices
Fig. 1.42 Elema-Ericcson lead (Illustration with permis-
sion from Aquilina [1])
insulated with soft polyethylene (Fig. 1.42). It
was estimated to resist over 184 million flex
cycles, hence lasting for at least 6 years. The uni-
polar epicardial stimulation electrode was a plati-
num disc, 8 mm in diameter and insulated at the
back. Chardack also introduced spring-coil elec-
trodes and improvements in coil manufacturing
processes which caused lead fractures to dimin-
ish dramatically. Estimates were made that the
number of lead flexions without lead failure rose
from 100,000 to 10,000,000 following this devel-
opment in “electrode” design. The electrodes
would be encased within silicone rubber insula-
tion (Fig. 1.43).
The technique for inserting permanent trans-
venous bipolar pacing electrodes was developed in
1962 by Victor Parsonnet and colleagues (in the
USA) and by Lagergren and coworkers (in Sweden)
using fluoroscopic guidance and paved the way for
the replacement of epicardial leads by transvenous
leads – avoiding thoracotomy and general anesthe-
sia. The electrode was initially connected to an
external generator, but a few weeks later it was
then connected to a subcutaneously implanted
generator. Furman demonstrated that cardiac pac-
ing could be maintained for a prolonged period
19
Fig. 1.43 Improved epicardial attachments of electrodes
using such an intravenously-placed electrode
whose tip was placed into the right ventricular
apex. This development resulted in a broadening of
the indications for pacing, particularly because the
lower thresholds achieved by these newer endocar-
dial leads also resulted in extended pacemaker life.
By May 1963, the successful clinical use of a
wholly implantable bipolar endocardial pacemaker
system had been described by Parsonnet, Zucker
and colleagues and Medtronic introduced their
system for clinical use in December 1963.
Thus, the first decade of pacing demonstrated
the clinical value and feasibility of implantable
pacemakers in the revolutionary treatment of
complete heart block and syncope induced by
bradycardia, but there was much more work that
was needed to be done. Cardiologists demanded
improvements in reliability in order to avoid
reoperation due to exit block caused by lead frac-
ture or insufficient output energy of the generator.
Amplitude and rate programmability as well as
the hermetic seal of the electronics were pro-
posed – the latter in order to avoid body fluids
causing short circuits and increased energy loss.
Moreover, because it was soon recognized that
patients paced at a fixed rate exhibited diminished
20 1 History and Developments

exercise tolerance, thoughts were also turned to
developing a device that might allow the pace-
maker’s stimulation rate to be varied according to
the demands being placed on the heart by physi-
cal activity – but it would be sometime before
these particular dreams would be realized.
In the early 1960s, the mortality of pacemaker
insertion was significant (7.5%) and although this
would soon improve, the limitations of fixed-rate
devices – the significant incidence of ventricular
fibrillation and complaints of palpitations due to
competitive pacing – remained a problem.
Demand Pacing
the rectus sheath and without fear of inevitable
generator erosion through the skin. It would also
improve the cosmetic result. For a time, the
devices remained large (Figs. 1.44–1.47) and
would still be placed behind the rectus sheath
requiring a general anesthetic for implantation.
Cordis produced the Stanicor (142 g) and the
Omni Stanicor (145 g) pacemakers encased in
epoxy resin and in 1975 the programmable
Stanicor g (94 g). CPI’s Microlith-A appeared
with an elliptical shape and had its circuitry/bat-
tery coated in Parylene to protect it against mois-
ture before encasing it hermetically in the
stainless steel can. It weighed 76 g and had a

Further understanding of cardiac signals and

developments in electronics made it possible to
detect spontaneous cardiac depolarization. This
gave rise to the concept of demand pacing, where
the pacemaker would only stimulate the heart if
the intrinsic heart rate fell below a set level. This
would prevent competitive pacing on the heart’s
own QRS complexes and the risk of life-threatening
ventricular arrhythmias. At the same time a differ-
ent device emerged, using an algorithm whereby a
ventricular pacemaker was triggered by a sponta-
neous R wave, so that the stimulus fell in the abso-
lute refractory period of the ventricle (VVT mode).
However, if the R-R interval was less than a preset
limit (300 ms), the device functioned at a fixed
rate. The major application was for patients who
experienced pacemaker inhibition due to external Fig. 1.44 Telectronics 120 VVI pacemaker
stimuli such as electromagnetic interference and
repetitive mechanical or myopotential inhibition.
In May 1966, Parsonnet and colleagues were the
first to report on the clinical use of an implantable
demand generator.
The reliability of electronic circuitry was
greatly improved by packing all the components
into a hermetically sealed “can” in order to
exclude body fluids, and the use of “hybrid” tech-
nology instead of discrete components allowed a
significant reduction in size of the pacemaker.
The latter change would make the transvenous
implantation technique most attractive – allowing
the device to be placed superficially in the pecto-
ral area rather than deep in the abdomen behind Fig. 1.45 Medtronic 5945 VVI pacemaker
Demand Pacing
Fig. 1.46 Vitatron’s Vitalith™ VVI pacemaker
volume of 36 cc – a size more suited to prepec-
toral placement. Devices, a British company, pro-
duced a pacemaker but the company proved
unable to compete with the larger US manufac-
turers whose R&D departments received heavy
investment in the rewards that were to come.
Other developments, such as defibrillation-
protection diodes would protect the detection
amplifier of demand pacemakers against strong
electric fields which occurred during procedures
such as transthoracic defibrillation or during elec-
trocautery. Patient safety was improved by
designing automatic rate-limiting circuitry for
single-component failure – avoiding life-
threatening excessively high pacing rates. Most
of these developments occurred as a result of
close collaboration between the pacing industry
and the implanting cardiologists. When a prob-
lem arose, the engineers incorporated a change
within the device or its circuitry to fix it.
Lead design also improved: “tined” and
“flanged” tips for passive fixation (Fig. 1.48) and
“screw-in” for active fixation (Fig. 1.49) result-
ing in a fall in the displacement/malfunction rate.
The conductor material was made of corrosion-
resistant nickel alloy and space-wound in a heli-
cal configuration to minimize the possibility of
wire fracture during flexion. Tips were made
short and blunt to reduce perforation and trans-
parent silicone rubber was used for insulation for
21
Fig. 1.47 Devices UK pacemaker
the conductor material. The electrode tips were
made of platinum-iridium alloy.
Longevity of cardiac pacemakers was increa-
sed from 18 to 28 months with the mercury
oxide-zinc batteries to 3–6 years with the intro-
duction of lithium iodine batteries. Moreover, the
sudden loss of output and failure to pace as the
mercury/zinc cells became depleted became his-
tory following the introduction of lithium batter-
ies with their more predictable and gradual power
loss over time. These batteries also featured high
energy densities and allowed further reduction in
pacemaker size without shortening the genera-
tor’s life. Although lithium-powered pacemakers
were introduced in 1973, mercury/zinc-powered
devices continued to be used up until 1977 in many
pacing centers because of the significant addi-
tional cost of the lithium pacemakers (usually 1.5
times the cost). Similarly, fixed-rate devices were
significantly cheaper than demand pacemakers.
Programmability would lead to further increase
in the cost of devices over nonprogrammable
pacemakers and initially many centers chose
which device to use based on clinical criteria and
budgetary restrictions. In 1972, Medtronic/Alcatel
in Paris made a radioisotope-powered pacemaker
22
Fig. 1.48 Various designs of
lead tips for passive fixation
Fig. 1.49 Helifix electrode tip for active fixation
which was implanted by Parsonnet and cowork-
ers (Fig. 1.50). These nuclear pacemakers had an
expected life of >20 years but went out of fashion
before gaining a foothold in the market mainly
due to the need for extensive regulatory paper-
work and concerns over the long-term adverse
effects of radiation on the body. Perhaps of more
concern was that such devices would confine
1 History and Developments
Fig. 1.50 Medtronic/Alcatel nuclear-powered pacemaker
patients to a lifetime of old pacing technology.
In 1974, the Inter-Society Commission for Heart
Disease Resources (ICHD) recommended a
3-letter coding terminology to indicate the cham-
ber paced, sensed, and the mode of response of
the pacemaker to sensing of the P wave or QRS
complex. In 1987 this was developed further
into the 5-letter NASPE/BPEG (North American
Society of Pacing and Electrophysiology/British
Pacing and Electrophysiology Group) generic
Demand Pacing 23

code, which addresses the important functions pacing. The problems of pacemaker syndrome
of rate adaptive pacing and programmability, and due to loss of AV synchrony with VVI pacing
which remains in current use today. and atrial contraction against closed AV valves,
Titanium casing was developed by the resulting in venous regurgitation, atrial disten-
Telectronics pacing company in 1969 to enclose sion, impaired diastolic filling, hypotension, AV
the battery and circuitry. Cardiac Pacemakers valve incompetence, and atrial fibrillation, and
Inc. used stainless steel and Pacesetter Systems a symptoms of neck pulsation, dizziness, fatigue,
nickel alloy before moving to titanium. This light presyncope, and syncope, needed to be addressed
but very strong material replaced the epoxy resin by restoring AV synchrony. By the end of the
and silicone rubber that was previously utilized 1970s, dual-chamber pacemakers were introduced
to encase the internal components of the pace- to pace and sense in both atria and ventricles,
maker. Other innovations by Telectronics included
the introduction of integrated circuits, narrowing
the stimulating impulse to 0.5 ms, and using
microplasmic welding to join the two halves of
the pacemaker capsule and the Model 120 was
“the state of the art” in pacing in 1974 (see
Fig. 1.44). A slimline version, Model 160, fol-
lowed in 1976. Pacemakers were also made non-
invasively programmable in the mid-1970s using
hand-held and tabletop programmers (Figs. 1.51
and 1.52). Using a radio-frequency telemetry
link, a variety of pacing parameters could be
adjusted to follow the changing clinical needs of
the patient.
As the indications for pacing increased to
include sick sinus syndrome, problems of ventric-
ular sensing in the VVI mode resulting in pace-
maker inhibition required solving. Effects such as
capacitance feedback, P or T wave oversensing,
and external interference were shown to inhibit Fig. 1.51 Siemens handheld pacemaker programmer

Fig. 1.52 (Left) Spectrax™ – S Model 9700 hand- more functions than the handheld programmer and a built-
held pacemaker programmer (Medtronic). (Right) in printer for producing a permanent record for the
Spectrax™ – SX Model 9701 tabletop programmer with casenotes
24 1 History and Developments

but these remained sizeable devices (Fig. 1.53).

Synchronized timing made it possible to preserve
the atrial contribution to ventricular filling as well
as to track the intrinsic atrial rate.
During this period, the rate of pacemaker
implantation grew remarkably. In the USA in
1969, pacemakers were being implanted at the
rate of 71 per million. By 1978, the rate had
increased to 309 per million and in 1981 to 513
per million, and the rate of pacemaker generator
replacements decreased. The rate of implantation
would continue to increase.
It also became possible to transmit pacemaker
data and ECG from the patient’s home to the
ECG department within the pacing center using a
telephone receiver handset and a teletransmitter
in the patient’s home and a telereceiver in the
pacing center (Fig. 1.54).
Fig. 1.53 Medtronic 7000 dual-chamber pacemaker

Fig. 1.54 (Left) The Model 9410 TeleTrace® Receiver
(Medtronic®) is a telephone monitoring receiver for use
with single and dual-chamber pacing systems and com-
patible with the TeleTrace® Transmitters – Models 9407
(Upper right) and 9408 (Lower right). The 9407 was
equipped with bracelet wrist electrodes and the 9408 used
finger-tip electrodes or could be used against the bare
chest using electrodes on the back of the device. Parameters
such as atrial/ventricular pulse width, pacemaker rate, and
AV interval and ECG could be detected and transmitted
Flexibility, Programmability, and Physiological Pacing
Fig. 1.55 (Right) External ventricular demand pace-
maker (Model 5375) and (left) external AV sequential
demand pacemaker (Model 5330) from Medtronic® had
numerous features including output, rate, and sensitivity
settings, indicator lights showing pace and sense func-
tions, a battery test feature, and a safety-lock On-Off
switch to prevent inadvertent turn-off
In the area of temporary pacing, Medtronic
produced compact but versatile, battery-powered,
external demand ventricular and AV sequential
pacemakers for use in a wide variety of clinical
situations such as pre-, intra-, and postoperative
management of cardiac surgical patients, short-
term treatment of arrhythmias and heart block
and emergency cardiac pacing. Wide rate ranges,
adjustable output control, and calibrated sensitiv-
ity dial contributed to the versatility of the device
(Fig. 1.55).
Flexibility, Programmability,
and Physiological Pacing
With the development of CMOS (Complemen-
tary Metal-Oxide-Semiconductor) technology
and the low-power digital integrated circuit on
microprocessors, it became possible to provide
pacemakers with more functions without
significantly compromising size or service-life
(Fig. 1.56). Indeed, the devices became progres-
25
Fig. 1.56 CMOS − 1 Intermedics Inc. programmable
pacemaker
Fig. 1.57 Medtronic MINIX™ SSI pacemaker showing
the reduction in size of pacemakers as a result of advanc-
ing technology
sively smaller (Fig. 1.57). In 1978, Intermedics
had the Quantum VVI pacemaker in a titanium
can weighing only 42 g, and in 1980, Cordis
introduced Omni Stanicor g (VVI), also at 42 g
– a similar dramatic reduction in size – suitable
for a pre-pectoral pocket.
Telemetry (the use of wireless communica-
tion between devices) made the multi-program-
mable pacemaker possible, thereby offering the
increased flexibility needed to adapt the pace-
maker to the patient’s condition whenever
required. In 1977, ventricular demand pace-
makers were introduced with limited program-
mability and in 1978 dual-chamber devices
were implanted for the first time (Fig. 1.58).
Siemens-Elema produced the Vario 659 which
26 1 History and Developments

Fig. 1.59 Siemens-Elema 659 pacemaker

Fig. 1.58 Telectronics Autima® dual-chamber pacemaker

Threshold at
Start Vario test 6 Vario stens

The Vario test reveals that 6 pulses are not accompanied by

any depolarization. This indicates a sufficient threshold mar-
gin as the pacer stimulates whit 5 V and the acute voltage threshold
obviously is only 6 x 0.3 or 1.8 V. Paper speed 25 mm/s.

Fig. 1.60 Vario® (noninvasive) measurement of threshold

enabled noninvasive voltage threshold determi-
nation by application of a magnet (Figs. 1.59
and 1.60).
Figure 1.61 shows the progressive reduction
in size of pacemakers over two decades.
Programmability had major benefits to offer
patients and cardiologists. Reprogramming the
pacemaker’s basic rate made it possible to
increase a patient’s effort tolerance if necessary,
competitive pacing could be suppressed by repro-
gramming the sensitivity setting and exit block
eliminated by increasing stimulation energy by
either increasing the amplitude or pulse width.
Undersensing and oversensing problems could
also be dealt with by reprogramming. Such
maneuvers avoided the need to change the pace-
maker in the event of these not uncommon prob-
lems, and were both cost-saving and a more
acceptable alternative for the patient. The pro-
gramming of hysteresis, to allow patients with
intermittent heart block or sinus bradycardia to
maintain sinus rhythm and only pace at a higher,
determined base rate if the native rate fell below
a set rate, became a useful programmable tool.
Specific programmers were available from indi-
vidual manufacturers, and these too would
become more sophisticated as the technology
developed (Figs. 1.62–1.65).
Flexibility, Programmability, and Physiological Pacing
Maintaining atrioventricular (AV) synchrony
with or without variable-rate pacing based on
sino-atrial node information required a stable
atrial electrode. Progress in lead technology gave
rise to multifilar and coaxial coils plus new
insulating materials which made it possible to
produce thin, flexible leads – less prone to lead or
insulation breaks. The introduction of tines and
the “screw-in” electrodes reduced lead displace-
ment and the need for reintervention for lead
repositioning. The arrival of plastic introducer
kits (Fig. 1.66) made the subclavian vein approach
Fig. 1.61 Progressive reduction in size of pacemakers
Fig. 1.63 The 2035 portable
programmer from CPI®
27
for electrode introduction simpler for operators
and the use of the cephalic vein “cut-down” pro-
cedure (which was difficult if two high-profile
electrodes were necessary) became much less
common. These improvements resulted in an
expansion of pacing modes, including atrial
demand pacing (AAI), ventricular pacing with
atrial and ventricular sensing (VDD), and
atrioventricular sequential pacing (DVI, DDI,
DDD). In August 1982, the first QT-driven rate-
responsive pacemaker (invented by Dr. Anthony
Rickards) was implanted, based on the fact that
Fig. 1.62 Vitatron handheld programmer
28
Fig. 1.64 Pacesetter® Systems Inc. desk-top/semi-
portable programmer
Fig. 1.65 Cordis handheld “sophisticated” programmer
the QT-interval changed with both exercise and
emotion due to the influence of circulating cate-
cholamines. This investigational device, the
TX 1, was a multiprogrammable VVI pacemaker
which was able to sense and measure the duration
of the evoked endocardial T-wave via a conven-
tional pacing electrode. The pacemaker was
therefore able to continuously monitor variations
in stimulus-T interval and adapt the pacing rate
accordingly. The Rhythmx and Quintech® TX
911, 915, and 919 models (Vitatron) (Figs. 1.67
and 1.68) were introduced into an extensive clini-
cal program in the early 1980s and in the mid-late
1980s became commercially available. The TX
1 History and Developments
Fig. 1.66 Peel-away plastic introducer kits
Fig. 1.67 Vitatron’s Quintech® TX rate-responsive
pacemaker
model with its special parameters (upper and
lower rate limit, slope, detection window, and
T-wave sensitivity) was fully programmable.
Other rate-responsive devices such as the RS4
(CPI) and Activitrax™ pacemakers (Medtronic)
were subsequently designed, developed, and
released for clinical use in 1982–1985 (Fig. 1.69).
The RS4-SRT pacing system used a single tripo-
lar (orthogonal) lead for bipolar sensing of the
Flexibility, Programmability, and Physiological Pacing
Fig. 1.68 Quintech® TX 911 rate-adaptive, multipro-
grammable device
“floating” atrial electrogram and ventricular pac-
ing (Fig. 1.70). The RS4 pacemaker algorithm
was designed to vary the ventricular rate to a
maximum of 110 bpm according to the average
sensed P-wave rate. In the Activitrax™ system, a
piezoelectric crystal within the pacemaker can
detected body movement and used this as a sur-
rogate measure of activity. Signals from the sen-
sor were filtered and applied to an algorithm to
alter the pacing rate up or down. Thus, pacing
rate would change according to the patient’s
activity level (VVIR, AAIR, and DDDR).The
RS4-SRT device provided an unreliable rate-
response because of the variable atrial sensing
ability of the lead, but the activity-sensing device
would mature into a capable and sophisticated
rate-responsive pacing system (Fig. 1.71) which
would last.
Anti-tachycardia pacemakers, e.g., PASAR-
Model 4151 (Programmable Automatic Scanning
Arrhythmia Reversion), arrived in 1981 from
Telectronics for terminating supraventricular
tachycardia (SVT) (Fig. 1.72). Such a fully
implantable automatic scanning pacemaker rec-
ognized tachycardia and delivered one or more
extrastimuli which automatically scanned inward
if tachycardia continued. Other devices such as
the Orthocor II Model 284A and the Gemini II
Model 415R from Cordis were introduced for
29
Fig. 1.69 Medtronic’s Activitrax™, activity-sensing
rate-responsive pacemaker
treating and preventing tachycardia respectively.
These devices were rarely 100% successful with-
out additional drug therapy and although they
gained brief popularity among electrophysiolo-
gists, radiofrequency ablation would see the
demise of this technology for the treatment of
patients with re-entrant SVT.
Other changes took place rapidly during this
period of pacemaker/electrode development. The
development of the “In-line” connector concept
reduced the size of the pacemaker connector/
header and made systems sleeker and thinner.
New electrode tip materials and configurations
such as the ring, porous, and carbon tips resulted
in reduced atrial and ventricular thresholds and
improved sensing and new conductor materials
such as platinum/iridium and better insulating
materials, e.g., improved polyurethane and high-
performance silicone rubber all resulted in better
pacing performance. Consequently, the early rise
of capture threshold was blunted and safety was
enhanced. As a result, bipolar leads were pro-
duced which were of the same size as previous
unipolar leads and this led to increased usage and
a reduction in muscle/interference inhibition of
the pacing stimulus. In the early 1980s, steroid-
eluting leads were also developed. These slowly
released steroid from their tip and hence decreased
the inflammatory response evoked by the pres-
ence of the lead tip, abolishing the early thresh-
old rise and providing generally lower chronic
pacing thresholds. Lead and connector problems
became uncommon. The “slippery” polyurethane
coating made it easier to deliver two leads via the
30 1 History and Developments

c Case 1

120
Paced ventricular rate (bpm)

110
100

90
80

70

60

10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 01 02 03 04 05 06 07 08 09
Twenty four hour clock

Fig. 1.70 CPI’s RS4-SRT rate-responsive pacemaker.
(a) PA and lateral chest X-rays show the lead and device
in situ. The white arrow shows the bipolar pair of orthogo-
nally oriented, nonendocardial contacting atrial sensors
designed to optimize intra-atrial electrogram amplitude
and frequency. (b) SRT (segmented ring tripolar) lead.
White arrow shows the atrial sensing electrodes. (c) A
24 h ECG tape recording was used to show the frequency
of rate-response during daily activities
Flexibility, Programmability, and Physiological Pacing
same vein without one moving the other during
positioning.
Bi-directional telemetry links between the
pacemaker and programmer developed dramati-
cally and interrogation of the pacemaker’s
function and its reprogramming became an essen-
tial part of troubleshooting pacing problems in
clinical practice. In addition, a low energy-con-
suming memory made it possible for the pace-
maker to store the intervals between successive
cardiac events for the subsequent production of
histograms for analysis. During the 1980s, CPI
produced the Microthin-P1® (50 g) (Fig. 1.73)
Fig. 1.71 The Legend™ rate responsive activity-sensing
pacemaker was introduced in 1989
Fig. 1.72 The multipro-
grammable PASAR
antitachycardia device, its
handheld programmer, and
the external analyzer/
stimulator
31
and Command P5® (57 g) devices. The latter had
a slimline shape, programmable rate and pulse
width, and were available as uni- or bipolar
models. These stainless steel devices followed on
from the Microlith-P® (75 g), Microlith-A® (75 g),
and Microthin® (50 g) models. Telectronics pro-
duced the titanium-encased Optima®, Optima-MP®
and Autima II® devices and Cordis – the Omnicor®,
Multicor g®, and Stanicor® series (Fig. 1.74). The
Multicor g® was light (42 g) and 10 mm thin. It
had 5 programmable features, 4 output currents,
14 rates, 8 sensitivities, 3 pacing modes (VVI/
VVT/VOO) and was the first to offer uni-/bipolar
programmability. Pacesetter Systems Inc. had the
nonprogrammable Vivalith™ 5 and 10 series –
reflecting 5 and 10 years projected longevity
(Fig. 1.75), and Programalith™ which utilized
large-scale integrated circuitry and telemetry and
offered rate, pulse amplitude, pulse width, sensi-
tivity, refractory period and hysteresis program-
mability and was available in uni- and bipolar
models. Projected life expectancy of these gen-
erators varied between 8 and 10 years and end-
of-life was signified by a reduction of pacing rate
or magnet rate by 6 bpm, e.g., Microthin® D2,
32
a reduction in magnet rate by 10% below pacing
rate, e.g., Programalith™, or a magnet rate of
85 bpm, e.g., Microlith-P/Command P5® (begin-
ning of life magnet rate was 100 bpm).
The early dual-chamber devices (DDD)
included Versatrax® (Medtronic 7000), Sequicor®
(Cordis 233D), Diplos® (Biotronik), and Autima®
(Telectronics) and initially were relatively large
devices.
An even larger device, the automatic implant-
able defibrillator – the AID® from Intec Systems –
was implanted in 1980 for the treatment of life-
threatening ventricular arrhythmias (Fig. 1.76).
Although this initially required a thoracotomy to
insert the electrodes (patch electrodes on the left
ventricle and a spring electrode into the superior
vena cava), this technology would also develop
rapidly. The AID-B, the hybridized VENTAK®
and the VENTAK® 1550 (CPI), the latter released
in 1988, would provide significant product
®
Fig. 1.73 CPI’s Microthin P1 0522 unipolar device
Fig. 1.75 Pacesetter® Systems
Inc. Vivalith™ 10 unipolar and
bipolar devices
1 History and Developments
enhancements while maintaining a high efficacy
of 98% survival from sudden cardiac death at
1 year. The VENTAK® 1550 combined enhanced
longevity with energy and detection criteria pro-
grammability, but these devices remained large
until the mid-1990s (Fig. 1.77). A handheld pro-
grammer enabled communication with the device
(using radiofrequency telemetry) in order to
interrogate the device’s activity, e.g., arrhythmias
detected, total patient shocks, etc., as well as
enabling adjustments in shock energy levels, rate
“cut-offs,” and morphology sensing. The prog-
ress in the developments of this technology would
continue apace over the ensuing 20 years such
that more sophisticated, smaller, longer-lasting
devices can now be implanted transvenously/sub-
cutaneously in the pectoral region rather than by
thoracotomy and burial of the device in the abdo-
men. In 2010, an implantable but entirely lead-
less implantable cardioverter-defibrillator (ICD)
Fig. 1.74 Telectronics Autima II® dual-chamber and
Cordis’ Stanicor single-Chamber device
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present)
Fig. 1.76 AID-B – first automatic implantable
defibrillator from INTEC
was released for clinical use (Cameron Health
Medical). Moreover, randomized clinical trials
would be performed to confirm the survival
benefits of ICD therapy.
Sophistication, Multifunctionality,
and Multiprogrammability
(1990–Present)
Over the last 15 years or more, microprocessor-
driven pacemakers have resulted in further dra-
matic change in the pacing specialty. For
example, by 1992 the dual-chamber Minuet™
from Medtronic weighed only 24 g, was only
6 mm thick, had a longevity of 11 years at 2.5 V
output, boasted 11 pacing modes and full
programmability, AV interval flexibility, and
enhanced diagnostics. These included Real-Time
and Marker Channel™ telemetry and electro-
grams (EGMs) for patient monitoring. Moreover
the device was compatible with both 5 mm uni-
polar and IS-1 bipolar leads.
Devices have become very complex systems
capable of detecting and storing events utilizing
several algorithms such that they can now deliver
therapy and modify their internal pacing param-
eters according to the changing needs of the
patient in an automatic manner. The rate-response
pattern can also adjust itself automatically to the
patient’s activity level. With the increase in auto-
maticity, follow-up visits have become easier and
33
Fig. 1.77 (Top) The Ventak® PRx II was one of a series
of AICDs from CPI in the early 1990s. It was a large
device which could be used with epicardial or endocardial
electrodes. (Bottom) The Photon™ DR, dual-chamber
AICD from St. Jude was the thinnest AICD available
when it was first implanted in December 1999
briefer and pacemakers can also upload data tele-
phonically to a central server via the internet.
Moreover, much effort has been placed into
further understanding the advantages and disad-
vantages of correctly selecting the pacing mode
for patients with sick sinus syndrome or AV block
and that the mode should be prescribed for indi-
vidual patients. For example, AAI or DDD pac-
ing has been shown to reduce the incidence of
chronic atrial fibrillation over VVI pacing in
patients with sinus node disease, while algo-
rithms to minimize ventricular pacing by allow-
ing normal conduction whenever possible will
help to preserve ventricular function.
However, a disadvantage of dual-chamber pac-
ing, endless-loop pacemaker-mediated tachycar-
dia, when pacemakers track atrial activity (VAT,
VDD, DDD) resulting from retrograde atrial acti-
vation following a paced ventricular event was a
34
potentially serious adverse effect. This latter
problem was shown to be treatable by program-
ming pacing modes such as DVI or DDI (such
that the atrium is either not sensed or not tracked).
A variety of algorithms that increase the post-
ventricular atrial refractory period (PVARP), drop
ventricular paced events after periods of pacing at
the upper rate limit, or shorten the AV interval
were also introduced to deal with this problem.
The hemodynamic importance of AV synchrony
and of the AV interval also became appreciated and
more recently pacemakers have been introduced
that have the facility for programming a rate-
adaptive AV interval function to offer hemody-
namic benefit and enable a shorter total atrial
refractory period (TARP) with higher maximal
tracking rates during exercise. In rate-adaptive pac-
ing (available in single-chamber pacemakers since
1986 and dual-chamber pacemakers since 1988),
this has been shown to be advantageous for patients
with chronotropic incompetence for improving
exercise tolerance and has become the program of
choice for such cases although programming and
follow-up are inevitably more complex.
For optimal pacing in patients with atrial tach-
yarrhythmias, which are not uncommon in pace-
maker patients, several options have been
developed to deal with the potential disadvantage
of a DDD pacemaker from the tendency to track
the arrhythmia. Automatic mode switching is one
such mechanism available in DDDR pacemakers.
When criteria are met that the pacemaker identifies
as a nonphysiologic atrial rhythm, the pacemaker
automatically switches from DDDR to VVIR pac-
ing mode until a physiologic atrial rhythm is
restored when the device switches back to DDDR –
ensuring maintenance of rate adaptation.
In a different approach to rate responsive pac-
ing, attempts were made to use a single lead
atrial-sensing, ventricular pacing pacemaker.
Although the floating, unipolar, atrial-sensing
electrode could sometimes be effective in pro-
ducing a good rate response with exercise from
CPI’s RS4 pacemaker, atrial sensing was often
suboptimal and the rate response unpredictable.
The disadvantage of unipolar sensing (myopoten-
tial and other far-field signal oversensing) led to
the development of a VDD lead incorporating
1 History and Developments
bipolar atrial sensing. Other sensors of movement
and acceleration were investigated thoroughly
during the 1980s and the possible advantages of
accelerometer-based sensors over vibration-based
sensors demonstrated during exercise and pos-
tural changes. Biotec International produced the
multiBIOrate® MB1 (following extensive experi-
ence with the RDP-3 device introduced in 1982)
which detected respiration based on the imped-
ance principle. A small auxiliary lead was
implanted subcutaneously in the thorax, and a
train of low voltage constant current impulses
sent between the tip of the auxiliary electrode and
the pacing can. Variation of electrical impedance
occurred during respiration and was proportional
to tidal volume (Fig. 1.78). The output of the
impedance detector device produced a waveform
from which the rate and volume of respiratory
activity could be detected, and programming used
to optimize sensing. Other sensors of minute-
ventilation, e.g., META MV® (Telectronics/
Cordis), of the rate-of-rise of ventricular pressure
(dP/dt), pre-ejection interval, of autonomic ner-
vous system activity derived from filtered intrac-
ardiac impedance measurements (so-called VIP
or ventricular inotropic parameter), of QT-interval,
e.g., Rhythmyx® (Vitatron), central venous tem-
perature, O2 saturation, and of depolarization gra-
dient were also extensively investigated. Some of
these have become incorporated within modern
systems. Dual-sensor technology was pursued to
get around the problem that no single sensor
offers a perfect physiologic response to all exer-
cise and non-exercise requirements, by providing
“cross-checking” of appropriate sensor response.
The classic development was of the combined
activity- and QT-sensor which was designed to
combine the fast response of activity-sensing
with the more proportional response to exercise
and non-exercise requirements of the QT-sensor
and to prevent inappropriate response of the activ-
ity pacemaker to environmental vibrations by
cross checking. Others have included activity/
minute ventilation, accelerometer/minute ventila-
tion, and even combinations of a fast acting activ-
ity sensor with a more proportional and specific
metabolic sensor. Present systems allow for the
automated tailoring of rate response, via self
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present)
Fig. 1.78 The MultiBIOrate® MB1 respiratory rate
detector. (Bottom panel) Impedance lead and trochar sys-
tem for tunneling the wire across the chest wall subcuta-
neously. (Top right panel) System in place showing the
learning rate-response algorithms, or program-
ming of a target rate histogram on the basis of the
patient’s activity level and frequency of exercise.
Systems can facilitate storage of patients’ details
and diagnose rhythm disturbances using sophisti-
cated algorithms.
The indications for pacing have also expanded
beyond symptomatic bradycardia and now
include neurocardiogenic syncope, hypertrophic
obstructive cardiomyopathy, and cardiac resyn-
chronization therapy (CRT, biventricular pac-
ing) for congestive heart failure. There has also
been progressive refinement of antibradycardia-
pacing function in implantable cardioverter
defibrillators (ICDs). Recent ICDs capable of dual-
chamber and triple-chamber, rate-responsive pac-
ing provide state-of-the-art treatment (Fig. 1.79).
Shortcomings in early-generation devices have
35
train of pulses sent between the tip of the lead and the can
(---). (Top left panel) chest x-ray showing the sensing
lead, the pacemaker, and the pacing electrode
been corrected. Nevertheless, future research
will define the optimum pacing parameters/set-
tings for these sophisticated systems in patients
with various cardiac pathologies. Pacing to ter-
minate ventricular tachyarrhythmias requires a
back-up defibrillation facility via an ICD but pac-
ing to prevent ventricular tachyarrhythmias may
use continuous or intermittent (rate-smoothing
or stabilization) pacing (with ventricular cap-
ture) to suppress triggering of ectopic beats,
prevent re-entry, decrease dispersion of refrac-
toriness, and eliminate pauses that might induce
tachyarrhythmia.
Alongside these remarkable developments in
pacemaker technology and programmability, the
value of pacing at alternative sites to the right
atrial appendage and right ventricular apex has
become appreciated. For example, pacing of the
36 1 History and Developments

interatrial septum and pacing in the right ventric- amplitude safety margin and minimum voltage.
ular outflow tract using active-fixation leads may The Identity™ ADxDR pacemaker from St. Jude
prevent atrial arrhythmias and improve cardiac has a suite of diagnostic and therapeutic capa-
output respectively. In addition, left ventricular bilities aimed at managing patients with inter-
pacing via the coronary sinus has been shown to mittent atrial fibrillation besides being recently
be beneficial in patients with severe left ventric- claimed to be the world’s smallest dual-chamber
ular dysfunction and major left-sided intraven- pacemaker at 18 g and 8 cc (Fig. 1.82).
tricular conduction disorders such as left bundle Techniques for removing infected or redun-
branch block. This Cardiac Resynchronization dant pacing leads have also developed using spe-
Therapy (CRT), by resynchronizing contrac- cial sheaths to provide counterpressure and
tion of the right ventricle, left ventricular sep- countertraction as an extractor applies traction to
tum, and left ventricular lateral walls has been remove the lead from the myocardium. Locking
shown to improve LV contractility resulting in
improved morbidity and mortality (Figs. 1.79–
1.81). Moreover, programmable features such as
Managed Ventricular Pacing (MVP), AV Search
Hysteresis, and AAI-DDD safe modes may help
to reduce the amount of right ventricular pacing
and also reduce the incidence of atrial fibrillation.
Ventricular Capture Management (VCM) and
Atrial Capture Management (ACM) are achieved
by the device being designed to periodically test
ventricular/atrial thresholds, and reprogram ven-
tricular/atrial outputs based on a programmable

Fig. 1.80 Medtronic’s InSync® CRT device and leads

(Reproduced with permission of Medtronic, Inc.)

Fig. 1.79 Boston Scientific’s Cognis® CRT-D provides

enhanced CRT therapy, atrial arrhythmia management,
SmartDelay AV optimization, and high-energy defibril-
lation in a 9 mm thin, 35 cc can (Used with permission of
Boston Scientific Corporation, ©2010 Boston Scientific
Corporation/affiliates. All rights reserved)
Fig. 1.81 Boston Scientific’s Contak Renewal® TR2
(CRT) device (Used with permission of Boston Scientific
Corporation, ©2010 Boston Scientific Corporation/
affiliates. All rights reserved)
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present) 37

Fig. 1.82 St. Jude’s Identity® ADxDR device features

atrial fibrillation management, a suite of therapeutic and
diagnostic capabilities designed to help manage pacemaker
patients suffering from AF, e.g., AF suppression algorithm,
Auto-Mode Switch Log, and Physician Commanded Atrial
Therapy (NIPS – Non-Invasive Programmed Stimulation)
(Image provided courtesy of St. Jude Medical, ©2008
St. Jude Medical, Inc.)

stylets, telescoping sheaths, and excimer laser

sheaths are also now available to aid removal of
chronically adherent leads when mechanical
removal has failed (Fig. 1.83) and have been
found to be advantageous. These percutaneous
lead extraction techniques should be restricted to
experienced centers with cardiac surgical Fig. 1.83 Spectranetics® Laser extraction sheath for lead
back-up. removal
Another major development has been the
introduction of digital technology by Vitatron in
their C and T series (Fig. 1.84). They were able to
adapt Digital Signal Processing (DSP) for use in
a pacemaker platform with minimal energy con-
sumption. DSP switches the analogue signal into
a digital signal, allowing more accurate signal
analysis. This results in a high-quality intracar-
diac electrogram (IEGM) which enables the heart
rhythm to be identified more readily. Moreover,
this technology allows data storage within the
pacemaker and has made interrogation and pro-
gramming of the device rapid – using sophisti-
cated external devices (Fig. 1.85). It is also now
possible to interrogate pacing devices wirelessly
in pacing clinics as well as in the patient’s own
home using the World Wide Web. Traditionally, a
“wand” attached by a wire to the programmer is
positioned on the body’s surface over the device
implantation site in order to receive the telemetry
signal. However, the distance for radiofrequency Fig. 1.84 Vitatron’s C- and T-series of pacemakers were
communication has increased from 2–5 in. the world’s first to use digital technology
38 1 History and Developments

Fig. 1.85 Sorin’s desk-top

programmer/data analyzer –
Orchestra™

(5–12 cm) to 10–20 ft (3–6 m) and some devices

communicate without a wand. The longer dis-
tance telemetry is device-specific and employs
either the Industrial, Scientific and Medical (ISM)
band from 902 to 928 MHz or a subsection of the
Medical Implant and Communications (MICS)
band from 402 to 405 MHz. Use of telemetry in
these frequency spectra has allowed the telemet-
ric signal to be reliably and securely sent to and
from the programmer and device up to a distance
of 10 ft (3 m) distant. This has proved useful dur-
ing implantation, in the device clinic (using a
programmer), and also in the patient’s home as
part of remote monitoring (remote telemetry
device) (Fig. 1.86). Programmers now have inte-
grated printers to document the device settings,
but home monitor/communicators and program- Fig. 1.86 Merlin@Home is the home monitoring device/
mers can also communicate the interrogated data transmitter from St. Jude Medical (Image provided cour-
tesy of St. Jude Medical, ©2008 St. Jude Medical, Inc.)
to a remote printer for a hard copy presentation or
be transferred to a cardiac device database or
Electronic Medical Record (EMR). dependent on the ingenuity, vision, and drive of
Many of these innovative developments will be cardiologists and the engineers in the industry
described further in the chapters that are to follow. who remain focused on producing devices which
Suffice to say, as with all the developments and have the potential to improve patient survival and
improvements in the technology and practice of quality of life. Many of the important “Milestones
pacing described here, future advances will remain in pacing” are shown in Table 1.1.
Sophistication, Multifunctionality, and Multiprogrammability (1990–Present) 39

Table 1.1 Milestones in pacing

1928 Lidwell reports successful electrical restarting of the heart in a newborn
1932 Hyman presents the “artificial pacemaker” – a mechanical device for producing a DC current to stimulate
the right atrium directly using a bipolar needle
1949 Earl Bakken founds Medtronic Inc.
1949 Bigelow, Callaghan, and Hopps use endovenous electrode to stimulate the sino-atrial node during open
heart surgery
1952 Zoll demonstrates a transthoracic external pacemaker
1957 Transthoracic pacing performed using a pacing wire placed directly into the heart via a needle placed
through the chest wall
1958 Furman uses endovenous electrode to pace the right ventricle using a mains-powered electrical stimulator
1958 Weirich, Lillehei, and Bakken use battery powered stimulator to pace the heart via an endovenous electrode
1958 Ake Senning implants first pacemaker invented by Rune Elmqvist at Elema-Schonander in Stockholm,
Sweden, using a device powered by nickel-cadmium batteries/inductive recharging unit
Davies, Leatham, and Robinson reported “effective ventricular stimulation” in a patient with second
degree heart block in October 1958
1959 Hunter and Roth produce a stainless steel epicardial electrode with a small surface area and spikes that
could be pushed into myocardium/sutured in place
1960 Greatbatch and Chardack produce Medtronic’s first pacemaker powered by mercury batteries – recharging
unnecessary. Used clinically for first time in June 1960
Zoll implants permanent pacemaker in October 1960
1961 Noel Gray, New South Wales, Australia, founds Telectronics Company – becoming Telectronics Inc. in 1963
Lillehei et al. and Kantrowitz et al. implant permanent pacemakers in January and May 1961 respectively
1962 First Vitatron pacemaker
Lagergren and Johansson first used a unipolar endocardial electrode in the RV apex as a permanent lead.
Initially connected to an external generator for a few weeks, it was then connected to a subcutaneously
implanted generator
Wilson Greatbach patents implantable pacemaker in Buffalo, NY
1963 Zucker, Parsonnet and colleagues report the use of a wholly implantable bipolar endocardial pacemaker;
Siddons and Davies also reported use of endocardial ventricular pacing with a St. George’s generator
implanted in the axilla
First Biotronik pacemaker
1964 Telectronics facility for permanent pacemaker production established; first device, P1 (4 mercury-zinc
batteries) implanted
1965 Alfred E. Mann founds Pacesetter Systems Inc.; produce first rechargeable long-life pacemaker battery
developed by Robert Fischell at the Johns Hopkins University.
First Biotronik endocardial lead
1966 Ellis Epstein, Norman Coulshed, Charles McKendrick and colleagues in Liverpool report the use of
temporary RV pacing for the treatment of AV block complicating acute MI
1968 Vitatron demonstrate first noninvasive threshold measurement
1969 In USA, number of new pacemaker implants was 71 per million of population
1970 First nuclear-powered (Plutonium-238) Medtronic pacemaker implanted in Paris
1972 First lithium-iodine battery-powered pacemaker implanted
1972 Cardiac Pacemakers Inc. (CPI) of St. Paul, Minnesota, was formed
1973 Albert Beutel II creates Intermedics
1974 Elema-Schonander becomes Siemens-Elema
1976 Intermedics produce first small, lithium battery-operated pacemaker which tripled the life of currently
available generators
First Biotronik pacemaker with a lithium battery, a hybrid circuit, and an hermetic MP35N housing (Protasul)
1978 CPI acquired by Eli Lilly and rename the company Guidant
1979 Pacesetter Systems Inc. introduce first pacemaker to use bidirectional telemetry
1979 Anthony Rickards showed that at fixed pacing rates, the QT-interval changed on exercise and during
emotional stress due to catecholamines and that this phenomenon could be used to develop a
rate-responsive pacemaker
40 1 History and Developments

Table 1.1 (continued )

1980 First ICD, developed by Michel Mirowski and Morton Mower – the AID® from Intec Systems – implanted
in a patient by Dr. Levi Watkins, Jr (February 1980). Marlin Heilman, the founder of MedRad (a medical
device company) and Alois Langer, his chief biomedical engineer have been recognized for their pivotal
roles in developing a prototype automatic ICD alongside Mirowski and Mower from 1973 onward
1981 In USA, number of new pacemaker implants was 513 per million of population
1981 Vitatron produce world’s first microprocessor, software-driven pacemaker (DPG1), introduce “Flywheel”
mode for rate smoothing and first pacemaker diagnostics – long/short-term rate histograms
1982 Vitatron produce first rate responsive pacemaker – TX 1, a QT-sensing device which increased ventricular
pacing rate as the paced evoked-QT-interval changed with physiological demand. Devices implanted in
Europe
1983 Biotronik introduce Neos, the world’s smallest single-chamber pacemaker with bi-directional telemetry
1984 Vitatron introduce features such as “Conditional Wenckebach response,” night rate drop, rate-adaptive A-V
delay, automatic upper rate response (first mode switching), reduced ventricular tracking limit (during
paroxysmal AF). Quintech TX was introduced which improved T-wave sensing by altering the filter
characteristics (bandwidth) to favor the T-wave rather than R-wave frequencies
1985 Activitrax™ – a vibration-sensing, rate responsive pacemaker introduced by Medtronic
1985 Eli Lilly purchase Intec Systems defibrillator technology on behalf of its subsidiary CPI; Siemens,
AG purchase Pacesetter Systems Inc.
1986 CPI release VENTAK® ICD
1986 Telectronics becomes subsidiary of Nucleus Ltd., – Australian high technology health products
1986 Vitatron acquired by Medtronic
Biotronik introduce thermosol, a rate-adaptive pacemaker with a central venous temperature measurement
sensor
1988 Daily learn algorithm in Rhythmyx® introduced by Vitatron
1990 Biotronik introduce NEOS-PEP, a rate-adaptive pacemaker with a pre-ejection phase measurement sensor
1992 Vitatron produce world’s first dual-sensor rate responsive pacemaker; Sensor Cross-Checking™
1993 Vitatron produce dual sensor/dual-chamber pacemaker plus other features such as Automatic Scanning for
spontaneous AV conduction; AV delay hysteresis; Beat-to-beat mode switching; P-wave histograms
1994 St. Jude Medical purchase Siemens’ pacemaker division for $500 million
1995 ELA (a French company later acquired by Sorin) produce world’s first dual-chamber defibrillator
–DEFENDER®
1996 Pacific Dunlop sells Telectronic Pacing Systems to St. Jude Medical Inc., USA for $170 million
1997 Spectranetics introduce Excimer Laser Lead extraction device
1998 Vitatron produce 4 novel preventive pacing algorithms for preventing AF onsets
2000 Vitatron introduce new series of anti-atrial arrhythmia DDDRP pacing devices
2002 Vitatron introduce the Vitatron CRT 8000 for cardiac resynchronization therapy; Sorin Group produce
LIVING™ CHF, a CRT device with an endocardial acceleration sensor
2003 Vitatron produce world’s first digital pacemaker series – Vitatron C-series with fast and efficient digital
signal processing and a Therapy Advisor facility
Sorin introduce SafeR™ in SYMPHONY® pacemakers – the first pacing mode to limit unnecessary
ventricular pacing
2004 First Vitatron T-series released offering dual-channel electrograms
2005 Vitatron C-series models released
2006 Boston Scientific acquire Guidant for $27.2 billion
Sorin Group introduce a small ICD with the SafeR™ mode
2007 2nd Vitatron T-series released
2009 Medtronic introduce the first MRI-safe device – the Advisa MRI™
Surescan®; St. Jude Medical and Boston Scientific Ltd. introduce the first DF-4 standard leads for ICDs
2010 Quartet™ (the IS4, quadripolar LV pacing lead) is released by St. Jude Medical
2010 Biotronik launch The Evia premium pacemaker series and Biotronik ProMRI® a technology to allow MRI
scanning in their bradycardia device and leads portfolio
References 41

References 2. Furman S, Escher DJW. Principles and techniques of

cardiac pacing. New York: Harper & Row; 1970.
1. Aquilina O. A brief history of cardiac pacing. Images
Paediatr Cardiol. 2006;27:17–81.
 Permanent Pacing: Current
Overview
Today, approximately three million people
worldwide have a pacemaker and more than
600,000 pacemakers are implanted annually.
A responsibility of the International Cardiac
Pacing and Electrophysiology Society is a
worldwide quadrennial survey of cardiac pacing
and ICD practices. Fifty countries contributed to
the 2001 Worldwide Survey. Table 2.1 shows the
number of implanting centers per country, the
number of new and replacement pacemaker
implants by each country, and the number of new
implants per million population. The largest
implanting nation with 223,226 new implants
was the USA followed by Germany (69,823) and
France (37,250). Japan’s new implants totaled
26,700, Canada’s 18,376, and the UK’s 17,550.
Figure 2.1 shows the number of new implants
per million. Most countries showed an increase
in new implants per million compared with the
1997 survey. High degree AV block and sick
sinus syndrome were almost universally the
major indications for pacemaker implantation,
with <2% biventricular pacing in those countries
that implanted such devices in 2001. VVIR pac-
ing increased progressively in developing coun-
tries and values >40% were still common in
Europe. Most countries showed a significant
increase in the use of DDDR replacing the use of
VVIR systems. Single-lead VDD pacing systems
were used throughout the world although few
countries had greater than a 10% rate. The USA
and the UK, for example, implanted <1% of such
devices. AAIR systems were predominantly used
in less socioeconomically developed countries,
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_2, © Springer-Verlag London 2012
2
e.g., Lithuania. Pacing leads were predominantly
transvenous, bipolar and passive fixation elec-
trodes and active-fixation leads in the atrium are
being used with increasing frequency. There
were marked variations from country to country.
In the UK, the ratios of active- to passive-fixation
leads in the atrium and ventricle were 16:84 and
6:94, respectively, but in the USA the corre-
sponding figures were 73:27 and 38:62, respec-
tively. The 2001 Survey showed a progressive
increase in the number of ICDs worldwide with
the largest number of implants being in the USA
(48,127, or 169 implants per million). Dual-
chamber and biventricular ICD devices were
being used with increasing frequency and biven-
tricular pacemakers themselves were being
introduced in several countries. These devices
are so expensive that few are implanted in poorly
developed countries. Although the next survey is
likely to show a further increase in such implants
worldwide, the contrast between developed and
third-world countries is likely to persist. These
remarkable devices have been shown to have
life-saving benefits, but their expense is an
important issue and will continue to put a
financial burden on the health services of most
countries.
In a recent report by the Heart Rhythm Society
and the European Heart Rhythm Association, it
was estimated that in 2006 approximately
280,000 pacemakers and 160,000 ICDs (implant-
able cardioverter defibrillators) were implanted
in North America while the corresponding num-
bers for the countries of western and central
43
44 2 Permanent Pacing: Current Overview

Table 2.1 World survey 2001

New implants per
Country Population (million) No. of centers New implants million population Replacements
Germany 83 850 69,823 837 ?
USA 284 ? 223,226 786 51,616
Belgium 10 120 7,053 685 3,086
Italy 58 400 36,779 637 ?
France 59 600 37,250 628 5,871
Canada 31 125 18,376 591 1,218
Austria 8 64 4,666 583 1,232
Czech Republic 11 36 5,563 530 ?
Australia 20 105 9,498 486 1,536
Sweden 9 45 4,201 472 1,485
Denmark 5 14 2,429 467 967
Switzerland 7 65 3,014 415 846
Finland 5 24 2,128 411 ?
Spain 41 145 16,421 399 ?
Uruguay 3 12 1,160 362 496
Israel 6 18 2,009 335 663
Norway 4 29 1,472 329 301
Netherlands 16 106 5,016 314 1,891
Slovenia 2 2 621 312 142
UK 60 174 17,550 293 3,823
Lithuania 4 3 953 272 ?
Argentina 36 230 9,000 250 1,000
New Zealand 4 8 914 245 195
Croatia 4 11 1,049 238 157
Ireland 4 13 879 228 145
Slovak Republic 5 14 1,143 212 ?
Latvia 3 3 528 210 127
Japan 127 2,700 26,700 210 11,500
Hong Kong 7 16 1,004 143 92
Taiwan 22 22 2,290 102 193
Singapore 3 10 281 92 20
Brazil 170 243 15,167 89 7,182
Russia 144 97 10,950 76 100
South Africa 45 39 1,814 40 224
South Korea 45 65 1,162 26 322
Iran 60 27 1,469 24 211
Peru 25 20 550 22 80
Ecuador 12 18 180 15 15
Thailand 62 22 605 10 47
China 1,300 241 11,000 8 855
India 1,000 329 6,725 7 570
Pakistan 135 14 910 7 60
Philippines 79 10 348 4 12
Indonesia 220 21 220 1 30
Mond et al. [1]
Countries listed in order of implants per million
2 Permanent Pacing: Current Overview 45

Pacemaker implants per million worldwide − 2001 survey

1000

800

600

400

200

0
India Pakistan China Malaysia Peru S Korea S Africa Russia
Brazil Taiwan Hong Kong Japan Latvia Slovakia Ireland Croatia
Argentina Lithuania UK Slovenia Netherlands Norway Israel Spain
Finland Switzerland Denmark Sweden Australia Czech Rep Austria Canada
Italy Belgium USA Germany

Fig. 2.1 Number of new implants per million of population. Worldwide survey 2001 (Mond et al. [1])

Europe were 250,000 and 50,000 respectively.
They estimated the prevalence of these devices
in 2007 to be 564,074 pacemakers, 234,780 ICDs,
and 148,092 CRTs (cardiac resynchroniza-
tion therapy devices) in North America and
683,472, 87,747, and 62,010, respectively, in
Europe. The logistics of monitoring such large
numbers of devices is an ever increasing chal-
lenge for the cardiovascular community and the
group estimated that the number of follow-up
encounters annually for pacemakers (with or
without CRT) in North America and Europe was
3.2 million and for ICDs (with or without CRT)
2.5 million. Recently the HRUK Audit Group
(formerly the Network Device Survey Group)
published its sixth annual report for 2010 in the
UK. For England, this suggested a new pace-
maker implant rate of 528 per million, an ICD
implant rate of 72 per million and a total CRT
implant rate of 114 per million as against targets
of 700, 100, and 130 per million, respectively
(Figs. 2.2–2.4). There was considerable regional
variation within the UK. A comparison with
implant rates across Europe is shown in
Figs. 2.5–2.7.
The joint American College of Cardiology/
American Heart Association/North American
Society of Pacing and Electrophysiology
(NASPE) Committee’s Guidelines have been
updated. Generally, wherever possible, a pace-
maker device with atrial contribution, i.e., a
single-chamber atrial or dual-chamber device
should be used. It is justified by the additional
benefit expected from these devices, e.g.,
improved hemodynamics and a better quality
of life and reduced morbidity and mortality.
However, several controlled, randomized trials
on these issues revealed somewhat disappointing
results. Only the first trial, in Denmark, studying
255 patients with sinus node disease, showed a
significant reduction in mortality and morbidity
such as the incidence of atrial fibrillation, stroke,
and congestive heart failure with single-chamber
atrial pacing versus single-chamber ventricular
pacing. Other studies aimed at demonstrating the
survival benefits of dual-chamber pacing over
46
600
England
Wales
500 Scotland
N Ireland
400
Per million population
300
200
100
0
2000 2001 2002
Fig. 2.2 Trends of new pacemaker implant rates in the UK 2010 (HRUK Audit Group)
single-chamber ventricular pacing failed to do so.
These included the Pacemaker Selection in the
Elderly trial (407 patients), the Canadian Trial
of Physiological Pacing (2,568 patients), and the
Mode Selection Trial (2,010 patients). However,
the incidences of atrial fibrillation were less fre-
quently observed in the dual-chamber group in
all three trials. Mattioli and colleagues showed
similar results in their study, but the Pacemaker
Atrial Tachycardia trial failed to do so despite
showing a survival benefit with dual-chamber
pacing. Two large databases such as the Danish
and German pacemaker registries allayed fears
that complication rates were higher with dual-
chamber pacing compared to single-chamber
pacing and it is now accepted that an atrial lead
should be implanted where there is no contrain-
dication, e.g., atrial fibrillation.
An issue that has important practical implica-
tions is the question as to whether ventricular
pacing from the RV apex may be detrimental.
Studies have shown that permanently pacing the
2 Permanent Pacing: Current Overview
2003 2004 2005 2006 2007 2008 2009 2010
Year
RV apex results in an increased incidence of
atrial fibrillation, hospitalization for heart fail-
ure, and possibly death even when AV synchrony
is maintained. If these results are corroborated
by others, then RV apical pacing would have to
be avoided and sites elsewhere in the RV such as
the RV outflow tract (RVOT) or interventricular
septum using an active-fixation lead might prove
to be the best option. Thus, in patients with sinus
node disease, single-chamber atrial pacing or
dual-chamber pacing with sophisticated algo-
rithms which reduce RV pacing might be the
answer, and for those with AV block, RV pacing
from the RVOT might prove more beneficial. In
the past, in patients with sinus node disease but
without evidence of AV block, it was common
practice to check Wenckebach rate by pacing the
atrium at high rates to assess AV conduction in
order to decide whether or not to implant a ven-
tricular lead (especially in young patients with
sinus node disease) – unfortunately this appears
to have poor predictive value.
2 Permanent Pacing: Current Overview
140
England
120 Wales
Scotland
N Ireland
100
Per million population
80
60
40
20
0
2000 2001 2002
Fig. 2.3 Trends of new ICD implant rates in the UK 2010 (HRUK Audit Group)
During the last decade, many attempts were
made to apply pacing technology to the treatment
of problems other than symptomatic bradycardia
– mainly to prevent atrial tachyarrhythmias and
to improve the symptoms, the hemodynamics,
and possibly the survival of patients with con-
gestive cardiac failure. The initial interest in the
prevention and treatment of atrial tachyarrhyth-
mias with implantable devices fell as algorithms
designed to prevent paroxysmal arrhythmias
proved unsuccessful and then substantially
after publication of the results of the Atrial
Fibrillation Follow-up Investigation of Rhythm
Management Trial. This showed no survival
benefit for patients with vigorous rhythm control
(i.e., attempts to retain or restore sinus rhythm)
compared to simple rate control in sinus rhythm
or atrial fibrillation. Other studies supported
these findings, resulting in an uncertain future
for pacing to prevent atrial fibrillation. More
optimistically, pacing to deliver cardiac resyn-
chronization therapy in patients with congestive
47
2003 2004 2005 2006 2007 2008 2009 2010
Year
cardiac failure appears to hold much promise.
Trials such as Pacing Therapy in Congestive
Heart Failure trial, Multisite Stimulation In
Cardiomyopathies, and Multicenter InSync
Randomised Clinical Evaluation all demonstrate
that CRT can improve the symptoms, exer-
cise capacity, and the functional status of such
patients. CARE-HF showed a survival benefit for
CRT pacing therapy (CRT-P). The Comparison
of Medical Therapy, Pacing and Defibrillation in
Chronic Heart Failure trial showed a reduction
in mortality when CRT therapy was combined
with an ICD (CRT-D) and MADIT-CRT showed
a reduction in progression of mild (Class I and II)
to more severe heart failure (Class III and IV) as
well as a 34% reduction in the risk of all-cause
mortality or heart failure in patients treated with
CRT-D compared with ICD implantation alone.
Besides these and other newer indications for
pacing, developments in pacemaker program-
mability and novel diagnostic and monitoring
features of pacemakers and ICDs continue to
48 2 Permanent Pacing: Current Overview

140

England
120 Wales
Scotland
N Ireland
100
Per million population

80

60

40

20

0
2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
Year

Fig. 2.4 Trends of new total CRT implant rates in the UK 2010 (HRUK Audit Group)

make this subspecialty of cardiology exciting and
rewarding for those technicians and doctors
intending to develop an expertise and indeed a
career in this field. Opportunities for both clinical
research and device development and evaluation
alongside pacemaker manufacturers and their
engineers are numerous and limited only by the
imagination and enthusiasm of the individual.
Training of physicians in the techniques of
implantation of devices, their indication for use,
and their subsequent programming and trouble-
shooting in order to optimize their function, is
essential and should be of a high standard.
Similarly training of technical staff (cardiac
physiologists) that are essential for running a
comprehensive and high quality service both in
the pacing theater and in the out-patient clinic is
no less important. Training programs, examina-
tions, and qualifications as a testament to the
individual’s expertise are discussed in Chap. 22.
2 Permanent Pacing: Current Overview 49

Ireland
Norway
UK
Greece
Netherlands
Switzerland
Spain
Denmark
Portugal
Czech Republic
Finland
Austria
Sweden
France
Italy
Belgium
Germany
0 200 400 600 800 1000 1200 1400

Fig. 2.5 Comparison of all pacemaker implants in the UK versus rest of Europe in 2010 (HRUK Audit Group) (Sources:
Eucomed (2010))

Portugal
Spain
UK
Greece
France
Sweden
Norway
Finland
Switzerland
Ireland
Belgium
Austria
Czech Republic
Italy
Denmark
Netherlands
Germany
0 50 100 150 200 250 300 350

Fig. 2.6 Comparison of all ICD implants in the UK versus rest of Europe in 2010 (HRUK Audit Group) (Sources:
Eucomed (2010))
50 2 Permanent Pacing: Current Overview

Greece
Spain
Ireland
Portugal
Finland
Norway
Switzerland
Sweden
France
Austria
UK
Belgium
Denmark
Netherlands
Czech Republic
Germany
Italy

0 50 100 150 200 250

Fig. 2.7 Comparison of all CRT implants in the UK versus rest of Europe in 2010 (HRUK Audit Group) (Sources:
Eucomed (2010))

Reference
1. Mond HG, et al. The world survey of cardiac pacing
and cardioverter defibrillators: calendar year 2001.
Pacing Clin Electrophysiol. 2004;27:955–64.
 Pathology Associated with Need
for Pacing 3

Cardiac pacing is indicated for the treatment of
both bradyarrhythmias and tachyarrhythmias.
However, the major indication for pacing is
the treatment of bradyarrhythmias due either to
sick sinus syndrome, atrioventricular block, or a
combination of both, which result in symptoms
such as dizziness, near syncope or syncope.
Prophylactic pacing is also indicated in asymp-
tomatic individuals who have ECG evidence of a
significant intracardiac conduction defect which
may result in similar symptoms or death due to
asystole.
The commonest causes for cardiac conduct-
ing system disease are shown in Table 3.1 and
include idiopathic conducting tissue fibrosis,
myocardial infarction, myocardial infiltrative dis-
orders, myocarditis, infective endocarditis, cardi-
omyopathy, neuromuscular dystrophies, coronary
artery disease, cardiac surgery, and congenital
heart block (Figs. 3.1–3.5). Radiofrequency (RF)
ablation of the AV node to treat patients with
difficult supraventricular arrhythmias (e.g., atrial
fibrillation) that are unresponsive to drugs and
other RF ablative techniques may necessitate per-
manent pacing (Fig. 3.6) as may alcohol-septal
ablation in patients with hypertrophic obstruc-
tive cardiomyopathy (Figs. 3.7 and 3.8). Sick
sinus syndrome, a disorder of impulse formation,
is most commonly due to idiopathic fibrosis. It
also occurs after cardiac surgery, especially in
children undergoing corrective surgery for con-
genital abnormalities and rarely with myocardial
infiltrative disorders such as sarcoidosis, amyloi-
dosis, Chagas’ disease, and cardiomyopathies.

Table 3.1 Causes of cardiac conducting system disease that may necessitate pacing
Idiopathic conducting tissue fibrosis
Sick sinus syndrome/tachycardia–bradycardia syndrome
Coronary artery disease
Myocardial infarction
Myocardial infiltrative disorders/cardiomyopathy
Cardiac surgery, e.g., aortic valve surgery, repair of ventricular septal defect, surgery for correcting structural cardiac
defects in children
Radiofrequency ablation of the AV node
Infective endocarditis
Myocarditis
Congenital heart block
Alcohol septal ablation for hypertrophic obstructive cardiomyopathy
Percutaneous coronary rotational atherectomy – temporary pacing
Neuromuscular diseases, e.g., dystrophia myotonica, Kearns–Sayre syndrome
Drug toxicity

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 51

DOI 10.1007/978-1-4471-2939-4_3, © Springer-Verlag London 2012
52 3 Pathology Associated with Need for Pacing

I II III aVR aVL aVF

V1 V2 V3 V4 V5 V6

Fig. 3.1 Acute inferior myocardial infarction is sometimes hypotension, or symptoms of dizziness or syncope, tempo-
complicated by second or third degree heart block. When rary pacing is indicated. This 12-lead ECG and rhythm strip
associated with marked bradycardia, a fall in cardiac output, show inferior ST-elevation and Mobitz Type II AV block

Fig. 3.2 Muscular dystrophies such as dystrophia myo- conduction disturbances such as complete heart block
tonica (evidenced by frontal balding, bilateral ptosis, and when permanent pacing is indicated
a long, haggard facial expression) may be associated with
3 Pathology Associated with Need for Pacing
Fig. 3.3 Infective endocarditis, particularly involving the
aortic valve, may result in spread of infection and abscess
formation into the interventricular septum and result in
serious conduction disturbance, including complete heart
block and asystole. Patients with infective endocarditis
and septal abscess should have a temporary pacemaker
inserted especially if a conduction disturbance develops
on the ECG. (Top) Destructive infective endocarditis of
this bioprosthetic valve due to Staphylococcus aureus
caused severe aortic regurgitation. (Bottom left) 2D
53
echocardiogram shows a large vegetation on the aortic
valve which resulted in severe aortic regurgitation.
(Bottom right) 2D echocardiogram showing large inter-
ventricular septal abscess (AB) which was associated with
a progressively increasing PR interval and sudden onset
of complete heart block. Fortunately, a temporary pace-
maker was inserted when the PR interval was first noticed
to increase from 200 to 280 ms. VEG vegetation, AO aor-
tic valve, RA right atrium, RV right ventricle, LV left
ventricle
54 3 Pathology Associated with Need for Pacing

Fig. 3.6 AV Node ablation either requires temporary

pacemaker implantation prior to ablation and permanent
pacing thereafter or more commonly is done 8 weeks after
permanent pacemaker implantation

Fig. 3.4 Aortic valve surgery may be complicated by

heart block and require temporary and/or permanent pac-
ing. An artificial aortic valve is shown being deployed

Fig. 3.7 Patients with hypertrophic obstructive cardio-

myopathy may be helped by dual chamber pacemaker
implantation with an RV apical lead. The echocardio-
graphic features of asymmetric LV hypertrophy and LV
outflow tract obstruction are shown here

Fig. 3.5 Aortic valve bio-prosthesis in situ

3 Pathology Associated with Need for Pacing 55

Fig. 3.8 Alcohol septal ablation for hypertrophic obstruc-

tive cardiomyopathy (shown here by the small balloon
catheter inflated in the septal artery (green arrow)) is asso-
ciated with complete heart block in 8–10% of cases and
patients will require dual chamber permanent pacemaker
implantation. The procedure is covered by temporary pac-
ing with a pacing catheter placed in the right ventricular
apex (black arrow)

Some patients will require temporary pacing

only – when the conduction defect is considered
to be a temporary phenomenon, such as after
acute myocardial infarction (see Fig. 3.1) or to
protect them against the effects of higher degrees
of heart block if this should develop during gen-
eral anesthesia, surgery, or percutaneous coro-
nary intervention, such as rotational atherectomy
in the right coronary artery (Fig. 3.9), or as a
result of drug toxicity. Combined temporary atrial
and ventricular pacing (dual chamber pacing)
may help improve cardiac output in low output
states associated with AV block or severe sinus
bradycardia when single chamber right ventricu-
lar pacing fails to improve the hemodynamic
state (Fig. 3.10).
For tachyarrhythmias such as ventricular
tachycardia, right ventricular overdrive pacing
may be used as an interim measure to terminate
the arrhythmia if pharmacological treatment has
failed or is contraindicated (Fig. 3.11). Temporary
pacing is used in intracardiac electrophysiologi-
cal studies during the investigation of supraven- Fig. 3.9 Rotational atherectomy of calcified lesions in a
large, dominant right coronary artery should be covered by
tricular or ventricular arrhythmias and in the temporary pacing as plaque ablation with the high speed
identification of accessory pathways such as in Rotablator may result in severe bradycardia or heart block
56 3 Pathology Associated with Need for Pacing

the Wolff–Parkinson–White syndrome (Figs. 3.12

and 3.13).
For patients with severe heart failure due to
impaired cardiac function, biventricular perma-
nent pacing (cardiac resynchronization therapy)
may be indicated in order to re-establish synchro-
nous RV and LV contractility (Fig. 3.14) and the
indications, technique, and benefits of this are
discussed in Chap. 16.

Fig. 3.10 Patients with cardiogenic shock and AV

dissociation after severe myocardial infarction may favor-
ably respond hemodynamically to AV sequential pac-
ing using temporary atrial and ventricular electrodes.
Unfortunately, temporary atrial leads are unstable and
frequently displace and lose capture. In this situation,
permanent pacing using actively fixed atrial and ventricu-
lar electrodes may be extremely useful in stabilizing the
hemodynamics. The arrow points to the tip of a straight
atrial electrode actively fixed into the low right atrium
where sensing and pacing thresholds were acceptable

Fig. 3.11 RV overdrive pacing can terminate ventricular confirming AV dissociation and that the rhythm is ven-
tachycardia. The top ECG is a surface lead II. The second tricular tachycardia. The bottom two ECGs (lead II) show
recording is an intracardiac recording from a temporary that the VT is overdriven by rapid RV pacing and then
electrode within the RA. The arrow shows the P-waves, terminated
3 Pathology Associated with Need for Pacing 57

Fig. 3.12 Temporary pacing electrodes are used in

intracardiac electrophysiological studies during investiga-
tion and treatment of arrhythmias such as the Wolff–
Parkinson–White syndrome (see Fig. 3.13). Here catheters
are shown in the coronary sinus, in the left atrium, and
against the Bundle of His

Fig. 3.13 ECG showing Wolff-Parkinson-White syndrome Type B

58 3 Pathology Associated with Need for Pacing

Fig. 3.14 Cardiac resynchronization therapy (CRT) has (left) alongside a chest X-ray showing leads in the RA, RV
proved useful for treatment of patients with impaired car- septum, and in a branch vein of the coronary sinus (Image
diac function. Medtronic’s InSync® III CRT device is shown reproduced with permission of Medtronic, Inc.)
 Permanent Pacemaker Implantation
for Bradycardias: Indications
Permanent pacemaker implantation is indicated to
relieve symptoms of syncope, near syncope, dizzi-
ness, or dyspnea in patients with severe bradycar-
dia and to improve prognosis in asymptomatic
patients with impaired intracardiac conduction tis-
sue. Indications for permanent pacemaker implan-
tation are shown in Table 4.1. The ECG is the most
important guide to whether pacing is indicated.
First-Degree AV Block
First-degree AV block alone is not usually an
indication for cardiac pacing (Figs. 4.1 and 4.2).
However, if associated with syncope or near-syn-
cope, co-existent 2° or 3° AV block may be sus-
pected and investigations including continuous
ambulatory ECG monitoring or loop event record-
ing should be performed. A prolonged PR inter-
val (>200 ms) (especially lengthening of the PR
interval over time) in association with RBBB,
LBBB, or alternating BBB should be considered
an indication for permanent pacing (Fig. 4.3).
Second-Degree AV Block
Mobitz Type I AV block (Wenckebach) in young
people, especially if transient or nocturnal, is
probably due to increased vagal tone and pacing
is not indicated. In older people, the incidence of
symptoms and the prognosis is not dissimilar to
Mobitz Type II AV block and pacing is indicated
(Fig. 4.4). An exception may be adults who have
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_4, © Springer-Verlag London 2012
4
a high vagal tone, perhaps as a result of physical
training such as athletes and professional sports-
men/women.
Table 4.1 Indications for permanent pacemaker implantation
Second-degree AV block
Idiopathic/ischemic/persistent post MI/infiltrative/
post-surgery/traumaa
Complete AV block
Idiopathic/ischemic/persistent post MI/infiltrative/
post surgery/traumaa
Bifascicular blockb
RBBB + LAFB and normal PR interval
RBBB + LPFB and normal PR interval
Trifascicular block
RBBB + LAFB and prolonged PR interval
RBBB + LPFB and prolonged PR interval
LBBB + long PR interval (especially if progressive
lengthening of PR)
Alternating RBBB/LBBB
Junctional bradycardiab
Severe sinus bradycardiab
Sick sinus syndromeb
Sinus arrest (>3 s pauses)
Carotid sinus hypersensitivityb
Malignant vasovagal syndromesb
Hypertrophic obstructive cardiomyopathy – if septal
ablation is complicated by 2° or 3° AV block or slow
junctional rhythm; or in drug-refractory patients
unsuitable for septal ablation
Cardiac resynchronization therapy
Post-cardiac transplantationa
Pediatrics and congenital heart diseasea
a
See text
b
In symptomatic patients or where considered that there is
a high likelihood of progression to 2°, 3° AV block, slow
junctional escape rhythm, or asystole
59
60 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.1 First-degree AV

block in a patient with
previous inferior MI

Fig. 4.2 First-degree AV

block in an asymptomatic
sportsman
Second-Degree AV Block 61

Fig. 4.3 Alternating LBBB

(left upper panel) and RBBB
(right upper panel), followed
by complete heart block
(central lower panel)

Fig. 4.4 Wenckebach Mobitz

Type I second-degree AV
block
62 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.5 Mobitz Type II AV

block

Fig. 4.6 Third-degree AV

block or complete heart block

Mobitz Type II AV block is associated with a
high incidence of complete AV block and patients
with this arrhythmia should be paced permanently
(Fig. 4.5). Perhaps the only exception is follow-
ing an acute inferior MI, when second- and third-
degree AV block may resolve within the next
2 weeks. However, after an acute anterior MI,
these bradyarrhythmias reflect interventricular
septal infarction/necrosis and carry a high risk of
asystole, and those patients with persistent Mobitz
Type II AV block should be permanently paced.
For those patients in whom second-/third-degree
AV block resolves, the prognosis for future AV
block or ventricular asystole is even less certain
– but those having had anterior MI and transient
second-/third-degree infranodal AV block but
new onset BBB should probably also be paced.
Third-Degree AV Block
This is usually due to conducting tissue fibrosis
(Fig. 4.6). Frequently the QRS complex is wide.
Other causes are shown in Table 4.1. Patients
Sick Sinus Syndrome
Fig. 4.7 Bifascicular block –
RBBB + LAFB with a normal
PR interval
should be paced whether they are symptomatic or
not. Prognosis has been shown to be improved by
pacing (1-year mortality: 35–50% unpaced vs.
5% paced), and a first Stokes–Adams attack may
be fatal.
Complete AV block may be congenital. Here,
the level of block is higher in the His bundle or
AV node and the QRS is narrow. Any idioven-
tricular rhythm is usually faster than in the
acquired form, and it responds more to exercise
and other autonomic stimuli. Pacing is usually
only considered necessary if associated with a
wide QRS complex, the development of brady-
cardia-related symptoms, if the rate fails to rise
on exercise, or if the resting junctional rate is
<50 bpm.
Second-degree or complete AV block associ-
ated with myotonic muscular dystrophy, Kearns–
Sayre syndrome, etc., and when occurring after
catheter ablation of the AV node or after valve
surgery when block is not expected to resolve are
all indications for pacing.
Bundle-Branch Block
Patients with bradycardia-related symptoms
and evidence of bifascicular or trifascicular
block should be paced. Asymptomatic patients
should be treated conservatively unless evi-
dence of progressive AV conduction block, such
as progressive lengthening of the PR interval, is
evident.
63
Evidence of bifascicular block includes
RBBB + left anterior fascicular block (LAFB)
(Fig. 4.7) and RBBB + left posterior fascicular
block (LPFB) or complete LBBB alone
(Fig. 4.8).
Trifascicular disease means impaired conduc-
tion in all three branches at the same time, although
it has been used to describe bifascicular block
together with first-degree AV block (Figs. 4.9
and 4.10). Alternating RBBB + LBBB, RBBB +
alternating LAFB/LPFB, or LBBB +long PR in-
terval on the same or successive ECGs are prob-
ably evidence of trifascicular disease.
Sick Sinus Syndrome
Sinoatrial disease may result in sick sinus
syndrome or “tachy–brady” syndrome. Sick
sinus syndrome may be manifest as prolonged
sinus arrest (Fig. 4.11) or sino-atrial block
separately or combined with paroxysmal atrial
tachycardia, flutter or fibrillation (Fig. 4.12)
in the “tachy–brady” syndrome. It may also
coexist with AV block perhaps as a manifesta-
tion of generalized conducting tissue fibrosis
(Fig. 4.13) and even ventricular arrhythmias
(Fig. 4.14). Pacing is indicated for symptoms
associated with a bradycardia. Although prog-
nosis is probably not improved by pacing,
the incidence of stroke and the onset of atrial
fibrillation may be diminished by atrial-based
pacing.
64 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.8 Left bundle branch

block (LBBB)

Fig. 4.9 Tri-fascicular block

(RBBB + LAFB) with a
prolonged PR interval

Carotid Sinus Hypersensitivity charge as a result of stimulation of the carotid

and Malignant Vasovagal
Syndrome (MVS)
These two conditions, members of a group of
conditions known as neurocardiogenic syncope,
are relatively uncommon. Intense vagal dis-
sinus causes unusually profound sinus brady-
cardia/sinus arrest and in MVS profound
peripheral vasodilatation resulting in severe
hypotension (Fig. 4.15). Syncope after turning
the neck or on looking vertically upward should
alert one to the diagnosis. A ventricular pause
Carotid Sinus Hypersensitivity and Malignant Vasovagal Syndrome (MVS) 65

Fig. 4.10 Tri-fascicular

block (RBBB + LPFB) with a
prolonged PR interval

Fig. 4.11 Sick sinus

syndrome manifested by
prolonged sinus arrest.
First-degree and possible
Mobitz Type I (Wenckebach)
AV block indicate additional
AV nodal disease

lasting 3s or more and a fall in systolic blood
pressure of 50 mmHg or more is considered
abnormal and defines carotid sinus hypersensi-
tivity. Dual-chamber pacing may be indicated
for those with recurrent vasovagal syncope and
prolonged asystole during Holter recording
and/or tilt testing and might improve the symp-
toms. Loop recorders might help identify those
most likely to benefit from pacing by docu-
menting evidence of severe bradycardia/asys-
tole coinciding with the patient’s symptoms.
Measures such as support stockings and avoid-
ance of dehydration are essential in MVS. Patients
with MVS also require reassurance and education
regarding the benign nature of the condition, but
based on the medical history they should also be
informed of the likelihood of syncope recurrence.
Recognition of any associated premonitory symp-
toms which allows them to recognize an impend-
ing episode might prompt them to sit or lie down
or use isometric maneuvers to avert or limit the
consequence of a loss of consciousness.
66 4 Permanent Pacemaker Implantation for Bradycardias: Indications

Fig. 4.12 Sick sinus syndrome manifesting with sinus arrest and paroxysmal atrial flutter and fibrillation

Hypertrophic Obstructive apex alters septal motion significantly (Figs. 3.7

Cardiomyopathy
In symptomatic patients, AV synchronous pacing
with a short AV delay may help to reduce the sub-
aortic gradient in hypertrophic obstructive cardi-
omyopathy (HOCM) since pacing from the RV
and 4.16). This has been shown to reduce symp-
toms. However, recent randomized trial data
(M-PATHY) have suggested that pacing alone
may not benefit all patients with HOCM.
Although alcohol-induced septal ablation
may be very effective treatment for HOCM,
Hypertrophic Obstructive Cardiomyopathy 67

Fig. 4.13 Sick sinus

syndrome may be associated
with AV block as well. These
ECG strips show progressive
increase of PR interval and
sinus arrest (top) and
complete heart block
(bottom)

Fig. 4.14 The “tachy–brady” syndrome may manifest as atrial fibrillation with markedly variable ventricular rates and
ventricular arrhythmias

temporary pacemaker insertion is usually nec-
essary during the procedure because of an inci-
dence of AV block of 10%. In 7–10% of
patients, permanent DDD pacing will be
required for persistent 2° or 3° AV block or fol-
lowing the development of new bi- or tri-
fascicular block as a result of the septal
infarction and necrosis.
DDD pacing may also be considered in
patients with contraindications for septal ablation
or myectomy or in those requiring pacing for bra-
dycardia or with an indication for ICD implanta-
68 4 Permanent Pacemaker Implantation for Bradycardias: Indications
Fig. 4.15 Hypersensitive
carotid sinus syndrome.
Carotid sinus massage
produces sinus bradycardia
and then prolonged asystole
and near syncope
Fig. 4.16 Position of permanent right atrial and right
ventricular lead in a patient with HOCM
tion. It may also be indicated in elderly patients
with drug-refractory HOCM.
Cardiogenic Shock and AV Block
Post Myocardial Infarction
Occasionally in patients with 2º or 3º AV block post
myocardial infarction who are in cardiogenic shock,
only restoration of AV synchrony will lead to an
improvement in cardiac output and survival may be
dependent on maintaining it. Temporary atrial elec-
trodes are liable to displacement, and this may lead
to a sudden catastrophic deterioration in the
patient’s hemodynamic state. In such a situation,
insertion of actively fixed atrial and ventricular
electrodes and implantation of a permanent DDD
pacemaker may be lifesaving (see Fig. 3.10).
Post-Cardiac Transplantation
Symptomatic bradyarrhythmias due to sinus node
dysfunction or AV block 3 weeks after cardiac
transplantation or chronotropic incompetence
impeding quality of life are indications for pacing.
Pediatrics and Congenital
Heart Disease
Class I indications for pacing include congenital
3° AV block associated with any of the following
conditions: symptoms, ventricular rates <50–55/
min, ventricular rates <70/min in congenital heart
disease, ventricular dysfunction, wide QRS escape
rhythm, complex ventricular ectopy, abrupt ven-
tricular pauses >2–3× basic cycle length, prolonged
QTc, or presence of maternal antibodies-mediated
block. Other indications include 2° or 3° AV block
with symptomatic bradycardia or ventricular dys-
function, postoperative Mobitz type II 2° or 3° AV
block which persists at least 7 days after cardiac
surgery, and symptomatic sinus node dysfunction.
Class IIa indications include asymptomatic
sinus bradycardia in the child with complex
European Society of Cardiology and European Heart Rhythm Association Guidelines
congenital heart disease and resting heart rate <40/
min or pauses >3 s; bradycardia–tachycardia syn-
drome requiring antiarrhythmic drugs; long-QT
syndrome with 2° or 3° AV block, symptomatic
bradycardia, or pause-dependent VT; congenital
heart disease and impaired hemodynamics due to
sinus bradycardia or loss of AV synchrony. Class
IIb indications include congenital 3° AV block
without a Class I indication; transient postopera-
tive 3° AV block with residual bifascicular block;
asymptomatic sinus bradycardia in the adolescent
with congenital heart disease and resting heart
rate <40/min or pauses >3 s; and neuromuscu-
lar diseases with any degree of AV block without
symptoms.
European Society of Cardiology
and European Heart Rhythm
Association Guidelines
The ESC/EHRA and the ACC/AHA have issued
guidelines for the appropriate use of pacemaker
devices in sinus node disease, in acquired AV
69
block, in chronic bifascicular and trifascicular
block, after myocardial infarction, in carotid
sinus syndrome, in vasovagal syncope, in pedi-
atrics and congenital heart disease, after cardiac
transplantation, and in hypertrophic cardio-
myopathy. They also present their recommen-
dations for the use of biventricular pacemakers
(with and without ICD) for patients with heart
failure.
The ESC/EHRA present the Class of
Recommendation and the Level of Evidence for
each clinical indication, and these are available
on the ESC website: www.escardio.org. More
recently, the AHA/ACC 2008 guidelines were
similarly published on the HRS website: www.
hrsonline.org.
 Investigations Prior to Pacing
5

A classification of syncope is shown in Table 5.1 Table 5.1 (continued)

and guidelines on the diagnosis and management
of syncope have been produced by the ESC in
2009 and are available on the website www.
escardio.org.
A clinical history of sudden unprovoked diz-
ziness, faintness, or syncope should alert the
physician to the possibility of significant bra-
dyarrhythmias or tachyarrhythmias. The history
might suggest a reflex/neurally mediated cause,
syncope due to orthostatic hypotension, or true
cardiac syncope. A witnessed event should be
researched carefully by talking to the patient
and to the witness, if at all possible. The report
of “a very slow pulse” might suggest a need for
permanent pacemaker implantation although
a vaso-vagal episode might also explain the
event and pacing would then be inappropriate.
Carotid sinus massage producing prolonged
sinus arrest, ventricular asystole or 2° or 3° AV
block in a patient with symptoms suggestive
of cardiac presyncope or syncope may well be
Table 5.1 Classification of syncope
Reflex (neurally-mediated) syncope
Vasovagal
Mediated by fear, pain, emotional distress, instru-
mentation, blood phobia
Mediated by orthostatic stress
Situational
Cough, sneeze
Gastrointestinal stimulation (swallowing, defecation,
visceral pain)
Micturition
Post-exercise
Post-prandial
Others (laughing, playing brass instruments,
weightlifting)
Carotid sinus syncope
Atypical forms (without apparent triggers and/or
atypical presentation)
Syncope due to orthostatic hypotension
Primary autonomic failure
Pure autonomic failure, multiple system atrophy,
Parkinson’s disease with autonomic failure
Secondary autonomic failure
Diabetes, amyloidosis, uremia, spinal cord injuries
Drug-induced orthostatic hypotension
Alcohol, vasodilators, diuretics, antidepressants
Volume depletion
Hemorrhage, diarrhea, vomiting, dehydration, etc.
Cardiac syncope (cardiovascular)
Arrhythmia as primary cause
Bradycardia
Sinus node dysfunction
AV conduction tissue disease
Implanted device malfunction
Tachycardia
Supraventricular
Ventricular (idiopathic, secondary to structural
heart disease or to channelopathies)
Drug-induced bradycardia or tachyarrhythmias
Structural disease
Cardiac: valvular disease, acute MI/ischemia,
HOCM, cardiac tumors, pericardial disease/
tamponade, prosthetic valve dysfunction
Others: pulmonary embolus, acute aortic
dissection, pulmonary arterial hypertension

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 71

DOI 10.1007/978-1-4471-2939-4_5, © Springer-Verlag London 2012
72
CSM
Fig. 5.1 ECG during carotid sinus massage (CSM) shows inducible prolonged sinus arrest
evidence sufficient to justify pacing (Fig. 5.1).
However, generally speaking, unmonitored
patients with such symptoms and a negative
response to carotid sinus massage will require
further investigations to support the need for
permanent pacing. These investigations include
a 12-lead electrocardiogram, continuous Holter
ECG monitoring, event ECG recorders, exter-
nal ECG loop recorders and implantable ECG
loop recorders (Table 5.2). Tilt table testing is
indicated in the case of an unexplained single
syncopal episode in high risk settings, e.g.,
risk of injury, pilots, or recurrent episodes in
the absence of organic heart disease, or in the
presence of organic heart disease after cardiac
causes of syncope have been excluded. It is also
indicated for discriminating between reflex and
orthostatic hypotension induced syncope and
Table 5.2 Types of investigations available for detecting
bradyarrhythmias or tachyarrhythmias responsible for
dizziness or syncope
12-lead ECG
Continuous ECG “Holter” monitoring
Event recorders
External event recorder
Post-symptom onset
External loop recorders
Pre/post-symptom onset
Implantable loop recorders
Pre/post-symptom
Tilt table test
5 Investigations Prior to Pacing
in the assessment of patients with unexplained
syncope.
Electrocardiogram
A 12-lead ECG may demonstrate evidence of 2°
or 3° AV block or junctional rhythm which would
be sufficient to indicate the need for pacing in a
symptomatic patient. Evidence of bi- or trifas-
cicular block or progressive lengthening of the
PR interval in a patient with LBBB (on serial
ECGs) should raise suspicion of the need for pac-
ing (Fig. 5.2).
Holter Monitoring
Continuous ECG monitoring may be useful in
patients with fairly frequent symptoms but a
normal 12-lead ECG or abnormalities sugges-
tive of significant AV conduction abnormality,
e.g. RBBB, LAD, and long PR interval or evi-
dence of sick sinus syndrome, e.g., sinus arrest
or sino-atrial block. Mechanical tape recorders
still exist which magnetically record the ECG
as an analog signal on cassette tape (C60/C90)
(Fig. 5.3), but these have virtually been replaced
by “solid-state” devices which record the ECG
digitally on memory cards within the recorder.
Direct digital recordings avoid the artifacts that
may be produced by mechanical recorders and
Event Recorders
Fig. 5.2 12-lead ECG
showing bifascicular block
Fig. 5.3 Analog 24 h Holter ECG recorder using
cassette tape
the limitations of data recorded in analog for-
mat. Some can record continuous ECG from
between 24 h and 11 days. Some devices have
an “event-marker” button which the patient can
use to identify the onset of symptoms such as
dizziness.
The Vision™ 5L (Burdick®) weighs 112 g and
can record high quality 3-channel ECG for up to
48 h on a compact flash card. Data can be down-
loaded and analyzed rapidly using Vision Premier
software on a Windows-based PC (Figs. 5.4 and
5.5). Figures 5.6–5.9 show four examples of
downloaded ECG traces showing prolonged sinus
arrest, Mobitz Type I and Mobitz Type II second
degree AV block, and severe nodal bradycardia,
respectively. The Vista Plus device (Novacor)
73
can record 1–3 channel ECG for 8–11 days. This
device measures 8.6 × 5.4 × 1.9 cm, weighs 100 g,
and can be worn around the neck attached to the
patient by the special 5-lead cable (Fig. 5.10).
The HOLTERSOFT ULTIMA Windows™-
based software platform has fast analysis mod-
ules based on powerful technologies (Wavelets
Transform, Fractal Analysis) for providing
analysis of arrhythmias, heart rate variability,
ST, QT, and QT variability, pacemaker rhythms,
and automatic detection of AF episodes and sleep
apnea. The Vista Plus also has a microphone to
allow patients to record voice messages during
the recording.
Event Recorders
These devices are useful for patients with less
frequent symptoms of dizziness or presyncope.
External “Post-symptom” Event
Recorders
These small portable devices are kept in the
continual possession of the patient during the
prolonged monitoring period. During symptoms,
the patient places the device on the chest and
74
Fig. 5.4 Vision™ 5L Holter ECG recorder (Burdick®)
uses digital technology to store ECG signals on a memory
card (single arrow) which can be inserted in a card reader
(twin arrow) and displayed on a Windows-based PC
5 Investigations Prior to Pacing
Fig. 5.5 Vision™ 5L recorder and its card reader
(Burdick®)
starts the recorder by pressing an activation but-
ton. After a 10 s or so sample of ECG (usually a
single lead rhythm strip) has been recorded, this
can be transmitted to the monitoring station as
per instructions. The patient keeps the device
until several recordings have been made or for an
agreed period (maybe 2–6 weeks). These devices
only allow capture of data once the activation
button has been pressed and studies have shown
that short-lived arrhythmias may frequently be
missed by these “post-symptom onset”
recorders.
The CorDigital® Micro ER® (Instromedix®)
recorder/transmitter weighs only 42 g and
fits into a patient’s pocket, purse or handbag
(Fig. 5.11). At the onset of symptoms, the
patient simply holds the device on the chest and
presses the “record” button, which records and
stores 32s of real-time ECG in solid-state mem-
ory. Six events can be stored before it is neces-
sary to transmit the information to the receiving
center. The Cardiocall VS20 device
(SPACELABS Healthcare) can be used as a
Event Recorders 75

Fig. 5.6 3-channel ECG showing sinus arrest

Fig. 5.7 3-channel ECG showing Mobitz Type I second degree AV block

Fig. 5.8 3-channel ECG showing Mobitz Type II second degree AV block
76 5 Investigations Prior to Pacing

Fig. 5.9 3-channel ECG showing a slow ventricular escape rhythm. P-waves are probably visible with a rate similar or
slightly slower rate than the QRS complexes, but the P-waves and QRS complexes are independent of each other

Fig. 5.10 Vista plus device (Novacor)

simple event recorder. For “post-symptom”
event recorders, transmission of the ECG
rhythm is usually done by dialing up the receiv-
ing center, holding the recorder over the mouth-
piece of the patient’s own telephone handset
and pressing a “send” button on the recorder.
The Cardiobeeper shown in Fig. 5.12 is a simi-
lar, earlier Event Recorder. The ECG recording
is received and printed out at the receiving cen-
ter (Fig. 5.13).
Event Recorders
Fig. 5.11 The CorDigital MicroER ®
event recorder
(Instromedix®)
Fig. 5.12 The Cardiobeeper event ECG recorder is held
on the chest and activated by pressing a button
External “Pre-/Post-symptom” Event
Loop Recorders
These devices are useful for intermittent symp-
toms which are short-lived, when other recorders
have proved unsuccessful in capturing an event.
The patient wears the digital recorder and elec-
trodes over a period of a few days to several
weeks (2–4 weeks), constantly recording a 1–3
77
Fig. 5.13 The saved ECG strip is then played to a record-
ing center over a standard telephone line
lead ECG. When an arrhythmia is felt, he/she is
able to activate a record feature that has been pro-
grammed for that particular individual. For
example, this might enable capture of the ECG
for any set period up to and including the event
and after the event as a loop of ECG. If no event
is detected, the loop is continually renewed and
erased. Later, when a telephone is accessible, the
patient can transmit the captured information
from the memory to the monitoring station. These
devices are useful for patients with syncope,
since the record button can be pressed once con-
sciousness has been regained, which will capture
the ECG prior to, during, and after the symptoms.
Some devices can also be programmed to auto-
matically record one or more specific
arrhythmias.
The CorDigital Micro LR™ (Instromedix®)
(Fig. 5.14) can store up to 6 events totaling 524 s
and has a battery life of 62 days or 150 record-
ings. The King of Hearts Express™ (Instromedix®)
(Fig. 5.14) is a small and easy to use, program-
mable device and can be worn on the waist, in the
shirt pocket, or on a cord around the neck. To
record an event, the patient presses the RECORD
button and to transmit the event simply dials up
the receiving center by telephone and places the
device over the telephone’s mouthpiece to trans-
mit the stored ECG for analysis. The R Test
Evolution 3 (Novacor) weighs 45 g and is fully
programmable to automatically capture a variety
of cardiac arrhythmias, ST shifts, and pacemaker
78 5 Investigations Prior to Pacing

Fig. 5.14 (Top left) The Genesis™ (Lechnologies Research Inc.), (top right) CorDigital Micro LR™, (bottom left)
King of Hearts Express, and (bottom right) Express II external ECG loop recorders (Instromedix®)

spikes with programmable pre- and post-event
times (Figs. 5.15 and 5.16). It features transmis-
sion by transtelephonic modulation, either real-
time transmission of the ECG or transmission of
recorded strips using NovaDrive – a freeware
which allows R Test programming and reading.
The program can be installed on any PC and
transmission enabled by direct connection to
modem or by e-mail. The R Test Evolution 4
(Novacor) offers additional advantages, includ-
ing improved signal resolution of 200 Hz,
Advanced Wavelet Technology for improved
accuracy, greater loop memory from 4 to 5 min,
improved battery life allowing continuous moni-
toring, and automatic arrhythmia detection up to
16–32 days with a change of batteries (Fig. 5.17).
It has three times more programmable memory –
up to 60 min available for detected ECG strips
and the new R.TSoft software platform. The
recorders cost approximately £2,000, although
the monitor/analysis system is extra.
The Recollect™ mini Holter ECG recorder
can provide continuous looping ECG recordings
for a week or more or for patient-activated
application for longer. This device allows the car-
diologist to collect automatic recordings at
specified times in addition to patient-activated
recordings. Single- or dual-channel ECGs can
help in clarifying the nature of any arrhythmia.
The data is stored on a memory card which can
then be plugged into a Windows-based PC for
generation of a report.
Implantable Loop Recorders 79

Implantable Loop Recorders

The Reveal® loop recorder (Medtronic Inc.)

(Fig. 5.18) is an implantable, patient-activated
monitoring device which continually records sub-
cutaneous ECG and is indicated for patients who
experience transient symptoms that may suggest
an arrhythmia and for those with clinical syn-
dromes or situations that put them at risk of car-

Fig. 5.15 The R Test 3 Evolution external ECG loop

recorder can be worn around the neck (Novacor)

Fig. 5.16 The R Test 3 Evolution device (Novacor)

Fig. 5.17 The R Test 4 Evolution device (Novacor)

80
Fig. 5.18 The Reveal® Plus implantable loop recorder
(Medtronic Inc.)
Fig. 5.20 Chest X-ray shows a Reveal® device placed
parasternally
diac arrhythmias. The device is 6.2 × 1.9 × 0.8 cm,
9 cc in volume, weighs 15 g, and has two bipo-
lar sensing leads 3.7 cm apart within the shell of
the device. Under local anesthesia, the device
is placed vertically pre-pectorally in the left
parasternal region (Fig. 5.19). Often the position
of the device is marked before implantation by
analyzing the R-wave to ensure relevant data cap-
ture. Figure 5.20 shows a chest X-ray in a patient
with an implanted Reveal® device. When symp-
toms occur, the patient can place a hand-held
activator over the device to activate storage of a
memory loop of the cardiac rhythm (Fig. 5.21).
The pre-activation and post-activation periods
are programmable.
5 Investigations Prior to Pacing
Fig. 5.19 Implantation of a Reveal® device under local
anesthesia and asepsis
Fig. 5.21 Activator applied over Reveal® device can put
the recorded rhythm strip into a “memory loop” store
There are two models currently available from
Medtronic Inc. – Reveal® DX and Reveal® XT
(Fig. 5.22). Both have a patient activation (using the
Patient Assistant) and an autoactivation mode, when
rhythms may be automatically recorded when the
heart rate exceeds or falls below a certain preset
limit (see Fig. 5.22). Both possess 42 min of mem-
ory for standard ECG, have a high (60–88%) diag-
nostic yield, and are cost-effective compared to
conventional testing-based treatments. The device
Implantable Loop Recorders
a b
Fig. 5.22 Reveal® DX (top left) and Reveal® XT (top
middle) are the latest implantable loop recorders from
Medtronic. The Patient Assistant (top right) is the new
patient-held activating device. Automatic recording of
periods of asystole from an implanted Reveal® XT device
can be programmed and data is retrieved using the
portable Medtronic 9790 Programmer. Up to 3 years
of monitoring is possible. The Reveal® devices are
MR-conditional safe, i.e., safe in standard MRI con-
ditions. Ideally, however, patients should avoid
sources of diathermy, high energy sources of radia-
tion, electrosurgical cautery, defibrillation, litho-
tripsy, and radiofrequency ablation to avoid damage
to the device and/or inappropriate sensing.
The Reveal® DX can be set up to autoclassify
episodes as bradycardia, asystole, ventricular tach-
yarrhythmia, or fast ventricular tachyarrhythmia.
The Reveal® XT has an exclusive AF detection
algorithm for detecting episodes of atrial tachycar-
dia and atrial fibrillation. It can assess the AF bur-
den and the ventricular rates during episodes in
order to guide treatment. Cardiac Compass®
81
c d
are shown here (bottom). The recording is continuous
from a-d and resulted in permanent pacemaker implanta-
tion in this patient with infrequent syncope. It was detected
on routine interrogation prior to removal
Trends offers 14 months of rhythm data including
daily AF burden, ventricular rate during AT/AF,
heart rate variability, and average day and night
rates. Moreover, these devices can be remotely
monitored using the Medtronic Carelink® Network.
The devices should be removed under local anes-
thesia once the relevant diagnostic information has
been revealed or when the battery is depleted.
Their cost is approximately £1,450.
St. Jude Medical have the SJM Confirm™
(Model DM2100) implantable cardiac monitor
which is slightly smaller (Fig. 5.23). It measures
5.6 × 1.8 × 0.8 cm, has a volume of 6.5 cc, and
weighs 12 g, and has an excellent longevity of
3 years. It boasts Proven SenseAbility™ for
increased sensitivity, a number of data storage
options for flexibility as well as automatic and
82 5 Investigations Prior to Pacing

Fig. 5.23 The Confirm® device (St. Jude Medical)

patient-activated options for electrogram cap-

ture and storage. The patient-activated option
requires a “Patient Activator” which has to be
held over the device and activated by pressing a
button. It has additional programming options
for tachycardias, bradycardias, and asystole.
The Merlin™ Patient Care System provides
communication, data retrieval, and programming
capabilities (Fig. 5.24).

Cardionetics C.Net5000

The Cardionetics C.Net5000 is a 24-h ambula-

tory ECG monitor with instant automated anal-
ysis, designed specifically for use in general
practice to assist in the early detection of cardiac
arrhythmias. The three electrode configuration
is easy to fit (Fig. 5.25). A test is started with a
single button press. The C.Net5000 features fully
automatic ECG analysis. The C.Net5000 is able
to automatically detect significant arrhythmias
such as atrial fibrillation (AF), ventricular ecto-
pic beats, pauses and arrests, and wide-complex
tachycardias (including VT). The ECG trace is
shown in real time on the LCD screen, allow-
ing cardiac events to be observed as they occur
(Fig. 5.26). The C.Net5000 analyses the sig-
nal and automatically records examples of any
arrhythmia detected. The keypad and LCD screen
can be locked to prevent the patient from view-
ing the ECG trace or interfering with the monitor
during the test. The patient can press the symp-
tom button when they experience symptoms, and
the C.Net5000 will record an ECG trace. At the
end of the test, the analysis results can be viewed
on the LCD screen, without requiring connection
to a computer. The on-screen report shows
example traces of the most significant arrhyth-
Fig. 5.24 The Merlin™ Patient Care System (Image pro-
vided courtesy of St. Jude Medical, © 2008 St. Jude
Medical, Inc.)
mia detected. Using the included Cardionetics
Connect software, the report can be downloaded
to a PC for printing, review, and attaching to the
patient record.
Tilt Table Testing
Tilt testing enables the reproduction of a neu-
rally-mediated reflex in a laboratory setting.
Blood pooling and decrease in venous return
due to orthostatic stress and immobilization
trigger the reflex. The final effect, hypotension
and usually concomitant heart rate slowing, is
related to impaired vasoconstrictor capability
followed by sympathetic withdrawal and vagal
overactivity. The clinical situation correspond-
ing to tilt testing is reflex syncope triggered by
prolonged standing. However, this test can also
be positive in patients with other forms of reflex
Tilt Table Testing
Fig. 5.25 Cardionetics C.Net5000 Holter ECG recorder
attached to a patient using three electrodes
syncope and in patients with sick sinus
syndrome.
A modern tilt table will have a foot plate sup-
port and be electrically powered to allow rapid
achievement of upright and supine posture as
well as calibrated tilt angles of between 60–80°
(Fig. 5.27). ECG and blood pressure monitoring
should be continuous. A supine pre-tilt phase of
at least 5 min is recommended and after venous
83
Fig. 5.26 Cardionetics C.Net5000 ECG recorder
cannulation a further period of 20 min supine is
recommended. The tilt table is then tilted to
between 60–80° (Fig. 5.28) for 45 min during
careful ECG and BP monitoring (Fig. 5.29). The
induction of reflex hypotension/bradycardia with
reproduction of syncope or progressive orthos-
tatic hypotension (with or without symptoms)
are diagnostic of reflex syncope and orthostatic
hypotension, respectively. Isoproteronol or
glyceryl trinitrate can be given to further test
patients whose test remains normal after
40 min.
84
Fig. 5.27 (Left) This electric tilt table is comfortably
upholstered, has a foot rest, restraining straps, and an arm
rest. The table can be tilted electrically from the horizon-
tal to the vertical position and also into –15° head-down
tilt. The table is usually positioned between 70 and 85° for
the tilt phase of the test. (Right) The Task Force® Monitor
5 Investigations Prior to Pacing
(CNSystems) is ideal for tilt table testing offering a
6-channel display including a high resolution 3-channel
ECG and CNAP™ or continuous noninvasive arterial
pressure monitoring. A high-fidelity BP waveform is dis-
played alongside real-time SBP, DBP, and mean BP
Tilt Table Testing 85

Fig. 5.28 (Left) Patient secured in horizontal position on tilt table has pulse and BP measuring device on right arm/
hand. (Right) Patient is tilted to 70° while ECG and hemodynamics are monitored by two cardiac physiologists

Fig. 5.29 Task Force® monitor displays 2-channel ECG, arterial pressure waveform, and continuous SBP, DBP, and
mean BP – graphically and numerically
 Permanent Pacemakers and Leads
Permanent Pacemaker Code (NBG)
A 5-Position NBG (NASPE/ BPEG Generic)
Code is used internationally to describe the vari-
ous pacemaker functions (Table 6.1).
The first position identifies the chamber(s)
that is paced.
A = atrium; V = ventricle; D = Dual, when both
atrium and ventricle can be paced. O = None.
A device used to pace in only one chamber
will be represented by either the letter A (atrium)
or V (ventricle), whereas devices that are capable
of pacing in both chambers are represented by the
letter D (dual). Some pacemakers allow pacing to
be turned OFF for diagnostic purposes, and,
while turned off, the position 1 coding is O.
There is a code letter S that identifies the pace-
maker as a single chamber device, which can be
used to pace either the atrium or ventricle. This is
only used as the manufacturer’s designation and
is not valid once the pacemaker is connected to a
pacing lead.
The second position indicates the chamber(s)
whose intrinsic activity is sensed. A = atrium;
V = ventricle; D = both atrium and ventricle;
O = the pacemaker is incapable of sensing. For
example, VDD represents a pacemaker in which
the ventricle is the chamber paced, but that the
device is capable of sensing in both atrium and
ventricle. As for position 1, S identifies the device
as a single chamber device, which can be used in
either atrium or ventricle but is only used as the
manufacturer’s designation and is not used once
the pacemaker and lead are attached.
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_6, © Springer-Verlag London 2012
6
The third position denotes the response of the
pacemaker to the sensed information. This posi-
tion is directly tied into position 2. Without sens-
ing, there can be no mode of response to
sensing.
I = that the pacemaker output is inhibited by a
sensed event. Thus, in a VVI pacemaker, the
pacemaker senses a ventricular event and with-
holds the ventricular output. In DDI mode, the
pacemaker simply inhibits the output of the
device in the chamber where any signal is sensed.
In the presence of a fast atrial rate and heart block,
the DDI pacemaker rhythm will resemble a VVI
device.
T = that pacing is triggered by a sensed event.
This is rarely used now, but it can be useful for
observing the location of sensing of intrinsic
events. Thus if a sensing problem is suspected,
programming to a triggered mode may show
exactly where in the timing of the device the
sensing abnormality is occurring. Triggered pac-
ing will produce pacemaker spikes concurrently
with intrinsic sensed events (pseudo-fusion
beats).
D = that ventricular sensed events inhibit pace-
maker output while atrial sensed events trigger
ventricular stimulation. Thus, D indicates that the
device will respond to the sensed signal by inhib-
iting the pacemaker response, tracking the sensed
event, or inhibiting the output on the sensed chan-
nel and triggering an output to maintain AV syn-
chrony. For example, in a DDD pacemaker, a
sensed atrial signal will cause the device to inhibit
the atrial output, a timer then starts that will cause
87
88
Table 6.1 The NASPE/BPEG generic (NBG) code
Position I II
Category Chamber paced Chamber sensed
NBG code V = Ventricle V = Ventricle
A = Atrium A = Atrium
D = Dual (A&V) D = Dual (A&V)
O = None O = None
Manufacturer S = Single (A or V) S = Single (A or V)
designation
only
NASPE was the North American Society of Pacing and Electrophysiology – now Heart Rhythm Society (HRS)
BPEG was the British Pacing and Electrophysiology Group – now Heart Rhythm UK (HRUK)
a triggered ventricular output after a certain inter-
val unless an intrinsic ventricular complex arises.
If the patient has an intrinsic R wave during the
triggering period, the pacemaker will inhibit the
ventricular output.
O = that there is no response to sensed events.
During magnet application to most pacemakers,
the sensing function is temporarily switched
OFF and the device operates in an asynchronous
or fixed rate mode. AOO, VOO, and DOO are
examples of fixed rate modes. Clearly the sec-
ond and third positions are “tied together,” since
if there is no sensing, there is no mode of
response.
The fourth position indicates something about
the programmable parameters of the pacemaker,
whether it has a sensor to regulate the rate during
periods of physical activity, whether and how it
can be programmed, and whether it is possible to
communicate with. R = a rate responsive facility
whereby the pacing rate is adjusted by a sensor
that detects a physiological variable such as
physical activity or respiration. C = communicat-
ing and indicates that the pacemaker is capable of
transmitting and/or receiving data for informa-
tional or programming purposes. Most, if not all,
devices currently manufactured have a communi-
cating ability. M = multiprogrammable, indicates
that the device can be programmed in more than
three parameters. All DDD pacemakers are pro-
grammable. Typical programmable parameters
include: rate, sensing, output, refractory periods,
mode, and hysteresis. Dual chamber pacemakers
usually have many more programmable parame-
6 Permanent Pacemakers and Leads
III IV V
Mode Programmable Antitachycardia
of response functions functions
T = Triggered R = Rate Modulated O = None
I = Inhibited C = Communicating P = Paced
D = Dual (T&I) M = Multiprogrammable S = Shocks
O = None P = Simple programmable D = Dual (P&S)
O = None
ters available. P = simple programmable, usually
indicates that the pacemaker is limited to three or
fewer programmable parameters. This letter in
the fourth position is limited to single chamber
devices. Typical simple programmable parame-
ters include: rate, output, and sensing. O = none,
is rarely encountered now, and indicates that the
device has no programmable features.
It should be appreciated that the fourth posi-
tion is hierarchical in nature. For example, a VVIR
pacemaker can be assumed to be, in addition to
rate-responsive, communicating (the sensor needs
to be programmable) and multiprogrammable
(there are usually several things to be programmed
on sensor-driven devices). Similarly, a DDD pace-
maker can be assumed to be communicating and
multiprogrammable since many parameters need
to be programmed. Obviously, any device that is
labeled with a P or M in the fourth position must
also be communicating.
The fifth position indicates whether the device
has any anti-tachycardia features. Most bradycar-
dia devices do not and are automatically assumed
to be O devices. Some “brady-devices” do have
limited anti-tachycardia capability and this posi-
tion allows this to be identified. In the pacemaker-
only patient, the fifth position can only be
represented by O or P. The pacemaker either has
no anti-tachycardia feature or it can attempt to
pace the patient out of a tachycardia episode. The
fifth position is used fully by ICDs and their abil-
ity to pace or shock patients out of tachyarrhyth-
mias. Most current ICDs will be represented by
D (dual – shocks and paces) in this position.
Types of Permanent Pacemakers 89

Types of Permanent Pacemakers line battery self-discharge, current drain for

A pacemaker or pulse generator consists of a
power source connected to microcircuitry which
controls the characteristics and timing of the gen-
erated impulse. The whole is encased in a her-
metically-sealed titanium “can.” Pacemakers
weigh between 13 and 31 g. Their physical
dimensions are shown in Tables 6.2–6.6, but gen-
erally have a diameter of <50 mm and a thickness
of 6–8 mm. They are considerably smaller and
lighter than the original pacemakers from the
early 1970s and 1980s (Fig. 6.1). Almost exclu-
sively lithium-iodine cells are the power source
for pacemakers and they provide a lifespan of
between 5 and 15 years depending on the com-
plexity and versatility of the system, the pro-
grammed output, what features are programmed
“on” and how much the generator is being used.
For example, modern pacemakers use current not
only for pacing but also for other functions such
as obtaining measurements of diagnostic data,
measurements made by rate response sensors,
and implementation of algorithms, such as for
mode switching. Pacemaker battery life therefore
depends on a variety of variables, including base-
device housekeeping functions, current used to
pace the heart, and current to sense the underly-
ing heart rhythm. An average pacemaker battery
has about 0.5–2 Ah of battery life. Esprit™ S
(Sorin) is estimated to have a life expectancy of
10.5 years in SSI mode, set at 70 bpm, 2.5 V out-
put, 0.5 ms pulse duration, 500 Ω with the Holter
monitor turned “on” whereas the Esprit™ DR
(Sorin) accelerometer-driven, rate responsive
dual chamber device has an estimated life expec-
tancy of 9 years at the same settings. The power
sources have a predictable, progressive discharge
rate and the residual battery life and the end-of-
life (EOL) can be accurately estimated and
accessed by the external programmer in the fol-
low-up clinic. Unlike the earlier nickel-cadmium
and mercury-zinc batteries, sudden cessation of
pacing output does not occur with lithium-iodine
power sources.
The cost of pacemakers varies enormously
and relates to the complexity and versatility of
the device, its programmability, its additional
monitoring and diagnostic facility, and the size of
the generator. Costs may vary from £800 to
£5,000 depending on the features offered by the

Table 6.2 Single chamber pacemakers

Pacemaker manufacturer Dimensions
Series/model Weight (g) H × W × D (mm) Volume (cc) Connector (mm)
Biotronik
Talos S 24 51 × 39 × 6 9 IS-1
Effecta S 25 53 × 39 × 6.5 10 IS-1
Boston Scientific
Altrua 20 S206 SSIC 23.6 42 × 42 × 8 10.1 3.2/IS-1
Altrua 50 S508 SSI 21.5 39 × 42 × 8 9.2 IS-1
*Insignia™ devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and
Ecuador
*Discovery™, Jade™ series no longer available
Medtronic
Sensia SES01 21.5 40 × 43 × 7.5 9.7 IS-1
Vitatron E10 S 21.5 40 × 43 × 7.5 9.7 IS-1
*Sigma™ 100/300, Thera™, and Vitatron C series no longer available
Sorin
Esprit S 19 37 × 41 × 6 7.5 IS-1
St. Jude Medical
Verity XL SC 5056 23 42 × 52 × 6 10.5 IS-1
*Regency SC+ 2402L – limited availability outside of UK
90 6 Permanent Pacemakers and Leads

Table 6.3 Dual chamber pacemakers: atrial synchronized ventricular pacemakers (VDD)
Pacemaker manufacturer Dimensions
Series/model Weight (g) H × W × D (mm) Volume (cc) Connector (mm)
Biotronik
None available
Boston Scientific
Altrua™ 50 S504a 23.5 41 × 42 × 8 10 IS-1
*Insignia devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and Ecuador
Medtronic
Adapta® AD VDD01 23.6 45 × 43 × 7.5 11.1 IS-1
*Sigma 300 SVDD 301; Kappa 700 KVDD 701; Kappa 900 KVDD 901; and EnPulse E2 VDD01 and Thera VDD
(i-series) series no longer available
Sorin
None available
St. Jude Medical
None available
a
Model with 400 ms AV delay

Table 6.4 Dual chamber pacemakers (DDD)

Pacemaker manufacturer Dimensions
Series/model Weight (g) H × W × D (mm) Volume (cc) Connector (mm)
Biotronik
Talos D 26 51 × 42 × 6 10 IS-1
Effecta D 26 53 × 43 × 6.5 11 IS-1
Boston Scientific
Altrua™ 20 S209 (EL) 29.6 49 × 43 × 8 12.1 IS-1
Altrua™ 50 S503a 25.4 44 × 42 × 8 10.8 IS-1
*Insignia™ devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and
Ecuador; Discovery™ II DDD no longer available
Medtronic
Sensia® Midsize SED01 27.1 45 × 48 × 7.5 12.1 IS-1
Adapta® Midsize ADD01 27.1 45 × 48 × 7.5 12.1 IS-1
Vitatron E50D 27.1 45 × 48 × 7.5 12.1 IS-1
*Thera D (i-series); Sigma D 300 Series; Kappa 700 DDD Series; Kappa 900 DDD Series; EnPulse and Ruby 3
DDD Series; and Vitatron C50 no longer available
Sorin
Esprit™ D 20 41 × 41 × 6 8 IS-1
Reply™ D 20 41 × 41 × 6 8 IS-1
St. Jude Medical
Identity® ADx XL DC5286 23.5 44 × 52 × 6 11 IS-1
Verity™ ADx XL DC5256 23.5 44 × 52 × 6 11 IS-1
*Affinity™ series no longer available
EL extended life
a
Model with 400 ms AV delay
Table 6.5 Single chamber rate adaptive pacemakers
Pacemaker manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector (mm)
Biotronik
Talos SR 24 51 × 39 × 6 9 Accelerometer IS-1
Effecta SRa 25 53 × 39 × 6.5 10 Accelerometer IS-1
Estella SR/SR-Ta,b 25 53 × 39 × 6.5 10 Accelerometer IS-1
Evia SR-Ta,b 24 53 × 39 × 6.5 11 Accelerometer + CLS IS-1
Axios SLR, Philos II SLR, Protos VR, and Talos SLR no longer available
Types of Permanent Pacemakers

Boston Scientific
Altrua™ 20 S201 23.6 42 × 42 × 8 10.1 Accelerometer 3.2/IS-1
Altrua™ 20 S204 24.9 44 × 47 × 8 11.0 Accelerometer 5/6
Altrua™ 40 S401 23.4 42 × 42 × 8 10 Acc + MV IS-1
Altrua™ 50 S501 23.4 42 × 42 × 8 10 Accelerometer IS-1
Altrua™ 60 S601 23.4 42 × 42 × 8 10 Acc + MV IS-1
*Insignia devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and Ecuador. Pulsar Max™ II and Discovery™ II SR series no
longer available
Medtronic
Sensia® Midsize SSIR SESR01 21.5 40 × 43 × 7.5 9.7 Accelerometer IS-1
Adapta® Midsize ADSR01 21.5 40 × 43 × 7.5 9.7 Accelerometer IS-1
Adapta® Midsize ADSR06 22.5 43 × 43 × 7.5 11.0 Accelerometer 5/6
Adapta® Midsize ADSR03 22.5 43 × 43 × 7.5 10.5 Accelerometer 3.2
*Sigma300 SSIR Series; Kappa400/700/900 SSIR Series; Thera i-series; EnPulse SSIR Series no longer available
Vitatron G20 SR 21.5 40 × 43 × 7.5 9.7 Accelerometer IS-1
*Clarity SSIR, Topaz 3 SSIR, Vitatron T20SR, and Vitatron C20SR devices no longer available. Clarity SSIR used QT-interval and Accelerometer for providing rate
response
Sorin
Esprit™ SR 19 37 × 41 × 6 7.5 Accelerometer IS-1
Reply™ SR 19 37 × 41 × 6 7.5 MV + accelerometer IS-1
St. Jude Medical
Accent™ SR PM1110 18 42 × 52 × 6 9.5 Accelerometer IS-1
Accent™ SR RF PM1210 23 52 × 52 × 6 12.8 Accelerometer IS-1
Identity® ADx SR5180 17 41 × 44 × 6 8 Accelerometer IS-1
*Identity SR 5172, Integrity ADx SR5160, Integrity SR 5142, Integrity mSR 5136 no longer available
91

(continued)
 92
Table 6.5 (continued)
Pacemaker manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector (mm)
Microny IISR+ 2525T 12.8 33 × 33 × 6 5.9 Magnetic ball IS-1
Microny K 2535Kc 12.8 33 × 33 × 6 5.9 Magnetic ball IS-1
*Microny SR + 2425T no longer available ; Regency SR models have limited availability outside of UK; Affinity™ SR models no longer available
Verity™ ADx XL SR5156 23 42 × 52 × 6 10.5 Accelerometer IS-1
Verity™ ADx XL SRM/S5157 23 42 × 52 × 6 11 Accelerometer 5/6 mm
Victory® SR 5610 17 41 × 44 × 6 8 Accelerometer IS-1
Zephyr™ SR 5620 17 41 × 44 × 6 8 Accelerometer IS-1
Zephyr™ XL SR 5626 23 42 × 52 × 6 10.4 Accelerometer IS-1
a
Remote monitoring possible
b
Estella and Evia devices are MRI conditional safe
c
For high base rates in small subjects – requires special order
6
Permanent Pacemakers and Leads
Table 6.6 Dual chamber rate adaptive pacemakers (DDDR)
Pacemaker manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector
Biotronik
Talos DR 26 51 × 42 × 6 10 Accelerometer IS-1
Effecta DR/DR-Ta 26 53 × 43 × 6.5 11 Accelerometer IS-1
Estella DR/DR-Ta 25 53 × 44.5 × 6.5 12 Accelerometer IS-1
EviaDR-Ta,b 25 53 × 44.5 × 6.5 12 Accelerometer + CLS IS-1
Axios™ DR, Philos II DR, Cylos DR, and Protos™ DR/CLS are no longer available
Types of Permanent Pacemakers

Boston Scientific
Altrua™ 20 S203 25.4 44 × 42 × 8 10.8 Accelerometer IS-1
Altrua™ 20 S205 EL 32.3 54 × 49 × 8 14.9 Accelerometer 5/6 mm
Altrua™ 20 S208 EL 29.6 49 × 43 × 8 12.6 Accelerometer IS-1
Altrua™ 40 S403 25.4 44 × 42 × 8 10.8 Acc + MV IS-1
Altrua™ 404 EL 29.6 49 × 43 × 8 12.6 Acc + MV IS-1
Altrua™ 50 S502c 25.4 44 × 42 × 8 10.8 Accelerometer IS-1
Altrua™ 60 S603c 25.4 44 × 42 × 8 10.8 Acc + MV IS-1
Altrua™ 60 S602c EL 29.6 49 × 43 × 8 12.6 Acc + MV IS-1/3.2
Altrua™ 606 EL 29.6 49 × 43 × 8 12.1 Acc + MV IS-1
*Insignia devices are only currently available in Germany, Italy, China, Mexico, Indonesia, Taiwan, Peru, and Ecuador
Medtronic
Sensia® DDDR SEDR01 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Adapta® Midsize ADDR01 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Adapta® Small size ADDRS1 23.6 45 × 43 × 7.5 11.1 Accelerometer IS-1
Adapta® Midsize ADDR06 28.5 50 × 48 × 7.5 14.2 Accelerometer 5/6 mm
Adapta® Midsize ADDR03 28.1 47 × 48 × 7.5 13.0 Accelerometer 3.2 mm
Adapta® Oversize ADDRL1 31.3 45 × 52 × 7.5 13.1 Accelerometer IS-1
Versa® DDDR VEDR01 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Ensura DR MRI Surescan™d 22 45 × 51 × 8 12.7 Accelerometer IS-1
Advisa DR MRI™ SureScan™d,e 22 45 × 51 × 8 12.7 Accelerometer IS-1
*AT500™; Prevent AF series; Prevent AF 920; Selection 9000 AF3.0; and Diagnose AF 910 are no longer available
*Sigma DDDR series; Kappa 400/700/900 DDDR series; EnPulse DDDR series; Thera DR i-series; and EnRhythm DDDR are no longer available
(continued)
93
Table 6.6 (continued)
94

Pacemaker manufacturer Dimensions

Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector
Vitatron E60 DR 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
Vitatron G70 DR 27.1 45 × 48 × 7.5 12.1 Accelerometer IS-1
*Vitatron C60 DR, Vitatron T60 DR, and Vitatron T70 DR are no longer available
*Clarity DDDR series and Diamond DDDR series are no longer available
Sorin
Esprit™ D 20 41 × 41 × 6 8 MV IS-1
Esprit™ DR 20 41 × 41 × 6 8 Accelerometer IS-1
Reply™ D 20 41 × 41 × 6 8 MV IS-1
Reply™ DR 20 41 × 41 × 6 8 MV/Accelerometer IS-1
* The Rhapsody DR, Symphony DR, Newliving DR, Neway DR models are no longer available
St. Jude Medical
Accent® DR PM2112 19 46 × 52 × 6 10.5 Accelerometer IS-1
Accent® DR RF PM2212 23 52 × 52 × 6 12.8 Accelerometer IS-1
Zephyr™ DR 5820 18 43 × 44 × 6 8.5 Accelerometer IS-1
Zephyr™ XLDR 5826 23.5 44 × 52 × 6 11 Accelerometer IS-1
Identity® ADx DR 5380 18 43 × 44 × 6 8 Accelerometer IS-1
Identity® ADx XLDR5386 23.5 44 × 52 × 6 11 Accelerometer 3.2 mm
Verity™ ADx XL DR5356 23.5 44 × 52 × 6 11 Accelerometer 3.2 mm (IS-1/VS 1)
Verity ADx XL DRM/S5357 23 45 × 52 × 6 11 Accelerometer 5/6 mm M/S
Victory® DR 5810 18 43 × 44 × 6 8.5 Accelerometer IS-1
6

Victory® XLDR 5816 23.5 44 × 52 × 6 11 Accelerometer IS-1

*Entity DR, Affinity DR, Identity DR 5370, Identity XL 5376, Integrity ADx DR5360, Integrity ADx XLDR5366, and Verity™ ADx XL DC5256 models are no longer
available
EL extended life
a
Transfers Home Monitoring data including trend messages and event and patient reports to the Biotronik Service Centre
b
Myocardial contraction Dynamics (CLS)
c
Model with 400 ms AV delay
d
MRI compatible; Managed Ventricular Pacing; Optivol
e
Atrial therapies, e.g., reactive ATP; Atrial arrhythmia preventive therapies; High VTR up to 210 ppm
Permanent Pacemakers and Leads
Types of Permanent Pacemakers
Fig. 6.1 Pacemakers reduced in size progressively from
1970s to 1990s. The bottom picture shows the Microny
SR+ pacemaker compared to a postage stamp (Courtesy
of Pacesetter/St. Jude Medical, Inc.)
Fig. 6.2 Pacemakers should be kept in a store close to the pacemaker theater. Devices should be arranged in some sort
of logical order
95
device, but CRT and ICD devices are consider-
ably more expensive (CRT-P – £3,000–£4,000;
CRT-D – £18,000–£25,000).
Storage
In most specialist pacing centers, a whole range
of permanent pacemakers, pacing electrodes, and
pacing accessories are kept in a dedicated pace-
maker store close to the pacing theater (Fig. 6.2).
For ease of use, devices should be kept in some
sort of order, e.g., type of device – single or dual
chamber device ± rate response programmability
(Fig. 6.3), and those devices with special features,
e.g., mode-switching, Managed Ventricular
Pacing, or Atrial Capture Management should be
readily identifiable (Fig. 6.4). Bi-ventricular
devices (see Chap. 16) and ICDs (see Chap. 17)
and their accessories should be separated from
the other pacing devices (Fig. 6.5).
96
Fig. 6.3 The Vitatron C60 DDDR, Vitatron C20 SSIR, and the St. Jude Medical Verity™ ADx SSIR devices kept in
separate stacks
All devices are presented inside sealed boxes
(Fig. 6.5) and within a sterile package accompa-
nied by the appropriate screwdriver (Fig. 6.6).
Pacing leads should be kept separate from the
devices and with some semblance of order, e.g.,
active-fixation versus passive-fixation electrodes,
steroid-eluting leads, straight versus fixed-J-
shaped electrodes, and atrial versus ventricular
leads (Figs. 6.7–6.9). Electrodes are also pre-
sented in a sterile, transparent package along with
a selection of stylets, a “vein lifter” (Fig. 6.10),
and when appropriate a tool for active-fixation of
screw-in leads.
Pacing technicians should regularly check the
expiry dates on devices, leads, and accessories so
as to avoid wastage of devices that are soon to
pass their sterilization dates. The Omnicell® cabi-
net system offers a slightly more secure but more
expensive method for “intelligent stock manage-
ment” (Fig. 6.11).
A whole range of multiprogrammable pace-
makers are available from the major manufactur-
6 Permanent Pacemakers and Leads
ers and they are constantly being updated and
improved (Figs. 6.12 and 6.13). Permanent pace-
makers are generally available as single or dual
chamber pacemakers. Single chamber devices
will have one lead port to accommodate an atrial
or a ventricular lead, whereas a dual chamber
device will have two ports to accommodate sepa-
rate atrial and ventricular leads. It should be noted
that VDD devices (see below) will have two ports
to accommodate the atrial sensing electrode and
the ventricular sensing/pacing electrodes present
on the special single VDD lead required. Most
manufacturers have now stopped production of
these latter devices in favor of other rate-adaptive
pacemakers (see below).
Different modes of function are available in
today’s sophisticated multiprogrammable devices.
For example, VVIR, DVI, AAI, AAIR, DDD, and
VDD and other modes can be programmed in most
DDDR devices and this allows great flexibility to
the cardiologist for use in changing clinical situa-
tions in individual pacemaker patients.
Single Chamber Pacing (Table 6.2)
Fig. 6.4 Devices with special functions should be kept in
their own sections for practical purposes, e.g., the
ADAPTA™ ADDR should be stacked separately
Single Chamber Pacing (Table 6.2)
Fixed rate pacing devices (AOO, VOO, and
DOO) are very rarely used now as there is a risk
of pacing on a native “P” or “R” wave and there-
fore initiating atrial or ventricular arrhythmias
(Fig. 6.14). When a magnet is applied to most
pacemakers, VOO or DOO mode is produced
until the magnet is removed (Fig. 6.15).
Single chamber pacemakers are now gener-
ally either atrial or ventricular demand devices,
most are multiprogrammable, many have a rate
response feature, and others more sophisticated
monitoring facilities. An example of a single
chamber, demand pacemaker that may be used
for either atrial or ventricular pacing is the
Altrua™ 20 S201 (Boston Scientific) (Fig. 6.16).
The manufacturer labels the pacemaker with the
code SSI to signify that the device will sense and
97
Fig. 6.5 Devices are presented in sealed boxes, with the
relevant warranty, patient information booklet, and
physician’s technical information booklet
pace in a single chamber, but the code becomes
redundant once the device is connected to the
electrode and implanted.
Ventricular Demand Pacing (VVI, VVT)
In the absence of spontaneous ventricular beats, a
ventricular-inhibited pacemaker (VVI) delivers a
stimulus to the ventricles (usually via the RV) at
a regular rate, set by the programmer (Fig. 6.17).
If spontaneous activity is sensed via the ventricu-
lar electrode, the current stimulation cycle is ter-
minated, pacing inhibited, and competition avoided.
The pacemaker then starts a new cycle and will
pace again after the set interval from the last
sensed ventricular beat (Fig. 6.18).
In the less commonly used ventricular-trig-
gered pacing mode (VVT), a sensed event trig-
gers delivery of a pacing stimulus which will
98
Fig. 6.6 A device is sealed
inside a transparent sterile
packet with its own
screwdriver
Fig. 6.7 Pacing electrodes and accessories should be organized on a separate shelf from the devices
consequently fall during the myocardial refrac-
tory period and thus be ineffective (Fig. 6.19).
The next cycle will then start from delivery of the
triggered impulse.
Immediately after a paced or sensed event, the
pacemaker is rendered insensitive for an interval
which approximates the duration of myocardial
6 Permanent Pacemakers and Leads
activation and recovery in order to prevent sens-
ing the ventricular electrogram which is produced
by the event. This interval is referred to as the
refractory period and measures between 250 and
300 ms.
Ventricular demand pacing is indicated for
bradycardia associated with atrial fibrillation, in
Single Chamber Pacing (Table 6.2) 99

Fig. 6.8 Like all electrodes, the tined, steroid-eluting
atrial electrode from Medtronic comes sterile in its own
box. The type of lead fixation, polarity, and length are
indicated on the label. A selection of straight and
J-shaped stylets, a fixation tool, and “vein picker” are
available within each electrode packet
Fig. 6.9 This Tendril™ ST electrode has an active-
fixation mechanism, is bipolar, steroid-eluting at its tip,
and is 58 cm long – suitable for placement anywhere in
the right ventricle, interventricular septum, or RV
outflow-tract

Fig. 6.10 Electrodes are

presented in a molded,
transparent packet with
several stylets and a
“vein-picker.” Active-
fixation leads also have a
“fixing-tool”
100
Fig. 6.11 The Omnicell® cabinets provide secure stor-
age and the OptiFlex™ CL software system can help
track equipment and device usage to the physician and
patient on each case. The system provides an opportunity
to improve the restocking process, reduce inventory costs,
and improve charge capture. However, it is an expensive
luxury that requires time and training to use effectively
and its cost-effectiveness is unproven. (Top) Cabinets in
store room next to pacing theater. (Bottom) Keyboard and
screen for inputting a code to access the equipment and to
record what equipment has been removed from the cabi-
net and for which patient. (Middle left) Close-up of
devices inside the cabinet. (Middle right) Pacemaker
accessories including suture materials, guidewires, glue,
etc., can also be stored in the Omnicell® cabinets to aid
inventory and cost-per case assessments
6 Permanent Pacemakers and Leads
Fig. 6.12 Some currently available pacemakers (with per-
mission): (Top left) Altrua™ 20 DR (Boston Scientific); (Top
right) Microny K SR (St. Jude Medical); (Middle left) Reply™
DR (Sorin Group); (Middle right) Talos DR (Biotronik);
(Bottom left) Advisa DR MRI™ (Medtronic Ltd.)
second and third degree AV block in patients
who are physically limited for other reasons such
as fraility, stroke, or other musculoskeletal
abnormalities and for those with very infrequent
bradycardia who simply require a “back-up” or
“stand-by” device.
Atrial Demand Pacing (AAI, AAT)
The timing cycles of AAI and AAT pacing are as
described above for VVI and VVT pacing
(Fig. 6.20).
The atrial refractory period is usually longer
than the ventricular refractory period in order to
avoid inappropriate inhibition of the pacemaker
by sensing the ventricular electrogram via the
atrial lead.
Dual Chamber Pacing
Fig. 6.13 (Left) The earlier Sigma™ series from
Medtronic had a range of models offering different pac-
ing modes – VDD, SSIR, DDD, SSI, VVI, and DDDR.
In recent times, manufacturers have reduced the number
of available models which can each offer a range of
mode programmability. (Right) The Kappa DDDR 900
series pacemaker and its programmer. The CapsureFix®
Fig. 6.14 Fixed rate VOO pacing is illustrated here. A ventricular ectopic beat does not delay the next paced beat as it
would in a ventricular demand system
Atrial pacing is indicated in symptomatic sick
sinus syndrome (SSS) unless AV conduction is
impaired. This may be evidenced by the presence
of bifascicular block, bundle branch block, or if
atrial pacing at a rate of 120 bpm causes second
degree AV block (Wenckebach rate). In these
situations, a dual chamber pacemaker should be
implanted. By stimulating the atria rather than
the ventricles, the normal sequence of cardiac
chamber activation and cardiac output is main-
tained. Atrial pacing may reduce the incidence of
101
pre-shaped, bipolar, active-fixation “J” lead, and the
bipolar, active-fixation ventricular lead are shown
attached to the pacemaker. This device has also been
superceeded by the Sensia™ and Versa™ models from
Medtronic Ltd. (Images reproduced with permission of
Medtronic, Inc.)
atrial fibrillation, stroke, and heart failure in
patients with SSS compared to those undergoing
VVI pacing.
Dual Chamber Pacing
Dual chamber pacing improves cardiac output
over VVI pacing as a result of the addition of atrial
transport with consequent increase in stroke vol-
ume, the prevention of deleterious hemodynamic
102 6 Permanent Pacemakers and Leads

Fig. 6.15 Fixed rate DOO pacing occurs when a magnet is applied externally to a dual chamber pacemaker (arrow)

influence due to ventriculoatrial conduction,

and the provision of a chronotropic response to
exercise. It results in improved survival in patients
with symptoms of heart failure compared to VVI
pacing. Moreover, although a comparable car-
diac output during exercise can be achieved with
single chamber rate-responsive pacemakers (see
below), dual chamber pacing can spare cardiac
reserve especially at low work load.

Atrial Synchronized Ventricular

Pacing (VDD) (Table 6.3)

In VDD, ventricular pacing is triggered by

a sensed atrial event after an interval simi-

Fig. 6.16 Altrua™ 20 (S201) is an SSIR device which

can be used as an AAI or VVI, AAIR, or VVIR device
Dual Chamber Pacing
Fig. 6.17 VVI pacing
Fig. 6.18 VVI pacing showing resetting of pacing cycle by intrinsic cardiac rhythm
lar to the normal PR interval (Fig. 6.21) and
the normal sequence of cardiac activation is
maintained. With normal sinus node func-
tion, a normal chronotropic response to exer-
cise should occur (Fig. 6.22). The upper rate
at which atrial activity will trigger ventricular
pacing (URL) is determined by the total atrial
refractory period (TARP), which consists of
the AV delay plus the post-ventricular atrial
refractory period (PVARP). Thus, if the AV
delay is 120 ms and the PVARP is 230 ms,
the TARP will be 350 ms and the URL will be
60,000/350 = 171 bpm.
VDD pacing is indicated in second or third
degree AV block when sinus node function is
103
normal. Atrial tachyarrhythmias and SSS are
contraindications.
If an atrial event is not sensed, ventricular
pacing continues at a set rate – otherwise atrial
asystole would lead to ventricular asystole. In order
to avoid rapid ventricular pacing should atrial
tachycardia, flutter, or fibrillation occur, an atrial
refractory interval renders the atrial channel insen-
sitive. This interval consists of the AV delay and a
period after ventricular stimulation, such that any
sensed atrial activity at a cycle length shorter than
this period will not trigger ventricular pacing.
Ventricular ectopic beats or ventricular
rhythms faster than the sinus rate will inhibit the
pacemaker unlike the earlier VAT systems.
104
Fig. 6.19 VVT pacing
Specific VDD devices are being phased out.
AV Sequential Pacing (DVI and DDI)
In DVI pacing, the atria are stimulated first
and after a short delay (approximately the
duration of the PR interval), the ventricles are
paced (Fig. 6.23). There is no atrial sensing
but ventricular pacing is inhibited by sponta-
neous ventricular activity. Although the pace-
maker is inhibited by an event sensed in the
ventricle, the first chamber to be stimulated is
the atrium. Pacemaker output may therefore
occur at the same time as spontaneous atrial
activation because its ventricular depolariza-
tion has not yet occurred. Hence, fusion beats
are common during DVI pacing. They should
be recognized as such and not misinterpreted
as a malfunction.
6 Permanent Pacemakers and Leads
In DDI pacing, sensing occurs in both atrium
and ventricle and competitive atrial pacing is
avoided.
AV Universal Pacing (DDD) (Table 6.4)
In DDD pacing, both sensing and pacing takes
place in the atrium and ventricle. Thus depending
on the heart rhythm, the pacemaker can function
in atrial demand (AAI), AV sequential (DVI,
DDI), or atrial synchronized (VDD) modes
(Figs. 6.23 and 6.24).
Therefore, in sinus bradycardia, a DDD pace-
maker will function as an atrial demand pacemaker.
If AV conduction is impaired, ventricular pacing is
triggered by either spontaneous atrial activity or a
paced atrial beat. When sinus node function is nor-
mal, the pacemaker functions in atrial synchro-
nized mode and a chronotropic response to exercise
Atrial Synchronized Ventricular Pacing (VDD, DDD)
Fig. 6.20 AAI pacing
follows. Pacemaker output will be inhibited by
atrial and ventricular ectopic beats.
DDD is indicated in second or third degree AV
block. It is relatively contraindicated if atrial
tachyarrhythmias are present unless “mode-
switching” is available, otherwise the fast atrial
rate will trigger a fast ventricular rate.
Physiological Pacing
Physiological pacing is a generic term for sys-
tems which allow a chronotropic response to
exercise by either maintaining AV synchroniza-
105
tion as the sinus node rate changes and/or by the
use of one or more non-atrial sensors (rate-
adaptive pacing).
Atrial Synchronized Ventricular
Pacing (VDD, DDD)
As indicated above, both VDD and DDD pacing
will maintain AV synchronization and allow a
chronotropic response to exercise in patients with
normal sinus node function (Fig. 6.22). Compared
to VVI pacing, cardiac output increases with
physiological pacing both at rest and during exer-
106
Fig. 6.21 VDD pacing is demonstrated by the first 8 beats on this ECG strip
cise. Exertional dyspnea, dizziness, and palpita-
tions are less than with VVI or VOO pacing.
Atrial Synchronized, Rate-Adaptive
Pacing (VDDR)
The Verity™ ADx XL VDR pacemaker (St. Jude
Medical) (Fig. 6.25) is a multiprogrammable,
mode-switching, rate-adaptive pacemaker designed
to operate with the AV Plus DX Model 1368 sin-
gle-pass bifurcated lead. Other manufacturers have
phased out these single lead devices.
Rate-Adaptive (or Rate-Responsive)
Pacing (VVIR, DDDR) (Tables 6.5–6.7)
The ability to increase heart rate with exercise is
as important as maintaining AV synchrony.
Exercise tolerance has been shown to be as good
in rate-adaptive ventricular pacing as with AV
synchronized pacing. Pacing systems are now
available that can produce a rate-response to exer-
cise which is independent of atrial activity. An
increase in pacing rate is usually in response to
6 Permanent Pacemakers and Leads
some parameter that alters with exercise. These
parameters include body vibrations, QT interval,
respiration, blood temperature, oxygen saturation,
RV pressure, and a number of these sensors have
now been incorporated into pacemakers, either
individually e.g., Vitatron C and T series (acceler-
ometer) or in combination, e.g., Reply™ DR
(Sorin Group) uses an accelerometer and a respi-
ratory minute volume sensor in order to allow an
appropriate chronotropic response to exercise.
Such rate-adaptive ventricular pacemakers can
achieve an enhanced exercise tolerance without
having to implant an atrial electrode. Ventricular
demand and dual chamber rate response pacemak-
ers are given the codes VVIR and DDDR respec-
tively, e.g., Victory™ SR and Victory™ XL DR
(St. Jude Medical) (Fig. 6.26). Some devices, e.g.,
Kappa series (Medtronic Ltd.) (Fig. 6.27) have a
Sensor Cross Check feature which verifies exer-
tion before allowing high sensor-driven pacing
rates. The Sensia™ pacing system (Medtronic
Ltd.) (Fig. 6.28) combines physiologic pacing
with automaticity. Moreover, using Search AV +,
the device automatically and continuously
searches for natural intrinsic conduction and
reduces unnecessary RV pacing to <20%.
Rate-Adaptive (or Rate-Responsive) Pacing (VVIR, DDDR) (Tables 6.5–6.7) 107

Fig. 6.22 VDD pacing

showing rate response with
exercise

Fig. 6.23 AV sequential

pacing
108 6 Permanent Pacemakers and Leads

Fig. 6.24 DDD pacing showing a rate response. (Bottom) plex). (Top) As the sinus rate increases to 79 bpm, the
As the sinus rate falls below 60 bpm, atrial pacing occurs ventricular pacing rate increases appropriately with nor-
at the base rate (60 bpm) which is followed by ventricular mal AV conduction (VDD)
pacing spike (fused with a normally conducted QRS com-
Rate-Adaptive (or Rate-Responsive) Pacing (VVIR, DDDR) (Tables 6.5–6.7) 109

Body Motion Sensors

These are the most widely used sensors. A piezo-

Fig. 6.25 Verity™ ADx VDR pacemaker (Image pro-
vided courtesy of St. Jude Medical, ©2008 St. Jude
Medical, Inc.)
electric crystal attached to the inside of the pace-
maker unit (so-called Activity Sensor) or an
accelerometer bonded to the circuitry within the
pacemaker (but not to the can itself) senses body
vibrations as a result of physical activity and via a
specific algorithm increases the pacing rate in line
with the level of sensed activity. The sensitivity of
the response can be adjusted by programming
several parameters using an external programmer.
These include the reaction time, the time to the

Table 6.7 Dual chamber A-V sequential rate responsive pacemakers

Pacemaker
manufacturer Dimensions
Series Weight (g) H × W × D (mm) Volume (cc) Sensor Connector
Biotronik
Talos SLR VDDR 26 51 × 42 × 6 10 Accelerometer IS-1
Boston Scientific
None available
Medtronic
Clarity VDDR/660 and Saphir 3/640 are no longer available
Sorin
None available
St. Jude Medical
Identity ADx 18 43 × 44 × 6 8 Accelerometer IS-1
VDR 5480 DC sensing/SC
pacing
Verity ADx XL 23.5 44 × 52 × 6 11 Accelerometer 3.2 mm (IS-1
VDR5456a or VS 1)
*Affinity VDR 5430 model is no longer available
a
Multiprogrammable, mode-switching, rate-responsive pacemaker for use with the AV Plus DX model 1368 single-pass
bifurcated lead. It has extended life

Fig. 6.26 Victory™ SR and

Victory™ DR rate respon-
sive pacemakers (Image
provided courtesy of St. Jude
Medical, ©2008 St. Jude
Medical, Inc.)
110
Fig. 6.27 The Kappa® DR 700 series pacemaker (Image
reproduced with permission of Medtronic, Inc.)
Fig. 6.29 Rate response seen soon after start of exercise
initial increase in sensor-driven pacing; the slope,
which determines the rate at which the pacing rate
increases following the onset of detection of
increased body activity; and the recovery time,
the time taken to return to standby rate after activ-
ity has ceased. It is possible also to program the
sensitivity of the pacemaker’s sensor to body
activity. The Kappa 700 series DDDR pacemaker
is an example of a system that used an accelerom-
eter as its sensor (Fig. 6.27). Although many of
these devices have been implanted worldwide, the
models are being replaced by the Versa™ series.
Evoked QT Response
This sensor was the first to be used by Vitatron in
their TX/Rhythmx and subsequently Quintech TX
pacemaker when it was discovered that the
QT-interval shortened with increasing heart rate
6 Permanent Pacemakers and Leads
Fig. 6.28 The Sensia™ DR device (Image reproduced
with permission of Medtronic, Inc.)
(see Fig. 1.67). Moreover, it shortens with increased
sympathetic activity and during exercise activity
when VOO pacing. This pacemaker senses, via the
ventricular electrode, the interval between the pac-
ing spike and the apex of the evoked T wave.
A decrease in the interval leads to an increase in
the pacing rate. Unlike the activity-sensor rate
responsive devices described above, the QT-sensing
pacemakers will allow a rate response to emotion
as well as exercise. The Vitatron T20 SR pace-
maker is an example of a current QT-sensing rate
responsive pacemaker. Figure 6.29 shows the
beginning of heart rate response from a VVIR
device in a patient climbing stairs.
Respiration
An estimate of respiratory minute volume (MV) –
change in intravascular impedance – is monitored
Multisensor Pacing
by a conventional bipolar pacing electrode. As
respiratory rate increases with effort, the pace-
maker’s algorithm allows the pacing discharge
rate to increase proportionately and decrease again
as the respiratory rate falls after exercise. Unlike
some other sensors, MV sensors also respond to
stress and emotion. However, pacemakers using
this sensor alone are used infrequently. Minute
volume sensors have been combined with
accelerometers in multisensor pacing devices, e.g.,
Altrua™ series (Boston Scientific) (Fig. 6.30).
Closed Loop Stimulation (CLS)
CLS uses myocardial contraction dynamics to
evaluate the patient’s specific pacing demand.
The sensor converts this value to an optimal pac-
ing rate. The device determines the impedance
waveform at the onset of each ventricular con-
traction and compares it with the reference curve
measured at rest. Differentiation between imped-
ance waveforms at rest and while the patient is
engaged in physical activities delivers a specific
parameter for individual metabolic needs. Studies
have already demonstrated CLS’s clinical perfor-
mances. The CLS rate is thought to be much
closer to the sinus rate of a healthy heart in every
tested situation, adapting to the hemodynamic
need on a beat-to-beat basis. It is another technol-
ogy that adapts the heart rate in response to emo-
Fig. 6.30 The Altrua™ 40 DR device uses a respiratory
minute volume sensor to perform as a rate-responsive
pacemaker (©2010 Boston Scientific Corporation/
affiliates. All rights reserved. Used with permission of
Boston Scientific Corporation)
111
tional activity. Select Biotronik pacemakers such
as the Evia DR–T device have this facility.
Alternative Sensors
Other direct and indirect metabolic parameters
such as body temperature, right ventricular pres-
sure, oxygen saturation, and blood pH have been
investigated as sensors for rate responsive pacing
systems. These have not been established to be of
any additional value to activity, QT-interval, and
respiration and have not become commercially
available. The use of an additional lead with a
special sensor is disadvantageous.
Multisensor Pacing
Over the last few years, single chamber pacemak-
ers have used combinations of sensors in order to
enhance and optimize the rate response to exer-
cise. The Clarity™ SSIR (Vitatron) uses a combi-
nation of an accelerometer to provide a prompt
response to physical activity and a QT-interval
sensor to ensure that the rate response is propor-
tional to the exercise load. The Reply™ DR (Sorin
Group) (Fig. 6.31) uses an accelerometer and a
respiratory minute volume sensor and the
Clarity™ DDDR (Vitatron) again combines an
accelerometer with a QT-interval sensor in order
to provide an appropriate rate response to exercise
(Fig. 6.32). These are ideal for patients with chro-
Fig. 6.31 The Reply™ DR uses multisensor blending
accelerometer and minute ventilation to optimize rate
response to exercise (Courtesy of Sorin Group)
112
Rest
Post
Exercise
Fig. 6.32 Rate response seen with the Clarity™ activity-sensing pacemaker
notropic incompetence due to sinus node disease,
who will have AV synchrony at rest from sensed
atrial activity via the atrial lead and an appropriate
sensor-adjusted rate response during exercise.
Advanced Programmability
Pacemaker manufacturers continue to produce
series and models of pacemakers with increasing
degrees of sophistication in pacing, sensing,
diagnostics, and other functionality. For example,
Guidant’s series of Insignia® – Entra, Plus, AVT,
and Ultra – had various capabilities with the
6 Permanent Pacemakers and Leads
Insignia® Entra Single Sensor System (SSI)–
Model 484 having the fewest pacing and diag-
nostic features, and the Insignia® Ultra Blended
Sensor System (DDDR)–Model 1290/1291 hav-
ing the most. Although still available in some
countries, these devices are being replaced by the
Altrua™ series (Table 6.6).
Special Functionality
Device manufacturers continue to develop and
produce for clinical use pacemakers with special
functions. When these functions are proven to be
Special Functionality
Fig. 6.33 The EnRhythm™ and Adapta™ pacemakers
(Image reproduced with permission of Medtronic, Inc.)
useful and worthwhile, they may become incor-
porated as standard features in the next genera-
tion of devices produced by the company. Thus
many of these “new” devices are soon replaced
by subsequent “improved” versions with greater
versatility and programmability. Some examples
of recently produced “novel” devices are given
here only soon to become obsolete with their
“special” features subsequently becoming “stan-
dard” in the companies’ next models.
EnRhythm™ and Adapta™ (Medtronic) use
Managed Ventricular Pacing (MVP) to promote
intrinsic conduction and minimize unnecessary
right ventricular pacing (Fig. 6.33). They operate
in AAI(R) pacing mode while providing the
safety of DDDR back-up pacing support if
necessary (Fig. 6.34). Minimizing RV pacing
may result in reduced risks of heart failure and
AF. Moreover, Reactive atrial Antitachycardia
Pacing (ATP) therapies and intervention algo-
113
rithms for atrial tachyarrhythmias offer more
opportunity to restore and maintain sinus
rhythm.
EnPulse™ (Medtronic) was labeled an “auto-
matic” pacemaker (Fig. 6.35). In this device,
Atrial Capture Management (ACM) automati-
cally and regularly adapted atrial threshold levels
and Search AV™+ continuously searched for
intrinsic conduction and automatically adapted
programmed AV delays to minimize chronic RV
pacing. Cardiac Compass™ Trends also auto-
matically monitored for arrhythmias and helped
in diagnosis and assessing the effects of
therapies.
Diagnose AF (Vitatron) was a full featured
dual chamber pacemaker, specially adapted to
function as a very sensitive, accurate detection
device for gathering and analyzing valuable car-
diac data. It managed the ventricular rate during
atrial arrhythmias with beat-to-beat mode
switching and provided dual sensor rate response.
Prevent AF (Vitatron) was another revolution-
ary pacing device which not only offered brady-
cardia pacing but which had novel sensing and
pacing capabilities and a series of sophisticated
new preventive pacing algorithms aimed at sup-
pressing the onset of AF. These features have
been incorporated into newer models.
Selection 9000 AF 3.0 offered a series of AF
monitoring diagnostics, new AF prevention pac-
ing therapy and new rate control therapies. It
included four algorithms for triggered overdrive
pacing which react to onset triggers of AF – PAC
suppression, PAC response, post-AF response,
and post-exercise response. In addition, there
were two more algorithms for continuous over-
drive pacing which aimed to condition the atrial
activation pattern by dynamically overdriving the
atrial rate: Pace Conditioning and Rate Smoothing.
This combination of continuous AF monitoring
and six preventive pacing therapies enabled fine-
tuning. AF preventing pacing therapies are aimed
at promoting and maintaining normal sinus
rhythm, improving hemodynamics, and reducing
risk of stroke.
The Symphony® DR (Sorin) introduced an
AAIsafeR™ mode which offered a unique and
comprehensive means of achieving optimal phys-
iological pacing in all types of AV conduction
114 6 Permanent Pacemakers and Leads

b Single Backup Pace

c AAI(R) to DDD(R)

d
DDD(R) to AAI(R)

Fig. 6.34 AAI safe mode: (a) AAI(R) mode – atrial- the presence of transient loss of conduction. (c) DDD(R)
based pacing allowing intrinsic AV conduction. (b) switch – ventricular support if loss of AV conduction is
Ventricular backup – ventricular pacing only as needed in persistent. (d) Switching from DDD(R) to AAI(R)

disorders, including permanent first degree AV
block, thus contributing to a reduced risk for heart
failure, AF, and death (Fig. 6.36). AAIsafeR™ is
a unique pacing mode suitable for the manage-
ment of AV conduction disorders. Like AAI,
AAIsafeR™ preserves AV conduction while con-
stantly monitoring ventricular activity, and pro-
vides critically needed dual chamber pacing in
case of advanced AV block. In addition to the
suppression of unnecessary ventricular pacing,
Symphony® DR offered advanced diagnostic
functions, including 7 min of intracardiac ECG
recordings and expeditious follow-up tools, such
as AIDA (Automatic Interpretation for Diagnosis
Assistance).
Most devices cannot be exposed to MRI for
fear of damage and malfunction of device and
lead. However, the Advisa DR MRI™ SureScan®
pacing system (Medtronic) is an MRI condi-
tional safe pacemaker that offers MVP®, com-
plete automaticity including VCM and ACM,
and automatic sensing (Fig. 6.36). Its sophisti-
Special Functionality
cated therapies include ATP and diagnostics
include Cardiac Compass Report™ and tachyar-
rhythmia management tools to assist in the early
detection and termination of atrial fibrillation. It
also offers Remote Follow-up via the Medtronic
CareLink® Network and OptiVol® Fluid Status
Monitoring which reports fluid changes using
intrathoracic impedance measurements, Rate
Drop Response which identifies abrupt brady-
cardia and responds by pacing at an elevated rate
– especially useful for those with cardioinhibi-
tory vasovagal syncope and high upper tracking
rates (up to 210 bpm). This may be useful for
pediatric patients and older active patients. The
EnRhythm MRI™ SureScan® and the Model
5086 CapSureFix MRI™ lead are similarly
“MRI safe” or “MR conditional” because of the
use of significantly reduced ferromagnetic com-
Fig. 6.35 The EnPulse™ pacemaker (Image reproduced
with permission of Medtronic, Inc.)
Fig. 6.36 (Left) The
Symphony® DR pacemaker
(with permission of Sorin
Group). (Right) The Advisa
DR MRI™ SureScan®
pacemaker (with permission
of Medtronic, Inc.)
115
ponents, changes to the internal circuitry, and
device design to minimize the gradient field
energy coupled to the lead tip, as well as changes
to the lead body geometry to prevent lead tip
heating. Conditional usually means that certain
conditions should also exist before MRI scan-
ning takes place even with these devices. These
are outlined in Chap. 10. The Accent MRI™
pacemaker and Tendril MRI™ lead from St.
Jude Medical, Inc. have recently been approved
as MR-Conditional in Europe and been released
for use in India. This system features an MRI
Activator™ device that provides a simple alter-
native option for programming the device to the
appropriate MRI mode for use during the scan.
Since it does not require a programmer, this
increases both clinical and personnel efficiency.
The pacing parameters are preselected by the
patient’s physician and stored in the Accent MRI
pacemaker. The MRI Activator can then be used
to program the device back to its original set-
tings after the scan has been completed.
Boston Scientific Corporation have recently
released the Ingenio™ MRI and Advantio™
MRI rate-responsive pacemakers (employing
RightRate™ MV sensor and ImageReady™
technology). When used in conjunction with
Fineline II leads, they are safe for use in patients
requiring MRI scanning by programming the
device into MRI Protection Mode.
With the advent of radiofrequency ablation for
the treatment of re-entrant supraventricular
arrhythmias, specific antitachycardia pacemakers
116
are now rarely used. The Stratos® LA (Biotronik)
is currently the only device available for specific
bi-atrial pacing (using RA/LA and RV leads)
which can be used for preventive overdrive
pacing.
Advanced Diagnostic Features
In recent years, devices have become equipped
with advanced diagnostic features which can be
interrogated easily at follow-up. Many of these
features prove invaluable during troubleshoot-
ing of suspected pacemaker malfunction (see
Chap. 21).
Automatic Daily Measurements
Approximately every 24 h, intrinsic P- and
R-wave amplitudes and atrial and ventricular
lead impedances are measured. Data for the last
52 weeks can be saved in the device memory.
Arrhythmia Detection
The frequency, type, and rate of arrhythmias can
be detected by some devices, such as the
Kappa™ 900 and Versa™ devices (Medtronic)
(Fig. 6.37).
Fig. 6.37 The Versa™ DR pacemaker is a sophisticated,
multiprogrammable pacemaker which is suitable for use
with Medtronic’s CareLink™ home monitoring service.
The Versa™ is the successor to the Kappa™ series from
Medtronic (Image reproduced with permission of
Medtronic, Inc.)
6 Permanent Pacemakers and Leads
Atrial Tachy Response
The percent of time mode-switched, maximum
and average mode-switch time, and number of
mode-switches can be retrieved from the memory.
Battery Status
Some pacemakers automatically evaluate battery
status every 12 h or so. It may be displayed in the
form of a gauge (showing BOL, ERT, and EOL)
and longevity remaining (>5 year to <6 months
in 6 month increments) at 100% pacing.
Remote Monitoring
The CareLink® Network (Medtronic) using
Conexus® Wireless Telemetry is available for
patients with EnPulse™, Kappa™ 900/700
series, and Versa™ pacemakers (Fig. 6.38). This
Internet-based remote monitoring service – com-
parable to a pacing clinic check, enables patients
who are housebound or infirm to connect to a
center for over-the-wire pacemaker checking.
The Medtronic CareLink® Monitor (weighs about
1 lb) connects to a standard phone line, gathers
the information from the device by placing an
antenna over it, and sends the data to a secure site
for access by technician or physician (Fig. 6.38).
Physicians can quickly access device data any-
time from any Web-capable PC.
The Evia™ and Estella™ pacemakers from
Biotronik (Fig. 6.39) transfer Home Monitoring
data automatically as trend messages, event
reports, and patient reports to the Biotronik
Service Centre using the Cardio-Messenger II®
device. The cardiologist then receives the detailed
report via the cellular telephone network. Similar
systems such as LATITUDE® (Boston Scientific)
and Merlin@home™ (St Jude Medical) are also
available and all are described in Chap. 11.
Intracardiac EGMs and Markers
Continuous atrial and ventricular intracardiac
EGMs and annotated event markers available
Digital Pacemaker Technology 117

Fig. 6.38 CareLink™

(Image reproduced with
permission of Medtronic,
Inc.) enables secure data
transfer from patient to clinic
in minutes. The medtronic
programmer/analyzer is
shown (top right)

The Medtronic Care Link Monitor and Antenna

Fig. 6.39 The Evia™ SR-T

and Estella™ DR-T pacemak-
ers allow transfer of Home
Monitoring data using the
CardioMessenger II® system
(Images courtesy of
Biotronik)

during testing and follow-up simplify evaluation
(Fig. 6.40).
Trending Evaluation
Rate and sensor trending available with graphic
display allows replay of rate based on new param-
eter settings while sensitivity trending shows
measured intrinsic events and sensitivity levels.
Digital Pacemaker Technology
Recently introduced pacemakers use Digital
Signal Processing (DSP) to convert analogue sig-
nals into a digital signal which provides precise
sensing and analysis of the cardiac signal. DSP is
much faster, it allows for more storage capacity
and all diagnostics are available during initial
interrogation. The Vitatron C-series were an
example of the efficient use of digital technology
within pacemakers. Using the programmer,
Therapy Advisor can analyze the pacemaker data
and translate it into therapy by giving suggestions
to optimize programming settings. A complete
technical follow-up can take as little as 3 or 4 min.
The pacemakers store useful information such as
EGM digitally – up to 12 min of digital EGM in
single chamber mode and 3 min with atrial and
ventricular monitoring. The high quality digital
EGM shows the actual signal that the pacemaker
uses as input signal which aids interpretation of
ECGs, diagnosis of the heart rhythm, and appro-
118 6 Permanent Pacemakers and Leads

01-DEC-2008 Lead-II (10 mm/mV) Boston 25 mm/s 01-DEC-2008 Lead-II (10 mm/mV) Boston 25 mm/s
12:28 Atrial Scientific Filter On 12:28 Atrial Boston Scientific Filter On
Vent Vent Scientific

(AS) (AS) (AS) (AS) (AS) (AS)

(AS) (AS) (AS) (AS) (AS) (AS)
VP VP VP VP
VP VP VP VP
VP VP VP VP

Fig. 6.40 Dual chamber pacemaker showing atrial sensing and ventricular pacing – confirmed by the atrial and ven-
tricular electrograms and the annotated event markers AS (atrial sense) and VP (ventricular pace)

priate adjustment of sensitivity according to the
signal amplitude of the EGM.
Moreover, the technology is energy-efficient
and allows for the EGM storage to be turned on
throughout the entire lifetime of the pacemaker
without affecting its longevity.
Permanent Pacemaker Leads (Table 6.8)
A permanent pacemaker lead consists of an
insulated wire or conductor with an electrode
at its distal tip which attaches to the myocar-
dium. Its function is to deliver the pacing stim-
uli produced by the generator as well as to
sense underlying myocardial activity and to
send this information back to the pacemaker
(Fig. 6.41). At the proximal end of the lead is
the connector pin which is fixed by a screw
mechanism to the pacemaker generator at the
time of implantation (Fig. 6.42). The screw is
reached through a silicone cover which self-
seals on removing the screwdriver. All leads
have a suture collar (Fig. 6.42) for anchoring
the lead to the pectoral fascia and preventing
the suture from cutting through the lead’s
insulation.
The last 25 years have seen much progress in
the development of permanent pacemaker leads,
in terms of their profile, flexibility, durability,
conductivity, shapes, fixation options, lengths,
and choice of tip types, besides the improved
materials used for the conductor, the electrode
tip, and the lead insulation.
A lead is presented in its individual box
whose labels indicate the model number, the
lead’s length and tip shape, the type of fixation
mechanism and polarity, and whether the tip is
steroid-eluting. The sterile package containing
the lead is transparent and also contains various
stylets, a “vein lifter,” and a fixation tool in
leads with an active-fixation mechanism
(Fig. 6.43).
Atrial and ventricular pacing electrodes cost
between £300 and £600 but left ventricular leads
for CRT and defibrillation leads for ICD devices
are significantly more expensive (£2,000 and
£3,000).
Electrode Insulation and Tip Structures
Electrodes have basically similar anatomy. They
usually consist of a multifilar, helically-coiled
wire (the conductor) that is insulated by a material
that does not cause tissue reaction or thrombosis.
The conductor is normally made of a nickel alloy
or platinum-iridium, and the two commonest
insulating materials are silicone rubber and poly-
urethane which are covered in a lubricious coat-
ing. For example, modern leads such as the
Flextend®2 (Boston Scientific) has a conductor
material of tri- and quad-wound helical coils of
MP35N, a non-magnetic, superalloy, or multiphase
Table 6.8 Permanent pacemaker endocardial leads
Pacemaker manufacturer Length (cm) Steroid Elec. tip
Electrode Polarity Placement Fixtn Tip shape Diameter Insulation Elution Connector SA mm2
Biotronik
Setrox S 45/53/60 Bi A/V Active Helix/straight 6.7F 45/53/60 Yes IS-1 4.5
Selox ST 53/60 Bi V Passive Straight/tines 6.5F 53/60 Yes IS-1 1.3
Selox JT 45/53 Bi A Passive J-shaped/tines 6.5F 45/53 Yes IS-1 1.3
Siello S 45,53,60 Bi A/V Active Straight/helix 5.6F 45/53/60 Yes IS-1 4.5
Siello JT 45,53 Bi A Passive J-shaped/tines 5.6F 45/53 Yes IS-1 2.1
Digital Pacemaker Technology

Siello T 53,60 Bi A/V Passive Straight/tines 5.6F 53/60 Yes IS-1 2.1
Safio S ProMRIa,b Bi A/V Active Screw 6.7F 53/60 Yes IS-1 4.5
Solia ProMRIa,c Bi A/V Active Screw/straight 5.6F 45/53/60 Yes IS-1 4.5
(Solia S)
Solia ProMRIa,c Bi A/V Passive Tines (Solia T) 5.6F 53/60 Yes IS-1 4.5
Solox Bi VDD Passive Straight/tines 9F 58/65 Si Yes IS-1
Boston Scientific
Dextrus®
4135/4136/4137 Bi A/V Active Helix/screw 6.7F 45/52/59 Si Yes IS-1 4.5
Flextend®2
4095/4096/4097 Bi A/V Active Helix/screw 7.2F 45/52/59 Si Yes IS-1 5.7
Fineline™ II Sterox
4456/4457 Bi A/V Passive Straight 5.4F 52/58 PU Yes IS-1 5
4458/4459 Bi A/V Passive Straight 6F 52/58 Si Yes IS-1 5
4479/4480 Bi A Passive Helix/screw 5.4F 45/52 PU Yes IS-1 5
Fineline™ II Sterox EZ
4469/4470/4471 Bi A/V Active Helix/screw 5.4F 45/52/58 PU Yes IS-1 5
4472/4473/4474 Bi A/V Active Helix/screw 6F 45/52/58 Si Yes IS-1 5
Medtronic
CapSure® SP Novusd
4092-52/58 Bi V Passive Straight/tines 5.3F 52/58 PU Yes IS-1 5.8
4592-45/53 Bi A Passive J-shape/tines 5.3F 45/53 PU Yes IS-1 5.8
5092-52/58 Bi V Passive Straight/tines 6F 52/58 Si Yes IS-1 5.8
5594-45/53 Bi A Passive J-shape/tines 6F 45/53 Si Yes IS-1 5.8
(continued)
119
Table 6.8 (continued)
120

Pacemaker manufacturer Length (cm) Steroid Elec. tip

Electrode Polarity Placement Fixtn Tip shape Diameter Insulation Elution Connector SA mm2
CapSure®Z Novus (High Efficiency)d
5054-52/58 Bi V Passive Straight/tines 6F 52/58 Si Yes IS-1 1.2
5554-45/53 Bi A Passive J-shape/tines 6F 45/53 Si Yes IS-1
*CapSure®SP-4023/4; 4523/4; 5024M; and 5524M leads are no longer available
CapSureFix® Novus (small-bodied, steroid-eluting, active-fixation lead)d
4076-45/52/58/65/85 Bi A or V Active Helix/screw 5.7F 45/52/58/65/85 PU Yes IS-1 4.2
5076-45/52/58/65/85 Bi A or V Active Helix/screw 6.1F 45/52/58/65/85 Si Yes IS-1 4.2
CapSureFix® MRI
5086MRI-45/52/58 Bi A or V Active Helix/screw 6.9F 45/52/58 Si Yes IS-1 4.2
CapSureFix®
5568-45/53 Bi A preformed J Active Helix/screw 7.2F 45/53 Si Yes IS-1 6.3
SureFix® (steroid-eluting, non-retractable fixation)
5072-45/52/58 Bi V/A straight Fixed screw 7.2F 45/52/58 Si Yes IS-1 6.3
CapSure Sense®
4073-45/52/58 Uni V/A Passive Straight/tines 3.6F 45/52/58 PU Yes IS-1 2.5
4074-45/52/58 Bi V Passive Straight/tines 5.3F 45/52/58 PU Yes IS-1 2.5
4574-45/53 Bi A Passive J-shape/tines 5.3F 45/53 PU Yes IS-1 2.5
Other active fixation leads
4058M-85 Bi A/V Active 85 PU No IS-1
4557M-53 Uni A preformed J Active 53 No IS-1
6

4558M-53 Bi A preformed J Active 53 No IS-1

Select Secure®
3830-59/69/74 Bi A/V Active Fixed helix 4.1F 59/69Si/ETFE Yes IS-1 3.6
Sorin
Stelid II
BTF25/26D Bi A or V Passive Tines 8F 52/59 Si Yes IS-1 2vc
UTF25/26D Uni A or V Passive Tines 8F 52/59 Yes IS-1 2vc
BJF24D Bi Atrial J Passive Tines 8F 45 Yes IS-1 2
BJF25D Bi Atrial J Passive Tines 8F 52 Yes IS-1 2
Stelix Bi A or V Active Helix/screw 9F Yes IS-1 2vc
Stelix II
BRF25/26D Bi A or V Active Helix/screw 8F 52/59 Si Yes IS-1 2vc
Permanent Pacemakers and Leads
 X-Fine™TX25D/26D Bi V Passive Tines 4.8F 52/58PU Yes IS-1 2
Beflex RF44D/45D/46D Bi A Active Screw/straight 6F 45/52/58Si Yes IS-1 4
Tilda JT Bi Atrial J Passive Tines 6.5F 45/53Si Yes IS-1 1.3
Tilda T Bi A or V Passive Tines 6.5F 53/60Si Yes IS-1 1.3
Tilda R Bi A or V Active Retract screw 6.7F 45/53/60Si Yes IS-1 4.5
Digital Pacemaker Technology

St. Jude Medical

Tendril® ST 1788TCe Bi A/V Active Helix/screw 6F 40/46/52/58/65 Yes IS-1
Tendril® ST 1782TCe Bi Atrial J Active Helix/screw 7F 40/46/52 Yes IS-1
Tendril® ST Optimf Bi A/V Active Helix/screw 6F 46/52/58 Yes IS-1
1888TC
Tendril® ST Optimf Bi Atrial J Active Helix/screw 7F 40/46/52 Yes IS-1
1882TC
Tendril™ STS 2088TCf Bi A/V Active Helix/screw 6F 46/52/58 Yes IS-1
OptiSense™ Optim™ Bi Atrial Active Helix/screw 7F 40/46/52 Yes IS-1
1999f
Isoflex Optim™ 1944f Bi Atrial J Passive Tines 7F 46/52 Yes IS-1
Isoflex Optim™ 1948f Bi A/V Passive Tines 7F 46/52/58 Yes IS-1
Isoflex 1646Tg Bi A/V Passive Tines 7F 34/40/46/52/58/85 Yes IS-1
Isoflex 1642Tg Bi Atrial J Passive Tines 7F 40/46/52 Yes IS-1
Isoflex 1644Th Bi Atrial J Passive Tines 7F 34/40/46/52 Yes IS-1
Isoflex 1648Th Bi A/V Passive Tines 7F 34/40/46/52/58/85 Yes IS-1
AV Plus DX VDD 1368g Bi VDD Single Pass/ Tines 9F 52/58/65 Yes IS-1
bifurcated
a
ProMRI – MRI conditional safe lead
b
Silicone insulation
c
Silicone/polyurethane insulation
d
Length of lead in cm is indicated after hyphen. Custom lengths of some leads are available at a surcharge
e
Silicone-insulation, endocardial, steroid-eluting, active-fixation leads
f
Optim insulation
g
Silicone insulation
h
Polyurethane insulation
121
122
Fig. 6.41 “Tined”
passive-fixation and
“screw-in” active-fixation
leads
Fig. 6.42 (Top) IS-1 Bipolar connector pin with arrow
on suture collar. (Bottom) The suture collar (arrow) for
anchoring the lead to the pectoral fascia can be slid along
alloy of nickel/cobalt/chromium/molybdenum
giving it ultra high strength, toughness, ductility,
and corrosion-resistance. The anode is made of
IROX (Iridium oxide-coated titanium) and the
cathode of platinum-iridium.
The advantages and disadvantages of silcone
and polyurethane as lead insulating materials
are shown in Table 6.9. The smaller the lead
profile, the smaller the introducer can be. A
small profile enables easier insertion into smaller
veins and allows two leads to be inserted via one
introducer–which may be useful in certain
situations.
6 Permanent Pacemakers and Leads
the electrode and is usually fixed as close to the lead’s
venous entry point as possible
At the lead tip is the cathode which is composed
of an inert meterial such as platinum-iridum, stain-
less steel, Elgiloy or vitreous carbon. The tips have
a variety of designs and are sometimes “porous”
aimed at improving the surface area of contact with
the endocardium and minimizing the development
of inflammation and fibrous tissue which may
increase the pacing threshold. “Porous tips” increase
contact with the electrolytes, reduce polarization
voltage, promote rapid tissue in-growth (Fig. 6.44),
secure fixation and lower thresholds. This results in
reduced current drain and increased longevity of the
pacemaker.
Digital Pacemaker Technology 123

Fig. 6.43 Electrodes are presented in a sterile, sealed transparent package (upper left) inside a sealed box which is
labeled in detail on the front and side (right and bottom left)

Table 6.9 Comparative advantages and disadvantages of exposure to body fluids, the steroid elutes from
silicone and polyurethane insulation on pacing leads the collar into the cardiac tissue, lowering acute
Silicone Polyurethane and chronic pacing thresholds and maximizing
Advantages Advantages sensing potentials. The CapSure® family of
Inert Biocompatible leads (Medtronic) employ similar steroid-elut-
Biocompatible High tear strength ing and platinization technology to provide sta-
Biostable Low friction coefficient ble, low pacing thresholds and a thin lead body
Less fibrotic while Stelix II (Sorin Group) has a vitreous car-
Small lead diameters bon tip and a steroid-eluting collar and the
Disadvantages Disadvantages Fineline II Sterox series (Guidant/Boston
High friction Environmental stress Scientific) have electrode tips coated with irid-
coefficient (sticky) Cracking
Handling damage Metal ion oxidation ium oxide (IROX™) to help reduce acute and
Size (for some types) Oxidative degeneration chronic pacing thresholds.
of the polyurethane The amount of energy required to pace the
insulation heart is related to the surface area of the cathode
tip. The lower the surface area, the higher the cur-
Activated carbon, sintered platinum-iridium, rent density at the tip/myocardium interface, the
and sputtered titanium-nitride are examples of higher the impedance and the lower the current
materials used to make porous tips. Many leads drain on the pacemaker batteries. This allows low
elute steroid, e.g., dexamethasone, from their output programming and increases longevity of
tips to minimize tissue reaction and a rise in the generator. Low surface area electrodes range
stimulation threshold. For example, the from 1.2 to 5 mm2.
Flextend® active fixation leads (Guidant/Boston Leads are available in various diameters (5.3–
Scientific) have a collar at the base of the helix 9.0 Fr), which enable smaller introducer sheaths
that contains dexamethasone acetate. Upon to be used. Their distal ends may be straight for
124
Fig. 6.44 Porous tip of pacing electrode promotes tissue
ingrowth
placement in the right ventricular apex or pre-
shaped into a “J” for attachment into the right
atrial appendage and may be passively or
actively-fixed to the endocardium. MRI-safe
leads are 6–7F diameter and ICD leads are 7–9F
diameter.
Passive Fixation
Passive fixation is achieved in the RV apex by
wedging the tip of the lead within the trabeculae
with the tip in direct contact with the endocar-
dium. This may be helped by a wedge-shape end
to the lead tip or by the use of “tines,” “flanges,”
or “fins” close to the lead tip (Figs. 6.45 and
6.46). Passive fixation of atrial leads in the RA
appendage is best achieved by a pre-shaped “J”
and tined lead (Figs. 6.46 and 6.47) which can
usually be positioned in the appendage by remov-
ing the straight stylet within the lead. The tines
on the atrial “J” cling onto the trabeculae within
the appendage (Fig. 6.48). Straight leads bearing
tines can also be placed in the atrial appendage
using the “J-shaped” stylet, and there is surpris-
ingly little tendency for the lead to detach itself
from the endocardium during removal of the sty-
let. The CapSure® SP Novus 4092 is an example
of a straight, tined lead that can be placed by pas-
sive fixation into the RV apex and the CapSure®
SP Novus 4592 is a pre-shaped, tined atrial “J”
lead that can be passively fixed in the RA
appendage.
6 Permanent Pacemakers and Leads
Fig. 6.45 “Tined” passive-fixation lead
Fig. 6.46 Fixed “J-shaped” tined electrode for passive-
fixation in the RA appendage
Active Fixation
Active fixation is achieved in the RV apex, RV
free wall, RV septum/outflow tract, RA append-
age, or anywhere else within the RA by the
deployment of an extendable/retractable helix/
coil from the distal end of the lead (Fig. 6.49).
The helix is extended and screwed into the endo/
myocardium using a fixation tool (Fig. 6.50). The
tool is attached to the terminal pin and rotated
clockwise (the number of turns depends on the
manufacturer) which protrudes the helix and
fixes it to the endocardium (Fig. 6.51). The tip
is electrically active which allows the implanter
to find an optimal placement site before fixing
the lead to the chamber wall. Fluoroscopy mark-
ers provide visible confirmation of helix posi-
tion and whether it is fully extended (Fig. 6.52).
The Fineline™ II Sterox EZ active fixation leads
(Boston Scientific) have a capsule of mannitol
Digital Pacemaker Technology 125

Fig. 6.47 (Upper) The “J”

electrode is straightened by
inserting a straight stylet
down the electrode’s fine
inner lumen. (Lower) Pulling
back the stylet once the tip is
in the RA appendage allows
the fixed “J” to take up its
shape and allow its tines to
fix on the trabeculated
muscle there

Fig. 6.48 Close-up view of this bipolar, passive fixation
lead. (a) Proximal end of lead showing the two poles, with
the most proximal, cathode pole being covered by a remov-
able plastic funnel. The latter makes it easier to introduce a
stylet into the electrode’s fine inner lumen. (b) Distal
“J”-shape of this atrial electrode is shown, with its distal ste-
roid-eluting tip, its tines for passive-fixation and the two
poles of the electrode being easily seen. (c) The distal portion
of the same electrode after inserting a straight stylet within
it
126
which covers the distal helix but which dissolves
within 4 min of introduction into the heart. It has
no moving parts.
Fig. 6.49 Active-fixation mechanism showing the
“screw” within and extended from the distal tip of this
active-fixation lead
Fig. 6.50 Fixation tool on connector pin
6 Permanent Pacemakers and Leads
Atrial Leads
Atrial leads may be actively fixed using an
extendable helix from a pre-shaped “J” lead or
from a straight lead with an extendable helix
using a “J” stylet to aid screwing the tip into the
endocardium of the RA appendage (Fig. 6.53).
Alternatively, a straight active-fixation lead can
be placed elsewhere within the RA and screwed
into position using the fixation tool. The
CapSureFix 4568 and 5568 (Medtronic) are
examples of a pre-shaped “J” actively-fixed lead
which is ideal for reducing the incidence of atrial
lead displacement (see Fig. 6.53). The Stelix II
(Sorin) and the CapSureFix 4076 and 5076 are
straight leads which can be actively fixed to the
RA using a “J” stylet and the fixation tool.
Polarity
Both unipolar and bipolar leads are available,
although bipolar leads are most commonly used.
Digital Pacemaker Technology 127

Fig. 6.51 Mechanism of deployment of active-fixation helix in Medtronic’s 5078/5079 electrodes (Image reproduced
with permission of Medtronic, Inc.)

Unipolar leads have a single pacing conductor

and the pacemaker “can” acts as the sensing
electrode (anode). Bipolar leads have one pac-
ing conductor and one sensing conductor. The
anode and cathode are within the cardiac cham-
ber to be paced – the cathode being at the lead
tip and the anode just proximal to it. The charac-
teristics of each type of lead are shown in
Table 6.10.

Terminal Pin Sizes

Before the implant procedure, it is important to
be certain that the terminal pin on the proximal
end of the lead(s) will fit into the header port of
the pacemaker (Fig. 6.54). These may be IS-1
(3.2 mm, short pin with sealing rings), 5 or 6 mm
in size, and pacing leads that are compatible with
the pacemaker should be chosen for the
implantation procedure. Adaptors are available
to enable upsizing or downsizing of the connec-
tor pins to fit into a particular generator at the
time of generator change, although most manu-
facturers have made the IS-1 connector pin and
port on the header unit standard features to leads
and generators, respectively (Fig. 6.55).
Fig. 6.52 X-ray showing fixation of helical coil into RV
myocardium
Special Leads
A single VDD lead is available which is bipolar
and has an atrial sensing electrode 13–15 cm
proximal to the distal tip to enable sensing of
atrial activity without the need for a second lead
(Fig. 6.56). The Solox® from Biotronik is 9F
compatible and has a fractal electrically active
surface of iridium. The CapSure® VDD2 Steroid-
eluting, single-pass lead (Models 5038, 5038S
and 5038L) from Medtronic provides a similar
function. It allows for atrial tracking and main-
128 6 Permanent Pacemakers and Leads

tains AV synchrony using a single, steroid-eluting

lead. This special lead is available as uni- and
bipolar configuration for the ventricular lead but
the atrial sensing electrode is bipolar (Fig. 6.57).
An MRI-conditional safe lead – the 5086
CapSureFix® MRI™ Lead – is available from
Medtronic for use with the EnRhythm DR MRI™
SureScan® and Advisa DR MRI™ Surescan®
pacing systems which are MRI safe. The lead and
pacemaker are identifiable on X-ray as being
MRI-conditional safe (see Chap. 10). The bipo-
lar, active-fixation lead has an helix/ring elec-
trode of titanium nitride coated platinum alloy, a
conductor of MP35N nickel alloy, and insulation

Table 6.10 Characteristics of unipolar and bipolar leads

Unipolar Bipolar
1 pacing conductor 1 pacing + 1 sensing
conductor
Sensing from pacemaker Arranged coaxially,
“can” co-radially, or as parallel
coils within lead body
Large pacing spike on Small pacing spikes
surface ECG
Small diameter lead body Larger diameter lead body
Less rigid lead body Stiffer lead
More susceptible to Less susceptible to
Fig. 6.53 (a) Fixed “J,” unipolar, active-fixation atrial oversensing oversensing
electrode showing the extended “screw” (b) (Medtronic May produce muscle/ Less likely to cause muscle/
Model 4557) nerve stimulation nerve stimulation

Fig. 6.54 Connector pins

inside header unit of
generator
Pacemaker Lead Accessories 129

Fig. 6.55 IS-1 connector pin

Fig. 6.56 CapSure VDD

lead (Image reproduced with
permission of Medtronic,
Inc.)

Fig. 6.57 Close-up view of the atrial sensing and ventricular sense/pacing electrodes of the Capsure® VDD lead. The
atrial electrode is bipolar but the ventricular electrode is available as a unipolar (bottom) or bipolar (top) connector

made of treated silicone rubber. It is available in
three lengths: 45, 52, and 58 cm.
Pacemaker Lead Accessories
A variety of useful accessories are available
from both pacemaker manufacturers and other
sources (e.g., Oscor® Inc.). These include a
range of “upsizing” and “downsizing” unipolar
and bipolar adaptors and lead extensions to
enable physicians to exchange pacemaker pins
to connect to different size header ports during
generator-exchange procedures (Fig. 6.58).
Others such as the “iLink-BLV-10” bifurcated
implantable lead adaptor enable the adaption of
one bipolar LV-1 connector and one bipolar IS-1
connector to one bipolar IS-1 header unit, and
130
Fig. 6.58 Four of the many useful accessories from Oscor®
Inc. (a) The VKU/V lead extender extends an implanted
unipolar lead (whose connector is removed) to a pacemaker
with an IS-1 port – available in 10, 20, and 40 cm lengths.
(b) B/IS implantable lead adaptor consists of two unipolar
5 mm receptacles and one bipolar IS-1 connector. Standard
Fig. 6.59 (Upper) iLink-BLV-10 bifurcated implantable
lead adaptor enables the adaption of one bipolar LV-1
connector and one bipolar IS-1 connector to one bipolar
IS-1 header unit. (Lower) the Dyad-LV bifurcated implant-
the Dyad-LV bifurcated implantable lead adap-
tor enables the adaption of one unipolar LV-1
(1.8 mm) connector and one bipolar IS-1 con-
nector to one bipolar IS-1 pacemaker header
unit (Fig. 6.59).
In certain circumstances, they also allow oper-
ators to repair fractured electrodes or leads with
broken insulation without having to explant the
entire lead – particularly important in leads that
6 Permanent Pacemakers and Leads
lengths are 15 and 20 cm. (c) BIS/BIS implantable lead
extension consists of one IS-1 receptacle and one IS-1 con-
nector – 10 and 40 cm lengths are available. (d) M/IS
implantable lead adaptor consists of one 5 mm receptacle
and one IS-1 connector – 10 and 40 cm lengths are available
(Courtesy of Oscor Inc., Palm Harbor, Fl, USA)
able lead adaptor enables the adaption of one unipolar
LV-1 (1.8 mm) connector and one bipolar IS-1 connector
to one bipolar IS-1 pacemaker header unit (Courtesy of
Oscor Inc., Palm Harbor, Fl, USA)
have been in-situ for many years and where a
difficult or challenging lead extraction procedure
is anticipated. Figure 6.58 shows examples of the
sort of adaptors and lead extensions that are
available.
Silicone “end-caps,” for insulating and sealing
redundant 5 or 3.3 mm connector pins; adaptor
sleeves, for adapting a 5 mm connector to a 6 mm
connector; ligature sleeves (of various lengths)
Pacemaker Prescription 131

Fig. 6.60 Accessories include lead end-cap kits, screwdrivers, and pin-plug kits

Fig. 6.61 All the accessories are presented in well-labeled sterile packaging. Screwdriver kit, pin-plug kit, and stylet-
kit are shown

for protecting lead insulation from their anchor- Pacemaker Prescription

ing sutures; “VV-plugs” for plugging up an empty
header cavity; spare PY fixation tools, straight
and “J” stylets, screwdrivers and repositioning
kits containing stylets and fixation tool are avail-
able and worth having in a busy pacing center
(Figs. 6.60 and 6.61).
The type of pacemaker required for each indi-
vidual patient depends on the type of conduction
disturbance that is present, e.g., sinus node dis-
ease, AV block etc., the basic rhythm that is pres-
ent, whether atrial tachyarrhythmias are present
132
and whether chronotropic incompetence is pres-
ent or absent. It is accepted that unnecessary RV
pacing may adversely affect heart failure morbid-
ity and overall mortality and so it is important to
try and reduce RV pacing as much as possible
without compromising hemodynamics. Ideally,
RV pacing should be reduced to below 40% and
as close to 10% as possible in order to maximize
the beneficial effects on reducing heart failure
morbidity. Algorithms in devices, such as MVP®
(Medtronic) and SafeR™ (Sorin Group), are
designed to minimize RV pacing. Unfortunately,
several factors may hamper achieving the 10%
target. These include the presence of complete
heart block, progression of AV node disease, and
episodes of atrial fibrillation with a slow ventric-
ular response. Closed loop stimulation pacing
(see above) may offer some advantages in this
regard. The Biotronik Evia device may be useful
in higher risk groups.
Guides to prescription for patients with sinus
node disease and for those with acquired AV
block, chronic bifascicular block, and trifascicu-
lar block are shown in Figs. 6.62 and 6.63. Correct
pacemaker prescription must now be recognized
as an issue for Clinical Governance committees
and physicians and pacing centers should be
shown to be practicing to recommended national/
international standards.
In general, every effort should be made to
minimize ventricular pacing. AAIR pacing should
be used in patients with SND, a normal PR inter-
val, and an intraventricular conduction delay of
<120 ms, where the progression to AV block is
approximately 0.6% per year. In patients without
chronotropic incompetence, back-up VVI pacing
(40–50 bpm) may be appropriate as most cases
will require pacing <1% of the time. Alternatively,
as indicated above, one could consider a device
with an algorithm that adapts the AV delay to
promote intrinsic conduction or that mode
switches from AAI to DDD pacing.
In patients with AV block, the choice of pac-
ing device depends on whether the block is per-
manent or intermittent and whether the ventricular
function is normal or not. For example, for inter-
6 Permanent Pacemakers and Leads
mittent AV block, dual chamber pacemakers with
algorithms to minimize RV pacing are indicated
and rate adaptation should not be used unless
there is evidence of symptomatic chronotropic
incompetence. For those with complete AV block
and normal systolic ventricular function, alterna-
tive RV pacing sites may be chosen over the RV
apex. In patients with symptomatic LV dysfunc-
tion and AV block, CRT should be considered
(see Chap. 16). Whether this should be CRT-P or
CRT -D depends on a variety of clinical factors,
the etiology of the LV dysfunction, the risk of
sudden cardiac death, and other comorbidities
that influence survival.
Simply leaving a device set at the nominal
parameters at the time of implant is unaccept-
able. An attempt must be made to preserve
spontaneous atrial activity and to promote
intrinsic conduction. Thus rate adaptation
should only be used when clinically indicated
and the device must be programmed to promote
intrinsic conduction.
Pacemaker Analyzers/Programmers
Device specialists and technicians must be famil-
iar with current pacemaker programmers which
are computer-based, complex devices them-
selves. Currently available devices are listed
in (Table 6.11). Programmers enable both pro-
grammability and telemetry of data including
programming commands, administrative data,
measured data, diagnostic data, and programmed
data (Fig. 6.64).
Data can be input using a keyboard, light pen
and/or “touch-screen” facility (Fig. 6.65). The
telemetry interface between pacemaker and pro-
grammer/analyzer may be a “wand” placed
directly over the pacemaker and connected
directly to the programmer (Fig. 6.66) or more
commonly by wireless telemetry. Radiofrequency
energy allows for rapid transmission of large
volumes of data through high frequency waves
emitted by the programmer’s antenna and
received by the pacemaker’s antenna.
Pacemaker Analyzers/Programmers 133

Sinus node disease

Sinus bradycardia

Atrioventricular block

No Yes

Chronotropic Chronotropic Chronotropic

Incompetence: Incompetence: Incompetence:
absent present/absent present/absent

Atrial Atrial Atrial

tachyarrhythmias: tachyarrhythmias: tachyarrhythmias:
present absent absent

DDDR + MPV AAIR DDDR + MPV

Class IIa Class I Class I
Level of evidence C Level of evidence C Level of evidence C

DDDR + MPV DDDR + MPV

+ ANTITACHY Class IIa
Class IIb Level of evidence C
Level of evidence C

ANTITACHY = antitachycardia algorithms in pacemaker; MPV = Minimization of Pacing in the Ventricles.

Note: In sinus node disease WIR and VDDR modes are considered unsuitable and are not recommended.
Where Atrioventricular block exists AAIR is considered inappropriate.

Fig. 6.62 Guide for prescription of pacemaker in sinus node disease (Courtesy of European Society of Cardiology)
134 6 Permanent Pacemakers and Leads

Atrioventricular
block, chronic bifascicular
and trifascicular block

Sinus rhythm

NO YES

Chronotropic Chronotropic
Incompetence Incompetence

No Yes No Yes

VDD/DDD* DDDR*
WI WIR Class IIa Class IIa
Class I Class I Level of Level of
Level of Level of evidence A evidence A
evidence C evidence C
WI WIR
Class IIb Class IIb
Level of Level of
evidence C evidence C

When atrioventricular block is not permanent, pacemakers with algorithms for preservation of native
atrioventricular conduction should be selected.
* WIR could be an alternative, especially in patients who have a low level of physical activity and in those
with a short expected lifespan.

Fig. 6.63 Guide for prescription of pacemaker in atrioventricular block, chronic bifascicular block, and trifascicular
block (Courtesy of European Society of Cardiology)
Pacemaker Analyzers/Programmers 135

Table 6.11 Pacemaker programmers/analyzers

Programmer Manufacturer Features
Orchestra Sorin SmartView – user-friendly; automatic recognition; color coded
interrogation and programming; easy retrieval of follow-up data;
one-touch/one screen – promotes easy navigation through
follow-up session
Merlin St. Jude Medical Three channel PSA; beat-to-beat analysis; allows bi-ventricular
testing at implantation
Zoom® Boston Scientific/Guidant Quick start-up, rapid device interrogation, touch screen, high
quality ECG
CareLink® 2290 Medtronic/Vitatron Automatic measurement of P- and R-wave amplitudes and slew
rates and lead impedance
Real-time display of atrial and ventricular EGM, rapid atrial
stimulation to 800 ppm
Antegrade and retrograde conduction tests, pulse width versus
amplitude threshold analysis; measurement reports
Renamic Biotronik Wireless antenna, fast follow-up, bluetooth file transfer, bluetooth
printing, automatic R and P wave measurement, auto-threshold,
retrograde conduction measurement, NIPS, overdrive pacing,
internal data archiving, GSM connectivity, PSA module

Fig. 6.64 Programmers/analyzers from the various manufacturers

136 6 Permanent Pacemakers and Leads

Fig. 6.65 Light-pen,

touch-screen programming
facility of the Medtronic
programmer/analyzer

Fig. 6.66 Wand placed

directly over the patient’s
pacemaker during interroga-
tion and reprogramming
 Implantation Technique
Permanent pacemaker implantation is most com-
monly performed via the left or right subclavian or
axillary vein. A cephalic vein may be used, and
although it has advantages this approach has limita-
tions. If the leads are inserted by either of these
routes then the generator is placed between the sub-
cutaneous fat and the surface of pectoralis major
muscle in a prepectoral pocket. In very thin or ema-
ciated patients or in those who wish the generator to
be hidden completely from view, the generator may
be placed behind the pectoralis muscle. An alterna-
tive site is the axilla, but this is rarely used. Epicardial
Fig. 7.1 Sterile operating theater should be appropriately ventilated and fully equipped
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_7, © Springer-Verlag London 2012
7
devices are usually buried behind the rectus abdo-
minis muscle. In patients with an occluded superior
vena cava, pacing electrodes can be inserted via a
femoral vein and the generator buried subcutane-
ously in the lower abdominal wall.
Operating Theater/Pacing Room
Pacemaker implantation should be performed
in a sterile operating theater with appropriate
ventilation and lighting (Figs. 7.1–7.3). A “clean”
137
138
Fig. 7.2 An operating table suitable for X-ray screening,
anesthetic equipment, piped gases, and oxygen and physi-
ological monitoring equipment are essential
catheter laboratory is a poor substitute for a dedi-
cated pacing theater and a poor use of the
resource. The room should have the recom-
mended 20 air changes per hour with positive
pressure relative to adjoining space. The room
should be adequately protected for radiation with
2 mm lead-equivalent lining for walls and
doors.
Equipment and Personnel
The room should be fully equipped with a high
quality fluoroscope, such as a mobile C-arm
fluoroscope or image intensifier, e.g., Philips BV
Pulsera (Fig. 7.4), and ideally operated by a fully
trained radiographer. The intensifier should have
excellent image quality with good image resolu-
7 Implantation Technique
Fig. 7.3 An operating light whose angle is easy to adjust
is particularly helpful
tion for visualization of fine guidewires and have
dose-saving features (Fig. 7.5). It should have a
9 inch field size with three magnification fields,
14, 17, and 23 cm available and a foot pedal is
ideal to allow the operator to screen the chest
during lead positioning. The system should be
easy to maneuver. The angles of rotation of the
C-arm should range from 45° left anterior
oblique (LAO) to lateral, with cranial and caudal
angulations of 20° as a minimum standard.
Ideally it should have a low-dose program for
extended screening procedures, a rotating anode,
pulsed fluoroscopy and digital acquisition. A
facility for archiving images acquired during
implantation and a split-screen facility for road-
mapping is useful (especially for CRT implants)
but not essential. The archiving for the system
could be onto CD ROM or networked via a PACS
(Picture Archiving and Communications System)
Equipment and Personnel
Fig. 7.4 A mobile C-arm fluoroscope or image intensifier, e.g., Philips BV Pulsera
Fig. 7.5 Excellent image quality with good image reso-
lution, the facility for archiving images acquired during
implantation and a split-screen facility for road-mapping
is available from Philips
139
and image transfer for static and dynamic images
should be available.
ECG monitoring is essential as is a trained
physiological measurement technician/clinical
physiologist experienced in pacing whose task
will be to perform and record the stimulation
and sensing threshold tests and lead impedance
measurements from atrial and/or ventricular
leads once they have been positioned by the car-
diologist (Fig. 7.6). Facilities for defibrillation
and external transthoracic pacing must be present
and readily available during pacemaker implan-
tation (Fig. 7.7).
An experienced theater nurse familiar with
pacing procedures is an essential member of the
pacing team. He or she will be responsible for
providing the equipment necessary for the
implantation and will be fully familiar with the
type of procedures being performed in the center.
A “scrub-nurse” or “runner” is sadly now a lux-
ury. Access to an anesthetist should be readily
available.
Staff should be trained and validated to deliver
advanced life support.
An operating table specifically designed to
allow X-ray screening is necessary for temporary
140 7 Implantation Technique

Fig. 7.6 Physiological measurement technician/clinical physiologist, pacemaker analyzer and ECG monitor/defibrillator

and permanent pacemaker implantation

procedures (Fig. 7.8). It should be constructed
of radiolucent carbon fiber, have a floating top,
have the facility for Trendelenburg/reverse tilt-
ing the patient into a “head-up” or “head-down”
position (±25°), be height-adjustable, and have
the pivot support of the table offset to allow
free movement and easy positioning of the
fluoroscope around the patient. The Stille
ImagiQ™ Imaging Table is a good example. A
lead shield hangs from the operator’s side of the
table to reduce radiation scatter to the operator
(Fig. 7.9).

Instrument Pack

A typical pack containing instruments that are

Fig. 7.7 Medtronic’s pacemaker analyzer and Lifepak 12
ECG monitor/defibrillator
useful for implantation of pacemakers is shown
in Figs. 7.10–7.12. A list of the contents is
shown in Table 7.1. Included in the pack or
available as a separate item is a large specially
designed pacemaker drape with adhesive back-
ing surrounding a window through which the
skin incision is made (see below). This is usu-
ally large enough to drape the whole of the
Instrument Pack 141

Fig. 7.8 The Stille ImagiQ™ imaging table, specifically designed to allow X-ray screening is ideal for temporary and
permanent pacemaker implantation procedures

Fig. 7.9 A lead screen hangs from the side of the table to protect the operator against X-ray scatter
142
patient and create a sterile field for the operator.
The head of the fluoroscope is covered with a
sterile plastic cover – with asepsis in mind
(Figs. 7.13 and 7.14).
Fig. 7.10 Sterile Instrument pack
Fig. 7.11 The number and
type of instruments in the
tray is usually chosen by the
device specialists responsible
for implantation
7 Implantation Technique
Preprocedure
If not already obtained, consent for the procedure
should be obtained from the patient after due
explanation of the benefits and risks of the proce-
dure. The risks and their approximate incidence
are shown in Table 7.2. The patient should be
fasted from food for at least 6 h before an elective
procedure. Patients are generally allowed to drink
water up until 2 h prior to the procedure – as per
local sedation policy. The practice of giving anti-
biotics prophylactically pre- and postprocedure
in an attempt to prevent pacemaker wound infec-
tion is widespread, but the published literature on
its efficacy is somewhat contradictory. However,
antibiotics are no substitute for a sterile operating
theater and meticulous aseptic technique before
and during implantation.
If antibiotics are to be given, anti-staphylococcal
agents should be the treatment of choice, e.g., 1 G
flucloxacillin IV at or ½ h before implantation and
500 mg qds orally for 2 days afterward. 1.5 G cefu-
roxime given IV just prior to the procedure may be
just as effective. For those allergic to penicillin, 1 G
of vancomycin IV in 500 ml of normal saline over
2 h followed by erythromycin 500 mg qds for
2 days is reasonable, although 800 mg teicoplanin
IV 30–60 min preprocedure and again 4 h postpro-
cedure is perhaps more convenient.
Preprocedure 143

Fig. 7.12 The ShortStop®

(Merit Medical) is a useful
safety device into which all
needles and scalpel blades
can be inserted after use

Table 7.1 Equipment provided within a typical pacemaker

pack
Instruments
2 sponge-holding forceps
2 towel clips
2 Halsted Mosquito artery forceps curved 12.5 cm
1 straight scissor 13 cm
1 Kilner needleholder 16.5 cm
1 McIndoe dressing forcep 15 cm
1 Gillies toothed dissecting forcep 15 cm
1 self-retaining retractor blunt
2 Gallipot polypropylene 60 ml
Two 6″ polypropylene bowls
Scalpel
18 gauge needle
10 ml syringe
20 ml syringe
Dressings/swabs
2 towel dressing crepe fld 2 ply 45 × 50 cm N/ST Fig. 7.13 An elasticated sterile plastic cover (arrow) is
2 swab XRD gauze 32 ply 10 × 7.5 cm T5 N/ST used to cover the head of the fluoroscope
Covers/drapes
1 large disposable drape – 205 cm wide × 262 cm long –
e.g., Guardian BDF ltd., Girvan, Ayrshire, Scotland
1 plastic elasticated cover for head of fluoroscope
57 cm diameter
144 7 Implantation Technique

Fig. 7.14 Sterile plastic cover on fluoroscope head (arrow)

Table 7.2 Approximate incidence of complications during

permanent pacemaker implantation as quoted to patients
during consent procedure
Arrhythmias 1%
Pneumothorax 1%
Hematoma 1%
Lead displacement 1–2%
Infection 1%
RV perforation – hemopericardium/ £1%
tamponade

Fig. 7.15 “Scrub-up” room is adjacent to the pacing theater

It is our practice to wash the upper chest/pro-
posed pacemaker implantation site with chlor-
hexidine or povidone-iodine solution on the ward
prior to the procedure.

Procedure

After thorough hand washing in a scrub-up room

(Fig. 7.15), the operator should wear hat, gown,
gloves, and mask and use strict aseptic technique
in order to minimize the chance of infection
(Fig. 7.16).
The patient should lie comfortably on the
operating table and a pillow is provided for head
support. The skin is again washed with 0.5–2%
chlorhexidine solution, povidone-iodine solution,
or both and the area allowed to dry (Figs. 7.17–
7.19). A sterile drape should then be placed
underneath the patient’s head before covering the
patient with the large drape designed specially
for the procedure, e.g., Guardian pacemaker
drape (Guardian Ltd., Ayrshire) (Figs. 7.20– Fig. 7.16 Operator is gowned and gloved and wears hat
7.25). Some operators like to cover the “window” and mask
Procedure 145

Fig. 7.17 Antiseptic solution can be colored with a red

dye (arrow) to help ensure that the appropriate area of
Fig. 7.19 The axilla, neck, and supraclavicular region
skin is painted
should be included in the area being cleaned

Fig. 7.20 Sterile drape from Guardian showing the adhe-

sive section and the “cut-out” window to be placed over
the operation site

Fig. 7.18 Left pectoral region is cleaned with antiseptic

146
Fig. 7.21 Covering the patient with the sterile drape
Fig. 7.22 The top of the drape is made of clear plastic
which is elevated above the patient’s face by a horizontal
pole fixed to the table (see Fig. 7.24)
7 Implantation Technique
Fig. 7.23 The drape covers the patient’s feet and creates
a large sterile field
Fig. 7.24 The patient’s face is covered with a clear plastic
section of the drape, with the latter elevated off the face
in the drape with Ioban™ (3M Health Care) for
added protection (Fig. 7.26).
Between 20 and 40 ml of 1% lignocaine (3 mg/
kg) is then infiltrated in and around the skin and
subcutaneous tissue over the pectoralis major as
well as around and under the clavicle where the
subclavian vein is to be punctured (Fig. 7.27).
Procedure
Fig. 7.25 Positioning the window over the site of incision
Fig. 7.26 Ioban™ (3M Health Care) may be placed over
the drape and skin at the operating site
Within 5 min, the area should be anesthetized
sufficiently to proceed with implantation.
Subclavian Approach
This approach is widely used and the route of
choice for most cases and especially when more
147
Fig. 7.27 1% lignocaine is infiltrated into the operation site
than one lead is to be inserted. Leads are inserted
via an infraclavicular subclavian vein puncture,
anchored with sutures and then connected to the
generator which is then placed in a subcutaneous
pocket fashioned by blunt dissection over pecto-
ralis major.
The left subclavian vein is usually preferred to
the right because of the straight course it takes to
the superior vena cava. There are exceptions, for
example, when a left-sided SVC is encountered
(see below). An incision is made 2 cm below the
junction of the middle and inner thirds of the
clavicle and the incision extended in a lateral and
inferior direction for approximately 4–6 cm
(Fig. 7.28). A prepectoral pocket large enough to
accommodate the generator and attached elec-
trodes is created by blunt dissection (Figs. 7.29–
7.31). The pocket should be deep enough to take
the generator and attached leads away from the
skin edges. Any bleeding should be stopped by
tying-off significant vessels by direct ligature with
a suitable suture or by the use of diathermy. The
148
Fig. 7.28 Skin incision
Fig. 7.30 The fingers are used effectively for blunt
dissection
pocket may be packed with a wet gauze swab until
the leads are ready to be attached to the generator.
Entry into the subclavian vein (SCV) is made
easier if the vein is distended. Dehydration, which
reduces venous pressure should be corrected.
Tilting the table into a head-down position will
help to achieve distension of the SCV (Fig. 7.32).
7 Implantation Technique
Fig. 7.29 A retractor may be used to help dissection
(identify the cephalic vein if necessary) and make a pocket
Fig. 7.31 Making the pacemaker pocket
An 18 (1.2 mm) gauge 7 cm long needle that
comes with the introducer pack is inserted into
the SCV just below the inferior border of the
clavicle at the junction of its middle and inner
thirds and the tip aimed at the sternoclavicular
joint, so that it passes behind and close to the pos-
terior surface of the clavicle (Fig. 7.33). When
Procedure
Fig. 7.32 Top: Head-down tilt is useful to distend the
left subclavian vein prior to needle puncture. Bottom:
Table is clearly seen to be in a “feet-up”/“head-down”
the needle punctures the vein, venous blood is
aspirated easily. In patients with bowed chest
walls, or where the clavicle bows anteriorly, the
SCV puncture should be performed slightly more
laterally and aimed slightly more posteriorly than
described above. Cannulation of the vein is then
done by introducing a flexible 0.035″ (0.97 mm)
149
Trendelenberg position to help distend the subclavian
vein prior to needle puncture
guidewire with a “J-shaped” tip through the nee-
dle (Seldinger technique) (Figs. 7.34 and 7.35)
and into the SVC. No resistance to guidewire
passage should be felt; resistance usually means
that the guidewire is not in the vein. Fluoroscopy
can be used to check that the tip of the J-wire is in
the SVC/RA. The needle is then removed
150
Fig. 7.33 Puncture of the subclavian vein. Top:
Landmarks: The subclavian vein passes between the junc-
tion of the medial and middle thirds of the clavicle and
the suprasternal notch/sternoclavicular joint. Bottom: The
needle is kept parallel to the frontal plane and close to the
deep surface of the clavicle/sternum in order to avoid
puncture of the pleura and subclavian artery
(Fig. 7.36). If a second lead is being inserted, a
second SCV puncture is made and a second
guidewire inserted as just described (Figs. 7.37
and 7.38). Some operators screen the wire to
7 Implantation Technique
Fig. 7.34 Inserting “J” guidewire into needle
Fig. 7.35 Guidewire inside needle within subclavian vein
Fig. 7.36 Needle removed and guidewire left within the
subclavian vein
below the diaphragm in order to ensure that the
guidewire has not been inadvertently placed into
the subclavian artery – before advancing the
introducer sheath. This may be particularly help-
ful in patients with low systemic pressures.
A 20 cm long vessel dilator/sheath combina-
tion is then placed over each guidewire in turn
Procedure 151

Fig. 7.37 A second needle puncture is performed if a Fig. 7.38 Two guidewires within the subclavian vein
second lead is to be inserted

Fig. 7.39 Top: Vessel

dilator and peel-away
sheath (St. Jude Medical).
Bottom: Vessel dilator
and peel-away sheath
being advanced over a
guidewire

and pushed through the subcutaneous tissue
and fascia and into the SCV and on into the
SVC (Figs. 7.39–7.42). The wire and vessel
dilator are then removed (Fig. 7.43) and the
lead is inserted into the remaining “splittable”
sheath (Figs. 7.44– 7.46). This is best done in a
slightly head-down position so that air embo-
lism is avoided. Getting the patient to stop talk-
ing and breathing during this maneuver also
helps. Once the lead tip is in the upper SVC,
the sheath can be withdrawn and “peeled away”
from the lead (see below) leaving the electrode
152 7 Implantation Technique

Fig. 7.40 Vessel dilator and sheath being advanced over Fig. 7.43 Vessel dilator (blue) and guidewire being
the guidewire and through the clavipectoral fascia under removed from sheath (white)
the clavicle into the subclavian vein

Fig. 7.41 Firm pressure is necessary to advance the Fig. 7.44 The ventricular lead is inserted into the intro-
introducer into the subclavian vein ducer sheath

Fig. 7.42 Introducer fully inserted over one of the Fig. 7.45 Lead is advanced through the sheath and into
guidewires the right atrium
Procedure
Fig. 7.46 Lead fully inserted into sheath
Fig. 7.47 The ventricular lead within the subclavian vein
and the “peel-away” sheath removed
within the circulation (Fig. 7.47). If a second
lead is to be introduced into the left SCV, a sec-
ond sheath/vessel dilator is then placed along
the second guidewire into the SVC and the sec-
ond lead inserted as described above
(Figs. 7.48–7.52). The sheath can then be
“peeled away” (Fig. 7.53).
Alternatively, a guidewire can be left in the
first sheath and a second vessel dilator/sheath
combination placed over the wire next to the first
electrode and then the outer sheath “peeled-away”
as described. The only drawback to this technique
is that the two leads tend to move each other dur-
ing positioning of the electrodes, unlike when
two separate punctures are made – but it does
reduce the number of SCV punctures.
153
Fig. 7.48 Second vessel dilator and sheath being intro-
duced over the guidewire
Fig. 7.49 Introducer fully inserted
The right SCV is accessible in a similar way
to the left SCV described above. However, the
SCV may make an almost 90° descent into the
SVC.
A range of “peel-away” introducer sheaths
which are available from Medtronic is shown in
Table 7.3. Some have a hemostatic valve and a
side-port for drug infusion.
Cephalic Vein Approach
This approach was commonly used before plastic
introducer sheaths were available and is still used
routinely by some operators. After administration
of local anesthetic to the pectoral region, it involves
154 7 Implantation Technique

Fig. 7.50 Vessel dilator being removed

Fig. 7.53 “Peel-away” sheath being removed

Table 7.3 “Peelable/splittable sheath” pacemaker lead

introducers (Medtronic)
Model no. Size
Single chamber introducersa
6207/6208/6209/6210-S1 7F/8F/9F/10F
6211/6212/6214-S1 11F/12F/14F
Dual chamber introducers (2 sheaths per kit)b
6208/6209/6210/6211-D1 8F/9F/10.5F/11F
Hemostatic, “tear-away” percutaneous lead introducer
with infusion side port (Medtronic)c
HLS 1007/1008/1009/ 7F/8F/9F/10.5F/11F
Fig. 7.51 Atrial lead being introduced into sheath
10105/1011M × 13 cm tear-away
valved sheath w/side
port
a
Cost approximately £27
b
Cost approximately £40
c
Cost approximately £45

border extending over the deltopectoral groove.

Fig. 7.52 Atrial lead within the sheath
cutting down onto the cephalic vein (using an
oblique incision) in the deltopectoral groove, which
can sometimes be identified by the presence of fatty
tissue between pectoralis major and deltoid mus-
cles (Fig. 7.54). Alternatively, a horizontal incision
2 cm below the clavicle can be made with its lateral
The vein is then dissected free from the fat and
sutures should be placed proximally and distally
(Figs. 7.55, and 7.56) and a cut down performed.
This should enable a guidewire and 7 Fr dilator to
be placed within the vein and then an electrode can
be introduced to the right atrium/ventricle
(Figs. 7.57–7.62). If there is difficulty in advancing
the guidewire, venography can be done via the dila-
tor in order to demonstrate the anatomy. Unfor-
tunately the vein is sometimes too small to be used
or only large enough to accommodate one elec-
trode. This technique eliminates the risk of pneu-
mothorax during lead implantation and reduces
the subsequent risk of “subclavicular crush.”
Procedure 155

Fig. 7.54 Self-retaining retractor can be used to help Fig. 7.57 A “vein-picker” (yellow) is used to help inser-
identify and anchor the cephalic vein tion of a guidewire into the cephalic vein and beyond

Fig. 7.58 “Vein-picker” or “vein-lifter”

Fig. 7.55 Suture is placed around the distal end of the

cephalic vein

Fig. 7.59 Guidewire being advanced

Fig. 7.56 A second suture is placed around the proximal

end of the cephalic vein

Fig. 7.60 Guidewire further advanced

156
Fig. 7.61 Vessel dilator and sheath being inserted into
the cephalic vein over the guidewire
Fig. 7.62 Lead being inserted into the cephalic vein
Axillary Vein Approach
The axillary vein is an alternative conduit for the
placement of pacing and defibrillation leads for
several reasons. Unlike the cephalic vein, the
axillary vein is almost always large enough to
accommodate multiple pacing leads. When com-
pared to the subclavian vein, the axillary vein
affords a less acute course. This potentially
decreases mechanical stress on the implanted
leads or catheters and results in a lower incidence
of mechanical lead failure. Additionally, subcla-
vian access is associated with the risk of inadver-
tently accessing the noncompressible subclavian
artery and the potential for increased mechanical
stress on the lead from crossing the subclavius
muscle and the clavipectoral fascia. Finally, use
of the axillary system does not require tunneling
of the leads over or under the clavicle.
A thorough understanding of the regional
anatomy is essential to successful cannulation of
7 Implantation Technique
IJV IJV
EJV EJV
RIV LS-CV
RS-CV
LIV
AxV SVC
BV
CV
MBV
MCV
Fig. 7.63 Venous anatomy of the upper limb/upper medi-
astinum relevant to pacing. MCV median cephalic vein,
MBV median basilic vein, BV basilic vein, CV cephalic
vein, AxV axillary vein, RS-CV right subclavian vein, RIV
right innominate vein, LIV left innominate vein, LS-CV
left subclavian vein, EJV external jugular vein, IJV inter-
nal jugular vein, SVC superior vena cava
the axillary system. The axillary vein begins at
the lower margin of the teres major muscle as a
continuation of the brachial vein. It continues its
course proximally until it terminates at the lateral
margin of the first rib to become the subclavian
vein. Along its course, it receives tributaries from
the cephalic and basilic veins (Fig. 7.63). The
vein is accompanied, along its course, by the
axillary artery, which lies slightly superior and
posterior to the vein. Overlying the vein are the
pectoralis minor and clavipectoral fascia, fol-
lowed more superficially by the pectoralis major.
A clinician can thus accurately and reliably can-
nulate the target vessel while minimizing the
chance of injury to adjacent structures. Techniques
for accessing the axillary and subclavian system
with the aid of ultrasonographic imaging have
also been used. However, because fluoroscopy is
Electrode Positioning 157

Fig. 7.65 Steel stylet

Fig. 7.64 Fluoroscopic-guided axillary vein puncture.

The arrow shows the tip of the needle just lateral to the
medial border of the first rib

an essential component of pacemaker and ICD

insertion, ultrasonography is rarely, if ever, used
for gaining access to the axillary system for these
procedures. In essence, this is a modified subcla-
vian approach and involves a fluoroscopically-
guided infraclavicular puncture, lateral to the
medial border of the first rib (Fig. 7.64). This
ensures an extra-thoracic puncture of the vein, Fig. 7.66 The stylet has a straight tip
thus eliminating the risk of pneumothorax. All of
the above precautions and tips for subclavian
vein puncture apply to the technique of axillary
vein lead placement.

Unusual Anatomy

Implanters of pacemakers and ICDs should be

fully familiar with the anatomy of the great veins
and the possible existence of congenital anoma-
lies (see Chap. 14).

Fig. 7.67 The tip is curved by gently curving the distal

Electrode Positioning stylet with the thumb and forefinger of the right hand

Ventricular Leads
Pacing leads are very soft and flexible and can
only be positioned in the RV by use of a stiffen-
ing steel stylet (Fig. 7.65). A gentle curve should
be shaped on the distal end of the stylet to help
maneuverability (Figs. 7.66–7.68) before placing
it within the hollow central lumen of the pacing
lead (Figs. 7.69 and 7.70). Stylets are available in
different lengths and variable degrees of stiffness
(Fig. 7.71).
158 7 Implantation Technique

Fig. 7.68 This curve on the distal end of the stylet will Fig. 7.69 Steel stylet being introduced into the lumen of
help the operator to get the pacing lead across the tricus- the lead via the plastic “funnel”
pid valve and the lead’s tip into the RV apex. A bigger
curve can be made on the stylet to help in positioning the
tip of an active-fixation lead onto the interventricular sep-
tum or RV outflow tract

Fig. 7.70 Gray knob on the proximal end of the stylet

which is inside this bipolar lead. Note the plastic “funnel”
which helps to place the stylet into the lead’s lumen

Fig. 7.71 Stylets of various lengths and tip-stiffness are available

Electrode Positioning
Fig. 7.72 Positioning the lead under fluoroscopy I
Fig. 7.73 Positioning the lead under fluoroscopy II
After entering the RA, using fluoroscopy the
lead can usually be advanced across the tricuspid
valve into the RV by advancing the whole lead
with the stylet slightly withdrawn making the
distal segment of the lead flexible (Figs. 7.72–
7.74). A diagrammatic representation of the tech-
nique of ventricular lead placement is shown in
Fig. 7.75. Sometimes the tip can be directly
placed into the RV apex. The stylet can then be
fully introduced into the lead and the latter pushed
gently into the apex. The stylet can then be half
withdrawn and the lead observed by fluoroscopy
to confirm a good anatomical stable position,
with the tip pointing slightly downward and ante-
riorly (especially for passive-fixation leads)
(Fig. 7.76). The latter position can be confirmed
by lateral fluoroscopy if necessary (Figs. 7.77
and 7.78). Tines or a conical shape on the lead’s
tip usually ensure passive fixation among the RV
159
Fig. 7.74 Retracting the stylet while advancing the lead
across the tricuspid valve en route toward the RV apex
trabeculae. Once satisfactory measurements are
confirmed (see below), the stylet is withdrawn
further into the brachiocephalic vein and atten-
tion is paid to examining the shape of the lead in
the RV and RA for the amount of slack in the lead
during inspiration and expiration. An example is
shown in Fig. 7.76.
More often the lead does not fall straight into
the RV apex. A loop or curve of distal lead should
be formed by withdrawing the stylet slightly and
impinging the lead tip on the lateral wall of the
RA, advancing the lead a little further and then
rotating the lead in order to flick the tip across the
tricuspid valve and into the RV. Ventricular ecto-
pic beats usually occur on entering the RV. If the
tip points upward, the lead may be in the pulmo-
nary artery or in the coronary sinus. If in the PA,
the lead can then be withdrawn and turned down
into the RV apex. Again, the lead tip is negotiated
into the RV apex by a process of lead rotation,
advancement and withdrawal. A satisfactory,
stable position should be confirmed by checking
for continuous pacing at 1 V during coughing,
deep inspiration, and expiration. The lead shape
and movement within the RA and RV should be
observed during these respiratory movements.
The right anterior oblique (RAO) view is optimal
for visualization of the full length of the lead, as
the PA view foreshortens the lead. Ideally, the
lead should straighten slightly in the RA/RV dur-
ing inspiration but not appear to pull on the api-
cal segment, and should form a gentle curve
through the tricuspid valve during expiration but
160 7 Implantation Technique

LIV LIV

RIV RIV
SVC SVC

PA PA

RA RA
TV TV

RV
RV

IVC IVC

a b

LIV LIV

RIV RIV
SVC SVC

PA PA

RA
RA
TV TV

RV

IVC IVC RV

c
d

Fig. 7.75 Technique for placing a permanent ventricular
lead into the right ventricular apex. (a) The lead and its sty-
let are inserted via the axillary or subclavian vein, innomi-
nate vein, and SVC into the Right atrium. Notice the position
of the tip of the stylet (---) within the lead. (b) With the
stylet withdrawn further into the lead, the lead is pushed
against the wall of the RA in order to form a generous curve
which (c) with further advancement can be advanced across
the tricuspid valve and into the RV cavity. (d) Rotation of
the lead and advancement of the curved stylet will flick the
distal part of the electrode toward the right ventricular
outflow tract (RVOT)/pulmonary artery (see Fig. 7.75e). (e)
Once the lead tip has been shown to enter the RVOT, there
is no doubt that the lead is not in the coronary sinus or in the
low RA. (f) The lead/stylet can then be withdrawn slightly.
(g) The curved stylet may then be advanced to the tip of the
lead and the two advanced forward into the RV apex with
gentle pressure. (h) With the stylet withdrawn slightly, the
lead can be further advanced gently in order to try and
wedge the tip between trabeculae and against the RV endo-
cardium RIV Right Innominate Vein; LIV Left Innominate
Vein; SVC Superior Vena Cava; RA Right Atrium; RV
Right Ventricle; IVC Inferior Vena Cava; TV Tricuspid
Valve; PA Pulmonary Artery
Electrode Positioning 161

LIV LIV

RIV RIV
SVC SVC

PA PA

RA
TV RA TV

RV RV

IVC IVC
e f

LIV LIV

RIV RIV
SVC SVC

PA PA

RA RA
TV TV

RV RV

IVC IVC
h
g

Fig. 7.75 (continued)

162
Fig. 7.76 PA chest X-ray showing satisfactory “down-
ward-pointing” position of this passively-fixed ventricular
lead (arrow). The chest X-ray also shows appropriate
amounts of “slack” in the atrial and ventricular leads – best
assessed by screening during inspiration and expiration
Fig. 7.77 This active-fixation lead points downward into
the RV apex (arrow)
not produce a redundant amount of lead in the
RA. Pacing at 5 V is advisable to rule out dia-
phragmatic stimulation. An LAO view will
ensure that the lead is in the RV and not in the
coronary sinus. Once the operator is happy with
the lead position (Figs. 7.79 and 7.80), measure-
ments, and stability, the lead should then be
7 Implantation Technique
Fig. 7.78 Lateral screening shows the lead tip to be posi-
tioned anteriorly in the RV apex (arrow)
Fig. 7.79 A “downward-pointing” lead tip is not always
essential to obtain, as in this case with excellent electrical
and positional stability
anchored by placing the short sleeve around the
lead near its entry point into the SCV and sutur-
ing it to the fascia over the underlying muscle
with two nonabsorbable sutures, e.g., Ethilon®.
Fixing the lead at this point should protect against
displacement.
Electrode Positioning
Fig. 7.80 The lateral X-ray again shows the lead point-
ing anteriorly toward the apex of the RV
Fig. 7.81 Actively-fixing the lead tip using the “lead-
fixing” tool attached to the distal connector pin
If active fixation leads are to be used, the
anchoring maneuver with the fixing-tool is per-
formed once the electrode tip appears to be in an
anatomically satisfactory position. With the sty-
let still within the lead, the fixing tool is attached
to the lead’s connector pin and rotated 12–15
times in a clockwise direction (Figs. 7.81–7.83).
This maneuver extends the helical/spiked distal
lead tip which becomes “screwed” into the adja-
cent myocardium (see Fig. 6.51). This may be
checked by fluoroscopy when a characteristic
feature is evident (see Fig. 6.52). The tool and the
163
Fig. 7.82 Rotating the tool during active-fixation
Fig. 7.83 Fixation tool on the distal connector pin after
fixing the distal tip of the lead to the myocardium and
removal of the stylet
stylet are then removed from the lead and
fluoroscopy used to ensure a stable position of
the lead’s tip and that there is the right amount of
slack in the RV and RA during inspiration and
expiration (see Fig. 7.76).
Recently, pacing the RV outflow tract (and in
particular the RV septal portion of the RVOT)
rather than the RV apex is becoming more
popular on the basis that this creates more
physiological conduction and some hemody-
namic advantage. In particular, it is thought that
long-term ventricular remodeling and dysfunc-
tion, cardiac failure, and atrial fibrillation are
less likely to occur with RV outflow tract pac-
ing compared to RV apical pacing. This may be
more important in children and younger adults
than in the elderly. Clearly, an active-fixation
164
Fig. 7.84 Chest X-ray showing active-fixation of atrial
lead into the RA appendage and of the RV lead into the
interventricular septum
lead is required for RV outflow tract pacing. A
typical appearance is shown in Fig. 7.84.
However, there is little data to support the theo-
retical advantages of RV septal pacing over RV
apical pacing and indeed it is often not possible
to know for certain whether the lead is fixed to
the septum or to the anterior or free walls.
Moreover, some patients, for example, those
with patch repairs of ventricular septal defects,
are not suitable for alternative-site pacing. A
left bundle branch block pattern QRS morphol-
ogy confirms RV apical pacing. Occasionally, a
right bundle branch block morphology may be
seen with pacing from the RV septum. If RV
apical pacing is accepted, then the pacemaker
should be programmed to minimize ventricular
pacing if at all possible. Clinicians frequently
attempt to minimize RV pacing while maintain-
ing a dual chamber mode by programming the
device to very long paced and sensed AV delays.
However, this practice has potential problems.
First, very long AV delays, even when followed
by intrinsic ventricular conduction or fusion,
may compromise atrial transport function.
Second, RV pacing may not be significantly
reduced especially at high pacing rates associ-
ated with rate responsive pacing. Many modern
dual chamber devices contain an AV hysteresis
7 Implantation Technique
function that can reduce RV pacing by tran-
siently increasing the AV delay in an attempt to
search for intrinsic conduction. An advantage is
the return to the programmed AV delay if the
device does not verify intrinsic conduction and
activates RV pacing. RV pacing, if necessary, is
performed in conjunction with a more physio-
logic AV delay. More recently, manufacturers
have introduced algorithms consisting of
modified AAI pacing modes that can be switched
from an atrial-based mode (AAI or AAIR) to a
dual chamber mode when a device detects AV
block. This results in a dramatic reduction in
RV pacing, e.g., SafeR™ (Sorin Group) and
MVP™ (Medtronic). In patients with a high
degree of AV block, reducing the percentage of
RV pacing is not really feasible, and in this pop-
ulation, alternative pacing sites from the RV
apex may provide a more physiological situa-
tion e.g., from RVOT.
There is little evidence that dual-site RV pac-
ing offers any significant advantage. Biventricular
pacing is advantageous in patients with poor LV
function (see Chap. 16).
Atrial Leads
The usual site for atrial pacing is the RA append-
age, and active and passive fixation leads may be
used in this site. Elsewhere in the atrium, such as
the atrial free wall or the interatrial septum,
active fixation leads must be used. A lead with a
J-shaped distal portion is usually used. Cases in
which inter-atrial septal pacing should be pre-
ferred include those with atrial arrhythmias and
those requiring atrial-based bi-ventricular pac-
ing with inter-atrial conduction delay, thus syn-
chronizing the right and left AV delay. Passive
fixation leads usually have tines to hold the tip
against the atrial myocardium, whereas active
fixation leads must be screwed into the myocar-
dium using a helix within its tip, as described
above.
With passive-fixation leads with a pre-shaped
“J,” a straight stylet is first placed within the hol-
low lead which straightens the distal portion of the
lead for advancement through the introducer
sheath to the mid-RA. The straight stylet is then
Electrode Positioning
Fig. 7.85 “J” stylet for use in deploying a lead into the
RA appendage
Fig. 7.86 Inserting “J” stylet into the atrial lead
Fig. 7.87 Advancing the “J” stylet into the atrial lead
withdrawn allowing the lead to assume its J-shape.
Slight withdrawal of the lead may enable the lead
tip to enter the RA appendage. If this is unsuccess-
ful, a J-shaped stylet (Fig. 7.85) may be introduced
165
Fig. 7.88 “J” stylet fully inserted into atrial lead
Fig. 7.89 Positioning the tip of the atrial lead into the RA
appendage requires careful maneuvering of the lead and
rotation of the stylet/lead combination
down the center of the lead which will help the
lead tip to be pulled up into the appendage
(Figs. 7.86–7.89). Several “J” stylets are usually
provided with each atrial lead. These have differ-
ent degrees of stiffness and curve to allow for the
variation in shape/size of a patient’s atrium/
appendage (Fig. 7.90). A diagrammatic represen-
tation of atrial lead placement is shown in Figs. 7.91
and 7.92. The use of the “J-shaped” stylet is always
necessary in straight leads being actively-fixed in
the RA. Correct positioning in the RA appendage
is usually evident by the lead tip moving from
side-to-side (“windscreen-wiper motion”) during
each atrial systole. Lateral screening shows the
lead tip pointing anteriorly. A good position is usu-
ally associated with a tall P-wave amplitude – ide-
ally >2 mV, recorded directly from the distal pole
of the electrode. The pacing threshold should be
low (ideally <1 mV but 1–2 mV is acceptable). For
active fixation leads, this is the appropriate time to
166
Fig. 7.90 Top left: Three “J” stylets accompanying the
Capsurefix® Novus 5076 lead (Medtronic) are presented
within a plastic guard. Top right: They have different
characteristics identifiable by the color of the knob on the
proximal end of the stylet. Bottom left: The Blue knob
signifies a thin stylet which provides a “J”- shape to the
lead for positioning in the RA. The White knob signifies a
slightly thicker/stiffer stylet for a “J”–“U”-shape, and the
LIV
RIV
SVC
PA
RA
TV
RV
IVC
a b
Fig. 7.91 Technique for placing a permanent, “active-
fixation,” atrial lead into the RA appendage. (a) A straight or
pre-shaped “J” lead is inserted into the RA via the subclavian/
axillary vein, innominate vein, and superior vena cava (SVC)
using a straight stylet (---) within the lead. (b) The straight
stylet is replaced by a “J” stylet which will allow the lead tip
to be rotated toward the RA appendage (c). (d) With the
7 Implantation Technique
Gray knob a stylet with a longer curve forming almost a
“U”-shape to the stylet and lead once it is placed within.
These alternative stylets are useful for lead positioning in
the right atrium of different sizes and shapes. The “J”
shape itself enables the lead to be maneuvered within the
RA when searching for the optimal position for sensing/
pacing. Bottom right: Left to right – Blue stylet, white
stylet, and gray stylet
LIV
RIV
SVC
PA
TV
RA
RV
IVC
lead/“J” stylet combination pulled up against the atrial myo-
cardium, the “U-bend” will open slightly. The tip of the lead
can then be actively-fixed to the myocardium using the tool
provided and the stylet can then be removed (e) RIV Right
Innominate Vein; LIV Left Innominate Vein; SVC Superior
Vena Cava; RA Right Atrium; RV Right Ventricle; IVC Inferior
Vena Cava; TV Tricuspid Valve; PA Pulmonary Artery
Electrode Positioning 167

LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

c d

LIV

RIV

SVC

PA

RA TV

RV

IVC

Fig. 7.91 (continued)

screw the lead’s helical tip into the myocardium
using the fixation tool – with the “J-shaped” stylet
still within the atrial lead (Figs. 7.93 and 7.94).
Protrusion of the helix can be seen on fluoroscopy.
The J-stylet has then to be removed from the lead
and this is a good test of successful fixation of the
lead to the myocardium.
Formal testing of the electrode (see below) should
now take place, and if satisfactory, stability testing of
the lead should follow. Lead stability is tested by
asking the patient to cough or perform deep inspira-
tion/expiration while pacing the atrium. Failure to
capture probably means that the lead is not fixed to
or held against the myocardium and the lead should
168
LIV
RIV
SVC
PA
RA
TV
RV
IVC
a b
Fig. 7.92 Technique for placing a permanent, “passive-
fixation,” atrial lead into the RA appendage. (a) As in
Fig. 7.91a, the pre-shaped atrial “J” lead is inserted into
the RA using a straight stylet (---) within the lead. (b) As
the straight stylet is removed, the pre-formed “J” lead will
take up its “J” shape in the RA appendage and becomes
Fig. 7.93 With the stylet in situ, the active-fixation tool
is attached to the distal connector pin
be repositioned and the above tests repeated. During
inspiration the J-shape should straighten slightly and
take up its J-shape on expiration. It is possible at this
stage to check that an appropriate amount of slack is
present on the lead when the lead (at its point of
appearance in the pacemaker incision) can then be
fixed to the fascia overlying pectoralis major using
the suture-collar and two nonabsorbable sutures as
described above for the ventricular lead. Ideally, the
collars should lay side-by-side and be as deep as
7 Implantation Technique
LIV
RIV
SVC
PA
RA TV
RV
IVC
passively-fixed to the trabeculated myocardium with the
aid of tines at the lead’s tip RIV Right Innominate Vein;
LIV Left Innominate Vein; SVC Superior Vena Cava; RA
Right Atrium; RV Right Ventricle; IVC Inferior Vena
Cava; TV Tricuspid Valve; PA Pulmonary Artery
Fig. 7.94 The lead is actively fixed to the RA appendage
by rotating the tool clockwise
possible away from the skin. Before attaching the
generator to the electrode pins, the stimulating and
sensing thresholds and lead impedance measure-
ments should be made.
If another site in the atrium is to be paced, a
straight active fixation lead should be chosen
and a straight stylet should be shaped by the
operator to enable the site of choice to be
reached and then the lead actively fixed using
the fixation tool.
Lead Measurements at Implantation
Fig. 7.95 Disposable wire connections for lead parame-
ter testing during implantation. The black/red connec-
tions in the left hand are inserted into the pacemaker
analyzer while the other black/red connections (arrow)
are attached to the distal and proximal electrodes on the
pacemaker lead
Fig. 7.96 Connection wire stretched across the operating
drape
It is recommended to check lead locations by
fluoroscopy in the RAO and left lateral views
before anchoring the leads.
169
Fig. 7.97 Close-up of the connecting wire and its terminals
Lead Measurements at Implantation
For satisfactory long-term pacing, low stimula-
tion and sensing thresholds should be present at
implantation. High thresholds or poor R- or
P-wave amplitudes suggest that the cathode tip is
not abutting excitable myocardium. If this is the
case, the leads should be repositioned.
Thresholds rise after pacemaker implantation,
and usually peak 1–3 months after lead fixation.
Thresholds are measured using a commercially
available pacing systems analyzer (PSA) – ideally
matched to the generator to be implanted. This
should ensure that they both have similar sensing
and generating circuits. It is important that the unipo-
lar or bipolar electrode configuration should be the
same as that being used in the implanted system.
A sterile bipolar lead is used to connect the
uni/bipolar electrodes on the pacing leads to the
PSA (Figs. 7.95 and 7.96). For a bipolar lead, the
positive (red) lead (anode) is connected to the
positive electrode on the pacemaker lead and the
negative (black) lead (cathode) is connected to
170
Fig. 7.98 Close-up view of the analyzer’s lead being
attached to the distal (black) and more proximal (red)
electrodes of this bipolar lead
Fig. 7.100 Technician
performing lead sensing,
pacing and impedance
checks
the distal tip negative electrode on the lead
(Figs. 7.97–7.99). The technician then begins the
sensing and pacing measurements using the PSA
(Fig. 7.100). For unipolar leads the negative
(black) PSA lead is connected to the single distal
electrode on the pacemaker lead and the positive
PSA lead (red) is connected to a metal instrument
which is placed inside the pacemaker pocket.
Measurements are first made on the ventricu-
lar lead (Fig. 7.101) and then on the atrial lead
(Figs. 7.102–7.105).
Sensing Threshold
The intracardiac electrogram resulting from
spontaneous activity of the cardiac chamber to be
7 Implantation Technique
Fig. 7.99 The black and red “crocodile clips” are seen
attached to the distal and more proximal electrodes on the
pacemaker lead during lead assessment
paced must be of sufficient amplitude if
satisfactory sensing is to be ensured. The PSA
should record an atrial and/or ventricular electro-
gram of >2 and >4 mV, respectively. ST-segment
shift due to current of injury indicates good endo-
cardial contact of RV and can be recorded as a
unipolar electrogram from the electrode tip
(Figs. 7.101 and 7.104). It should ensure a low
pacing threshold.
Pacing or Stimulation Threshold
The pacing threshold is the smallest electrical
impulse delivered by the cathode of the lead
that consistently activates or “captures” the
myocardium.
Lead Measurements at Implantation
Fig. 7.101 Left: Fluoroscopy shows satisfactory lead
position; Upper right: Ventricular electrogram shows
acute injury current (green arrow) and tall R-wave indica-
Fig. 7.102 Atrial lead
measurements: Pacemaker
analyzer’s crocodile clips
are attached to the two
electrodes of the atrial lead
during sensing, pacing, and
impedance measurements
To measure the pacing threshold, the PSA is
set to deliver impulses at 70 bpm or 10–15 bpm
above the patient’s own atrial or ventricular rate if
there is no bradycardia at the time. The impulse
duration or pulse width should be similar to that
which the pacemaker will likely deliver (usually
0.5 ms) and a voltage output of 5 V. The threshold
is then measured by steadily reducing the
171
0.3V
tive of good endocardial contact; Lower right: Pacing
threshold test: ventricular capture is lost at 0.3 V (blue
arrow)
output until “failure to capture” occurs (Fig. 7.101).
Care must be taken to then promptly increase the
output if the patient has no or little underlying
rhythm to avoid the consequences of asystole. A
phenomenon known as the Wedensky phenome-
non refers to the fact that the pacing threshold is
substantially greater when increasing from a sub-
threshold level and the technician should promptly
172 7 Implantation Technique

increase output by at least 2 V once there is failure

Fig. 7.103 Technician doing atrial lead tests using the
pacemaker analyzer/programmer
to capture.
With a pulse duration of 0.5 ms, a voltage
threshold of <1 V is considered acceptable in the
RV and <1.5 V in the RA. It will often be <0.5 V
in the RV if the lead is well positioned. With
active fixation leads, the pacing threshold may be
high, e.g.,1.5 V in the RV or even 3 V in the RA,
but it should fall within 5 min of fixation.
When testing bipolar leads, it is important to
ensure that the distal and proximal poles of the
electrode are connected to the PSA’s cathode (−ve)
and anode (+ve), respectively. If the poles are
reversed, the pacing threshold will be higher. With
a longer duration of pacing impulse, the more
energy is delivered per pulse and hence the pacing
threshold will be lower. The relationship is not lin-
ear, however, and 0.25–1.0 ms is usually the range
of efficient impulse duration or “pulse width.”
When testing unipolar leads, the distal pole of
the lead should be connected to the PSA’s cathode
(−ve) and the proximal electrode (+ve) connected to
a metal object such as a retractor placed within the
wound. In this situation, the surface area of the
anode should be similar to that of the pacemaker can
otherwise falsely high thresholds will be obtained.
Pacing the RV apex will lead to a ventricular
complex with LBBB and left axis deviation and
pacing the RV outflow tract, LBBB and right axis
deviation.

1.0V

Fig. 7.104 Top: Atrial electrogram shows some injury current and tall “P” wave (red arrows) suggestive of good endo-
cardial contact. Bottom: Atrial pacing threshold test shows lack of atrial capture at 1.0 V (blue arrow)
Lead Measurements at Implantation
Fig. 7.105 Top: Atrial threshold measurement. Bottom: Ventricular threshold measurement
Fig. 7.106 Anchoring the ventricular lead by inserting
two silk sutures around the lead collar
Lead Impedance
PSA will measure the resistance to current flow
down the lead – lead impedance. Although it
varies with each lead type, lead impedance should
be between 400 and 1,000 Ω at 5 V and 0.5 ms. A
very high impedance would suggest lead fracture
and a very low impedance a break in insulation
and leakage of current.
After the Lead Measurements
Once satisfactory measurements from the leads
have been confirmed and the atrial and/or
173
1.0V
0.3V
Fig. 7.107 Nonabsorbable 2:0 Mersilk is suitable for anchor-
ing the lead/collar although a nonbraided, nonabsorbable
suture such as “Ethilon” or “Ethibond” may be preferred
ventricular leads anchored using the protective
sleeves (Figs. 7.106–7.110), the leads should
be inserted into the generator’s respective ports
in the header unit. The generator has a screw-
driver within the sterile packet (Fig. 7.111).
The leads fit snugly into the ports (Figs. 7.112
and 7.113) and are fixed in place by tightly
screwing the respective retaining screws using
the screwdiver provided with the pacemaker.
The operator should visualize that the end of
each pin has passed the screw (Fig. 7.114)
before tightening it with the screwdriver
(Fig. 7.115). The self-sealing silicone cover
which covers the screws are shown in Fig. 7.116.
A small tug on each lead should confirm a
174 7 Implantation Technique

Fig. 7.108 Suturing the

ventricular lead to the fascia
over pectoralis major

Fig. 7.109 Suturing the

ventricular lead

Fig. 7.110 Anchoring the atrial

lead
Lead Measurements at Implantation 175

Fig. 7.111 The pacemaker

is usually accompanied by its
relevant screwdriver inside a
sterile package

Fig. 7.112 Once the leads have been anchored, the con- Fig. 7.114 The atrial lead is inserted into its relevant port
nector pins are inserted into the ports on the header of the and particular notice has to be taken to ensure that the
pacemaker distal pin has passed beyond the second securing screw

Fig. 7.113 Ventricular lead is inserted into its appropri- Fig. 7.115 The screwdriver is used to secure the leads
ate port inside the header

secure fix inside the pacemaker (Fig. 7.117). that the atrial and ventricular leads are inserted
Some operators check the serial numbers on into the correct respective ports in the pace-
each lead with the pacing technician to ensure maker header.
176
Fig. 7.116 The Altrua™ 50 has white self-sealing
covers over the screws (arrow). “A” and “V” indicate that
the atrial and ventricular leads are to be inserted into the
upper and lower ports respectively (©2010 Boston
Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)
Fig. 7.117 Once the leads are secured, a tug on the lead is
made to confirm that they are firmly fixed inside the header
Making the Pacemaker Pocket
and Inserting the Pacemaker
Most operators make the pocket before placing
the leads in the RA and RV. A pre-pectoral pocket
large enough to accommodate the generator and
attached leads is created by blunt dissection. The
pocket should be deep enough to take the genera-
7 Implantation Technique
Fig. 7.118 The pacemaker and leads are ready to be
implanted
Fig. 7.119 The generator and lead(s) are then wound
into a gentle circle before insertion into the pocket
tor and attached leads away from the skin edges
and ideally take the generator well down over
pectoralis major. In very thin or emaciated
patients, the generator may be placed under the
muscle. The generator should not be placed high
up, under the clavicle since erosion is then more
likely to occur. Any bleeding in the pocket should
be stopped by tying-off significant vessels by
direct ligature with a suitable suture or with
diathermy. The pocket may be packed with a wet
gauze swab until the leads are ready to be attached
to the generator. Once the leads are attached to
the generator and the pocket is dry, the leads
should be gently wound in a circle and placed
behind the generator as it is placed deep in the
pocket (Figs. 7.118–7.121) – preferably with the
header unit placed inferiorly. Placing the leads
behind the generator in this way makes it easier
to avoid cutting through the electrodes at the time
of generator replacement. The subcutaneous
Lead Measurements at Implantation 177

Fig. 7.120 The pacemaker is inserted into the pocket Fig. 7.123 Braided, absorbable Vicryl suture is suitable
ensuring that the header is placed inferiorly away from the for closure of this subcutaneous layer
skin edges

Fig. 7.121 The leads are placed behind the generator Fig. 7.124 The subcutaneous fatty tissue and pocket are
closed with interrupted absorbable sutures II

Fig. 7.122 The subcutaneous fatty tissue and pocket are Fig. 7.125 The subcutaneous fatty tissue is closed with
closed with interrupted absorbable sutures I interrupted sutures III

tissue is then brought together with interrupted absorbable Dexon® (Figs. 7.127–7.131). The
absorbable suture material (Vicryl®) (Figs. 7.122– wound should be cleaned with iodine or chlor-
7.126) and the wound edges either brought hexidine solution and dried with a sterile towel.
together with a neat subcuticular suture using The edges may then be glued together with
178 7 Implantation Technique

Fig. 7.126 The skin edges are now easy to approximate Fig. 7.129 Subcuticular suture being inserted

Fig. 7.127 Absorbable 3:0 Dexon II on a straight cutting Fig. 7.130 A pleasing end result is obtained by placing
needle is ideal for the subcuticular layer each subcuticular “bite” in close proximity to each other

Fig. 7.128 A continuous subcuticular suture is used to Fig. 7.131 The suture is completed by applying tension
bring the skin edges together to both ends of the subcuticular suture and the ends are
then removed

Dermabond® topical skin adhesive (Ethicon, Inc.) edges should preclude the need for plastic spray
or Nobecutane® plastic spray may be sprayed dressing (Figs. 7.132–7.134). It is ideal if ECG
over the wound to protect it from invading skin strips showing normal sensing/pacing are
microorganisms. Satisfactory gluing of the skin recorded and placed in the casenotes next to the
Lead Measurements at Implantation
Fig. 7.132 Dermabond® topical skin adhesive has a high
viscosity and an easy-to-use applicator
Fig. 7.134 Finished result
with glue applied
cardiologist’s notes on the procedure that has just
been performed (Fig. 7.135).
The procedure should take between 20 and
60 min depending on the type of pacemaker being
implanted and the ease/difficulty of entering the
central venous system and obtaining satisfactory
stable lead placement with favorable electrical
parameters.
A PA and lateral chest X-ray should be per-
formed to exclude pneumothorax and to check
179
Fig. 7.133 Dermabond® glue being applied to the skin
edges
satisfactory right ventricular, atrial, and left
ventricular lead positions prior to the patient’s
discharge.
A variety of accessories should be available in
a properly equipped pacing theater and these are
shown in Table 7.4.
The best defense against litigation is full doc-
umentation in the patient’s medical records of
every aspect of the implantation (or extraction)
procedure. This should include the indication for
180
Fig. 7.135 ECG strips showing DDD (upper) and VDD (lower) pacing after dual chamber pacemaker implantation.
This confirms atrial and ventricular pacing and satisfactory atrial sensing
Table 7.4 Accessories that should be available in the
pacing theater/lab during new pacemaker implants and
generator change procedures
Stylets for 52, 58, 65, 85, and 110 cm leads
J-Stylets for 45, 53, and 58 cm atrial leads
Lead anchoring sleeve
Lead end pin caps for 5, 3.2 mm, and IS-1 lead ends
“Pinch-on” tools for active-fixation leads
Screwdrivers for pacemaker generators
Medical adhesive
Adaptor kits:
Unipolar lead splice kit with IS-1 connector adaptor kit
for old generators (5866-9M)
Upsizing sleeve for 3.2 mm LP bipolar lead to 5 mm
bifurcated bipolar pacemaker (5866–22)
For changing a 5 mm unipolar to IS-1 unipolar lead
(5866-37M)
For changing two IS-1 unipolar leads to fit a IS-1
bipolar generator (5866-38M)
For changing a 3.2 mm LP bipolar lead to a IS-1
bipolar generator (5866-40M)
Sleeve for upsizing a IS-1 lead to 5/6 mm unipolar
single chamber pacemaker (5866–45)
For downsizing 6–5 mm (5866–21)
Lead extensions:
Unipolar, IS-1
Bipolar, IS-1
3.2 mm LP to IS-1, Bipolar
7 Implantation Technique
the procedure, the informed consent form, a
complete procedure note to include pacing
parameters achieved at implantation, and any
difficulties that were encountered. There should
be some evidence of what was done postopera-
tively, such as the programmed settings at dis-
charge, an ECG strip confirming satisfactory
pacing, and a note to indicate that the chest X-ray
excluded a pneumothorax. The arrangements for
follow-up should be clearly documented.
For extraction procedures, it is wise to docu-
ment what exactly was removed and why.
Pacemaker Programming
Immediately after pacemaker implantation, the
device should be programmed in the pacemaker
theater by the technician. Usually the pacemaker
prescription will have been decided beforehand
and the “factory settings” may even be repro-
grammed with the device still within the sterile
package. However, after implantation, the atrial
and/or ventricular sensitivity settings and outputs
can be changed according to the implant mea-
surements. A reduction in output will prolong
Pacemaker Programming
battery life. Upper and lower rate limits should be
set appropriately as should the AV delay/refrac-
tory periods if necessary. Pacing mode should be
set and rate response turned on and set appropri-
ately for each individual if necessary. Mode-
switching and Search AV facilities and diagnostic
tools can be turned on if appropriate but it should
be remembered that battery-life will be shortened
slightly in proportion to the number of diagnostic
and therapeutic programs in use.
For example, for patients who are predomi-
nantly in sinus rhythm, reduction of the base rate
181
will allow sinus rhythm to be maintained for lon-
ger periods. For those with angina pectoris, a
reduction in the pacing rate (and limitation of the
upper rate) may be important and a slightly faster
rate may be helpful in patients with cardiac fail-
ure or certain arrhythmias. For those patients
with paroxysmal atrial fibrillation, mode switch-
ing should be activated. The current device set-
tings should be noted in the case notes and entered
into the pacemaker database.
 Predischarge Pacemaker Checks
and Advice 8

Predischarge Pacemaker Checks isfactory pacing and sensing, if necessary by

The day after permanent pacemaker implantation
(or just prior to discharge if “day-case” pacing is
in operation), lead position should be checked by
performing a PA and lateral chest X-ray (see
Chap. 7). Pneumothorax and early lead displace-
ment should be excluded. A 12-lead ECG should
confirm satisfactory pacing in atrium, ventricle,
or both depending on the type of pacemaker
implanted, usually by application of the program-
mer head over the device to produce a “magnet
ECG strip.” The pacing threshold should ideally
be checked and the pacing parameters set appro-
priately by the clinical physiologist to ensure sat-
adjusting the pulse width (0.4–1.0 ms), output
(2.5–7.5 V), and sensitivity (0.25–8 mV) settings
(Figs. 8.1–8.3). The pacemaker’s upper (100–
180 bpm) and lower rate (30–100 bpm) limit,
pacing mode (e.g., AAI, VVI, DVI, DDD), rate
response, polarity (uni- or bipolar), refractory
period (200–500 ms), and AVD delay (0–300 ms),
etc., should also be confirmed by the clinical
physiologist using the programmer and the set-
tings documented in the case notes. For day cases,
these checks will be made by the technician
before the patient leaves the pacing theater.
Prior to discharge, the wound should be inspected
for signs of hematoma formation and integrity of

Fig. 8.1 Patient has device

interrogated/programmed before
discharge. Programming head is
placed over device

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 183

DOI 10.1007/978-1-4471-2939-4_8, © Springer-Verlag London 2012
184 8 Predischarge Pacemaker Checks and Advice

Fig. 8.2 Clinical physiologist uses

ECG machine and device programmer/
analyzer

Fig. 8.3 Company-specific programmer/analyzer from Medtronic (left) and Biotronik (right)
ID/Registration Card
Fig. 8.4 Pacemaker identification (ID) card
the wound incision and a follow-up appointment for
4–6 weeks should be given to the patient. This
should allow for early wound inspection and a fur-
ther assessment of pacing/sensing thresholds to
enable possible adjustments of the device settings.
Issues to Be Considered When Setting
the Initial Program
In those patients in sinus rhythm, the base rate
should be set to allow sinus rhythm to be main-
tained for longer periods to extend battery life and
help minimize RV pacing and its long-term disad-
vantages. Setting a low base rate, e.g., 50–60 bpm,
is useful for patients with angina pectoris. Bipolar
sensing and pacing should help prevent oversens-
ing and help prolong battery life respectively.
Atrial pacemakers require a higher sensitivity
than ventricular devices because the atrial electro-
gram is usually lower than the ventricular electro-
gram and the atrial sensitivity setting should be
set appropriately. Mode-switching should be
turned on if there is a history of paroxysmal AF
and the type, extent, and onset of rate response
can be set depending on the patient’s age, medical
185
condition, fitness, and activity level. The upper
rate limit should be set with these factors also in
mind. Adjustments to the pacemaker program set-
tings can be made at the first pacemaker clinic
visit at 4–6 weeks post-implantation.
ID/Registration Card
Patients should be given a pacemaker ID card
(Fig. 8.4) and asked to carry it with them. It should
provide important data such as: name, address,
date of birth, implanting center telephone number
and hospital number, type of pacemaker, pace-
maker mode and parameters at last programming,
and indication for implantation. The details and
coded information are filled in by the clinical
physiologist at the time of implantation and car-
bon copies are created. The white card is folded
and inserted into a plastic wallet and given to the
patient (Fig. 8.5). A green copy is provided for the
patient’s hospital file, a blue copy sent to The
National Registration Centre, and a yellow copy
(Manufacturer File) is given to the relevant sales
representative or sent to the pacemaker company
and acts a warranty application (Fig. 8.6). In the
186 8 Predischarge Pacemaker Checksand Advice

Fig. 8.5 ID card is folded

and placed in a plastic wallet

Fig. 8.6 Green, blue, and yellow carbon copies of the pacemaker data are created
Advice for Patients
Fig. 8.7 ID card for ICD
UK, the information is sent electronically to the
Central Cardiac Audit Database (CCAD) and the
blue copy is discarded. Adhesive stickers with the
serial number (SN) of the implanted device are
provided with most devices and should be attached
to each page of the European Patient ID card and
in the patient’s hospital file. Similar ID cards
(Figs. 8.7 and 8.8) and color-coded carbon copies
(Fig. 8.9) are available for ICD implantations.
A print-out of the pacemaker’s program at the
time of the patient’s discharge (Fig. 8.10) should
be placed in the patient’s casenotes and also
entered into the Pacing Database available within
the Centre.
187
Advice for Patients
General Advice
Patients should be advised to mobilize normally
from day 1 but to restrict vigorous arm move-
ments (on the pacing side) and avoid carrying
heavy weights over the next 2 weeks or so. They
should be asked to wash around the pacemaker
wound for the first week, and report to the
implanting center any undue pain, tenderness,
redness, swelling, gaps in the wound, or discharge
from the wound that appears so that an urgent
inspection can be made by a member of the spe-
188
Fig. 8.8 ID card for ICD
cialist pacing team. Except in unusual circum-
stances, such as a patient’s residence being a large
distance from the pacing center or severe frailty or
immobility, should any other doctor be given the
responsibility of treating these problems. Once
there is evidence of wound dehiscence or infec-
tion, the pacing center must be made aware of the
situation. It is suboptimal practice for anyone else
to simply prescribe antibiotics, resuture, or “ster-
istrip” the wound edges without discussion with
the cardiologist who was responsible for the pace-
maker implant. Once pocket infection has devel-
8 Predischarge Pacemaker Checksand Advice
oped, usually as a result of late, inadequate, or
inappropriate treatment, the pacing system is
probably doomed, in that it will have to be
removed and a new system implanted.
Patients will be given an information booklet
about their pacemaker (Figs. 8.11 and 8.12), told
about the need for regular checks in the pace-
maker clinic, and the approximate life expectancy
of their pacemaker. Discussion about the possi-
bility and potential for home monitoring can be
left until the first visit to the pacemaker clinic
4–6 weeks after implantation.
Advice for Patients 189

Fig. 8.9 Colored carbon copies of the ID card for ICD

Fig. 8.10 (continued)

Fig. 8.10 “Printout” of the pacemaker’s program at the

time of discharge
190
Fig. 8.11 Patient informa-
tion booklets from
Medtronic (left) and Boston
Scientific Ltd. (right)
Implanted
pacemaker
Lead in right
ventricle
a b
Fig. 8.12 The booklets are illustrated to help patients gain an understanding of their pacing system and the implantation
procedure itself (a) single chamber right ventricular pacemaker (b) dual chamber, atrial and ventricular pacemaker
Driving
In the UK, patients must refrain from driving or
riding a motor cycle for 1 week after uncompli-
cated pacemaker implantation or generator
replacement providing there is no other disquali-
fying condition. Professional drivers of HGVs,
buses, taxis, ambulances, or emergency vehicles
cannot drive for 6 weeks after implantation.
Although seatbelts may press on the pace-
maker of drivers or front-seat passengers, they
have not been shown to damage them.
8 Predischarge Pacemaker Checksand Advice
Implanted
pacemaker
Lead in
right atrium
Lead in right
ventricle
Dispensation to allow pacemaker patients not to
have to wear seatbelts may be given by the DVLA
in the UK, but the person must accept the poten-
tially serious consequences if an accident should
occur. For their front-seat passenger, the driver
may be held responsible for injury or death to
that person if they do not “belt-up.” Some patients
have found wearing a soft pad between the safety
belt and the pacemaker of some comfort.
Insurance premiums should not be increased
for pacemaker patients, unless they choose not to
wear a seatbelt!
Advice for Patients 191

Anticoagulant Therapy Specific Advice

Anticoagulant therapy with IV heparin or LMWH Specific advice about living and working with a
should be avoided for at least 12 h after implant. pacemaker and the precautions that should be taken
If anticoagulation is deemed necessary within the in order to avoid damaging the generator, uninten-
first week of implantation, dosing should be cau- tional reprogramming, or inhibition of pacemaker
tious to avoid a hematoma developing in the function is presented in Chap. 10, but guidance to
pocket. Warfarin may be started the day after the patients is found in the patient information booklet.
procedure but it is best to increase the dose grad-
ually rather than give large loading doses in an
attempt to reach an INR >2.5 quickly – which
will increase the likelihood of pocket hematoma
necessitating drainage.
 Programmable Functions
and Terminology
The rapid developments in technology and
pacemaker research have enabled pacemak-
ers and other implantable devices to become
more sophisticated. Devices have numerous
programmable features and can store sub-
stantial amounts of diagnostic information
related to device function, arrhythmia detec-
tion, cardiovascular hemodynamic parameters
including transthoracic impedance and patient
activity. Bi-directional telemetry using encoded
and encrypted radiofrequency signals allows
transmission of information to the implant-
able device from the programmer and to the
programmer from the device. This process
permits review of the programmed parameters
and stored diagnostic data and reprogramming
of device parameters to correct identified mal-
functions and/or to optimize device function
(Fig. 9.1).
It has gone far beyond simply reprogramming
pacing rate, upper and lower rate limits, mode of
pacing, electrode polarity, output and sensitivity,
but has evolved into clever mechanisms of
improving function and performance to optimize
the patient’s rest and exercise cardiac physiology
and abolish symptoms and exercise limitations.
For example, the ReplyTM DR DDDR pacemaker
(Sorin Group) which weighs 20 g and has a vol-
ume of only 8 cc offers the following: basic
parameters – mode, basic rate, rest rate, maxi-
mum tracking rate, rate hysteresis, rest AV delay,
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_9, © Springer-Verlag London 2012
9
exercise AV delay, AV delay extension; pacing
and sensing parameters – atrial and ventricular
amplitude, atrial and ventricular pulse width,
atrial and ventricular sensitivity, atrial and ven-
tricular sensing and pacing polarity; SafeR™
parameters – Pause (max), Long PR (max and
min), and AVB I switch (Rest + exercise vs. exer-
cise). Special features include: Fallback Mode
Switching (FMS), PMT protection, rate smooth-
ing, Atrial or Ventricular Autosensing, Ventricular
Autothreshold, Min. Ventricular Amplitude,
Post-Ventricular Atrial Blanking (PVAB); Atrial
arrhythmia prevention parameters – Overdriving,
Max Overdriving rate, Pause suppression, PAC
acceleration; Rate-adaptive parameters – Sensor
choice (MV + G, MV or G), Rate response mode,
physical exercise (very low, low, medium, high,
very high) (Fig. 9.2). Twenty minutes after
implantation, the pacing mode is automatically
programmed to SafeR™. The rate response
mode will be programmed to Learn, and Diagno-
stics will be ON. The latter includes Diagnostic
AIDA – Automatic Interpretation for Diagnosis
Assistance, offering Intracardiac ECG/annotated
markers, ECG triggers for mode switching, atrial/
ventricular bursts, switches in SafeRTM mode,
Histograms and counters for A and V rate, %
Pacing, atrial arrhythmias (number and time
in mode switch, bursts, Premature Atrial
Contractions (PACs), Ventricular bursts and
Premature Ventricular Contractions (PVCs),
193
194
Fig. 9.1 Interrogation of Reply™ DR pacemaker. First screen on Orchestra™ programmer displays all essential basic
programmed data (Courtesy of Sorin Group)
Pacing threshold follow-up, amplitudes of normal
and abnormal P and R waves and 24-h rate curve
(Fig. 9.3).
CRT and ICD devices are also extensively
programmable (Figs. 9.4 and 9.5).
The other major manufacturers offer a simi-
larly wide range of programmability.
Programmers
Pacing technicians or clinical physiologists use
manufacturer-specific analyzers/programmers to
adjust the pacemaker’s settings and change its
function (Figs. 6.64 and 9.6). Most are user-
friendly and individual pages display the param-
eter settings as well as offering the facility to
reprogram the device (Figs. 9.7 and 9.8) A
12-lead ECG machine is useful to document nor-
mal function of the implantable device after any
reprogramming (Fig. 9.9).
The programmer is a computer with specific
software and associated hardware modifications
9 Programmable Functions and Terminology
that provide for the highly reliable exchange of
the encrypted information and precise communi-
cation with the implantable device. The program-
mer uses bi-directional telemetry to receive the
stored information from the device and to modify
(program) the settings of the device if desired.
Usually a “wand,” attached by a wire to the pro-
grammer, is positioned on the body over the
implanted device to receive the telemetry signal
(see Fig. 8.1). The distance for radiofrequency
communication has increased from several centi-
meters to several meters (10–20 ft) and some now
communicate without a wand – wirelessly. The
longer distance telemetry is device-specific but
uses either the ISM (Industrial, Scientific and
Medical) band from 902 to 928 MHz or a subsec-
tion of the MICS (Medical and Implant and
Communications) band from 402 to 405 MHz
which allows reliable and secure signals to be
sent to and from the programmer and the device
>10 ft away. This is useful in the out-patient clinic
using a programmer, in pacing theater when pro-
gramming is required over a newly-implanted
Programmers 195

Fig. 9.2 Programmable parameters for the ReplyTM DR DDDR device with an estimated longevity of 9 years
DDDR pacemaker are wide-ranging and the diagnostic (Courtesy of Sorin Group)
capability impressive for a 20 g, 8 cc rate responsive
196
Fig. 9.3 Automatic Interpretation for Diagnosis Assistance (AIDA) showing 7 day Holter ECG recording illustrating
frequency of rate response from this Reply™ DR system (Courtesy of Sorin Group)
device, or over an open wound or at home as part
of remote monitoring (remote telemetry device).
However, when the encrypted data has to be
transmitted over a distance of miles, the commu-
nication is done via telephone lines or cell phone
technology – typically from the home monitor/
communicator to the ECG department’s pacing
clinic or data repository (see Fig. 6.38).
Programmers have integrated printers to docu-
ment the device settings (Fig. 9.10), and home
monitor/communicators and programmers can
communicate the interrogated data to a remote
printer for a hard copy presentation or be trans-
ferred to the device database or Electronic
Medical Record (EMR). The data are saved and
transferred via disc, CD ROM, USB drive,
directly by a network cable, Bluetooth, or WIFI
communication to an Internet or intranet connec-
tion and then downloaded to the Database or
EMR. The ISM and MICS radiofrequency com-
munication is used only for connecting the
implanted device to the programmer or remote
telemetry device and not for connecting the
programmer to printers, saved files, the database,
EMR or registries.
9 Programmable Functions and Terminology
It is essential to understand the meaning of the
terminology used in pacing in order to be compe-
tent in programming and troubleshooting and in
order to provide the best possible function from
today’s sophisticated devices. Figures 9.11 and 9.12
illustrate some basic pacemaker timing intervals.
Basic Pacing Terminology
Accelerometer
A type of activity sensor used in a rate-responsive
pacemaker that detects motion along a geometric
plane.
Acute-Chronic Threshold Change
The observed change in stimulation threshold from
implant to 2 months post-implant. This begins low,
trends sharply upward at 2–4 weeks, and then
decreases slightly and levels off at 8 weeks. Large
changes in acute-chronic thresholds are unusual in
modern leads and steroid-eluting leads.
 Basic Pacing Terminology
197

Fig. 9.4 Programmable parameters for the Paradym CRT 8750 biventricular device (Courtesy of Sorin Group)
 198
9

Fig. 9.5 Programmable parameters for the Paradym DR 8550 ICD (Courtesy of Sorin Group)
Programmable Functions and Terminology
Basic Pacing Terminology 199

Fig. 9.6 The Medtronic programmer being used to interrogate an implantable device in the follow-up clinic and
reprogram the device to optimize function and conserve battery life

Fig. 9.7 Parameters settings and programming screen for the Reply™ DR pacemaker – taken from the Orchestra™
programmer (Courtesy of Sorin Group)
200
Fig. 9.8 Parameters screen from the Medtronic program-
mer displaying live annotated ECG with simultaneous
intracardiac atrial and ventricular electrograms (EGM),
along with the current pacemaker and lead settings and
Fig. 9.9 A 12-lead ECG machine is ideal to see and
confirm with a “print out” that pacing is satisfactory from
one, two, or three chambers, and that any major program
changes appear to be functioning as expected
9 Programmable Functions and Terminology
“buttons” to allow further interrogation of patient data,
lead threshold testing, and trend data. From the Medtronic
Advisa DR MRI SureScan™ pacemaker (Image repro-
duced with permission of Medtronic, Inc.)
Algorithm
A specially designed form of pacemaker behavior
intended to achieve a specific goal, e.g., the AF
Suppression algorithm is a special form of dynamic
atrial overdrive pacing designed to suppress AF.
Asynchronous Pacing
Pacing mode (AOO, VOO, DOO) in which the
pacemaker paces but does not sense. This results
in properly-timed output pulses that are delivered,
irrespective of any intrinsic activity. Rarely used
clinically. Also known as “fixed-rate” pacing.
A-V Interval or Delay
Described for dual-chamber pacemakers, it is
equivalent to a native PR interval. It represents the
time (ms) between an atrial event and a paced or
sensed ventricular event. During this time, the pace-
maker discerns whether or not to pace depending
Basic Pacing Terminology 201

Fig. 9.10 Printout from Vitatron’s programmer showing data retrieved from a Clarity DDDR device
202 9 Programmable Functions and Terminology

a (i) (ii) b
LRI LRI

VP VP AP VP AP VP
VP VP
VRP

c BP
AV VA
d
AV VA AV

AP VP AP VP

AP VS AP VS

e
AV VA f
AV VA

AS VP AS VP
AS VS AS VS

Fig. 9.11 (a) (i) Lower rate interval (LRI) VP–VP is the
lowest rate at which the pacemaker will pace (base rate set-
ting) in the absence of intrinsic ventricular events. (ii)
AP–AP is the lowest rate at which the pacemaker will pace
in the absence of intrinsic atrial events. (b) Ventricular
Refractory Period (VRP) is initiated by a paced or sensed
event. During the first portion of the VRP, the Blanking
Period (BP), the pacemaker is “blind” to any activity. It is
designed to prevent oversensing the pacing stimulus or “far-
field” signals and crosstalk. (c) Atrial Pace (AP), Ventricular
Pace (VP), Ventriculo-Atrial Interval (VA), and Atrio-
Ventricular Interval (AV). (d) Atrial Pace (AP) and
Ventricular Sense (VS). (e) Atrial Sense (AS) and Ventricular
Pace (VP). (f) Atrial Sense (AS) and Ventricular Sense (VS)

upon sensing a native R wave and allows the ven- Auto Rest Rate
tricle time to fill following an atrial contraction.
A type of pacemaker response designed to mimic
the normal physiologic rate slow-down during
AV Synchrony sleep.

The mode in which there is 1:1 correspondence

between atrial and ventricular activity. Base Rate

The lower rate (bpm) at which the clinician/tech-

Automatic (Basic) Interval nician programs the pacemaker to pace. Typical
base rates are 50–75 bpm. It is also known as the
This is the stimulus-stimulus interval during reg- “lower rate limit.”
ular pacing.
Basic Pacing Terminology 203

Fig. 9.12 (a) Atrio-Ventricular Interval a

(AVI). Paced AV Interval (PAV) and PAV SAV
Sensed AV Interval (SAV). (b) Atrial
Escape Interval (VA Interval) is the
interval from a paced or sensed ventricu-
lar event to the next atrial event.
Ventricular Pace (VP). Atrial Pace (AP). AP VP AS VP
(c) Refractory Periods. Ventricular
Refractory Period (VRP) and Post- b
Ventricular Atrial Refractory Period VA interval
(PVARP) are initiated by sensed or paced
ventricular events. VRP is intended to
prevent self-inhibition such as by T-wave
sensing. PVARP is intended to prevent
sensing of retrograde P waves and the AP VP AP VP
inadvertent initiation of Pacemaker
Mediated Tachycardia. A PVARP of c
300 ms usually protects against this but AV interval
programming a long PVARP may limit
the upper rate limit. (d) Total Atrial
Refractory Period (TARP) equals the sum
of the AV interval (SAV) and PVARP.
Atrial Sense (AS), Ventricular Pace (VP), AP VP AP VP
Upper Tracking Rate (UTR). (e) Blanking
Periods. Atrial blanking (AB) (nonpro- AVI PVARP
grammable), Post-Ventricular Atrial
Blanking (PVAB), Post-Atrial Ventricular
Blanking (PAVB), Ventricular Blanking d
(VB) (nonprogrammable), Post-
Ventricular Atrial Refractory Period
(PVARP) Cross-Talk Sensing (CTS)
window: Inhibition of pacemaker output
by crosstalk may result in asystole. To
AS VP AS VP
prevent this, if a signal is sensed in the
CTS window a pacing spike is delivered SAV PV ARP
(safety pacing) TARP
UTR

e AVI PVARP

AP VP AP VP

Atrial
channel
AB PVAB
Ventricular
channel VB
PAVB CTS VRP
204
Bipolar Pacemakers
Most temporary pacing leads are bipolar with a
proximal ring electrode at approximately 1 cm
from the tip and a distal (tip) electrode. The prox-
imal electrode is the anode (positive) and the distal
electrode, the cathode (negative). Most perma-
nent pacing leads are bipolar. Generally, the pac-
ing spikes from bipolar leads are small on the
surface ECG.
Blanking Period
The “Blanking Period” is the time interval after
a pacing impulse during which the pacemaker
is insensitive to signals from the heart or from
the other channel (avoiding so-called cross-
talk).
Capture
Depolarization and resultant contraction of the
myocardium in response to a pacemaker gener-
ated electrical stimulus.
Cardiovascular Implantable Electronic
Device (CIED)
Includes pacemaker, ICD, CRT device, implant-
able loop recorder (ILR), and implantable cardio-
vascular monitor (ICM).
Coaxial Lead
Type of bipolar lead in which one conductor is
wrapped around another conductor.
Committed
A dual-chamber pacing system in which the
delivery of an atrial stimulus forces the delivery
9 Programmable Functions and Terminology
of a ventricular stimulus after a programmed AV
delay.
Cross-Talk
In DDD units, sensing of electronic events from
one channel by the other channel, e.g., an atrial
stimulus sensed by the ventricular channel result-
ing in dangerous inhibition of the ventricular
impulse. This is avoided by programming the
blanking period.
Demand Pacing (Inhibited)
Unlike the fixed-rate mode, spontaneous car-
diac activity is sensed and inhibits the pace-
maker, which delivers a stimulus only after a
pre-set interval if no further impulse is
sensed.
DF-1
High-voltage lead connection of ICD lead (defi-
brillation coil) into port on the header of the ICD.
DF-4/SJ4
New design of ICD lead which incorporates
four conductors into a quadpole, in-line con-
nection replacing the defibrillation coil DF-1,
and pace-sense IS-1 connections with the “DF-
4” connection. The ICD header has one port to
accommodate the dual-coil lead instead of three
and is thus smaller. The lead is 7–10 cm shorter
because no “yoke” is required to bring the IS-1
and DF-1 connections to a single lead body.
This development has two advantages: a more
streamlined header connection for these devices
and simplification of connection to the device
reducing pin-to-port mismatch, e.g., SJ4 Durata
lead (St. Jude Medical), ENDOTAK RELIANCE
4-SITE (Boston Scientific).
Basic Pacing Terminology
Entrance Block
Entrance block represents the failure of a pace-
maker to sense cardiac events. This may be
because the sensitivity of the pacemaker is too
low, the signals are of too low an amplitude, or
the electrode is fractured.
Escape Interval
The escape interval is the interval between a
spontaneous cardiac impulse which is sensed
and the next pacing stimulus. This is usually the
same as the automatic pacing interval unless the
pacemaker is programmed to hysteresis mode, in
which case the escape interval is longer than the
automatic interval.
Exit Block
Exit block occurs when excessive tissue growth
between the tip of the lead and the endocardium
increases the threshold to pace sufficiently to cause
failure to capture without lead displacement.
Filar
A strand of wire used in the conductor in a lead.
Some leads are unifilar (one strand), while others
are multifilar (many strands).
Fixed-Rate Pacing
Regular constant pacing of the heart at a fixed
rate which is independent and not affected by
spontaneous cardiac activity.
Housekeeping Current
The amount of energy a device consumes even
when it is not in use (including preimplantation).
205
Hysteresis
The takeover rate of the pacemaker is lower than
the pacing rate, e.g., a pacemaker with a pacing
rate of 70 bpm and hysteresis mode set at 60 bpm
will not start pacing until the patient’s heart rate
falls below 60 bpm when the pacing rate jumps to
70 bpm.
It is also defined as an intentionally prolonged
pulse interval in order to allow the generation of
a spontaneous-intrinsic electrical depolarization
event.
Intracardiac Electrogram
ECG taken from an electrode placed within the
heart. It contrasts with a surface ECG, which
records signals from the skin’s surface. Pacemakers
deliver intracardiac electrograms to the program-
mer. The intracardiac electrogram is what the
pacemaker “sees” and may be more useful than a
surface ECG for assessing pacing behavior.
IS-1
Abbreviation for International Standard 1, a lead
and connector standardized size that accommo-
dates leads with a 3.2 mm diameter pin. IS-1
leads and pacemaker connectors are the most
common used today.
IS-4
International standard in-line quadripole elec-
trode for use in low-voltage applications, e.g.,
quadripole LV lead, e.g., Quartet™ LV lead (St.
Jude Medical).
Lead Impedance
The lead impedance reflects the electrical resis-
tance of the lead and its tip-tissue interface. The
206
lead impedance is also influenced by the size of
the electrode tip; the larger the tip, the lower the
impedance. The lower the impedance/resistance
in the lead results in greater current flow and a
greater drain on the battery power. Thus low-
impedance leads result in early battery depletion.
Average lead impedance is 550 W. Conversely,
the higher the resistance/impedance in the lead,
the lower the current flow and less of a drain
on the battery of the generator. An electrode
whose tip has a small geometrical surface area,
enables the current applied to the myocardium to
be concentrated (high current density); in turn a
smaller current will be required to gain capture
and hence battery drain will be minimized. Newer
electrodes have smaller electrode tips 1.2–5 mm2.
Magnet Rate
Application of a magnet over pacemakers con-
verts them into fixed rate mode at a predictable
rate which depends on battery life. The response
depends on the type of pacemaker. This magnet-
testing is used to test battery life in the follow-up
clinic and to test satisfactory pacing when there is
competition at a slower demand rate. For exam-
ple, if a patient’s heart rate is 75 bpm and the
demand rate is 60 bpm, the pacemaker can be
made to pace at a set rate, e.g., 100 bpm (defined
by manufacturer) by application of a magnet over
the generator.
Maximum Tracking Rate (MTR)
The rate over which the pacemaker will not allow
the ventricles to be paced in response to atrial
activity.
Minute Ventilation
A sensor system used in rate-adaptive pace-
makers which detects respiration rates (based on
chest movements) and adjusts the pacing rate in
response to sensed need.
9 Programmable Functions and Terminology
Missing
This term is used to describe failure of the atrial
or ventricular lead to capture or pace the atrium or
ventricle respectively. There are multiple causes
including lead displacement, too low an output
voltage setting, and exit block. With a temporary
pacemaker, simply increasing the output voltage
and/or pulse width may help in the short-term, but
repositioning is likely to be necessary. With a per-
manent system, the cause must be sought. Lead
displacement will require repositioning of the
lead. Exit block may be overcome by reprogram-
ming the pacemaker to a higher output, or if this
is not possible by the use of oral prednisolone
therapy for 2–3 weeks. A primary lead problem
such as lead fracture or insulation break necessi-
tates explantation and implantation of a new
system.
Mode
Indicates pacemaker’s capabilities, e.g., fixed rate
or demand; atrial, ventricular, or dual-chamber
system.
Mode Switching
Special feature of many dual-chamber pacemak-
ers which allows the device to change modes in
the presence of rapid, intrinsic atrial activity,
e.g., AF. Mode switching “switches off” the
atrial channel of a dual-chamber pacemaker dur-
ing periods of very high, intrinsic atrial activity.
Also known as Automatic Mode Switching
(AMS).
Multisite Pacing
Device-based treatment which involves pacing
and sensing both the RA and LA (multisite atrial
pacing), the RV and LV (biventricular pacing), or
RV apical/RV outflow tract pacing (multisite RV
pacing).
Basic Pacing Terminology
Myocardial Lead
A pacing lead designed to be attached to the epi-
cardium, either by screwing into the heart’s exte-
rior or suturing on a patch – usually requiring
thoracotomy.
Myopotential Inhibition
Electrical myopotentials from skeletal muscle
close to the pacemaker (usually from pectoralis
major) may be sensed by the sensing circuit of
unipolar pacemakers during physical activity
involving use of this ipsilateral muscle.
Pacemaker output will be inhibited if the pace-
maker is programmed to a demand mode.
Reprogramming to bipolar sensing or a fixed rate
or triggered pacing mode will solve the problem.
Reducing the pacemaker’s sensitivity is rarely
effective.
Non-committed
This term describes a dual-chamber pacemaker
in which the sensing of ventricular activity dur-
ing the AV interval can inhibit the delivery of a
ventricular impulse.
Optimal AV Delay
The optimal AV delay in a dual-chamber pace-
maker refers to the AV interval that can lead to
closure of the mitral valve due to elevation of iso-
volumic pressure after atrial contraction and
resulting in maximizing the stroke volume.
Output Pulse
The electrical energy generated by the pace-
maker and delivered to the heart. This output
pulse is defined by pulse amplitude (voltage) and
pulse duration (length of time, measured in
milliseconds).
207
Oversensing
Inhibition of the pacemaker by inappropriate
sensing of myopotential signals (myopotential
inhibition), by nonphysiological electromagnetic
interference, or of “T” waves is often referred to
as “oversensing.” Reducing the pacemaker’s sen-
sitivity using the appropriate external program-
mer is the first option.
Pacemaker-Mediated
Tachycardia (PMT)
A rapid ventricular rate facilitated by the pres-
ence of a pacemaker. A PMT is not caused by
the device, but facilitated by the retrograde
conduction of atrial activity with subsequent
ventricular pacing. Once a re-entry tachycardia
gets started, the pacemaker acts like a re-entry
path.
Pacemaker Wenckebach
A type of upper rate response in which the AV delay
gets longer and longer until one of the P-waves falls
into the PVARP and is not followed by a ventricular
event. Also called pseudo-Wenckebach.
Pacing Interval
The amount of time between paced events (ms),
e.g., when a pacemaker is programmed to pace at
60 bpm the pacing interval is 1,000 ms (i.e.,
60,000/number of ms).
Pacing System Analyzer (PSA)
Small, handheld device that can be used to gather
intra-operative measurements of the pacing system.
These are being replaced by the device programmer/
analyzer available from the specific device manufac-
turer which are made available in the pacing
theater.
208
Pacing Threshold
Minimum amount of energy required to reli-
ably capture (cause depolarization of) the
heart. Also called stimulation or capture
threshold.
PMT Termination Algorithm
A special feature to help prevent or interrupt
PMTs.
Post-Ventricular Atrial Refractory
Period (PVARP)
PVARP is intended primarily to prevent sensing
of retrograde P waves. Initiated by sensed or
paced ventricular events.
Programmed Standby Rate
Heart rate at which pacing will commence if
native heart rate falls below this rate.
Pulse Amplitude
A programmable pacemaker setting which
defines the output pulse of the device. It is set in
volts. Increasing pulse amplitude increases out-
put pulse energy.
Pulse Interval
The total time of the AV and VA intervals. The
time between pulses (ms).
Pulse Width/Duration
The duration of the pacing stimulus (0.5–1.0 ms)
can be altered by the external programmer for
9 Programmable Functions and Terminology
permanent pacemakers and by adjusting the
dial/knob on a temporary pacing box. The
broader pulse width setting may aid atrial/ven-
tricular capture when narrower pulse widths
fail, but as a consequence will lead to greater
current drain and shorter battery life of the
generator.
Relative Threshold
The relative threshold is the minimum percentage
of total available voltage required to pace the
heart. Thus a relative threshold of 20% with max-
imum unit voltage of 5.0 V is 1.0 V.
Rate Drop Response
A special feature in some dual-chamber pacemak-
ers which may be useful for patients with neurocar-
diogenic syncope. The device is programmed to a
high hysteresis rate, so that pacing is mainly inhib-
ited; should a syncopal episode occur and the
patient’s intrinsic rate fall markedly, pacing com-
mences at a higher-than-normal rate to help com-
pensate for the temporarily diminished cardiac
output.
Rate-Responsive Pacing
(Rate Adaptive Pacing)
These pacemakers allow the pacing rate to
increase and decrease in response to certain phys-
iological stimuli such as vibration, respiration,
and QT interval. Pacemakers may be single-
chamber (AAIR/VVIR) or dual-chamber rate
responsive (DDDR) systems.
Rate-Responsive AV Delay (RRAVD)
A timing cycle in dual-chamber pacemakers that
automatically shortens the AV delay in response to
higher atrial rates. Often used with rate-responsive
Basic Pacing Terminology
systems, RRAVD can also be useful for patients
with high intrinsic atrial rates.
Reed Switch
A small reed-like metal component within the
pacemaker which can close to create an electrical
circuit that causes the pacemaker to revert to
magnet mode.
Refractory Period
A defined period of time (ms) during which the
heart will not contract. A refractory period may
be physiological or it may be part of a pacemaker
timing cycle. This is further subdivided into abso-
lute refractory period, when a contraction is
impossible, and a relative refractory period, when
there is limited response.
Safety Margin
An increment used to program output settings for
a pacemaker in which the pacing threshold is
increased. A safety margin ensures capture, even
with changes in pacing threshold over the course
of the day or longer. Commonly used safety mar-
gins involve finding the pacing threshold and dou-
bling the voltage setting or tripling the pulse
width.
Sensing
Dependent on the amplitude, slew rate, and sig-
nal frequency, it describes the pacemaker’s abil-
ity to recognize a native electrical signal.
Sensitivity
The minimum intracardiac signaling required by
the pacemaker to initiate a pacemaker response.
209
Sequential Pacing
Pacing of the atrium followed at a pre-set interval by
pacing of the ventricle allows “physiological” pacing.
Slew Rate
This represents the rate of rise of the endocardial
potential (dV/dt). Those with a low slew rate may
not be sensed by the pacemaker.
Strength-Duration Curve
A chart which plots the various voltage settings
(pulse amplitude) in relationship to pulse width
settings (ms) that capture the heart.
Synchronous Pacing
A mode of pacing in which the pacemaker times its
output pulses with the heart’s own intrinsic events.
Threshold
Minimum quantity, of either amplitude (milliam-
peres, volts), pulse duration (ms), charge (mcou-
lombs), or energy (mjoules) produced by the
pacemaker that persistently produces an action
potential and myocardial contraction.
Total Atrial Refractory Period (TARP)
Total atrial refractory period or the PVARP + AV delay.
TARP is not directly programmable, but can be adjusted
by modifying the PVARP or AV delay setting.
Triggered Pacing
Triggered pacing occurs when a sensed spontane-
ous R wave results in the immediate delivery of a
210
pacing stimulus into the R wave. The heart is obvi-
ously refractory and is not paced. Triggered pace-
makers have a built-in refractory period to protect
against ventricular tachycardia should fast electrical
interference be sensed. It used to be chosen to avoid
myopotential inhibition and when a TPM was being
used to cover a failing permanent pacemaker. In the
latter situation, stimuli from the failing unit will
trigger the external pacemaker to fire an impulse in
the absolute refractory period (assuming the inter-
nal unit’s impulse depolarized the heart) or alterna-
tively pace the heart if the permanent pacemaker’s
impulse fails to depolarize the myocardium.
Undersensing
A common sensing problem in pacing in which
the pacemaker inappropriately fails to sense sig-
nals it ought to see. This causes the pacemaker to
pace even when it should be inhibited. Under-
sensing typically leads to overpacing and shows
on the ECG in the form of intrinsic events along
with inappropriate, paced activity.
Unipolar Pacing
Here, the pacemaker “can” behaves as the anode
and the electrode tip as the cathode. Pacing spikes
are usually large on the surface ECG.
Upper Rate Behavior
The way in which a dual-chamber pacemaker
will perform when trying to deal with a high
intrinsic atrial rate. If the intrinsic atrial rate
exceeds the MTR and the TARP value, then pace-
maker “multiblock” will occur. If the atrial rate
exceeds the MTR but not the TARP value, then
pacemaker Wenckebach will occur. Pacemaker
Wenckebach is preferred over “multiblock.”
Ventriculoatrial (VA) Interval
Described for dual-chamber pacemakers.
Represents the time (ms) between a ventricular
event and a paced atrial event.
9 Programmable Functions and Terminology
Ventricular Refractory Period
VRP is intended to prevent self-inhibition such as
sensing of T-waves. Initiated by sensed or paced
ventricular events.
Voltage Threshold
Minimum voltage which will pace the heart.
VS-1
Voluntary Standard, an older standard for lead
and pacemaker connectors. Two main varia-
tions on VS-1 exist: VS-1A (for leads without
sealing rings) and VS-1B for leads with sealing
rings.
Advanced Pacemaker Function
and Terminology
Advanced Hysteresis Response
Manages special rate situations including sudden
rate drop. Available in many pacemakers now,
e.g., Identity ADx™ (St. Jude Medical).
Advanced Sensor Technology
Combining sensors such as accelerometer and
minute ventilation sensors adapt the pacing rate
to the patient’s changing metabolic demand. The
cardiologist can choose either one or other sensor
or a unique blend of the two.
AF Suppression Algorithm
Program in pacemaker designed to prevent onset
of AF.
AF Suppression Histogram
Allows evaluation of the success of the AF sup-
pression algorithm.
Advanced Pacemaker Function and Terminology
AIDA Diagnostics
Automatic Interpretation for Diagnosis Assistance
is a feature of devices from the Sorin Group. The
diagnostic aids may include Automatic analysis of
stored data providing advice on device manage-
ment regarding basic functioning, arrhythmia
management, and AV conduction; Trending, e.g.,
summary screen with 6 month trends of heart rate,
percentage pacing activity, and AF burden; Sensing
monitor to provide autosensing histograms of P
and R wave amplitudes; Lead monitor for lead
impedance and continuity curves; Arrhythmia
diary provides A and V arrhythmia episode distri-
bution and therapy analysis per zone; AV conduc-
tion analysis to include type of block, circadian, or
activity distribution and progression over time;
Arrhythmia episode documentation for multiple
episodes using EGM and Markers on V and A
arrhythmias as well as significant other events,
e.g., mode switch, AV block switch, lead imped-
ance rise, and PhD which provides monitoring of
respiratory and activity status, with day-by-day
analysis over the previous 6 months. All of these
are available among the many other programma-
ble features in the Paradym DR 8550 ICD device.
Arrhythmia Management
Mode switching from DDD to VVI or VVIR at
the onset of atrial arrhythmias such as atrial
fibrillation can be programmed to happen auto-
matically. Each atrial event is assessed individu-
ally, providing beat-to-beat mode switching on
AF and PACs to keep the ventricular rate as stable
as possible and minimize palpitations. When AF
ends, the pacemaker immediately resynchronizes
atrium and ventricle to prevent retrograde con-
duction and pacemaker syndrome. Some devices
have an Atrial Flutter Response (AFR) which
allows immediate reaction to rapid atrial rates. A
programmable (130–230 ppm) trigger rate pre-
vents atrial tracking above the trigger rate.
Arrhythmia Logbook
Some pacemakers automatically store events in a
logbook, each with a unique event number, date/
211
time, onset rate, maximum rate, and storage
trigger.
AT/AF Diagnostic Suite
AT/AF burden trend, AT/AF stored EGM
Trigger, AT/AF Histogram, and AT/AF Episode
Log.
Auto-Initialization
A feature of Biotronik’s Effecta series. This
allows automatic activation of a series of func-
tions after lead connection. A&V Capture Control,
Autosensing®, Auto Lead Check, Statistics and
IEGM recordings are functions that are activated
within 10 min.
Autolifestyle/Daily Learning™
This was a feature of the Insignia Ultra (Guidant)
and now of the Altrua™ series (Boston
Scientific) and optimizes the MV blended sen-
sor. At implant, Autolifestyle automatically
programs initial response factors at a very con-
servative level based on age. After implantation
it automatically adjusts the MV response factor
based on patient exertion level over several
weeks – so called coarse adjustment. The fea-
ture then automatically makes minor adjust-
ments to MV and accelerometer response factors
as needed based on patient exertion – “fine
adjustment.”
The Clarity™ rate-adaptive pacemakers (Vitatron)
combined the physiological QT-interval sensor
with a fast-responding activity sensor to provide a
rate that closely resembles that of a healthy sinus
node. Daily learning™ of the sensors continu-
ously adapts rate response to individual needs.
Children and young, more active individuals reach
higher sinus rates during exercise and their sinus
variations from one beat to the next are larger.
Clarity’s unique combination of tracking these
higher sinus rates while distinguishing sinus
rhythm from atrial arrhythmia over the entire rate
range allows these younger patients to be normally
active.
212
Automatic Capture
This function – a feature in Boston Scientific’s
Altrua™ and Guidant’s Insignia Ultra™ pacing
system – automatically adjusts pacing output to
maintain ventricular capture and maintains out-
put voltage at 0.5 V above capture threshold. The
pacemaker confirms capture on a beat-to-beat
basis, checks threshold every 21 h when loss of
capture is detected during beat-to-beat analysis,
and provides safety backup pulses as needed to
maintain ventricular capture.
A similar feature called Active Capture Control
(ACC) is available in the Talos SLR (Biotronik)
and permits energy efficient therapy and maxi-
mizes the generator’s longevity. Medtronic pace-
makers feature Atrial Capture Management
(ACM) and Ventricular Capture Management
(VCM) which provides complete long-term thre-
shold management automatically and ensures
pacing outputs remain at safe levels by adapting
programmed outputs to maximize longevity.
Automatic Post-Ventricular Atrial
Refractory Period Adjustment
The promotion of AV synchrony with automatic
PVARP adjustments reduces the likelihood of
palpitations and protects against pacemaker-
mediated tachycardia (PMT).
Auto Sense
Auto Sense is designed to automatically adjust the
pacemaker’s sensitivity to cardiac signal changes
without the cardiologist’s intervention. Sensitivity
is adjusted based on the measured amplitude of
previously sensed events, the type of cardiac cycle
(paced or sensed), and a measurement of the cur-
rent myopotential/environmental noise level.
Automatic AV Search Hysteresis
Designed to reduce unnecessary RV pacing with-
out dropping beats, e.g., Dplus (Sorin Group)
9 Programmable Functions and Terminology
Conducted Follow-Up
Automatic interrogation of stored data, two-chan-
nel, real-time intracardiac (IC) ECG with markers
can be helpful in troubleshooting. An indication
of battery life is always available at follow-up.
Diagnostic Memory Functions
Event counters, histograms, trends, and sensor
simulation are available on pacemakers such as
Biotronik’s Axios DR pacemaker. Diagnostic
Observations™ available in Vitatron’s Clarity™
pacemaker alerts to anomalies recorded in the
diagnostics, e.g., rhythm disturbances, and rec-
ommends appropriate therapy adjustments. In
addition Selected Event Recording allows the
causes and details of symptom-related events to
be captured for analysis and diagnosis.
(IRSplus) Intrinsic Rhythm Support
IRSplus is a featured algorithm of Biotronik’s
Effecta pacemakers which automatically pro-
motes intrinsic conduction with a full hysteresis
package. After 180 consecutive pacing cycles,
the AV scan hysteresis searches for intrinsic con-
duction by prolonging the AV delay to 400 ms.
Managed Ventricular Pacing® (MVP®)
Program to allow best pacing therapy available to
minimize RV pacing – feature of Medtronic’s
Adapta® and Ensura™ pacemakers.
Other devices offer multiple programming
options to provide increased flexibility to help
minimize unnecessary RV pacing. For example,
the Altrua™ 60 series (Boston Scientific) offer
a fixed AV Delay of 10–400 ms, a Dynamic AV
Delay extendable up to 400 ms, and AV Search
Hysteresis (AVSH) extendable to 400 ms maxi-
mum, allowing more time for intrinsic ventric-
ular conduction to occur after an atrial event.
Medtronic’s Versa™ and Sensia™ offer long
programmable AVDs and “AVD extension.”
Advanced Pacemaker Function and Terminology
SafeR™
A pacing algorithm from the Sorin Group that
maximizes intrinsic conduction by ensuring DDD
pacing when needed for all types of AV block,
provides AAI pacing while continuously monitor-
ing AV conduction and switch back to AAI mode
whenever possible. For example, if 7 long PR
intervals are observed, DDD pacing is initiated
(AVB I criteria); for 3 blocked P waves out of 12,
DDD pacing will be initiated (AVB II criteria); and
for 2 consecutive blocked P waves, again DDD
pacing will be initiated (AVB III criteria).
Adjustments can be made to cope with normal rest
and exercise such as the ability to suppress the
AVB I criteria at rest and to rapidly switch to DDD
during exercise if required. Similarly, it is possible
to reduce nocturnal pacing by allowing a long PR
and to test for AV conduction each morning if in
DDD.
Stored Intracardiac Electrograms
This useful feature helps in troubleshooting pace-
maker problems, such as an insight into arrhyth-
mia origination. Some allow patients to trigger
their own ICECG for event recording. In some
pacemakers, stored electrograms are initiated by
any of the following programmable triggers:
patient-applied magnet, Atrial Tachy Response
(ATR) mode switch, clinician-defined ventricular,
and/or atrial tachycardia and nonsustained tachy-
cardia (>3 PVCs), sudden bradycardia response,
and PMT.
Sudden Bradycardia Response (SBR)
with Minute Ventilation (MV) Offset
SBR is designed to respond to sudden decreases
in intrinsic atrial rates by applying dual-chamber
pacing at an elevated rate. MV Offset provides
the ability to inhibit SBR therapy to allow appli-
cation only when a patient’s minute ventilation
meets or exceeds a programmed level. This fea-
ture is present in the Altrua™ 50 and Altrua™ 60
series (Boston Scientific).
213
Support of Intrinsic Rhythm
AV and rate hysteresis can optimize pacing
function.
Triggered and Continuous
Overdrive Pacing
A broad range of preventive pacing algorithms to
stop AF from starting by recognizing the onset
mechanism in individual patients. They include
Post-Exercise Response, PAC Suppression, Post-
PAC Response, Post-AF Response, and continu-
ous overdrive pacing. These features were
available in Vitatron’s T-series, Prevent AF, and
Selection 9000 AF 3.0, and have been incorpo-
rated into the more recent models.
Ventricular Safety Pacing
Ventricular safety pacing (VSP) is an algorithm
used to prevent crosstalk inhibition and ventric-
ular capture during the vulnerable period.
Crosstalk is the inappropriate detection of a
spontaneous or pacemaker-generated event in
one channel by the other channel, which can
cause the inhibition of the second channel’s out-
put. There are two functions designed to prevent
crosstalk inhibition. One is the ventricular
blanking period that coincides with the atrial
stimulus and prevents the detection of the atrial
spike or activation that coincides with the atrial
stimulus. The second – VSP – delivers short-
coupled ventricular stimuli after atrial pacing
when sensing any activation in the ventricular
lead after the end of the ventricular blanking
period (see Chap. 21).
Ventricular Rate Regulation (VRR)
or Ventricular Rate Stabilization (VRS)
This feature is designed to regularize the ventric-
ular response to conducted atrial arrhythmias
using a historic weighted average method of
establishing the VRR pacing rate.
 Precautions After Permanent
Pacemaker Implantation
Patients often ask about what precautions they
should take to avoid damaging or affecting the
function of their pacemaker. The commonest
issues discussed by patients are set out below and
are most often seen with unipolar systems.
Table 10.1 lists sources of electromagnetic inter-
ference and the possible effects on pacemakers.
Electromagnetic Interference (EMI)
External EMI can cause reprogramming or dam-
age to the pacemaker circuitry. It may also cause
inhibition or a switch to the fixed rate mode.
Pacemakers are well shielded and protected by
appropriate filters and so generally problems are
an unusual occurrence. Although patients can be
reassured that the risks of EMI are small, if they
feel dizzy in close proximity to electrical equip-
ment, they should walk away from the device.
Possible sources of EMI include radio transmit-
ters, motor car engines, microwave ovens, and
electric motors inside some household equip-
ment. Theft detection devices in shops and stores,
metal/weapon detection devices in security set-
tings, for example, at airports, and radar can also
cause interference.
CB and “HAM” radios, electric drills, electric
blankets and shavers, heating pads, metal detec-
tors, microwave ovens, TV transmitters, and
remote TV controls have not been shown to dam-
age pulse generators, change pacing rates, or
totally inhibit pacemaker output. Although they
have the potential to cause occasional interference
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_10, © Springer-Verlag London 2012
10
and perhaps inhibit a single beat, this does not
appear to be of practical importance.
Bipolar sensing/pacing is essential if a patient’s
work is likely to bring the individual into contact
with strong sources of EMI such as internal com-
bustion engines, radar, and arc welding. Arc
welders have to take special precautions, such as
avoid working in wet areas, avoid high currents
(<400 A), and should wear nonconductive gloves.
Connecting the ground clamp to the metal close
to the welding point is advisable.
Magnets
Magnets held over a pacemaker may put the
device into fixed-rate mode by activation of its
reed-switch. Inappropriate sensing by the pace-
maker due to noise artifact created by electric
cautery will be avoided by magnet application.
Removal of the magnet is all that is required to
restore normal function.
Magnets held over ICDs do not inhibit sensing
function but do inhibit delivery of any antitachy-
cardia therapy, such as ATP or high-energy
defibrillation. Magnet application may therefore
be used to prevent inappropriate ICD therapies
during use of electrocautery that may produce
noise artifact sensed by the lead as VT or VF.
Such a patient should be monitored, so that appro-
priate, programmed ICD therapy can be delivered
if required by removing the magnet. In the UK,
the Medicines and Healthcare products Regulatory
Agency (MHRA) suggested that local policies
215
216 10 Precautions After Permanent Pacemaker Implantation

Table 10.1 Sources of electromagnetic interference and their possible effects on pacemakers
Item Safe Precaution Avoid
Personal items Electric blankets Cell phones Body fat measuring scales
Electric toothbrushes Keep 6″ from device (handheld)
Electric razors Keep 12″ from device Magnetic mattresses or
Hair dryers if transmits >3 W chairs
Heating pads Hold phone to ear on Electrolysis (hair removal)
Pagers opposite side of body from
Patient alert devices device
Personal digital assistants Do not carry phone in breast
(PDAs unless used as cell phones) pocket within 6″ of device
Radio-controlled clocks/ Cordless phones
watches Safe if not placed directly
Tattoos over device
Thermolysis (hair removal) Handheld massagers
Safe if not placed directly
over device
Kitchen, Air purifiers
tabletop, and Blenders
household items Clothes dryers
Convection ovens
Electric can openers/knives
Electric ovens and stoves
Food processors
Gas ovens and stoves
Microwave ovens
Portable space heaters
Sewing machines
Toasters
Vacuum cleaners
Washing machines
Office, shop, Copy machines Arc welding equipment Jackhammers
and yard Electric invisible fences Keep 24″ from device
equipment Fax machines Running motors/alternators
Personal computers especially those found in
vehicles and high-power
generators
Keep 24″ from device
Avoid leaning over running
motors/
alternators of a running vehicle
For the following items, keep
12″ from device
Battery-powered cordless
power tools
Chainsaws
Corded drills/power tools
Lawn mowers/hedge
clippers
Leaf blowers
Shop tools (drills, table
saws)
Snowblowers
Magnetic Resonance Imaging (MRI) 217

Table 10.1 (continued)

Item Safe Precaution Avoid
Entertainment AM/FM radios Bingo game magnetic wands
items CD/DVD players Keep 6″ from device
Hot tubs/whirlpool baths CB and police radio antennas
Laser tag games Keep 24″ from device
Multimedia players Slot machines
e.g., iPods/MP3 players Keep 12″ from device
Remote controls (TV, garage Stereo speakers
door, stereo, camera/video Keep 12″ from device
equipment) SCUBA diving
Tanning beds
TVs and VCRs
Video games
Travel/ Amusement parks/roller Security systems (airports, jails, Stun guns
environment coasters courthouses etc.)
Walk through security
archways normally
Tell security personnel that
you have a device and show
Medical Device ID card
Security wand should not be
held over device for >30s;
ask for hand-search
Theft detection systems
(store/library entrances)
Walk through theft detection
systems at a normal pace
Do not lean against or linger
near these systems
Magnetic fields
Transformers
High voltage lines
TV/radio towers
Radiofrequency transmitters
Residential power generators
Dental/medical CT scans Radiation therapy, MRI scansa
tests and Dental drills/cleaning equipment electrocautery used in surgery, Diathermy
procedures Diagnostic X-rays TENS unit
ECG Contact doctor in charge
Mammography (tell technician so Contact pacemaker company
that the device is not compressed) for further information
Ultrasound Cardioversion
Defibrillation
Lithotripsy
© Boston Scientific; http://www.bostonscientific.com/templatedata
a
The Advisa DR MRI™ Surescan® device (Medtronic Ltd.) is MRI safe

should be put in place to allow ICDs to be deacti-
vated prior to routine surgery and reactivated
afterward and that “magnet deactivation” should
only be used in an emergency situation. Detailed
advice can be found on www.mhra.gov.uk.
Magnetic Resonance Imaging (MRI)
In general, pacemaker patients should not
undergo MRI scanning and only in exceptional
circumstances after consulting the pacemaker
218
manufacturer. The appropriate device’s sensor
and magnet responses should then be turned off
with the external programmer in order to try
and avoid inappropriate reversion to fixed-rate
mode or to fast rates which may be potentially
dangerous. The latter may be due to the pulsing
radiofrequency field owing to the antenna effect
Fig. 10.1 The MRI-conditional safe Advisa DR MRI™
Surescan® pacemaker and leads from Medtronic Ltd.
(Image reproduced with permission of Medtronic, Inc.)
Fig. 10.2 The MRI-conditional safe electrode is
identifiable by X-ray. A radiopaque helix in the proximal
end of the CapSureFix MRI™ SureScan™ Pacing Lead
10 Precautions After Permanent Pacemaker Implantation
of the electrode system. MRI at 1.5 T can cause
major temperature rise at the tissue-electrode
interface, tachycardia, and even ventricular
arrhythmias.
In patients who definitely need MRI, it might
be cautiously undertaken as long as the pace-
maker is checked before and after MRI and
dependency status checked. In those who are not
dependent, the pacemaker should be turned off if
possible and a low magnetic field used (0.5 T).
Monitoring of the patient is essential.
Recently, Medtronic Ltd. released the
EnRhythm DR MRI™ SureScan® and Advisa
DR MRI™ Surescan® pacing system which are
MRI “conditional safe” (Fig. 10.1) and an MRI-
safe lead – the CapSureFix MRI™ Lead. The lat-
ter is identifiable on X-ray (Fig. 10.2). To safely
scan patients with these devices several condi-
tions must be satisfied. These include:
• The system has been implanted for >6 weeks
• The device was implanted in the pectoral
region
• No additional active implantable device(s) are
present
• Device and leads are labeled “MR Conditional”
• Leads are electrically intact (impedance
200–1,500 Ω)
(Model 5086) identifies the lead as MRI compatible (blue
arrow). The radiopaque code (green arrow) identifies the
pacemaker
Radiation
• Abandoned or additional leads or wires are
not present
• No lead extenders or adaptors are present
• Capture thresholds do not exceed 2 V at 0.4 ms
• SureScan® is programmed ON before the scan
and programmed OFF after the scan
Biotronik have released the Estella series of
pacemakers which are MR “conditional safe”
(Biotronik ProMRI®) and need to be used with
MRI conditional safe leads, e.g., Safio S and
Solia.
St. Jude Medical Inc. have produced the Accent
MRI™ pacemaker and Tendril MRI™ lead which
have been approved as MR-Conditional in Europe
and released for use in India and the Sorin Group
are developing the Reply MR-conditional pace-
maker and Filtrea pacing lead.
Boston Scientific Corporation have recently
released the Ingenio™ MRI and Advantio™
MRI rate-responsive pacemakers (employing
RightRate™ MV sensor and ImageReady™ tech-
nology). When used in conjunction with Fineline
II leads, they are safe for use in patients requiring
MRI scanning by programming the device into
MRI Protection Mode.
Diathermy
Short-wave or microwave diathermy uses high-
frequency, high-intensity signals, and may perma-
nently damage the generator, cause inappropriate
inhibition, or cause ventricular fibrillation by trig-
gering ventricular pacing due to atrial oversens-
ing. Surgeons should ideally use a bipolar system.
If a unipolar diathermy is used, the output should
be kept low, the active electrode kept >2–3 in.
from the pacemaker, and the indifferent electrode
kept as far away as possible so that its dipole is at
right angles to the pacing system.
The heart rhythm should be monitored so that
diathermy can be stopped if prolonged inhibition
occurs. Interference can be avoided during sur-
gery by reprogramming the generator to a fixed
rate (DOO or VOO) mode at the start of the oper-
ation and reprogrammed to a demand mode at the
end. Bipolar pacing systems may be less suscep-
tible to inhibition.
219
Besides inhibition, resetting/reprogramming
or damage of/to the pacemaker, upper-rate pacing
(in Minute Ventilation rate-responsive systems),
and internal burns and scarring as a result of the
current induced in the lead may occur. The latter
may lead to a higher pacing threshold or exit
block.
The pacemaker program and function should
be checked postoperatively.
Radiofrequency Ablation (RF)
Most pacemakers are not affected by RF catheter
ablation of intracardiac tissue, but it is usually
worth checking the pacemaker’s function and
program settings after the procedure. Both sens-
ing and pacing failure have been reported and
care should be taken to establish whether the
patient is pacemaker dependent prior to the pro-
cedure and the program adjusted accordingly to
allow for potential problems that may rarely
occur.
Generally, the rate response function should be
turned off and the RF applications should be as brief
as possible and remote from the pacing lead tip.
Radiation
Diagnostic X-rays do not affect pacemaker func-
tion but radiotherapy may damage the circuitry. It
probably causes damage to the thin oxide layers
and transistors by accumulation of positive charge
inside the circuitry leading to failure of various
battery components or accelerated battery deple-
tion. Changes in sensing capability, failure of
telemetry function, runaway function, and total
shutdown may occur. Positioning the radiation
field at an angle oblique to the pacemaker in order
to minimize the amount of radiation delivered at
the pacemaker site is advisable. A total accumu-
lated dosage limit of 2 rad should be estimated
and additional shielding of the pacemaker with a
1 cm margin may be required. If it cannot be
shielded because it is in the path of the desired
beam, then the pacemaker should be resited.
Certainly, the device’s function should be checked
220
after each therapy session and the pacemaker
replaced if found to be faulty.
Cellular Phones
Mobile phones should be kept at least 6 in. away
from the pacemaker and the opposite ear should
be used. There is a possibility that transient inter-
ference with pacemaker function could occur
when using a mobile phone held close to the
pacemaker. A study of 980 patients found that
ventricular tracking of signals sensed on the atrial
channel, noise reversion, and inhibition of ven-
tricular output were the most common types of
interference – clinically significant in 6.6% of
patients. Interference is more common in dual
chamber (25.3%) compared to single chamber
(6.6%) systems and in digital telephones (24%)
compared to analog ones (3%).
Electronic Article Surveillance
Systems (EAS)/Metal Detectors
Such devices which use RF scanners or magnetic
sensors could transiently inhibit or reprogram a
pacemaker, but this is a rare occurrence. Pacemaker-
dependent patients should be told not to linger
near such systems but that merely passing through
them should not cause a problem. Handheld metal
detectors should not be held over the pacemaker
and an alternative body search should be requested
by pacemaker-dependent individuals.
Cardioversion/Defibrillation
In order to prevent damage to the pacemaker, the
paddles should be kept >6 in. from the pacemaker.
Positioning the paddles at right angles to the pacing
system should minimize the current induced in the
lead and antero-posterior rather than antero-apical
paddle placement might minimize the risks.
Unipolar pacemakers are more susceptible
than bipolar devices. The pacemaker program and
function should be checked after the procedure.
Defibrillation/cardioversion may cause under-
sensing due to alteration of the intracardiac sig-
nal, failure to capture due to an increase in the
10 Precautions After Permanent Pacemaker Implantation
stimulation threshold, erasure of the programmed
settings in the pacemaker’s memory, back-up
pacing, and myocardial burns with cardiac
enzyme release. Most have a built-in protection
called “Power On Reset” which automatically
reprograms the pacemaker to a safe set of values
(usually VVI mode). It can then be reprogrammed
to its desired parameters.
Electroconvulsive Therapy (ECT)
ECT should not cause interference with pace-
maker function.
Transcutaneous Electrical Nerve
Stimulation (TENS)
The ECG should be monitored when initially
using a TENS machine. Unipolar pacemakers
may be inhibited during TENS applied close to
the pacemaker.
Lithotripsy
Shocks should be aimed well away from the gen-
erator, and because of the vibrations the rate-
adaptive mode should be turned off. The
piezoelectric crystal of activity-driven pacemak-
ers can be irrevocably destroyed if placed in the
focal point of an extracorporeal shock wave litho-
tripsy. The latter should be at least 25 cm away
from the pacemaker. It is best avoided in abdomi-
nal pacemakers.
SCUBA Diving
Many pacemakers may be affected beyond depths
of 11 m as the pacemaker titanium can may be
compressed by severe hydrostatic pressure.
Vigorous Sports
Vigorous contact sports are best avoided, to avoid
injury to the generator. Rugby, boxing, wrestling,
judo and karate should be avoided.
Other Sources of Electromagnetic Interference
Cremation
All pacemakers must be explanted before crema-
tion since they are likely to explode.
Other Sources of Electromagnetic
Interference
Hospital pagers may disturb telemetry in the form
of inaccurate battery voltage, current, and imped-
ance measurements, disturbances in intracardiac
221
ECGs, or complete interruption of telemetric
communications.
Some dental instruments, e.g., ultrasound
scalers/cleaners and electrosurgical instruments
can cause transient inhibition of pacing output.
Some cardiac monitoring systems used for
recording continuous ECGs in hospitalized
patients can cause inappropriate rate changes in
patients in whom rate response is as a result of
sensing minute ventilation.
 Follow-up After Pacemaker
Implantation 11

Patients who have undergone permanent pacemaker,
ICD, or CRT device implantation should be
regularly followed-up. Follow-up normally
takes place in a specifically designated, out-
patient pacing clinic – the pacemaker clinic –
although increasing numbers of patients in
Europe and USA are being monitored at home
using a variety of remote monitoring systems.
According to the HRS/EHRA expert consensus,
follow-up should include the assessment of the
device and lead status, as well as the review of
detected episodes and hemodynamic measure-
ments or recordings of any other programmed
parameters. The details of their joint recom-
mendations can be found in the journal Europace
2008;10:707–725.
The aims of a pacing clinic are set out in
Table 11.1. The reason for such attendance is to
check that the pacemaker is functioning normally,
to troubleshoot and solve any pacemaker prob-
lems (see Chap. 21), to optimize the pacing sys-
tem’s programmed settings and function to each
patient’s needs, and to download information
stored in the pacemaker. It is useful to ensure no
new symptoms have developed since the implant
(e.g., angina), to examine the wound and check
for any pacemaker complications, to check the
battery life and maximize longevity by adjusting
the settings, and to plan the next date for atten-
dance. It is appropriate to confirm the patient’s
contact details in case of manufacturer-recom-
mended pacemaker recall. Following discharge

Table 11.1 Aims of a pacemaker clinic

Optimization of the pacing system to each patient’s needs together with safe maximization of generator life.
Monitor implant site and wound status
Identification of abnormalities in the pacemaker system (generator and any lead) and any complication to permit
prompt treatment
Prediction of end-of-life of the pulse generator to permit elective change of the pulse generator
Provision of patient support and education: provide information about the device and therapies set
Keep appropriate records of follow-up
Accumulation of a database that offers information on present and past pacing systems for each patient and general
data on the function of pulse generators and leads from as wide a field as possible (including a link to the CCAD/
NPDB).
Provision of training opportunities for medical and paramedical staff.
Provision of a clinical cardiological follow-up service where this is appropriate. In some cases, this is provided by a
separate clinic or, alternatively, at another medical facility.
To liase with MHRA (Medical Health Regulatory Agency) and pacemaker manufacturer in relation to device and
lead problems when appropriate

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 223

DOI 10.1007/978-1-4471-2939-4_11, © Springer-Verlag London 2012
224 11 Follow-up After Pacemaker Implantation

Fig. 11.1 Initial steps Confirm patient identity

carried out by pacing
technician in follow-up
clinic Identify pacemaker model/manufacturer

Select appropriate programmer

Attach patient to ECG (limb leads, I, II, III & V1, V2 for CRT patients)

Record ECG and magnet strip

Review wound (especially at first visit or if any problem reported)

If wound inflamed/tender If wound OK

Arrange medical review Interrogate Device

+/– FBC, CRP using wand Telemetry/
+/–antibiotics radiofrequency

Review trends
Organise early follow-up/review
Check intrinsic amplitudes, impedances,
and need for further treatment
thresholds, events, battery life/warnings

If Battery at ERI–list for “box Measurements OK

change”
If Battery at EOL (should not
happen!)–urgent medical review
and prompt admission for “box
change”

Arrange subsequent follow-up appointment

from hospital after pacemaker implantation, the
patient should be told to contact the pacing center
if the pacemaker becomes painful or very tender,
if the wound becomes red and/or swollen, or if
they become unwell with pyrexia. If the wound
edges gape, again the patient should return to the
center without delay if serious infection is to be
avoided.
The clinic should be in or close to the ECG
department, staffed by an experienced pacing
technician or clinical physiologist with immedi-
ate access to a cardiologist familiar with normal
and abnormal pacemaker function. Guidelines
for a physiologist-led pacemaker clinic are avail-
able on the HRUK website. Practical algorithms
for technicians working in pacing clinics are
illustrated in Figs. 11.1–11.4. The equipment and
facilities necessary in a pacemaker clinic are
listed in Table 11.2, and the routine tasks to be
performed in Table 11.3. Programmers compati-
ble with the devices implanted in the center
should be present in the clinic (see Fig. 6.64) and
the telephone numbers for technical support of
all the relevant pacemaker manufacturers should
be available.
The cardiologist or technician should first
request to see the patient’s ID card and the details
should match what data are in the casenotes or on
the pacemaker database. A brief interview about
the presence of symptoms since last reviewed
should be accompanied by inspection of the pace-
maker wound. It should then be established
whether the patient is “pacemaker-dependent”
and to what degree. The patient’s history and case
records and a 12-lead ECG should help answer
this question. Application of a magnet to
Follow-up After Pacemaker Implantation 225

Fig. 11.2 Lead Lead measurements

amplitude sensitivity,
pacing threshold, and Impedance Amplitudes Thresholds

impedance measurement
algorithm
(400–1,500 Ω) At 4−6 weeks
Review trends R Wave > 5 mv V threshold
Allow 20% variation P Wave > 2 mv < 1 v @ 0.4 ms
between follow-ups A threshold
< 1.5−1 v @ 0.4 ms

P & R wave sensitivity should

Check in both unipolar
be approx. 1/2 of measured Switch on Automatic
and bipolar modes
P & R wave amplitude Capture Management

Outputs should be
High impedance Low impedance reduced > 6 weeks
suggestive of suggestive of 2.5 V @ 0.4 ms or 2x voltage
conductor failure insulation failure threshold – whichever is greatest
obtain PA & Lat CXR difficult to see on CXR

Oversensing = Undersensing = If acute rise in threshold

Medical review & CXR
underpacing overpacing (> 1.5 V @ 0.4 ms after 6 weeks):
Symptoms eg: syncope,
dizziness, palpitation. Exclude:
Lead displacement – CXR
Exit block – consider steroid
therapy
Decide on need for Reprogram to reduced Reprogram to increased Medication contributing to
lead replacement sensitivity sensitivity increased threshold e.g., flecainide

Histograms & EGMs

AF, SVT, VT

VT > 6 beats
AF
How many episodes have
What is the frequency
there been, beats & rate?
of arrhythmia?
Is the device set up
Is there appropriate
optimally to record
mode-switching?
arrhythmias?
Rate response
Is there adequate
Percentage V
chronotropic response?
paced > 40%?
Histograms should show
Is this true pacing,
a range of ventricular
fusion or pseudofusion?
rates – not mostly
base rate activity

Is there documented Is there a documented

history of AF? history of VT? Check indication
Are there symptoms
Symptoms − do they relate Symptoms − do they relate for pacing.
of fatigue or
to EGM date/time? to EGM date/time? Is AV node
exertional dyspnea?
Is the rate controlled or ? Syncope, disease present?
fast conducted AF? ? EF < 35% or CAD

Thromboprophylaxis: Is patient on Check “rate-response”

Is RV pacing
Is the patient taking antiarrhythmics? is enabled and/or
avoidable?
anti-coagulation? i.e. Beta-blockers, adjust response
i.e. Warfarin, Aspirin Amiodarone sensitivity

Rate/rhythm control Arrange for review of

Consider adjusting
Is an antiarrhythmic/ symptoms and possibly
Assess AV delay
rate-controlling drug further adjustments
LV function +/– using RV pacing
Fig. 11.3 An assessment prescribed eg: flecainide,
reduction algorithm
of rate-response
β-blocker sensitivity
is made of the occurrence
and frequency of AF,
SVT, VT, frequency of
ventricular pacing, and Medical review
frequency and appropri-
ateness of rate response
226 11 Follow-up After Pacemaker Implantation

a CRT implant b Three month follow-up

ECGs recorded
RV, LV, BiV (Lead 1) CRT device check
Leads I and V1 as above
are most useful
Full device check
including wound check > 90% True BIV paced
Pacing OK? Y/N
Sensing OK? Y/N
AVD appropriate? Y/N
Yes No

No Yes
Medical review
Clinical response
AF/AT
Medical review > 90% True BiV paced VEs
Reprogram
CXR No Yes
Yes No

Clinical response % V sensed Living advice Y/N

ECHO optimization
NYHA Class VE’s Driving advice
AV and V-V delays
HF symtoms/diagnostics/ AF/AT Remote follow-up
heart failure meds ? reprogram
prescribed
Confirm rehab referral

? CXR ICD PPM

Yes No
LV lead position 3−6/12 follow-up 6−12/12 follow-up

Driving advice Trigger HF nurse/

Remote follow-up medical review

Medical review
ICD PPM
3/12 follow-up 6/12 follow-up

Fig. 11.4 Technician’s algorithm for use with patient with a CRT device on (a) first and (b) 3 month follow-up visits

Table 11.3 Routine pacemaker follow-up – tasksa

Table 11.2 Equipment and facilities necessary for a
pacemaker/ICD follow-up clinic Patient assessment
Resuscitation equipment including defibrillator and Symptoms
external pacemaker device Skin overlying the pacemaker system
Cardiac arrest team “call button” 12 s multichannel ECG rhythm recording with and
12-Lead ECG machine without a magnet applied over the generator to:
Magnet Verify automatic interval with/without magnet
Relevant range of pacemaker/ICD programmers/ Estimate degree of pacemaker dependence
analyzers for the devices used in the center Verify appropriate depolarization sequence, capture,
Manuals/information booklet for all relevant pacemak- sensing, fusion/pseudofusion beats
ers/ICDs and programmers Lead stability testing. Respiratory tests and lead
Contact telephone numbers of all relevant manufactur- integrity by generator manipulation – when intermittent
ers or their local agencies lead problem suspected
File of technical notes and notices from manufacturers End-of-life battery check (EOL). Use of a device
specific programmer is essential
Computerized patient database
Acquisition of generator telemetry concerning lead
Access to X-ray facilities, exercise stress testing, and
functions where available
ambulatory ECG monitoring
Verification of pacing and sensing functions by
24 h telephone answering facilities manned by
threshold assessment using the programmer and/or
competent staff
magnet application
Access to temporary pacing facilities
Recording and communicating all the above as
Access to a cardiologist appropriate in casenotes/letter to GP
A robust process for listing patients for device Recording of data on database
replacement or system revision a
Each device implanting/follow-up clinic should have a
Facilities to admit patients as emergencies at any time
protocol for the procedure to be followed
Follow-up After Pacemaker Implantation 227

Fig. 11.5 Interrogating

the device by placing the
magnetic wand or
programming head of the
programmer over the
implant site

Fig. 11.6 The program

can be adjusted appropri-
ately and saved in the
pacemaker

pacemakers usually results in reversion to an wand. Interrogation includes verification of the

asynchronous pacing mode (AOO, VOO, or
DOO), which can be recorded on ECG and which
confirms that the lead(s) can pace the myocar-
dium (see Fig. 11.13).
The technician/clinical physiologist can then
begin to interrogate the pacemaker by placing the
magnetic wand or programming head of the pro-
grammer over the pacemaker (Fig. 11.5), although
increasingly more common, pacemakers can be
interrogated wirelessly without the need for a
administrative data, a check on the programmed
data, examination of the measured or real-time
data on output, battery life and lead impedance
measurements. Data collected by the pacemaker
are sent into the programmer and can be dis-
played (see Fig. 9.6). The program can be adjusted
appropriately and saved in the pacemaker using
the touch screen on the programmer (Fig. 11.6).
A printout of the program and an ECG showing
satisfactory pacing should be inserted in the
228 11 Follow-up After Pacemaker Implantation

Fig. 11.7 A printout of the program and an ECG showing satisfactory pacing should be inserted in the patient’s
case records

patient’s case records (Figs. 11.7–11.11). Data should be tested and the pacemaker program
should be entered into the Pacing Database and a adjusted if necessary (Figs. 11.13 and 11.14).
copy of the recent entry placed in the casenotes Modern pacemakers and their programmers allow
(Fig. 11.12). Sensing and pacing thresholds for non-invasive pacing stimulation (NIPS) test-
Follow-up After Pacemaker Implantation 229

Fig. 11.8 Satisfactory

DDD pacing

Fig. 11.9 Satisfactory VDD

pacing

Fig. 11.10 A summary of the pacemaker check is provided for the case records
230 11 Follow-up After Pacemaker Implantation

Fig. 11.11 Lead data should include amplitude, threshold, and impedance measurements

Fig. 11.12 A typical printout

following pacemaker interrogation
Follow-up After Pacemaker Implantation 231

Fig. 11.13 Application of

magnet to this dual-chamber
pacemaker results in DOO
pacing at a rate of 100 bpm
(arrow)

Fig. 11.14 Testing the

ventricular lead threshold
shows loss of capture at 0.4 V
(arrow)

ing of pacing, sensitivity, and impedance to be
displayed on screen (Fig. 11.15). A useful, time-
saving facility available on most programmers is
the Overview Screen or “First Page,” which pres-
ents all useful indicators gathered in one screen
when no further testing may be required
(Fig. 11.16). “Pages” may display live annotated
ECG with simultaneous intracardiac atrial and
ventricular electrograms (EGM), along with the
current pacemaker and lead settings and “but-
tons” to allow further interrogation of patient
data, lead threshold testing, and trend data
(Fig. 11.17). Figures 11.18 and 11.19 show the
pages that can demonstrate lead data over time.
Changes in lead impedance are important to
note. Lead impedance tends to fall in the first
2 weeks after implantation, but then reaches a pla-
teau and remains relatively stable at approximately
15% higher than the implantation value. Fluctuations
of impedance by as much as 300 Ω are considered
normal. Generally, an increase in impedance by
>300 Ω suggests conductor fracture, whereas a
decrease of >300 Ω suggests insulation break. A
chest X-ray should be done if either is suspected.
232 11 Follow-up After Pacemaker Implantation

Fig. 11.15 Screen on the Orchestra™ programmer for NIPS (Non-Invasive Pacing Stimulation testing of a Reply™
DR pacemaker. Courtesy of Sorin Group)

Fig. 11.16 Interrogation of Reply™ pacemaker. First impedance measurements, device statistics and battery sta-
screen provides information on pacing mode, basic rate tus at a glance. Further interrogation is obtained by enter-
and maximum rate, sensing and pacing settings, lead ing the next series of pages (Courtesy of Sorin Group)
Follow-up After Pacemaker Implantation 233

Fig. 11.17 Page from the Medtronic programmer dis- tons” to allow further interrogation of patient data, lead
playing live annotated ECG with simultaneous intracar- threshold testing and trend data (From the Medtronic
diac atrial and ventricular electrograms (EGM), along Advisa DR MRI SureScanÒ pacemaker) (Image repro-
with the current pacemaker and lead settings and “but- duced with permission of Medtronic, Inc.)

Fig. 11.18 Quick Look II Screen from the Medtronic interrogation of this Medtronic Advisa DR MRI™
programmer showing the facility for trending lead data SureScanÒ pacemaker. It includes links to more detailed
and the amount of time atrial sensing/pacing and ventricu- status and diagnostic information stored in the device
lar sensing/pacing. This is the initial screen shown upon (Image reproduced with permission of Medtronic, Inc.)
234
Fig. 11.19 Continuous atrial and ventricular lead threshold
and impedance data can be displayed on a page of the
Medtronic programmer. This allows an assessment of the
performance and integrity of the leads. The “last measured”
CRT and ICD devices are interrogated in simi-
lar fashion and the programmer used to print out
details of the retrieved data (Figs. 11.20 and 11.21).
Modern programmers present a series of “pages”
as screenshots which can be accessed by “touch
buttons” to reveal data on program settings, lead
and battery data, arrhythmia detection settings,
information on therapy delivery, etc.
(Figs. 11.22–11.25).
Specific diagnostic functions should be
checked and evaluated. For example, heart rate
histograms can assess rate adaptive function,
sleep rate, hysteresis function, and automatic
mode switching. Event histograms include ecto-
pic counts as well as the percentage of time spent
in a particular pacing state such as AS-VP activity.
AT/AF histograms can show the frequency of
high atrial rates and how the device responded.
11 Follow-up After Pacemaker Implantation
values represent the most recently measured threshold or
lead impedance value for the particular lead, while the graph
represents measurements taken over the previous 12 months
(Image reproduced with permission of Medtronic, Inc.)
Devices can show peak atrial rate histograms, %
AT/AF burden, and the details of each and every
episode. AF suppression diagnostics can show
how often this was required, what circumstances
provoked it, and how well it performed.
Intracardiac EGMs are really useful diagnosti-
cally and should be downloaded at follow-up.
These may be single-channel EGM or dual-
channel EGM in dual-chamber systems. EGM
triggers are programmable and may include high
atrial rate activity, PVCs, and mode-switch
events. Some devices allow patient-triggered
EGM recordings. Most devices seen in clinical
practice today also offer annotated ECG strips
which allow one “to see events” exactly as the
device interprets them. Generally, the letter codes
are AS (for atrial sensed events), AP (for atrial
paced events), VS (for ventricular sensed events),
Follow-up After Pacemaker Implantation
Fig. 11.20 Interrogation of Contak Renewal CRT device – summary for case notes
and VP (for ventricular paced events) (Fig. 11.26).
Intervals are stated numerically, often with hori-
zontal lines, to help identify where they belong.
Where sensing problems are suspected, evidence
may be sought for crosstalk, myopotential inhibi-
tion, and retrograde VA conduction.
At the end of the session, the technician should
be able to answer the following questions. (1) Are
235
the programmed settings consistent with the
patient’s ECG recordings? (2) Does every pacing
spike lead to capture and a depolarization? (3) Is
the QRS normal or are there fusion beats? (4) Is
sensing appropriate, does sensing lead to inhibi-
tion of an output pulse, and does sensed atrial
activity lead to sensed or paced ventricular activ-
ity? (5) What is the patient’s underlying rhythm?
236 11 Follow-up After Pacemaker Implantation

Fig. 11.21 Interrogation of Contak Renewal CRT device – detailed summary of data printed from programmer

Fig. 11.22 “Therapy guide” page on the Medtronic programmer interrogating the Protecta CRT-D device (Image
reproduced with permission of Medtronic, Inc.)
Follow-up After Pacemaker Implantation 237

Fig. 11.23 Battery and lead data are available on a separate page on the Medtronic programmer when interrogating the
Protecta CRT-D device (Image reproduced with permission of Medtronic, Inc.)

Fig. 11.24 Ventricular arrhythmia detection settings for this Protecta CRT-D device are shown on this page (Image
reproduced with permission of Medtronic, Inc.)
238
Fig. 11.25 The “ventricular therapies” program for this Protecta CRT-D device is shown on this page (Image repro-
duced with permission of Medtronic, Inc.)
Fig. 11.26 Pacemaker interrogation of a possible rhythm
disturbance. Interpretation is aided by the ECG in Lead II
(6) Would the patient benefit from having particu-
lar features turned on, for example hysteresis, AF
suppression, or sleep rate function? (7) Are the
diagnostic data consistent with the programmed
settings and is there anything unusual in the
diagnostics? (8) Are the programmed algorithms
functioning appropriately? (9) Are there any sug-
gestions from the diagnostics of possible prob-
11 Follow-up After Pacemaker Implantation
(top), the atrial electrogram (middle), and the ventricular
electrogram (bottom), as well as the annotations AS and VS
lems that may require troubleshooting (e.g., sen-
sor-driven rates that seem inappropriate for that
individual’s activity, much high-rate atrial activity
with fast ventricular response)?
Besides the device’s diagnostics, other investi-
gations can be of use during follow-up in order to
try and identify suspected problems or optimize
function.
Frequency and Timing of Follow-up 239

Fig. 11.27 Holter ECG

monitoring confirms that this
patient’s palpitations are due
to pacemaker-mediated
tachycardia

Fig. 11.28 Checking the

pacemaker wound for
evidence of infection is an
important advantage of
“in-person” follow-up

Holter monitoring and treadmill exercise Frequency and Timing of Follow-up

testing may be useful for assessing exercise toler-
ance, chronotropic competence, exercise-induced
arrhythmias/pacemaker-mediated tachycardia, and
maximal heart rate achievable – paced or unpaced
(Fig. 11.27). Although Holter monitoring may be
arranged on the same clinic day, exercise testing is
often best arranged on a separate occasion.
After interrogation is complete and the data saved
and printed, the diagnostic counters should be
cleared so that new follow-up data can be collected.
The first follow-up appointment after pace-
maker implantation should be at approximately
4–6 weeks unless some specific concern
demands an earlier review. Examination of the
pacemaker wound is important at this stage
(Fig. 11.28), and antibiotics should be given for
any superficial wound infection. Pacing thresh-
old should be assessed and the pacemaker out-
put programmed to at least twice the stimulation
240
threshold or three times pulse width. If there is
any suggestion of pacing or sensing loss, a chest
X-ray should be performed to check the
electrode(s) position. Lead impedance should
be checked. If all is well, a further appointment
at 6 months should be arranged and then annu-
ally until any reduction in battery life appears
when 1–3 monthly checks should then be rein-
stituted. If at anytime lead, generator, or wound
concerns occur, follow-up can be adjusted
accordingly.
Manufacturers recommend follow-up for
ICDs and CRT devices at 3–6 monthly intervals,
and those patients with frequent arrhythmic epi-
sodes, shocks, and/or heart failure may need to be
seen more frequently.
The frequency of follow-up depends on a
number of patient-related, device-related, and
disease-related factors. These are shown in
Table 11.4. Troubleshooting in the event of car-
diac-sounding symptoms or possible pacemaker
malfunction will require experience and exper-
tise from technicians and cardiologists.
Troubleshooting is discussed in Chap. 21.
Pacemaker Reprogramming
to Preserve Battery Life
A pacemaker that is programmable for rate,
pulse width, and output may have its battery
life prolonged by reducing these parameters
after confirming low pacing thresholds
3–4 months after implantation to allow estab-
lishment of the chronic threshold. If a pace-
maker with hysteresis mode is available, the
takeover rate may be set lower than the basic
pacing rate in order to conserve battery life.
Turning off unused sophisticated monitoring/
11 Follow-up After Pacemaker Implantation
Table 11.4 Factors determining frequency and type of
follow-up after device implantation
Patient factors
Cardiovascular symptom stability
Rhythm stability
Patient, family or physician issues, e.g., patient
distance from F/U clinic, medical/social issues
High/unstable pacing thresholds
Change in antiarrhythmic drug or heart failure
treatment
Frequency of ICD therapies
Device factors
Reliability of the device and lead(s)
Programmed parameters that are switched “on” and
that influence battery life, e.g., frequency of shock
therapy, pacing frequency, pacing threshold
Age of device
Complexity of device
Drugs that may influence pacing or defibrillation
threshold
Arrhythmia/heart failure diagnostics, e.g., patient
activity, transthoracic impedance
Disease factors
Frequency and severity of symptoms, e.g., recurrent
dizziness/syncope/palpitations
Changes in cardiovascular therapy, e.g., b-blockade,
flecainide
Diagnosis of other serious/life-threatening conditions,
e.g., terminal cancer, stroke
sensing circuits and rate adaptation if not
required will also help. Anything that reduces
the % pacing will help prolong battery life.
Pacemaker Alerts/Recall
Pacemaker manufacturers occasionally report that
a fault has been reported in one of its pacemakers
or leads and that close monitoring of patients pos-
sessing the particular model (Fig. 11.29) is nec-
Pacemaker Alerts/Recall
Fig. 11.29 Urgent medical
device information from
manufacturer
essary. The MHRA also send out device alerts to
pacing centers (Figs. 11.30 – 11.32) with infor-
mation about which device(s) is being referred
to, what the problem is, what action needs to be
taken, and the frequency of follow-up required
for monitoring. The failure rate is usually very
low and only if potentially serious is it recom-
mended that generators should be recalled and
replaced. For patients who are pacemaker-depen-
dent, replacement is essential, but for those who
241
are not dependent, consideration of the benefits
and risks involved in a replacement procedure
is important especially in the elderly and infirm.
Each center should be able to identify a list of the
relevant patients using its own database. The lat-
ter can also be used by the center’s cardiologists
to assess any suspected trend in pacemaker fail-
ures ahead of any alert or recall. Each advisory
or recall should be managed separately and an
action plan developed by each implanting center.
242
Fig. 11.30 Medical device alert from MHRA
Battery Depletion/End-of-Life
Parameters
In the past, pacemakers were tested for battery
depletion by applying a magnet over the pace-
maker. A reduction in the fixed pacing rate to
the “end-of-life” (EOL) parameters set by the
manufacturer (usually 5–10% of the implant
or beginning-of-life (BOL) rate) – measured
precisely by the handheld device – was the
indicator to plan elective generator replace-
ment. The free-running rate may also decrease
according to design. Increase in pulse width
duration in some pacemakers to compensate
for a lower voltage output may be an elective
replacement indicator (ERI). Some devices
11 Follow-up After Pacemaker Implantation
Fig. 11.31 Medical device alert from MHRA indicates
the relevant device, the problem, and the action advised
change to simpler pacing mode, for example,
DDDR to VVI, VVIR to VVI or VOO to
reduce battery current drain may be an ERI or
EOL. Specific values of EOL and ERI vary
between manufacturers.
Most pacemakers can now be extensively
interrogated by telemetry using a handheld pro-
grammer. Large reductions in battery voltage and
increase in its internal resistance are indicators of
battery depletion. Recommended elective replace-
ment time (ERT) indicates that elective replace-
ment should be organized over the next 3 months
or so. The EOL parameters indicate that genera-
tor replacement should be performed without
delay. In some systems, a pacemaker battery
energy gauge can be displayed on interrogation.
Home Monitoring
Fig. 11.32 Medical device alert from MHRA regarding ICD
Home Monitoring
In addition to programmer-based interrogations in
a hospital-based follow-up clinic, device follow-
up has been expanded with a system of remote
interrogation tools. These home monitors/com-
municators employ telephone-based links to
extend the bidirectional telemetry links into the
patient’s home or with cellular technology unre-
stricted by landlines. Remote transmissions may
be completed by connecting the transmitter to any
form of telecommunication network (wired or
wireless). These bedside or handheld communi-
cation devices employ either a wand with short
distance radiofrequency communication with the
programmer or by the long distance ISM or MICS
band radiofrequency telemetry described earlier
in Chap. 9. This home monitor/communicator is
then linked by telephone to a central (Internet
based) data repository where the data are stored
and analyzed and disseminated electronically.
243
Older style remote monitoring of pacemakers
used transtelephonic monitoring using modem
technology. These devices transmitted the patient’s
heart rhythm recording by converting the ECG
information into sound and sending it over the
telephone line to a decoding machine which
changed the sound back into the “rhythm strip” at
the other end. Heart rate, rhythm and battery sta-
tus, and, to some degree, sensing and capture
function can be obtained. A typical protocol to be
followed by technical staff doing transtelephonic
device monitoring is shown in Table 11.5.
Such remote monitoring technology reduces
the need for some face-to-face clinic visits and
may facilitate, when needed, visits triggered by a
clinical event. In addition, remote monitoring and
the storing of monitoring data may facilitate the
detection of device system performance issues
and clinical conditions that may lead to the need
for increased frequency of in-person or remote
surveillance. However, although technically fea-
sible and probably reliable, remote reprogram-
244
Table 11.5 Procedure protocol for technician doing
transtelephonic follow-up
Single-chamber/single-chamber-rate-adaptive
pacemakers
Verify pacemaker performing according to pro-
grammed parameters
Determine the underlying rhythm – if possible
Review of programmed parameters
Mode
Ratea
Pulse width
Hysteresis (off/on)
Pacing polarity configuration
BOL/EOL characteristics
ECG analysis: single-chamber pacemaker
Verify pacemaker performing according to pro-
grammed parameters
Verify pacing spikes are present
Verify 1:1 capture is present
Check intrinsic activity sensed appropriately
Oversensing
Undersensing
Verify normal/abnormal function of the pacemaker
Monitor technician provide technical comment
Dual-chamber/ dual-chamber-rate-responsive pacemakers
Verify pacemaker performing according to pro-
grammed parameters
Determine the underlying rhythm
Review of programmed parameters
Mode
Rate (Lower programmed rate – maximum tracking)b
Pulse width
Hysteresis (off/on)
Pacing polarity configuration
BOL/EOL characteristics
Automatic mode switch – (off/on)
ECG analysis: dual-chamber pacemaker
Verify pacemaker performing according to pro-
grammed parameters
Check if atrial and/or ventricular spikes present
Verify 1:1 capture is present
Check intrinsic activity is sensed appropriately
Oversensing
Undersensing
a
Check lower programmed rate and maximum sensor rate
in rate-responsive pacemakers
b
Maximum sensor rates in rate responsive systems
ming of devices is not currently permitted – mainly
due to the limited ability to respond to potential
changes in the patient’s condition as a result of
11 Follow-up After Pacemaker Implantation
the change in the device’s parameters after
reprogramming.
The TRUST clinical study demonstrated the
safety and effectiveness of remote monitoring
and that it reduced 43% of in-office follow-ups
without any impacts on patients’ safety [1]. The
HRS/EHRA expert consensus on the monitoring
of cardiovascular implantable electronic devices
recommends in-person follow-ups after implan-
tation and annual follow-ups. However, during
the maintenance phase of follow-ups and when
the patient’s medical condition is stable and no
anticipated device programming is required, fol-
low-ups could be accomplished remotely.
Home monitoring is now available in the UK
from most of the device companies using wireless
or telephone technology and can help to reduce pac-
ing clinic visits – especially desirable for those
patients living remotely from the pacing clinic or
with poor transport links. It has been more widely
used in the USA for several years. Transtelephonic
pacemaker data collection has been available for
many years and can provide information with
respect to battery status, pacing threshold, lead
impedance, parameters, and diagnostic data. Intra-
cardiac electrograms showing events and mode
switching data showing AF can also be transmitted,
but lead testing cannot be performed via this tech-
nology. Patients with symptoms or changes in clini-
cal status and those requiring reprogramming and
optimization need to be seen in pacing clinic.
Medtronic’s CareLink® service was launched
in Europe in 2007 and is available in 14 European
countries with a few thousand patients on active
follow-up. In the USA, CareLink® is well estab-
lished with over 150,000 patients being followed-
up remotely (Figs. 6.38, 11.33 and 11.34). The
Medtronic CareLink® Network with Conexus™
Wireless Telemetry offers automatic data trans-
missions and customizable alert notifications.
With wireless device interrogation, routine follow-
ups occur automatically while the patient sleeps,
alleviating patient compliance issues (Fig. 11.35).
Using the Medtronic CareLink® Clinician web-
site, clinic staff can preschedule up to six auto-
matic device checks for each patient, minimizing
time spent rescheduling missed appointments and
the difficulties contacting patients by phone. The
Home Monitoring 245

patient’s implanted device can be programmed

to notify clinicians of programmed alerts. If the
device detects a potential problem, such as atrial
fibrillation or a lead integrity issue, it initiates a
data transmission and a Medtronic CareAlert®
notification via pager and/or voicemail/e-mail.
Physicians have flexibility and control in program-
ming both wireless and audible device alerts and
notification methods. Conexus™ Telemetry uses
the Medical Implant Communications Service
(MICS), a radio frequency band designated for
implantable medical devices. The MICS band
protects Medtronic’s wireless transmissions from
interference caused by cell phones or other com-
Fig. 11.33 Medtronic CareLink® monitor for home
mon electronic devices.
monitoring

Fig. 11.34 Inside the device

is the mains plug, the
telephone socket connection
and the “wand” which must be
placed over the implanted
device

Fig. 11.35 The Medtronic CareLink® Network with Conexus™ Wireless Telemetry offers automatic data transmis-
sions while the patient sleeps (Image reproduced with permission of Medtronic, Inc.)
246 11 Follow-up After Pacemaker Implantation

Fig. 11.36 Biotronik’s

CardioMessenger I offers a
bedside (CardioMessenger S)
and a portable version
(CardioMessenger I) for
home monitoring of devices
(Image reproduced with
permission of Biotronik)

Biotronik’s CardioMessenger was first used in

2001, and there are >60,000 Biotronik devices with
home-monitoring implanted worldwide (>50% in
the USA). The implant – pacemaker, CRT, or ICD
– transmits diagnostic, therapeutic, and technical
data to an exterior device, the CardioMessenger,
using an integrated antenna. The patient is not
required to do anything. The CardioMessenger II is
compatible with all Lumax ICD and CRT devices,
whereas the CardioMessenger I serves all other
implants. The CardioMessenger S is a bedside ver-
sion of the more portable CardioMessenger I
(Fig. 11.36). The CardioMessenger forwards the
data to the Home Monitoring Service Center via Fig. 11.37 CardioMessenger II® is also available as a
the cellular phone network. The Service Center bedside monitor (CardioMessenger II®S) and a portable
analyzes the data and edits a CardioReport. The device, CardioMessenger II® (Image reproduced with per-
mission of Biotronik)
information flow is entirely automated. The cardi-
ologist can evaluate the patient’s data at any time
using a secured website. Upon request, one can
receive customized additional information per fax,
e-mail, or SMS when selected events occur.
There are two versions of CardioMessenger
II® (Figs. 11.37). The portable CardioMessenger
II® offers patients unwavering assurance along
with complete mobility (Fig. 11.38). Its small
size, integrated Quad-band modem, and multi-
voltage transformer make it ideal for unrestricted
traveling in more than 50 countries. The
convenient belt clip and carrier strap along with
lithium ion batteries that last up to 72 h provide
increased freedom and mobility (Fig. 11.39).
With only one button and a simple LED icon dis-
play, the CardioMessenger II® is today’s small- Fig. 11.38 The CardioMessenger II® is the more porta-
ble version (Image reproduced with permission of
est, most advanced, remote monitoring system Biotronik)
available. All CardioMessenger II® devices also
contain a unique call-back function. It allows
physicians to request a patient call-back through ity of life. The CardioMessenger II®S is a
a flashing LED on the CardioMessenger, result- simplified bedside version of the CardioMessenger
ing in less patient disturbance and increased qual- II®, suitable for those patients requiring less
Home Monitoring
Fig. 11.39 The CardioMessenger II® can be clipped on a
waist belt (Image reproduced with permission of Biotronik)
mobility (see Fig. 11.37). It has all the features of
the portable CardioMessenger II® and can also be
used when traveling worldwide. Like the
CardioMessenger II® it is compatible with all
Lumax ICDs and CRTs and with all future
implantable cardiac devices.
Guidant/Boston Scientific’s LATITUDE®
home-monitoring system has only recently
become available in Europe, but >20,000 devices
are under active follow-up in the USA. This device
remotely collects data from Boston-Scientific’s
247
Fig. 11.40 Boston Scientific’s LATITUDE® home mon-
itoring device
CRT-D and ICD devices. It consists of a wireless
communicator that automatically collects infor-
mation from the implanted device at predeter-
mined times without any patient involvement
(Fig. 11.40). The LATITUDE® Communicator
then transmits the information via the phone line
(plugs into a standard phone jack and power out-
let) to a secure server that can be accessed by the
pacing clinic technicians or cardiologist via the
LATITUDE® website with a username and pass-
word. A “wanded Communicator” is also avail-
able but the patient must actively participate in the
data collection process. At scheduled times, a light
on the Communicator prompts the patient via the
Active Button to place the wand over their
implanted device. The Communicator will then
walk the patient through the appropriate steps that
are necessary to send the device data to the cardiac
center. Remote transmissions usually include
scheduled remote device follow-ups, where the
Communicator collects information similar to that
of a hospital-based device-check (without per-
forming any threshold testing) including a real-
time electrogram. In addition, LATITUDE® can
monitor for any alerts both during and between
follow-ups, for example, if the battery power of
the device reaches ERI status. It also allows
patients to send device data other than during
scheduled follow-up or remote monitoring check.
Patients receiving the Cognis® CRT-D device can
have changes in their weight and blood pressure
at home monitored using specific, dedicated
weighing scales and sphygmomanometer which
communicate with the LATITUDE® home
248
Fig. 11.41 Dedicated weighing scales and blood pres-
sure monitor for home monitoring of heart failure in
patients with the Cognis® CRT-D device and the
LATITUDE® home monitoring device (Boston Scientific)
monitoring system using Bluetooth technology
(Fig. 11.41). The website www.aboutlatitude.com
provides useful information for patients and their
families with links to technical support represen-
tatives. The LATITUDE™ NXT Remote Patient
11 Follow-up After Pacemaker Implantation
Management System has just been released in
Europe for use with Boston Scientific’s advanced
INGENIO™ and ADVANTIO™ pacemakers
and the INVIVE™ CRT-P device.
St. Jude Medical’s Merlin@home™ trans-
mitter allows patients to have their device
checked and monitored remotely at home (see
Fig. 1.86). The data are uploaded to Merlin.
net™ PCN a safe and secure web-based man-
agement system which can be accessed by the
technicians and cardiologist at the cardiac center
using a username and password. Connected to a
telephone line, the device can monitor, down-
load, and transmit the device’s data while the
patient is asleep.
Reference
1. Varma N, et al. Evaluation of efficacy and safety of
remote monitoring for ICD follow-up: the TRUST
trial. Circulation. 2008;118:2316, A4078.
 Complications of Pacemaker
Implantation 12

Complications associated with pacemaker implan- cavity and when positioning the electrode in the
tation are generally uncommon when temporary RV apex. They settle spontaneously and do not
and permanent pacing are performed by experi- require treatment. Sustained ventricular tachy-
enced personnel. cardia and ventricular fibrillation are unusual
Complications can be divided into early occurrences (Fig. 12.2) but may be more likely in
(intra-, peri-, or postoperative) (<30 days) and a clinical setting of myocardial infarction. DC
late (>30 days) complications (Table 12.1). Early cardioversion may be necessary, especially if
complications mainly consist of procedural com- hemodynamic compromise occurs.
plications occurring as a result of lead insertion Complete heart block and asystole may
and lead positioning which are similar for tempo- also occur during electrode insertion. Quick
rary and permanent pacing procedures. Late positioning of the pacing electrode and prompt
complications, occurring after hospital discharge, pacing is the ideal treatment but a precordial
are obviously only relevant to permanent pace- thump, cardiac massage, IV atropine or isopre-
maker implant procedures. naline, emergency transthoracic pacing, and
full cardiopulmonary resuscitation may be
required.
Early Complications
Table 12.1 Acute complications of pacemaker electrode
Arrhythmias insertion
Arrhythmias Atrial/ventricular
Atrial ectopic beats, atrial tachycardia, flutter or tachyarrhythmias
fibrillation may be produced by maneuvering the A-V block
Pneumothorax/hemothorax
electrode in the right atrium en route to the RV.
Myocardial perforation/
These arrhythmias usually settle/revert spontane- SVC perforation
ously, although atrial flutter/fibrillation may take Infection
several hours or more (Fig. 12.1). If AF fails to revert Hemorrhage
spontaneously, the arrhythmia can be addressed and Air embolus
treated by DC cardioversion. If AF develops after a Thrombophlebitis/venous
dual chamber implant, the pacemaker may be repro- thrombosis
grammed to a VVI or VVIR mode until sinus rhythm Brachial plexus injury
is restored, when DDD pacing can be reinstituted Thoracic duct injury
using the external programmer. Failure to pace Lead displacement
Ventricular ectopic beats and even couplets Lead disconnect
and triplets invariably occur on entering the RV Failure to sense

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 249

DOI 10.1007/978-1-4471-2939-4_12, © Springer-Verlag London 2012
250 12 Complications of Pacemaker Implantation

Fig. 12.1 Atrial fibrillation may occur during lead manipulation within the right atrium

Fig. 12.2 Ventricular tachycardia/ventricular fibrillation is an uncommon occurrence during pacemaker lead position-
ing and as shown above requires immediate DC cardioversion

Pneumothorax

The apical pleura may be punctured during sub-

clavian vein puncture prior to sheath/electrode
insertion (Figs. 12.3–12.5). Aspiration of air
indicates when this has happened, and a post-
procedure chest X-ray is essential. Pneumothorax
can be obvious and large (Figs. 12.6 and 12.7) or
localized if pleural adhesions happen to be pres-
ent. Percutaneous drainage using an underwater
seal drainage system is necessary if >50% of
the thoracic cavity is air-filled or if breathless-
ness or signs of tension pneumothorax develop.
Otherwise, a watchful, conservative approach Fig. 12.3 Left apical pneumothorax is visible (arrow)
after device implantation
with daily chest X-rays might suffice (Figs. 12.8
and 12.9).

rary pacing electrodes which are relatively stiff

Myocardial Perforation devices. Positioning a permanent pacing electrode
with the shaping stylette still in situ also makes it
Perforation of the RV myocardium may occur stiffer and increases the chance of perforation.
during manipulation and positioning of tempo- Screwing-in an active-fixation lead at the RV
Early Complications 251

Fig. 12.4 Underwater sealed chest drain (arrow) is

inserted
Fig. 12.6 Large pneumothorax (arrows) requires inser-
tion of chest drain

Fig. 12.5 Pneumothorax diminishing 12 h after chest

drain insertion (arrow)

apex can also result in myocardial perforation

(Fig. 12.10). Elderly patients with a thin RV
muscle wall are particularly at risk (Figs. 12.11
and 12.12). Sharp chest pain during the insertion,
evidence of cardiac tamponade with breathless-
ness, raised jugular venous pressure, falling sys-
temic blood pressure, and cyanosis are likely
sequelae and suggest hemopericardium that
Fig. 12.7 Reduction in size of pneumothorax (black
arrow) after chest drain inserted (green arrow)
requires emergency pericardiocentesis and pos-
sibly cardiac surgical repair. Echocardiography
should confirm hemopericardium (Fig. 12.13)
and may even show the electrode tip in the
252
Fig. 12.8 A smaller pneumothorax may be localized to
the apex (green arrow)
Fig. 12.9 Blood or serosanguinous fluid may result in
opacification if the air is replaced with fluid (arrow)
pericardial space (see Fig. 12.10). Other signs of
perforation may be loss of pacing or symptoms
and signs of pericarditis – including a pericardial
friction rub.
12 Complications of Pacemaker Implantation
Fig. 12.10 Transthoracic echocardiogram (subcostal
view) shows the helical coil tip (red arrow) of this active-
fixation lead protruding through the apex of the right ven-
tricle (RV). The green arrow shows the lead within the RV
cavity, and the yellow arrows the anterior, apical, and
septal portions of the RV. RV right ventricular free wall
Fig. 12.11 Frail elderly patients may have extremely
thin RV myocardium and RV perforation is not difficult,
especially when positioning the lead with the stiffening
stylet in position. RV lead is shown in situ with tip close
to perforation point
A less common cause of myocardial perforation
may occur during explant/implant procedures.
Actively fixed electrodes – especially attached to
the right atrial free wall – may be impossible to
remove by manual traction and persistence and
additional force may result in myocardial avulsion
(Fig. 12.14) and rapid demise as a result of sud-
den hemopericardium. This was more a concern
Early Complications
Fig. 12.12 Histology in this case shows a perforation track
into the epicardial fat and an atrophic RV myocardium. It
was not clear whether this had been caused by the emer-
gency TPM (removed) which had been placed during the
resuscitation of this elderly lady brought in unconscious in
complete heart block and a ventricular rate of 10 per min
Fig. 12.13 Echocardiography should confirm hemoperi-
cardium (arrow) and be helpful in determining the success
of pericardiocentesis
with the old “helifix” leads than the more modern
“screw-in” electrodes.
Hemorrhage
Serious bleeding only occurs if the subclavian
artery is punctured. Swift removal of the needle
will often solve the problem. However, if the
operator is unaware of the inadvertent arterial
puncture and the introducer sheath is pushed
into the artery, simply removing the sheath is
253
Fig. 12.14 Some active fixation leads are firmly fixed to
the myocardium and forceful traction may result in myo-
cardial avulsion and fatal, sudden hemopericardium unless
surgical drainage and repair is not urgently performed
unlikely to solve the problem and surgical inter-
vention is likely to be required. If the guidewire
is still in situ, an attempt can be made to close
such a perforation with the Angioseal™ device
or similar percutaneous closure device. Early
recognition and immediate vascular repair is
paramount.
Venous oozing from the insertion site of a
temporary electrode is more likely to occur if the
central venous pressure is raised, for example, in
patients with heart failure or if the patient is anti-
coagulated. Generally the subclavian route should
be avoided if the patient is anticoagulated with
heparin or coumarin anticoagulants and the
cephalic vein used instead.
After permanent pacemaker implantation,
continued bleeding into the pacemaker pocket is
usually as a result of a missed bleeding arteriole
or vein within the pocket. Hematoma formation
usually occurs within the first few hours and if
large/tense or if associated with pain requires
drainage by opening the pocket under sterile con-
ditions in theater without delay (Fig. 12.15).
Anticoagulant therapy should be stopped prior
to pacemaker implantation and the INR normal-
ized with vitamin K or fresh frozen plasma if
necessary. Wherever possible, aspirin and clopi-
dogrel should be stopped for 1 week before in an
attempt to minimize hematoma formation which
may increase the incidence of later pocket
infection.
254 12 Complications of Pacemaker Implantation

Fig. 12.15 Small hematoma

as a result of venous oozing
within pacemaker pocket

Hemothorax

Hemothorax may occur if the needle is inserted

through both walls of either the subclavian artery
or vein (Fig. 12.16) and especially if the intro-
ducer sheath is also pushed into the subclavian
artery and then withdrawn. A widening mediasti-
nal shadow, a new ipsilateral pleural effusion, or
total opacification of the ipsilateral thorax on the
chest X-ray might follow serious bleeding fol-
lowing subclavian artery puncture and suggests
hemothorax. A fall in hemoglobin and typical
signs on examination of the chest would support
this serious complication that demands urgent
surgical referral.
Fig. 12.16 Hemothorax is a serious complication –
usually caused by perforation of the subclavian artery.
Left-sided hemothorax is shown
Air Embolism

Air embolism is rare but may occur if the
patient is in a head-up position and/or hypov-
olemic with either the needle or the introducer
sheath in the SCV without the syringe attached
or the guidewire in place. In this situation, it is
more likely to occur on inspiration. It can be
avoided by having the patient in a head-down
position when detaching the syringe from the
needle and when removing the vessel dilator
prior to introducing the lead.
Brachial Plexus Injury
This is rare and due to the needle puncture being too
posterior. Symptoms usually resolve spontaneously
Early Complications 255

Fig. 12.17 PA chest X-ray showing normal “J-shape”

position of the atrial lead (arrow)

Fig. 12.18 Lateral chest X-ray showing normal “J-shape”

after a few weeks. Rarely, infraclavicular lignocaine and anterior pointing position of the atrial lead at implan-
can cause temporary plexus nerve paralysis. tation (arrow)

Thoracic Duct Injury

This is rare. The main thoracic duct drains into

the junction of the left subclavian and left inter-
nal jugular veins. Milky aspirate should give a
clue to the needle misplacement. Conservative
treatment is usually the correct management.

Lead Displacement

Displacement of a passively fixed atrial lead is a

not infrequent occurrence. It results in failure to
sense and pace the atrium and is confirmed by a
PA/lateral chest X-ray. It is unusual with actively
fixed atrial leads which are now more commonly
used in order to reduce the problem. However, it Fig. 12.19 PA chest X-ray showing the atrial lead to
have lost its “J-shape” and to be hanging down vertically
may still occur even after using a “screw-in” lead (arrow) into the right ventricle
(Figs. 12.17–12.20).
Displacement of a ventricular lead is less
common and indeed rare when using active- of the atrial lead. In pacemaker-dependent indi-
fixation or “tined” passively fixed leads but it viduals, this may result in ventricular stand-
is potentially more serious than displacement still or severe bradycardia if there is no or only
256 12 Complications of Pacemaker Implantation

Fig. 12.21 Chest X-ray shows normal position of ven-

tricular lead in the apex of the RV

Fig. 12.20 Lateral chest X-ray showing that the atrial

lead has become displaced and fallen into the RV close to
the tip of the RV lead (arrow). The ECG shows loss of
atrial capture

an extremely slow ventricular escape rhythm.

Microdisplacement results in a rising pacing
threshold, failure to sense and intermittent cap-
ture, or complete failure to pace. A PA and lateral
chest X-ray should be obtained post-implantation
whenever lead displacement is suspected and
repositioning of the lead should be done imme-
diately using fluoroscopy under sterile conditions
(Figs. 12.21–12.23). Although leads fixed in the
RV outflow tract are probably no more prone to
displacement than those fixed in the RV apex, lead
displacement can occur (Figs. 12.24–12.26).
Figures 12.27 and 12.28 show both atrial and
ventricular lead displacement in a patient with three
leads as part of cardiac resynchronization therapy.
Fig. 12.22 Chest X-ray shows that the reason for loss of
ventricular capture and syncope after pacemaker implan-
tation is displacement of the RV lead back into the right
atrium (arrow)
Connection Failure
Connections between a temporary pacemaker
box and temporary lead should be checked regu-
larly since disconnection could result in cata-
strophic loss of pacing and cardiac output.
Early Complications
Fig. 12.23 Chest X-ray shows restoration of the correct
RV apex position of the ventricular lead
Fig. 12.24 Chest X-ray in a patient with a dual chamber
pacemaker with the RV lead actively fixed into the inter-
ventricular septum rather than the RV apex
Inadvertent failure to secure the head screws
between the permanent pacemaker and its perma-
nent leads may result in intermittent or total fail-
ure to pace and will require the pacemaker wound
to be reopened (Fig. 12.29).
257
Fig. 12.25 Within 24 h, the patient’s ECG showed loss
of capture and the chest X-ray showed displacement of the
RV lead into the RV outflow tract
Fig. 12.26 Chest X-ray after repeat active fixation of the
RV lead into the interventricular septum
Infection
Pacing should be performed under sterile
operating theater conditions with full aseptic
technique. Pyrexia, local inflammation, and dis-
charge of pus from a temporary electrode inser-
tion site suggest infection which is commonly
258 12 Complications of Pacemaker Implantation

Fig. 12.27 The more leads that are inserted, the greater Fig. 12.28 However, within 12 h, both the atrial (black
the incidence of displacement! This patient underwent arrow) and ventricular leads (green arrow) had displaced –
cardiac resynchronization therapy requiring repositioning

Fig. 12.29 Failure to

secure the connector pin
with the screw in the header
unit will lead to sudden loss
of capture. X-ray of dual
chamber ICD in a patient
with intermittently high lead
impedance. Note the distal
pin of the ventricular IS-1
connector (arrow). Unlike
the atrial connector which is
seen immediately above, the
pin is not wholly engaged
within the female connector
in the header. This led to an
intermittent break in the
pacing circuit causing high
pacing impedances and
intermittent loss of capture
Early Complications 259

Fig. 12.30 Staphylococcus

aureus is usually responsible
for early pacemaker
infections. Agar plates
showing golden colonies of
Staphylococcus aureus (left)
and the white colonies of
Staphylococcus epidermidis
(right)

due to Staphylococcus aureus or Staphylococcus

epidermidis. It is best to remove the infected elec-
trode and proceed to permanent pacing as soon as
possible – if indicated – in order to avoid this
complication which can lead to septicemia. When
the temporary pacemaker is required to be left in
situ for >2 days, for example in acute MI, the
insertion site should be washed daily with chlor-
hexidine or povidone iodine solution and then
covered with a sterile, transparent dressing. When
infection is obvious or confirmed, the electrode
should be removed after inserting a new electrode
Fig. 12.31 Redness, pain, swelling, and tenderness of
via a different route. Blood cultures should be the pacemaker pocket are the usual signs of serious
taken and antibiotics administered intravenously. Staphylococcus aureus infection. Although antibiotics
Infection of a permanent pacemaker site diminish the signs of inflammation, chronic exudates/dis-
may occur in <1% of cases. Again the respon- charge from the wound forms a crust covering the wound
sible organism is nearly always staphylococcus
(Fig. 12.30). Superficial infection of the wound However, it should be avoided in patients with
edges can usually be promptly treated with anti- bacteremia and in younger/fitter individuals who
biotics. Pocket infection, however, will require will require a new pacing system, since persistent
lead and generator extraction, wound drainage bacteremia, tricuspid endocarditis, and infection
and prolonged systemic, anti-staphylococcal of the new system is likely to follow. Extraction
antibiotics (Figs. 12.31–12.33). Lead extraction procedures are discussed in Chap. 19.
may be not too difficult early after implantation,
although screw-in leads have to be unscrewed
from the myocardium before applying traction to Subclavian Vein Thrombosis/
the lead(s). Removal late after implantation can Thrombophlebitis
be very difficult and requires the use of a lock-
ing stylet, laser extraction, and even thoracotomy. This is an unusual occurrence with the relatively
Cutting the lead short, capping the proximal end, low profile temporary pacing leads used today. It
and suturing it away from the infected area some- is more likely if a temporary lead is left in situ for
times has to be the treatment of choice in patients >1 week or if it becomes infected.
who are unlikely to tolerate an explant/implant This complication is rare after permanent pac-
procedure or thoracotomy and especially if life ing, but is more common when redundant leads
expectancy is very limited for other reasons. are left in the same subclavian vein (perhaps
260 12 Complications of Pacemaker Implantation

Fig. 12.32 Opening the

wound releases bloody,
yellow pus

Fig. 12.33 Large globules

of pus (arrow) can be sent
for culture and antibiotic-
sensitivity testing. Leads and
generator have to be
removed

from an old pacing system that could not be
removed in entirety) (Fig. 12.34). It presents as
discomfort and swelling in the ipsilateral arm
and shoulder, often with distended veins in the
upper arm and in the subclavicular and pectoral
region and often an engorged external jugular
vein (Figs. 12.35 and 12.36). Venography of the
axillary/subclavian vein will confirm the diagno-
sis and the exact site of occlusion (Figs. 12.37
and 12.38).
Patients should be treated initially, at least, by
analgesia and anticoagulant therapy for
3–6 months. Usually the swelling, discomfort,
and signs of phlebitis will disappear as recanali-
zation of the thrombosed subclavian vein occurs
within the first 4–6 weeks.
In the rare event of persistent, progressive
edema and pain in the arm, removal of the pacing
leads and generator will be necessary and a new
system will be required on the contralateral side.
Late Complications
Complications seen after hospital discharge are
listed in Table 12.2.
Late Complications 261

Fig. 12.34 Multiple leads placed in the subclavian vein

(arrow) may lead to fibrosis and/or thrombosis and signs
of venous obstruction

Lead Displacement

Atrial and ventricular pacing leads may dislodge

from their implantation positions between dis-
charge and the first follow-up appointment. Loss
of atrial or ventricular pacing or sensing on the
ECG may be the first clue to a problem, although
a recurrence of dizziness/near syncope/syncope
may result from ventricular lead displacement if
the patient is pacemaker dependent. X-ray of the
chest in PA and lateral views should confirm the
diagnosis (see Figs. 12.21–12.23). Repositioning
of the leads will be necessary to restore the
function.
Twiddler’s syndrome can be a cause of early Fig. 12.35 Left subclavian vein thrombosis causes dis-
lead displacement. tended veins in the left pectoral region, left side of neck
(arrow) and left arm as well as discomfort and swelling of
the left arm

Failure to Sense

Most pacemakers will be programmed in a
demand mode, whereby the pacemaker senses
spontaneous atrial and ventricular activity and
only discharges a stimulus if a native beat has not
occurred within a pre-set period, which is pro-
grammable. Failure to sense spontaneous activ-
ity due to microdisplacement or tissue growth
may result in pacemaker discharge on intrinsic or
ectopic QRS complexes (Fig. 12.39). This may
be hazardous and risks causing ventricular
fibrillation, especially in patients with myocar-
dial infarction.
It may be solved by lowering the setting for
R-wave sensitivity, for example, from 5 to 2 mV,
thus making the pacemaker more sensitive. At
the 2 mV setting, the pacemaker will sense any
262 12 Complications of Pacemaker Implantation

Fig. 12.36 Distended veins

in the subclavicular/pectoral
region

Fig. 12.37 Venography of

the left axillary/left
subclavian vein identifies
subclavian/axillary vein
thrombosis (black arrow).
Distended collateral veins
are evident on venography
(white arrows)
Late Complications 263

Table 12.2 Late complications after pacemaker

implantation
Problem Consequence
Lead displacement Failure to sense, failure to pace,
diaphragmatic stimulation
Exit block Failure to pace
Inappropriate Intermittent failure to pace,
inhibition e.g., myopotential inhibition
Lead fracture Failure to pace
Insulation break Failure to sense/pace; muscle
twitching
Infection
Early Staphylococcus aureus
Late Staphylococcus epidermidis
Erosion Generator erosion
Lead erosion
Superior vena caval SVC obstruction syndrome
obstruction
Fig. 12.38 Long segment of thrombosis of the left sub-
Subclavian vein Pain, swelling of ipsilateral
clavian and axillary veins (between the black arrows).
thrombosis limb
Note the distended collateral veins which are visible clini-
cally as well as angiographically Premature generator Failure to pace
failure
Pacemaker syndrome Dyspnea, neck pulsation,
signal of 2 mV or more but not a signal of <2 mV. dizziness
At the 5 mV sensitivity setting, the pacemaker Twiddler’s syndrome Lead displacement/fracture
will sense signals of ³5 mV but not those <5 mV. “Rate-responsive” Inappropriate heart rate
system specific changes
Thus, lowering the sensitivity setting (e.g., complications
3–1.5 mV) makes the pacemaker more capable of Pacemaker-mediated Palpitations
sensing lower R-wave amplitudes, that is, 1.5 mV tachycardia
setting has a higher sensitivity than 3 mV.
Conversely, raising the sensitivity setting (e.g.,
from 1.5 to 4 mV) will make the pacemaker less If all these maneuvers fail, the lead will have to
sensitive – only sensing any signals of 4 mV or be replaced.
greater.

Inappropriate Pacemaker Inhibition

Exit Block
Excessive tissue growth between the tip of the
lead and the endocardium may increase the
threshold to pace sufficiently causing pacing
failure without lead displacement. The ECG
will show pacing spikes but no following QRS
complex (Fig. 12.40). This is an infrequent
problem now with modern leads with porous
electrodes and steroid-eluting tips. It is most
likely to occur during the first 3 weeks to
3 months after implantation. Usually the prob-
lem can be solved by reprogramming the pace-
maker to an increased output and/or pulse width.
External inhibition of a demand pacemaker
from myopotentials from the underlying
or nearby muscles or from electromagnetic
waves emitted from nearby electrical equip-
ment can sometimes inhibit pacemaker output
(Fig. 12.41). The ECG will show absent pac-
ing stimuli and usually the electrical poten-
tials that are responsible for the inhibition.
It can be demonstrated by asking the patient
to push their hands firmly together or push
against a wall. Myopotential (EMG) inhibition
may cause syncope or severe dizziness in a
pacemaker-dependent patient when using their
264
Fig. 12.39 Failure to sense
Fig. 12.40 Failure to
capture
Fig. 12.41 Myopotentials (arrow) from upper chest wall
muscles during arm exercises cause inhibition of pace-
maker output due to oversensing from this unipolar sys-
arms or upper body musculature such as pecto-
ralis major muscle, which are situated close to
the pacemaker (Fig. 12.42). Cutting a hedge,
hoeing the garden, carrying boxes, hanging out
the washing, and even hugging a loved one are
examples of such movements (Figs. 12.43–
12.45)! It is most likely to occur in pacemak-
ers programmed to unipolar sensing and can be
abolished by reprogramming to bipolar sens-
12 Complications of Pacemaker Implantation
tem – resulting in the onset of dizziness. Typical activities
are shown in Figs. 12.43–12.45
ing or by reducing the pacemaker’s sensitivity.
Reprogramming the pacemaker to fixed rate
mode (VOO) will also prevent inappropriate
inhibition and in days gone by surrounding the
generator in an insulating boot will also make
the phenomenon unlikely to occur.
False inhibition or oversensing may also occur
with spurious signals from lead fracture or be
due to large T-wave voltage. Increasing the
Late Complications 265

Fig. 12.42 Large myopotentials (arrow) when using the left upper arm cause pacemaker inhibition of this unipolar
system, asystole and transient presyncope

pacemaker’s sensitivity setting (e.g., from 2 to

5 mV) should make the device less able to sense
such spurious signals while maintaining the abil-
ity to sense normally conducted or ectopic R
waves.

Muscle Stimulation/Twitching

This usually only occurs in unipolar pacing and

is due to the can being the anode, which leads to
stimulation of the underlying pectoral muscle.
Reprogramming to a bipolar mode (if possible)
or reducing output and/or pulse width might
help. Diaphragmatic stimulation may occur
when a thin RV overlies the diaphragm and
phrenic nerve stimulation when thin atrial mus-
cle separates it from the atrial electrode. Reducing
the output and/or pulse width might stop the
problem; otherwise, the lead will need to be Fig. 12.43 Adduction of the arms, e.g., during carrying
repositioned. heavy weights
266
Fig. 12.44 Hoeing soil
Lead Fracture
Lead fracture is now rare with modern leads, but
may occur late after pacemaker or ICD implan-
tation. It often occurs at the point of entry of the
lead into the subclavian vein, at the site of liga-
ture fixation or at any point of excess angulation
of the lead (Figs. 12.46 and 12.47). It would
present as a recurrence of syncopal symptoms
in pacemaker-dependent patients and pacing
stimuli will be absent on the ECG. Lead imped-
ance will be very high (>1,000 Ω). X-ray of the
lead in PA and lateral views may show a gap or
fracture in the lead. It may still be a problem
12 Complications of Pacemaker Implantation
Fig. 12.45 Hugging a loved one can result in near syn-
cope/syncope
in pacemaker “twiddlers.” Replacement of the
pacemaker system will be necessary.
Poor/loose fixation of the lead’s connector pin
into the pacemaker may present after hospital
discharge, similarly with loss of stimuli on the
ECG or a high pacing threshold and high lead
impedance.
Late Complications 267

Fig. 12.46 The lead

insertion point is a vulnerable
site for lead fracture as in this
muscular weight lifter where
the leads lay between the left
clavicle and head of the left
first rib

Fig. 12.47 Subsequent lead

fracture (arrow)

Insulation Break leads may be more susceptible (Figs. 12.50 and

This is often due to the insulation being cut
through by a tight fixation ligature applied to the
lead without using the protective plastic collar,
and it may be possible to see the defect on a chest
X-ray (Figs. 12.48, and 12.49). Polyurethane
12.51). Insulation breaks will allow current leak-
age and may cause stimulation of nearby mus-
cles, twitching, and early battery depletion. Lead
impedance will be very low (<250 Ω). ECG
should show pacing spikes but capture may or
may not be preserved.
268 12 Complications of Pacemaker Implantation

Fig. 12.48 Insulation breaks

on leads can result in local
muscle twitching, premature
battery depletion, and loss of
capture. Careful scrutiny of
the chest X-ray might suggest
the problem (arrow)

Fig. 12.49 Magnified view

of the site in question
confirms a section of lead
without its insulation (green
arrow). Loss of capture and
low lead impedance result

Fig. 12.50 Tight silk

sutures applied to the lead
directly rather than over the
protective collar can cut
through lead insulation
Late Complications
Infection
Pacemaker pocket infection is a serious complica-
tion which invariably necessitates removal of the
whole system – generator and electrode(s), and
implantation of a new pacing system. It is usually
due to poor aseptic technique, poor skin prepara-
tion, and poor practical technique and prolonged
Fig. 12.51 Magnified view showing fractured lead insu-
lation at site of “anchoring” silk suture
Fig. 12.52 Swollen, inflamed area at site of
epicardial pacemaker implant suggests pocket
infection or even abscess formation in this case
269
procedures. Having to reopen the pocket because
of early lead displacement or hematoma forma-
tion increases the risk of infection.
Within the first month of implantation, the
commonest organism is Staphylococcus aureus.
Patients will present unwell with a pyrexia and
discomfort over the pacemaker pocket which
may be tender and usually inflamed (Figs. 12.52
and 12.53). The wound may discharge exudate
or pus and this will usually be revealed when the
pocket is incised. Blood cultures and swab from
the wound should be collected and intravenous
antibiotics, usually IV flucloxacillin, should be
started prior to removal of the pacing system.
IV antibiotics alone, even over prolonged peri-
ods, will invariably not solve this problem but
may give rise to fungemia, which is difficult to
treat. Echocardiography should be performed
to exclude tricuspid valve (TV) endocarditis
(Fig. 12.54). Every effort should be made to
remove the leads from such patients as not infre-
quently the electrodes are infected with bacteria.
If TV endocarditis develops, a prolonged
course of antibiotics should be given after removal
of the infected system. Tricuspid regurgitation
may develop and be demonstrated by echocar-
diography (Fig. 12.55). Only if vegetations fail
270 12 Complications of Pacemaker Implantation

Fig. 12.53 Close-up view showing

the infected pacemaker pocket with
impending generator erosion

Fig. 12.54 Transthoracic echocar-

diogram showing large vegetation on
the tricuspid valve in this patient with
infective endocarditis as a result of an
infected pacing system

Fig. 12.55 Transthoracic echocar-

diogram showing severe tricuspid
regurgitation in this patient with
vegetations on the tricuspid valve as a
result of an infected pacing system
Late Complications
to resolve and appear to be increasing in size
despite antibiotics should surgery be considered.
Pulmonary abscesses should resolve with effec-
tive IV anti-staphylococcal agents (Fig. 12.56).
If large vegetations are present on the lead(s) or
on the TV, fungal infection should be considered
and surgical removal of lead(s) should probably
be preferred to removal via the subclavian vein
(Fig. 12.57 and 12.58). Surgical removal of
the lead(s) may be required if traction or laser-
removal devices fail to free the leads from the
endocardium (Figs. 12.59–12.61).
Beyond 6 months after implantation,
Staphylococcus epidermidis is more commonly
Fig. 12.56 Chest X-ray showing a pulmonary abscess.
Note the fluid level (arrow) visible within the abscess due
to Staphylococcus aureus infection on the pacemaker,
pacing lead, and tricuspid valve
Fig. 12.57 Open heart
surgery is sometimes
necessary to remove infected
pacemaker systems whose
leads are fixed to the wall of
the great veins, tricuspid
valve, right atrium, or right
ventricle
271
responsible for pacemaker pocket infection.
This may present only as a swelling over the
generator, without much in the way of pain or
signs of inflammation (Fig. 12.62). Blood cul-
tures should be checked and, if positive, IV anti-
biotics – perhaps Teicoplanin or flucloxacillin
– should be commenced (Fig. 12.63) and plans
made to remove the infected system.
Superior Vena Caval Obstruction
Multiple leads placed in the SVC can cause cica-
tricial fibrosis where the leads are in contact with
the wall of the SVC. If blood flow is significantly
impaired past the obstruction, venous thrombosis
and SVC obstruction may occur. This will present
with fairly typical SVC obstruction syndrome
with engorged head and neck, suffused conjuncti-
vae, distended neck veins and prominent veins
over the upper chest (Fig. 12.64 and Fig. 12.36).
Venography of the SVC should clearly identify
the anatomical problem. Percutaneous balloon
angioplasty of the obstruction may relieve it and
the signs of SVC obstruction will disappear imme-
diately (Fig. 12.65). Anticoagulation with heparin
and then long-term warfarin should be given.
Alternatively, the pacing leads should be removed
and the system replaced by either an epicardial
system or a pacing system with leads placed in the
RV via the IVC from the femoral vein. The gen-
272 12 Complications of Pacemaker Implantation

Fig. 12.58 Atriotomy

showing infected tricuspid
valve with vegetations and
the pacing leads that are
about to be removed

Fig. 12.59 Infected

pacemaker and leads
removed at open heart
surgery

erator is then buried in the lower abdomen region suggest that diagnosis and anticoagulant
(Fig. 12.66). therapy should be commenced (see Fig. 12.35).

Subclavian Vein Thrombosis Pacemaker Lead or Generator Erosion

Clinical evidence of this is uncommon but This is less of a problem than it used to be
would present as a swollen arm that feels heavy with higher-profile leads and the older, larger
and tight or painful. Distended veins on the generators. Emaciated patients are most at
upper arm, chest in the sub/supra-clavicular risk (Fig. 12.67). Both lead and generator
Late Complications
Fig. 12.60 This infected system removed by open heart
surgery shows the excess tissue that can form around the
lead and make it completely adherent to the wall of the
RV/RA and even to the tricuspid valve. Such tissue has to
be resected surgically in order to free the lead sufficiently
to enable its removal
erosion through the skin may occur if the
pocket is too small and the system is too close
to the skin. Both are usually associated with
pocket infection.
Pre-erosion skin changes include a dusky pur-
ple or red discoloration of the skin, which is often
thin and tethered to the lead or generator
(Fig. 12.68). It may be tender to pressure. This is
an opportunity to promptly revise the pacemaker
pocket and move the whole system deeper
beneath the subcutaneous fat and away from the
skin. Once the skin has eroded and the electrode
or generator has been exposed through the skin, it
may be assumed that skin organisms have entered
the pacemaker wound and removal of the whole
system is inevitable (Figs. 12.69–12.71). Once
erosion is evident, merely trying to bury the lead
and/or generator rarely leads to a successful out-
come, although in certain situations, for example,
in very frail, elderly demented patients who
would have difficulty tolerating an explant/
implant procedure, it may be worth attempting, at
least initially.
273
Pacemaker Generator Failure
Unexpected recurrence of symptoms of dizziness
or syncope may be due to unexpected pacemaker
failure and loss of output (Fig. 12.72). This is
rare with modern lithium iodine batteries and
with regular follow-up of patients in a pacemaker
clinic. Regular checks on battery life in the clinic
enable safe planning for elective generator
replacement. However, for those patients who
fail to attend follow-up pacemaker checks, they
are at risk of sudden loss of pacing if the battery
reaches end-of-life (EOL) (Fig. 12.73).
Unexpected component failure is very rare. In
the event of such an occurrence anywhere in the
world, the pacemaker manufacturer will investi-
gate the case as an emergency, and if component
failure is thought to be possible they will send an
urgent warning of potential component failure to
all implanting centers. Elective generator replace-
ment may be advised and usually the generators
will be provided free of charge.
Several factors may lead to premature bat-
tery depletion. These include low lead imped-
ance with a large electrode tip, wide pulse width
or high amplitude settings, constant pacemaker
use or fast pacing rate and complex circuitry in
DDD units with two sensing and two pacing cir-
cuits or use of several monitoring facilities
using sophisticated microprocessors within the
pacemaker.
The EOL of most pacemakers used to be
indicated by slowing of the basic pacing rate or
magnet rate, an increasing pulse width or a decrease
in output voltage; however, routine interrogation
of the generator in the pacemaker follow-up clinic
will indicate the amount of battery life that remains
and the expected time for replacement.
Pacemaker Syndrome
Pacemaker syndrome occurs when a patient in
sinus rhythm but complete AV block undergoes a
VVI pacemaker implantation. At frequent intervals,
with loss of AV synchrony, the atria will contract
against closed A-V valves resulting in cannon
waves – often visible in the internal and external
274 12 Complications of Pacemaker Implantation

Fig. 12.61 This extracted, infected lead is covered in vegetations

Fig. 12.62 Late pocket

infection may only present
as slight discomfort around
a swollen pocket and no
other signs of local
inflammation

jugular veins. It is associated with an impaired car- Twiddler’s Syndrome

diac output during exercise, the unpleasant sensation
from the cannon waves, dizziness, and even syn-
cope. Hypotension is more marked on standing and
most severe during the first few seconds of ventric-
ular pacing. It can be corrected by implanting an
atrial electrode and restoring A-V synchrony.
Twiddler’s syndrome is characterized by rotation
of the pacemaker or ICD with subsequent coiling
of the lead(s). Rotation of the pulse generator is
made possible by the loose subcutaneous pocket
and the size and weight of the generator relative to
Late Complications 275

Fig. 12.63 After opening the

pocket and culturing fluid from
within it, Staphylococcus epider-
midis is the commonest cause found
at this stage. Antibiotic sensitivities
will help guide appropriate
treatment

the pocket. It may occur spontaneously or by will-

ful manipulation by the patient. Coiling of the
lead(s) may induce lead displacement or lead
fracture and may be a serious complication in a
pacemaker/ICD-dependent patient (Figs. 12.74
and 12.75). Lead displacement can produce muscle
stimulation or phrenic/brachial plexus stimulation.
Lead fracture requires lead replacement, and
lead displacement will require lead repositioning or

Fig. 12.64 Superior vena caval obstruction can occur

following fibrosis/thrombosis at the site of adherent leads.
The more leads that are present increase the likelihood of
this complication. A swollen, suffused face with engorged
veins in the neck and on the upper chest should suggest
this complication
276
Fig. 12.65 (Upper left) Venogram showing SVC obstruc-
tion by a critical stenosis at the site of pacemaker leads
which have become adherent to the wall; (upper middle)
angioplasty balloon to dilate the stenosis is severely
indented by this fibrotic narrowing; (upper right) balloon
removal if severe coiling/twisting of the lead has
occurred (Fig. 12.76). The opportunity should be
taken to create a tighter/smaller generator pocket
and to fix the lead(s) to the fascia by direct suturing.
Simply burying the generator behind the pectoralis
major muscle might also prevent further twiddling.
Pacemaker-Mediated Tachycardia
Pacemaker-mediated tachycardia (PMT) is defined
as any condition in which a pacing device paces
the ventricles at rates that are “inappropriately
fast.” This term was classically reserved for the
reentrant tachycardia occurring in patients with
12 Complications of Pacemaker Implantation
fully inflated at higher pressure dilates the stenosis; (lower
left) larger balloon fully dilated relieves the obstruction
immediately; (lower right) after balloon dilatation, the
SVC obstruction is immediately relieved and long-term
anticoagulant therapy is commenced
dual chamber pacemakers. The device forms the
anterograde (A → V) limb of the circuit, and the
atrioventricular node is the retrograde limb
(V → A) of the circuit. The patient must have
V → A conduction with an atrial activation time
that is longer than the programmed postventricu-
lar atrial refractory period (PVARP). A ventricu-
lar-paced beat or a properly timed PVC conducts
retrograde via the AV node (or accessory path-
way) to the atrium. If the atrial depolarization
occurs after the programmed PVARP, but before
the next timed atrial-paced beat, ventricular pac-
ing will be triggered at the programmed AV inter-
val. PMT tends to occur at or close to the
programmed URL and depend upon the pro-
Late Complications
Fig. 12.66 Dual-chamber Kappa™ (Medtronic) pace-
maker is implanted in the right inguinal region (arrow)
using CapSure Fix™ active-fixation leads in the right
atrium and ventricle, avoiding traversing the SVC in this
patient recently treated by balloon angioplasty for SVC
obstruction at the site of multiple previous pacing leads –
which were also removed
grammed AV delay and the PVARP. This gener-
ates an incessant reentrant arrhythmia (so-called
“endless-loop tachycardia”) that lasts for as long
as there is continuous VA conduction with atrial
activation outside the PVARP (Fig. 12.77). Atrial
undersensing can also result in PMT and interro-
gation of a modern device should be able to clarify
this is the mechanism. Modern devices possess
specific algorithms which can terminate PMT if
tracked rates persist at the URL. The device can
be programmed to lengthen the PVARP after a
277
Fig. 12.67 Pre-erosion of this right-sided pacemaker is evi-
dent (arrow). The area is usually painful, tender, and reddened.
Usually the skin is adherent to the underlying generator
PVC or with an incessant tachycardia at the URL
or prevent one atrial sensed event from being
tracked.
PMT may also be due to a too sensitive rate-
responsive setting, tracking of an atrial tachyar-
rhythmia related to the upper rate settings,
tracking of atrial noise (e.g., EMI) or with inap-
propriate pacemaker manipulation with the rate-
response turned on.
278
Fig. 12.68 (Top) At the site of purple discoloration, the
pacemaker is adherent to the skin only 14 months after
implantation. The area is usually tender to palpation. This
is a typical appearance of pre-erosion and the generator
should be resited or removed completely without delay.
(Bottom) Close-up view
12 Complications of Pacemaker Implantation
Fig. 12.69 Lead erosion in this rather superficially
placed pacemaker will necessitate the whole system to be
replaced on the opposite side. Subpectoral placement
should be considered in thin emaciated patients
Fig. 12.70 This permanent pacemaker lead could not be
extracted when an attempt was made to remove an infected
system and so the lead was simply cut and the pacemaker
wound closed. A few months later the lead/bare wire
eroded through the skin. The patient tried initially to cover
it with cotton wool but it was uncovered when she attended
for a routine pacemaker check. The lead had to be removed
via an atriotomy
Late Complications 279

Fig. 12.71 Severely eroded

and infected epicardial
pacing system

Fig. 12.72 Loss of capture (pacing spike but no ensuing QRS complex) and loss of output (absence of pacing spikes
and asystole) are both evident on this ECG in this patient whose device is at EOL

Fig. 12.73 Sudden loss of pacing spikes indicates loss of output due to impending battery failure – so-called “end-of-
life” or EOL

Troubleshooting should establish the mecha-
nism and allow preventive therapy.
Unwanted Symptoms Associated
with Rate-Adaptive Pacemakers
Sensors of Body Motion
Pacemakers with piezoelectric crystals attached to
the inside of the can (so-called activity sensors)
respond to pressure/vibrations applied to the device
and so the heart rate may increase without exer-
cise. Some examples include sleeping in a prone
position or turning in bed might cause inappropri-
ate tachycardia; horseback riding or riding in a car
or on a cycle over rough terrain; using hand-held
drills, for example, pneumatic or dental drills; in
close proximity to very loud rock music – deep
base/low frequencies. Postoperative shivering or
epileptic fits may also increase the pacing rate.
280 12 Complications of Pacemaker Implantation

Fig. 12.75 Twiddler’s syndrome. This young patient had

Fig. 12.74 Twiddler’s syndrome. This young man had a
a Maximo II DR ICD implanted 6 weeks earlier. Continual
Teligen™ ICD device (Boston Scientific) implanted
rotation of the device within its pocket caused the atrial
4 weeks earlier. By continual rotation of the device within
lead to be pulled out of the RA into the pocket itself.
its pre-pectoral pocket, he managed to place enough tension
Tension is also placed on the RV lead although it has not
on this active-fixation, Sprint Quattro, single, RV bipolar
yet been pulled off the RV myocardium. Note the coiling
lead (Medtronic) that it became detached from the RV myo-
of the leads around the ICD device. (Top) Active-fixation
cardium and retracted back into the left subclavian vein
leads placed in the RA and RV shown immediately after
implantation of this ICD. (Bottom) 6 weeks later, contin-
ual rotation of the device within the pocket has pulled the
RA lead off the RA myocardium and its tip is now in the
pocket. The RV lead has been stretched and the tip fixed to
the RV apex is also likely to soon come free from the
myocardium. Both leads had to be repositioned
Late Complications 281

Fig. 12.76 Defibrillator lead removed in a patient with the lead displaced into the left brachiocephalic vein. The
Twiddler syndrome. Constant rotation of the device within lead had to be extracted and a new lead inserted
the pocket eventually placed tension on the lead tip and

Fig. 12.77 Pacemaker-mediated tachycardia is initiated by an ectopic beat in the left-hand ECG and almost initiated
by several ventricular ectopic beats in the right lower ECG

Sensors of Minute Ventilation especially rotating shoulder actions on the side

Coughing, hyperventilation, and tachypnoea of the pacemaker may increase the pacing
can lead to an increase in pacing rate, as can an rate. Electrocautery may change transthoracic
increased ventilation rate during anesthesia. impedance and cause an increase in pacing
Vigorous movement of the ipsilateral arm and rate.
282
Fig. 12.78 Two lead tip fragments have been retained in
the wall of the left subclavian vein, having fractured from
the lead’s coil/insulation during attempted removal
by traction
12 Complications of Pacemaker Implantation
Q-T Sensors
Frequent ventricular ectopics may make T wave
detection difficult and the Q-T interval may be
affected by electrolyte disturbances, drugs, and
ischemic heart disease giving an unpredictable
rate response.
Dual sensors and sensor “blending” in pace-
makers and sensor “cross-checking” reduce the
frequency of false responses.
Retained Fragments
Occasionally when attempting to remove leads
from the heart and great veins, the lead may frac-
ture when under stress by forceful traction.
Fragments of the lead such as the tip may become
embedded in the wall of the right ventricle or a
vein wall and separated from the fine filaments of
the stretched/fractured electrode. These small
fragments usually cannot be retrieved and are
best left alone (Fig. 12.78).
 Temporary Pacing
Indications
Patients with significant intracardiac conduction
defects who are symptomatic with dizziness or
syncope due to bradycardia should have a tempo-
rary pacemaker (TPM) inserted if the defect is
thought to be reversible, or if when deemed irre-
versible, permanent pacemaker implantation
cannot be done immediately. After acute myo-
cardial infarction (MI) (see Fig. 3.1) or cardiac
surgery, evidence of new or extensive intracar-
diac conduction defect, prolonged sinus arrest or
asystole requires a TPM. Those with “at risk”
conduction defects require a TPM prior to gen-
Fig. 13.1 Temporary
epicardial pacing is not
infrequently required after
certain types of open heart
surgery such as aortic valve
replacement shown here
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_13, © Springer-Verlag London 2012
13
eral anesthesia as do patients with certain drug
overdosage associated with severe bradycardia,
for example, digoxin toxicity, b-blocker, or vera-
pamil overdosage.
Temporary pacing is also indicated during
interventional procedures such as percutaneous
coronary rotational atherectomy to a dominant
right or left circumflex coronary artery and for
AV node ablation (unless a permanent pacemaker
is present) since both may be associated with pro-
found bradycardia or heart block (see Fig. 3.9).
A TPM is indicated for patients with hypertro-
phic obstructive cardiomyopathy who are under-
going alcohol septal ablation, as this procedure
283
284
Fig. 13.2 Epicardial
pacing leads exit the
chest wound and are
attached to the connect-
ing cable which in turn
is connected to the
temporary pacing box
may be associated with AV block (see Fig. 3.8).
Temporary epicardial pacing may be necessary
after cardiac surgery, especially after surgery
close to the AV node or bundle of His (Figs. 13.1
and 13.2). TPMs are also used in electrophysio-
logical studies (see Fig. 3.12) and for overdrive
pacing in patients with ventricular tachycardia
(see Fig. 3.11).
Patients with infrequent bradycardias should
not routinely receive a TPM while awaiting per-
manent pacemaker implantation.
The clinical and electrocardiographic indica-
tions for TPM are shown in Tables 13.1–13.4.
AV Block in Acute MI
Complete AV Block
In anterior MI, complete AV block usually is a
result of septal infarction and requires tempo-
rary pacing. In inferior MI, complete AV block
most often occurs as a result of right coronary
artery occlusion with loss of the AV nodal
artery, and temporary pacing is necessary
(Fig. 13.3).
13 Temporary Pacing
Table 13.1 Clinical indications for temporary pacing
Dizziness or syncope due to chronic disease of the
conducting tissue (if permanent pacing is not immedi-
ately possible)
Hemodynamics compromised by bradycardia
Bradycardia-induced ventricular arrhythmias
Intracardiac conduction defects after acute myocardial
infarction (see Table 13.2)
Prior to general anesthesia in patients “at risk” of 2° or
3° AV block (see Table 13.3)
Prior to rotational coronary atherectomy in a dominant
right or left circumflex coronary artery
Post-cardiac surgery (see Table 13.4)
Termination of refractory tachyarrhythmias, e.g.,
ventricular tachycardia
During electrophysiological studies, e.g., initiation/
termination of arrhythmias
During AV node ablation
Drug toxicity, e.g., digoxin, B-blockers causing
symptomatic, severe or life-threatening bradycardia
Second-Degree AV Block
Mobitz Type I (Wenckebach), where there is a
progressive increase in the PR interval eventu-
ally leading to complete failure of a P wave to
AV Block in Acute MI 285

conduct and produce a QRS complex is usually adverse clinically significant hemodynamic
due to decremental conduction at AV node level. effects. It may respond to IV atropine (1 mg). In
In acute inferior MI, it usually does not require anterior MI, this type of AV block may be more
temporary pacing unless the bradycardia causes sinister and patients should be temporary
paced.
Mobitz Type II AV block is evident by a fixed
Table 13.2 ECG indications for temporary pacing in PR interval with sudden failure of conduction of
acute myocardial infarction
the atrial impulse (P wave). It frequently occurs
Alternating RBBB/LBBB in the presence of a wide QRS perhaps because it
Long PR + new RBBB + LAFB is commonly associated with more distal fascicu-
New RBBB + LPFB lar disease. It requires temporary pacing in both
Long PR + LBBB
inferior and anterior MIs as complete AV block
RBBB + new LPFB
often follows (Fig. 13.4).
Wenckebach (Mobitz type I) 2° AV Block in anterior
MI (in inferior MI if bradycardia poorly tolerated)
Mobitz type II 2° AV block in anterior MI and in
inferior MI if heart rate <40 beats/min or associated First-Degree AV Block
with hypotension or ventricular tachyarrhythmia
Complete AV block Although approximately 40% of patients with
Symptomatic junctional bradycardiaa first-degree AV block may eventually develop
Symptomatic sinus arrest (>3 s or if hemodynamically higher degrees of AV block, patients with first-
affected)a
degree heart block do not require temporary
Severe symptomatic sinus bradycardiaa
Asystole
pacing.
a
If unresponsive to atropine
Table 13.4 Types of cardiac surgery which are more
likely to be associated with the need for temporary
Table 13.3 ECG indications for temporary pacing prior pacing
to general anesthesia for noncardiac surgery
Aortic valve replacement for calcific aortic stenosis
Alternating RBBB/LBBB (with calcium extending into the septum)
Long PR + new RBBB + LAFB Aortic valve surgery/interventricular septal abscess
New RBBB + LPFB drainage/repair in infective endocarditis
Long PR + LBBB Tricuspid valve surgery/Ebstein’s anomaly repair
RBBB + new LPFB Repair of AV canal defects
Wenckebach (Mobitz type I) 2° AV block Ostium primum atrial septal defect repair
Mobitz type II 2° AV block Surgical repair of corrected transposition/AV discor-
Complete AV block dance defect
Sick sinus syndrome – severe sinus bradycardia/sinus Myomectomy for hypertrophic obstructive
arrest cardiomyopathy

Fig. 13.3 Complete heart block

286
Fig. 13.4 Mobitz type II AV block
Fig. 13.5 Trifascicular block manifested by 1° heart block, right bundle branch block and left axis deviation
Bundle Branch Block
Patients with trifascicular disease or so-called
nonadjacent bifascicular disease complicating
acute MI should receive temporary pacing.
Trifascicular disease (Fig. 13.5) includes
alternating RBBB/LBBB, long PR + new RBBB
+ LAFB, long PR and new RBBB + LPFB, and
long PR + LBBB.
13 Temporary Pacing
Nonadjacent bifascicular disease includes
RBBB + new LPFB. If LBBB + long PR develops
in acute anteroseptal MI, the LBBB is assumed to
represent LAFB + LPFB, although a His-bundle
study would need to be done to confirm this. RBBB
+ LAFB (left axis deviation) is not uncommon after
acute anterior MI as these two fascicles are in the
anterior portion of the septum. A long PR in this
situation should indicate the need for pacing.
Techniques
Fig. 13.6 Wenckebach 2° AV block in conjunction with prolonged sinus arrest
Sino-Atrial Disease
Marked sinus bradycardia or sinus arrest may
occur after acute MI, most commonly inferior MI.
Since this is likely to be vagotonically mediated,
it usually responds to IV atropine. Only if unre-
sponsive to atropine or poorly tolerated should
temporary pacing be considered (Fig. 13.6).
Prior to General Anesthesia
ECG abnormalities as listed in Table 13.3 should
indicate the possible need for prophylactic pacing
prior to general anesthesia, especially if there is
evidence of any recent deterioration such as a
lengthening PR or the development of new LAFB.
Holter ECG monitoring should be considered
prior to surgery to identify those possibly at higher
risk. As a minimum, ECG monitoring, IV access,
and an external transcutaneous pacing facility
should be available in theater if patients are thought
to be at risk of developing severe bradycardia or
higher degrees of AV block during general anes-
thesia. If a strong indication for permanent pacing
exists and the surgery is not urgent, permanent
pacemaker should occur first and the procedure
requiring general anesthesia postponed.
During or After Cardiac Surgery
Temporary epicardial pacing may be required in
cardiac surgery adjacent to the AV node and bundle
of His. Such surgery includes aortic valve replace-
ment for calcific aortic stenosis, particularly when
287
the calcium extends into the interventricular sep-
tum, aortic valve replacement in infective endo-
carditis especially when infection has caused septal
abscess formation – when permanent pacing is
indicated (see Fig. 3.3), tricuspid valve surgery and
Ebstein’s anomaly, repair of AV canal defects and
ostium primum ASD and closure of a VSD in cor-
rected transposition or of the ventricular compo-
nent of a complete AV canal defect.
Techniques
Temporary pacing may be performed transcutane-
ously by the application of external pacing elec-
trodes to the chest wall or by insertion of pacing
electrodes transvenously. The latter may be inserted
using a femoral, subclavicular, supraclavicular,
internal jugular, or antecubital approach. When
pacing is necessary in a patient who has received
thrombolytic therapy for acute MI, a TPM should
be placed via the femoral, brachial, or internal jug-
ular route – sites that are compressible. During car-
diac surgery, temporary pacing can be established
by direct attachment of special pacing wires to the
epicardium – so-called epicardial pacing.
Transesophageal ventricular pacing, devel-
oped in 1969, has been abandoned because of its
relative ineffectiveness compared to modern tran-
sthoracic, transcutaneous pacing. Transesophageal
atrial pacing is more reliable than transesopha-
geal ventricular pacing but is now rarely used and
has been replaced by transvenous atrial pacing
(see below).
A review of temporary cardiac pacing was
presented by McCann in 2007. He concluded that
288
Fig. 13.7 Lifepak 20 (Medtronic Inc.) is both a defibrillator and external pacemaker
cardiologists who implant TPMs have lower com-
plication rates and higher success rates than non-
specialists, that the internal jugular vein (R > L)
followed by the subclavian (L > R) and then femo-
ral vein were the most preferred route of access, and
that antibiotics and ultrasound probes should be
contemplated for all temporary wire insertions. The
commonest complications were sepsis, followed by
incorrect placement of the wire causing failure to
pace, arrhythmias, myocardial and lung perforation.
Training in the skills required to insert transvenous
TPMs is essential before accepting the responsibil-
ity for this potentially hazardous procedure.
External, Transthoracic Pacing
Modern transcutaneous, transthoracic pacemakers
function in demand mode and have a maximum
output in the region of 150 mA (Fig. 13.7).
Appropriate pacing electrodes (some which can
act as defibrillator pads) are required (Figs. 13.8
and 13.9), which are linked via a cable to a special
13 Temporary Pacing
connector which is then inserted into the external
pacing device (Fig. 13.10). One electrode pad is
placed on the front of the chest and a second on the
back over the right or left scapula (Figs. 13.11–
13.14), although anterior and lateral placement is
also effective. The arterial pulse should be moni-
tored for effective pacing as the ECG may not
show pacing spikes. Transthoracic pacing causes
chest wall muscle twitching, which is painful and
usually requires sedation.
This form of pacing should be considered only
as an emergency or rescue treatment and a more
stable and reliable transvenous pacemaker should
be placed as soon as possible
Transvenous Pacing
General Requirements
Written consent from the patient should be obtained
after due explanation of the risks and benefits of
the procedure – preferably in the presence of their
Transvenous Pacing
next of kin, although this may be impractical in a
serious or life-saving situation. The procedure
should ideally be performed in a sterile theater
dedicated to such procedures and specially
Fig. 13.8 Quik-Combo™ (Medtronic) external pacing/
defibrillator adhesive pads
Fig. 13.9 Quik-Combo™ pads removed from sealed packet
289
designed for the use of X-ray fluoroscopy. Cardiac
catheter laboratories are often used for insertion
but are at best clean areas rather than sterile envi-
ronments. A TPM may be inserted in a coronary
care unit when a “cath-lab” is not available on site.
However, the patient must be on a “screening bed”
and a mobile C-arm image intensifier must be
readily available (see Figs. 7.1 and 7.4).
Fig. 13.10 Pacing cable attached to the Lifepak 20 (arrow)
290
Fig. 13.11 One pad is placed over the precordium
Fig. 13.12 The second pad is placed on the back
A specially trained coronary intensive care
nurse or cath-lab nurse is required, as is a radiog-
rapher who is familiar with X-ray fluoroscopy and
who can set up and operate a portable fluoroscope
or cath-lab X-ray screening equipment. The oper-
ator should be trained in the technique and be able
to operate independently, possess a certificate
confirming his/her ability to use the X-ray equip-
ment, and ideally be able to perform advanced life
support procedures if necessary.
The operator must scrub carefully with anti-
septic, and put on a sterile gown, face-mask, and
gloves to perform this aseptic procedure
(Fig. 13.15). A wide area of skin around the
13 Temporary Pacing
Fig. 13.13 Connecting cable inserted into the fitting
attached to the disposable pads
intended puncture site should be cleaned with an
antiseptic solution of povidone iodine and/or
chlorhexidine (Fig. 13.16) and the area covered
with sterile drapes before administering the local
anesthesia (Fig. 13.17).
During insertion of the TPM, the heart rhythm
must be monitored and equipment for external
pacing and resuscitation should be available.
Methods
Temporary ventricular pacing is performed by
introducing a pacing lead into a systemic vein
and advancing it, with the help of X-ray
fluoroscopy, to the apex of the right ventricle.
Methods 291

Fig. 13.14 Cable attached to the

Lifepak 20

Fig. 13.15 The operator should

be in a sterile gown and gloves
and wear mask and hat
292
Fig. 13.16 The skin over the insertion site (inguinal
region for femoral vein insertion) is cleaned with chlor-
hexidine antiseptic solution
Fig. 13.17 The site is covered with a sterile drape with a
purpose-designed window
Techniques for reaching the right ventricular
apex with the lead tip are described below, but
once positioned (Fig. 13.18) the lead is connected
13 Temporary Pacing
Fig. 13.18 Fluoroscopic image showing a temporary
pacemaker in the right ventricular apex (arrow) from the
femoral vein. Permanent RA and RV leads are present in
this pacemaker-dependent patient undergoing a box-
change procedure
to an external pulse generator (Fig. 13.19) whose
pulse rate and energy output can be adjusted.
Several approaches are used and are described
below. Generally, access via the right internal
jugular vein is least hazardous but the complica-
tions of carotid artery puncture may be serious
and the lead position is often uncomfortable for
the patient.
Temporary atrial pacing is performed by intro-
ducing a J-shaped atrial lead (Fig. 13.20) into a
systemic vein (not femoral vein) and advancing
it, with the aid of X-ray fluoroscopy, to the right
atrium. The preformed J-shaped lead is pulled up
into the right atrial appendage and then sutured
to the skin at the skin puncture site (see below).
Atrial temporary pacing leads are frequently
unstable and capture/pacing of the atrium is then
lost. However, an active fixation temporary lead
is available for placement in the atrium which
should offer more reliable atrial sensing/pacing
for as long as is necessary (see below).
Temporary Pacing Leads
Extruded polyurethane bipolar pacing catheters
with stainless steel electrodes are most com-
monly used in catheter laboratories and coronary
care units for temporary pacing (Fig. 13.21). TC
Temporary Pacing Leads 293

Fig. 13.19 The bipolar temporary electrode’s pins are connected to the cable which is then attached to the temporary
pacing box

is the current bipolar temporary pacing catheter

Fig. 13.20 Temporary bipolar “J” lead for positioning in
the RA appendage
from Biotronik. It is easily visible on fluoroscopy
due to its coaxial shaft design. Its standard 2 mm
adapter pins allow direct connection to all com-
mon external pacemakers and EP devices. High-
quality NBIH and Goetz catheters with platinum
electrodes are also available in 4–7F sizes. The
Bard temporary pacing catheter is available in
6F, 7F, and 8F sizes and the catheter is shown in
Figs. 13.22 and 13.23.
Balloon flow-assisted catheters (Fig. 13.24) are
available for use when fluoroscopy is not immedi-
ately available and more specialist designs have
specific uses. The Zucker® catheter is ideal for right
heart bipolar pacing, intracardiac ECG sampling,
and infusion. The Myler® catheter is suited for pul-
monary artery pressure monitoring and sampling
while pacing the right ventricle and the Gorlin®
catheter for coronary sinus sampling while simul-
taneously pacing the right atrium. A CVP/pacing
lumen electrode catheter is ideal for pressure moni-
toring and sampling from the vena cava or right
atrium while simultaneously pacing the right ven-
294 13 Temporary Pacing

Fig. 13.21 Upper: Three

bipolar temporary ventricular
leads from Biotronik Ltd.
Lower: TB is a 110 cm long
bipolar temporary pacing lead
available as 4F, 5F or 6F
diameter, straight or preformed
“J” version (Courtesy of Oscor®
Inc., Palm Harbor, FL, USA)

Unshrouded
2 mm pin (non-USA)

Atraumatic tip

Shrouded 2 mm pin (USA)

Depth markings

Fig. 13.23 6F bipolar temporary pacing lead from Bard.

The distal tip is gently curved which aids placement into
Fig. 13.22 6F bipolar temporary pacing lead from Bard the RV apex from the femoral route. The proximal con-
is presented in a well-labeled sterile package nector pins are also shown
Temporary Pacing Leads 295

Quick release luer

activated valve Latex-free compliant balloon

Atraumatic
tip

Shrouded (USA)
or Unshrouded (non-USA) Depth markings

Fig. 13.24 Top: The floatation pacing lead has an pacing lead is a 5F latex-free radiopaque bipolar tempo-
inflatable distal balloon which helps delivery of the distal rary pacing lead (110 cm long) with 8 mm balloon
tip into the pulmonary artery and hence positioning of the (Courtesy of Oscor® Inc., Palm Harbor, FL, USA)
bipolar leads in the RV. bottom: The Helios™ temporary

Stylet, for better positioning

Shrouded 2 mm pin (USA)

Unshrouded 2 mm pin (non-USA)

Atraumatic tip
Depth markings

Fig. 13.25 The TAU 110 cm long bipolar electrode catheters have an inner lumen through which a stylet may
catheters (4–6F) are designed for EP studies – suitable for be inserted in order to help placement within the right
recording intracardiac signals and temporary pacing. The heart (Courtesy of Oscor Inc., Palm Harbor, FL, USA)

tricular apex. The TAU 110 cm long bipolar leads
(4–6F) are designed for EP studies – suitable for
recording intracardiac signals and temporary pac-
ing (Oscor® Inc.). The leads have an inner lumen
through which a stylet may be inserted in order to
help placement within the right heart (Fig. 13.25).
V-Pace™ (APC Cardiovascular, Ltd.) are also
bipolar temporary pacing leads for use in the
right ventricle. They are 110 cm long, are avail-
able in 4–7F size, and the electrodes are 1 cm
apart. The coaxial design, incorporating stainless
steel conductors along the length of the catheter,
ensures maximum strength and precise torque
control. The smooth polyurethane surface reduces
the risk of thrombosis and offers excellent
biocompatibility.
296
Fig. 13.26 The VascoStim
Screw 2/6F screw-in
temporary pacing lead
(VascoMed®)
The VascoStim bipolar semi-floating pacing
leads (VascoMed) are available in 4–6F diame-
ters and in a straight, curved, or J-shape. A tem-
porary screw-in lead is also available (VascoStim
Screw 2/6F) (Fig. 13.26).
External Pulse Generators
for Temporary Pacing
The external pulse generator allows adjust-
ment of pacing output (voltage ± current),
pulse width, pacing rate, mode and sensitiv-
ity to intrinsic activity (Figs. 13.27 and 13.28).
Dual-chamber generators will offer adjust-
ment of AV delay, PVARP, and MTR depend-
ing on stimulation rate (Figs. 13.28, 13.29, and
13.56) and a three-chamber temporary pacing
generator for biventricular pacing is also avail-
able from Osypka (Fig. 13.30). The Oscor®
PACE 203 H from Osypka provides easy mea-
surement of P/R wave amplitude and optional
AUTOSENSE function that automatically
13 Temporary Pacing
Fig. 13.27 Temporary pacing box from APC Medical
tracks P/R wave peak amplitudes and adjusts
atrial and ventricular sensitivities accordingly.
Most are now small enough to allow the patient
to be ambulant, although atrial lead stability
is the limiting factor in this regard. Generally,
however, patients should be confined to bed
when a temporary pacing lead is in situ. The
generator’s batteries should be checked daily
(a 9 V alkaline battery provides approximately
5 days of continuous operation in the PACE
203 H) and care should be taken to avoid drop-
ping the device and inadvertently pulling the
lead out of position. Some generators allow high
rate pacing – using a “x3” key, to allow for over-
drive pacing of ventricular tachyarrhythmias
(Fig. 13.31) or up to 1,000 ppm for rapid atrial
pacing (e.g., PACE 203 H).
Techniques of TPM Insertion
It is important to be familiar with the venous
anatomy (Fig. 13.32).
Internal Jugular Vein Puncture
The right internal jugular vein (IJV) is preferred
to the left. Injury to the thoracic duct is avoided.
The patient is tilted 15° head down and the head
turned toward the opposite side. The landmarks
are first identified. The IJV lies lateral to the
carotid artery. The sternocleidomastoid muscle
(SCM) overlies the IJV in the lower half of the
neck. The apex of the triangle where the clavicular
and sternal heads of the SCM meet is identified
External Pulse Generators for Temporary Pacing 297

Features

• Single-chamber pacing − 4 modes

• Rapid atrial pacing − 80−800 ppm
• Constant voltage output up to 12 V
• Pacing and sensing led indicators
• Low battery indicator − led and tone
• Larger faceplate and knobs − user friendly
• Built-in bedrail hanger
• Redel® terminal for quick easy connection
• Defibrillation protected
Features
• Single-chamber pacing − 4 modes
• Rapid atrial pacing − 90−450 ppm
• Constant voltage output up to 12 V
• Ten second operating time during battery change • Auto setting of atrial and ventricular refractory period
• Pacing and sensing led indicators
• Low battery indicator
• Light weight − user friendly
• Collet terminals
Features
• Single and dual chamber pacing − 11 modes
• Rapid atrial pacing − 100−800 ppm
• Suspended output and resume function
• Auto setting of av delay and mtr
• Constant voltage output up to 10 V
• LCD display with backlight
• Low battery indicator
• Keypad locking switch
• Collet terminals

Fig. 13.28 Current temporary pacing devices available pulse generator; right: MicroPace™ dual-chamber
from APC Medical. Left: Bedside™ single-chamber pulse external pulse generator
generator; center: Miniature™ single-chamber external

Fig. 13.29 Dual-chamber

temporary pacemaker
(Medtronic Inc.)

and local anesthetic should be infiltrated into this
area. “Scouting” for the IJV with an 18 gauge
needle is sometimes helpful and ultrasound-guided
access of the IJV is to be recommended. An
introducer needle is then inserted at a 45° angle
pointing toward the ipsilateral nipple of the
patient. As the needle is advanced, aspiration on
the syringe should yield venous blood on enter-
ing the IJV. Keeping a finger on the carotid artery
ensures that the puncture/needle direction is
always lateral to the artery (Fig. 13.33). Once the
needle is within the IJV lumen, a guidewire and
298 13 Temporary Pacing

Fig. 13.31 This temporary pacing box from APC cardio-

vascular has a key to enable X3 pacing for overdrive
pacing

IJV IJV
EJV EJV
RIV LS-CV

RS-CV
LIV
AxV SVC

BV
CV
Fig. 13.30 PACE 300 three-chamber temporary pace-
maker (Osypka) has a large range of features including MBV
AUTO SENSE for automatically tracking P/R wave peak
amplitudes and adjusting atrial and ventricular sensitivities. MCV
An optional function automatically adjusts the settings for
AV delay, PVARP and MTR depending on selected stimu-
lation rate. A wide range of pacing modes are available

introducer/sheath can be inserted over the wire

and the sheath then sutured to the skin. The pac-
ing lead can then be introduced through the
sheath and positioned in the right ventricle and/
or right atrium using fluoroscopy.

Subclavian Vein Puncture

This provides a suitable route of access to the
venous system. It is quick, infection and lead dis-
placement are unusual, and in experienced hands
complications are rare. However, if permanent
pacing is going to be required, then it is generally
accepted to use the internal jugular, antecubital,
Fig. 13.32 Venous anatomy of the upper limb/upper
mediastinum relevant to pacing. MCV median cephalic
vein, MBV median basilic vein, BV basilic vein, CV
cephalic vein, AxV axillary vein, RS-CV right subclavian
vein, RIV right innominate vein, LIV left innominate vein,
LS-CV left subclavian vein, EJV external jugular vein, IJV
internal jugular vein, SVC superior vena cava
External Pulse Generators for Temporary Pacing
Index
21G
18G
Guidewire
Fig. 13.33 Landmarks for puncture of internal jugular vein
or femoral vein so as to leave the subclavian veins
available for permanent lead placement.
The subclavian vein runs behind the medial
third of the clavicle and can be punctured using
either supra- or infraclavicular approaches. The
left subclavian venous approach is easier than the
right, because of the straighter run into the superior
vena cava (SVC). The technique of subclavian vein
puncture and lead insertion is shown in Chap. 7.
299
Sagittal
45°
20°
Frontal
Head
The patient lies flat or in a slightly head-down
position. A tiltable table is preferable so that the
legs can be raised to improve venous return and
distend the subclavian vein if the patient is hypo-
volemic (Fig. 13.34). Alternatively, intravenous
fluid can be given prior to puncturing the vein.
A needle is introduced through a 0.5 cm skin
incision just below the inferior border of the clav-
icle and just lateral to the mid-clavicular point
300 13 Temporary Pacing

Fig. 13.34 Head-down tilt

on the pacing table may be
helpful for avoiding
air-embolism during
temporary pacemaker
insertion from the subcla-
vian/jugular veins

Fig. 13.35 Landmarks for

subclavian vein puncture

and is directed toward the suprasternal notch so it
passes immediately behind the posterior surface
of the clavicle (Fig. 13.35). Feeling the undersur-
face of the clavicle with the needle tip during
entry helps to keep it superficial and avoid sub-
clavian artery puncture and pneumothorax (see
Chap. 7).
When the subclavian vein is entered, venous
blood will be easily aspirated from this large vein.
The syringe is removed (taking care not to move
the needle) and a soft-tipped J-shaped guidewire is
then inserted through the needle and into the sub-
clavian vein and advanced through the left bra-
chiocephalic vein into the SVC. The needle is then
External Pulse Generators for Temporary Pacing 301

Fig. 13.36 Local anesthetic being administered in region Fig. 13.37 Blood aspiration from the femoral vein
of femoral vein

removed and a sheath within which there is a

tapered vessel dilator is passed over the wire into
the vein. Care must be taken to ensure that the
guidewire always extends outside of the sheath
during its insertion in order to avoid losing the
guidewire within the venous system. The guide-
wire and dilator are then removed, leaving the
sheath in situ, and the pacing lead is then passed
through the sheath along the same route to the SVC
and right atrium. Ensuring a head-down position
during insertion and blood flow out of the needle
and sheath during insertion of the guidewire and
pacing lead, respectively, should prevent air embo-
lism from occurring. An alternative approach Fig. 13.38 Insertion of the guidewire
should be considered if the patient has received
thrombolytic therapy, is anticoagulated, or if the
contralateral subclavian vein has been used and common iliac veins and into the inferior vena cava
permanent pacing is likely to be required. and then into the right atrium using X-ray
fluoroscopy. Most leads are slightly curved and
Femoral Vein Puncture advancing the lead across the tricuspid valve into
This is perhaps the easiest and quickest venous the RV apex usually requires little manipulation
access route for establishing temporary pacing. (see Fig. 13.18). Figure 13.43 shows a diagram-
Using a similar needle/sheath technique to that matic representation of this usually simple maneu-
described above and local anesthesia, entry into ver. Unfortunately lead stability is not as good as
the femoral vein is usually easy, the femoral vein when inserted via the subclavian vein, and infec-
being located just medial to the femoral artery tion and venous thrombosis are slightly greater
pulse (Figs. 13.36–13.41). A splittable sheath can risks. It should be reserved for short-term emer-
also be used. The lead is then inserted into the gency pacing such as post-cardiac arrest/collapse
sheath (Fig. 13.42), passed up the external and complicated or caused by complete heart block,
302
Fig. 13.39 Setting up the
introducer sheath
severe bradycardia, sinus arrest, or asystole. Once
established, a subclavian pacemaker can then be
inserted more leisurely and then the femorally
placed lead removed. Electrophysiologists use the
femoral route for inserting one or more temporary
pacing leads during EP studies (see Fig. 3.12) and
when temporary pacing cover is required during a
generator change in a pacemaker-dependent
patient.
13 Temporary Pacing
Antecubital Vein Puncture
This route may be chosen if the patient has
received thrombolytic therapy or is anticoagu-
lated. A medially placed vein should be used such
as the median basilic vein. Although enticing,
laterally placed veins do not provide easy entry
into the SVC. Like the femorally placed leads,
lead stability is relatively poor and phlebitis and
infection are not uncommon.
External Pulse Generators for Temporary Pacing 303

Fig. 13.40 Inserting the

introducer sheath over the
guidewire

Fig. 13.41 Introducer sheath fully inserted into the fem-

oral vein

Positioning of the Lead

From the Antecubital, Subclavian,
or Jugular Vein
After placing the pacing lead into the venous sys-
tem, the lead is advanced into the SVC and into the
right atrium. There should be no resistance during
advancement. If obstruction is felt, the lead should
be withdrawn slightly, rotated and then advanced
Fig. 13.42 Inserting the temporary pacemaker lead into
the sheath
again under fluoroscopy. Occasionally congenitally
abnormal anatomy may be encountered such as a
left-sided SVC, when the course of the lead should
raise this possibility (Fig. 13.44). Contrast injection
can usually show the operator unusual anatomy or
304 13 Temporary Pacing

a b

LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

Fig. 13.43 (a) From the femoral vein, a temporary pacing
lead is simply advanced up the IVC and into the RA using
fluoroscopy. A gentle pre-shaped curve on the lead helps
to point the tip across the tricuspid valve. (b) The lead tip
can be simply advanced across the valve and into the RV
apex (arrow) RIV Right Innominate Vein; LIV Left
Innominate Vein; SVC Superior Vena Cava; RA Right
Atrium; TV Tricuspid Valve; IVC Inferior Vena Cava; RV
Right Ventricle; PA Pulmonary Artery

LSVC

CS

Fig. 13.44 Unusual route taken by pacemaker lead via a Fig. 13.45 Contrast injection can identify areas of obstruc-
left-sided SVC is confirmed by injection of contrast agent tion in the great veins resulting from fibrosis associated
CS Coronary Sinus; LSVC Left Superior Vena Cava with chronically implanted permanent leads (arrow)

venous obstructions that can sometimes occur in in the subclavian vein or SVC (Figs. 13.45 and
patients who have had several pacing leads placed 13.46).
External Pulse Generators for Temporary Pacing
Fig. 13.46 Multiple leads in the SVC (current and redun-
dant) are more likely to result in fibrosis and obstruction
of the SVC (arrow)
Once within the right atrium, a loop should be
formed by pushing the lead tip against the atrial
wall while simultaneously advancing the lead
(Fig. 13.47). The lead may then cross the tricus-
pid valve (TV) or this can be achieved by twist-
ing the lead in order to rotate the loop toward and
across the TV. Otherwise slight advancement or
withdrawal should allow the lead to cross the TV
into the RV. It can then be gently advanced and
slightly rotated into the RV apex. Further slight
withdrawal and advancement may be necessary
to position the lead tip in an optimal position
with a low pacing threshold. Alternatively if the
lead is advanced up into the pulmonary artery,
which confirms entry into the RV, the lead must
then be withdrawn into the body of the RV and
then rotated and advanced into the RV apex.
Fluoroscopy in anteroposterior view shows the
lead tip pointing toward the RV apex with a
gentle downwards curve (see Fig. 13.18).
Ventricular ectopic beats commonly occur on
entering the RV and nonsustained ventricular
tachycardia less commonly.
As indicated above, during lead positioning it
is often useful to cross the TV and advance the
lead into the right ventricular outflow tract before
withdrawing it and rotating the tip downwards
into the RV apex. Placement of the lead into the
coronary sinus looks similar to placement in the
305
RV outflow tract when screening in the PA pro-
jection. Correct placement can be confirmed by
fluoroscopy in the left anterior oblique or left
lateral view. If in the coronary sinus, the lead will
usually point posteriorly, whereas in the RV
outflow tract or apex the lead tip will point ante-
riorly (Fig. 13.48).
From the Femoral Vein
The lead is advanced up the inferior vena cava
into the right atrium. The “C”-shaped distal sec-
tion of most temporary pacing leads makes it
quick and easy to advance across the tricuspid
valve into the RV apex. Slight rotation of the
pacing lead may be necessary to cross the tricus-
pid valve (see Fig. 13.43).
Initiating Pacing
Once a stable pacing lead position is obtained,
the proximal and distal poles of the lead should
be connected to the external pacemaker
(Figs. 13.49–13.51). The proximal pole should
be connected to the pacemaker’s anode (+ve)
(red) and the distal pole to the cathode (−ve)
(black), respectively. If the poles are inadvertently
reversed, the pacing threshold will be significantly
higher.
The minimum voltage necessary for pacing
stimuli to capture or pace the ventricle consistently,
the pacing threshold should then be measured by
the technician (Fig. 13.52). Starting at 3 V, the
pacemaker amplitude or output is decreased by
0.1 V progressively until the pacing spike ceases
to produce a QRS complex (Fig. 13.53). This is
the pacing threshold and generally it should be less
than 1 V with a pulse duration of 1 ms. Usually, the
output is set at 2 V (or double the threshold) above
the pacing threshold. The stability of the pacing
lead is tested by observing the paced ECG during
deep inspiration or coughing. It is usually worth
looking at the lead by fluoroscopy during the deep
inspiration to ensure the correct amount of “slack”
is present in the right atrium. Figures 13.54 and
13.55 respectively show the ECG before and after
right ventricular pacing.
If pacing output needs to exceed 5 V or 10 mA,
repositioning should be considered.
306 13 Temporary Pacing

LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

a b
LIV LIV

RIV RIV

SVC SVC

PA PA

RA TV RA TV

RV RV

IVC IVC

c d

Fig. 13.47 Placement of a temporary pacing lead into
the RV apex from the internal jugular, subclavian or
axillary veins (a). Once into the SVC, the lead tip should
be pushed gently against the RA free wall in order to form
a “C-curve” (b). (c) Further advancement will prolapse
the lead across the tricuspid valve (TV) and into the RV.
(d) Once across the TV, the lead can be rotated in order to
turn the bipolar tip to point and be advanced upwards
toward the RVOT. (e) With the tip of the electrode point-
ing toward the RVOT, the lead can then be straightened by
gentle withdrawal (f) and then advanced toward the RV
apex (g). (h) Some slack should be left in the RA to allow
for straightening with inspiration and the tip should ide-
ally point slightly downwards and anteriorly RIV Right
Innominate Vein; LIV Left Innominate Vein; SVC Superior
Vena Cava; RA Right Atrium; TV Tricuspid Valve; IVC
Inferior Vena Cava; RV Right Ventricle; PA Pulmonary
Artery
External Pulse Generators for Temporary Pacing 307

LIV LIV

RIV RIV

SVC SVC

PA PA

RA
TV RA TV

RV RV

IVC
IVC

e LIV f LIV

RIV RIV

SVC SVC

PA PA

RA RA
TV TV

RV RV

IVC IVC

g h

Fig. 13.47 (continued)

308 13 Temporary Pacing

Fig. 13.48 Left (PA view): Contrast filling of the coro- such a lead is positioned posteriorly. Note the permanent
nary sinus (CS) shows how placement of a lead into the pacemaker lead in the apex of the RV and pointing anteri-
CS may look similar to an RV outflow tract position. Right orly (arrow)
(left lateral view): contrast filling of the CS shows that

Fig. 13.49 The temporary pacing lead and sheath are sutured to the skin and extended across the drape to be connected
to the pacing cable attached to the temporary pacing generator/box

In an emergency, if the position is not ideal
and the threshold high, repositioning the lead is
necessary. However, if the patient has become
pacemaker dependent, a second pacemaker lead
should be placed from the femoral vein until the
subclavian lead is safely repositioned.
The pacing lead is then sutured to the skin
with two sutures at its point of entry with separate
sutures securing redundant loops to the skin.
After cleaning the skin with povidone-iodine or
chlorhexidine solution, the site should then be
covered with a sterile dressing.
The pacing threshold should be checked daily
as should the battery and electrical connections.
Unnoticed accidental disconnection might lead to
ventricular standstill and death.
Paced patients should be monitored on a coro-
nary or intensive care unit.
External Pulse Generators for Temporary Pacing 309

Fig. 13.50 Operator gives the sterile connections to the technician who plugs them into the cable connections

Fig. 13.51 Pacing connections being made

310
AV Sequential Pacing
For patients with a low cardiac output and sinus
bradycardia or heart block, AV sequential pacing
can improve cardiac output by up to 30% more
than ventricular pacing alone. Two pacing leads –
a pre-shaped J lead placed in the RA appendage
and a straight pacing lead placed into the RV
apex – are necessary (see above). A special AV
sequential temporary pacing generator is required
to which the anode and cathode of each pacing
Fig. 13.52 Pacing threshold being tested using the ECG
on the Lifepak 12 as the voltage output from the tempo-
rary pacing box (Medtronic Inc.) is slowly reduced
Fig. 13.53 An example of a rhythm strip showing loss of ventricular capture at 0.27 V
13 Temporary Pacing
lead must be connected (Fig. 13.56). The atrial
pacing threshold tends to be higher than the ven-
tricular threshold.
Complications
Although transvenous temporary pacing is
superficially a simple procedure, complications are
not uncommon. They may be avoided by ensuring
that the procedure is only performed by experienced
or supervised operators and only when indicated.
Insertion and positioning of a temporary trans-
venous pacemaker lead may be associated with car-
diac arrhythmias such as atrial and ventricular
ectopic beats, atrial tachycardia, flutter or fibrillation,
ventricular tachycardia, ventricular fibrillation,
complete heart block, and asystole. Other compli-
cations include pneumothorax, hemothorax, right
ventricular perforation, hemopericardium and
cardiac tamponade and are all serious. Pericarditic
pain and a pericardial friction rub suggest RV
perforation. An “intracardiac signal” can be
recorded by connecting the TPM lead to the V lead
of an ECG machine. If the lead tip is against the
endocardium, a good endocardial potential of 1.5–
10 mV should be evident. After myocardial perfo-
ration and with the lead tip in the pericardium, the
endocardial signal is lost and ST-depression and
T-wave inversion will be recorded.
Injury to the brachial plexus and thoracic duct,
bleeding from the subclavian vein, and even
hemothorax as a result of subclavian artery punc-
ture are potential but rare complications when
pacing is performed via the infraclavicular route.
Lead displacement may result in failure to pace
and failure to sense and inappropriate pacing.
Microdisplacement (no obvious displace-
ment on CXR) may be overcome by increasing
the pacing output voltage and/or pulse width. If
Complications 311

Fig. 13.54 12-Lead ECG showing complete heart block prior to pacing

Fig. 13.55 12-Lead ECG showing VVI pacing

312
Fig. 13.56 Dual-chamber temporary pacing generator
(Courtesy of Oscor® Inc., Palm Harbor, FL, USA)
this fails, repositioning of the lead will be neces-
sary – as when lead displacement is obvious
radiologically.
Disconnection of the lead from the pacing box
or inappropriate settings may result in pacing fail-
ure as may breakage of the lead or its connections.
Once the TPM is placed in the RV, the patient
may become immediately pacemaker-dependent,
making repositioning difficult.
Infection is not uncommon when temporary
pacing is required for several days. At the first
signs of infection, swabs should be taken from the
site and antibiotics commenced. If pyrexia occurs,
blood cultures should be taken. Staphylococcus
epidermidis/aureus are the commonest organisms
responsible for infection, although coliforms may
be responsible when the femoral route has been
used. In the presence of pyrexia, IV antibiotics,
for example, IV flucloxacillin 1 G QDS should be
commenced once blood cultures have been sent to
the microbiology laboratory, since staphylococ-
cal septicemia is likely. A move should be made to
remove the infected TPM and replace it with a new
TPM on the opposite side if temporary pacing is still
required.
13 Temporary Pacing
Fig. 13.57 Semi-permanent pacing. Here a permanent
pacing lead is placed and actively fixed into the interven-
tricular septum via the right internal jugular vein and then
inserted into a nonsterile permanent generator attached to
the skin on the chest wall by adhesive tape
Deep venous thrombosis and thromboembo-
lism may be a complication when pacing is per-
formed from the femoral vein.
Semi-permanent Pacing
Occasionally, temporary pacing is required for
several weeks, for example, in patients with
infective endocarditis affecting the tricuspid
valve as a result of an infected pacing system and
requiring several weeks of IV antibiotics. In this
situation, a permanent lead may be placed into
the RV apex via the internal jugular vein, and
tunneled under the skin to the pectoral region
where it is inserted into a nonsterile permanent
generator attached to the skin by a tape and/or a
suture (Figs. 13.57 and 13.58).
Temporary Epicardial Pacing
If temporary pacing is indicated during cardiac
surgery, special myocardial pacing leads can be
sutured directly to the surface of the right atrium,
right ventricle, or left ventricle (Fig. 13.59) and
Temporary Epicardial Pacing
Fig. 13.58 Permanent pacemaker is fixed externally to
the skin above the clavicle by a clear adhesive dressing. A
lead is actively fixed to the right side of the interventricu-
Fig. 13.59 Epicardial leads from Medtronic. Top left:
Unipolar myocardial lead (Premium 6500); Top right:
Bipolar coaxial (Model 6495) lead with fixation coil;
Bottom left: Pediatric unipolar lead (Model 6491) has fea-
tures specifically useful for children, e.g., smaller fixation
313
lar septum and attached to the permanent pacemaker in
order to provide semi-permanent pacing
coil; Bottom right: The Convenience (Model 6494) unipo-
lar lead has some improved features such as smaller diam-
eter needles and color-coded wires (Image reproduced
with permission of Medtronic, Inc.)
314 13 Temporary Pacing

the proximal ends tunneled out through the skin

for connection to a temporary pacing box
(Fig. 13.2). The leads can be unipolar or bipolar.
Atrial epicardial leads are also available
(Fig. 13.60). The leads can be removed when no
longer required by simply applying firm traction
to the leads exiting the skin.

Fig. 13.60 Atrial epicardial unipolar lead from Medtronic

(Model 6492) is well suited for suturing to thin, delicate
atrial tissue (Image reproduced with permission of
Medtronic, Inc.)
 Pacing in Patients with Structural
Cardiac Abnormalities
Although most adult patients requiring pacemaker
or ICD implantation will have normal cardiac
anatomy, occasionally significant abnormalities
will be found only at the time of the procedure,
since they had not given rise to symptoms or any
obvious physical signs. These include persistent
left-sided superior vena cava (SVC) (with or
without a right-sided SVC), dextrocardia, atrial
septal defect, and patent foramen ovale. Such
abnormalities may give rise to practical prob-
lems during lead placement and operators should
be aware to recognize the problem immediately
and know how to deal with it. Patients (adults
or children) with congenital structural cardiac
abnormalities, such as transposition, corrected
transposition, tetralogy of Fallot, univentricular
heart, or post-operative “corrected” defects, will
require special consideration before proceeding
to the pacing theater. In particular, the opera-
tor will need to know whether the transvenous
approach is feasible, what problems might be
encountered during lead implantation, and how
to seek the best and most stable of electrode posi-
tions. Preoperative investigations, including tran-
sthoracic and transesophageal echocardiography,
CT and MRI cardiac imaging as well as angiog-
raphy, for example, left arm venography, should
be used to clarify the cardiac and venous anatomy
in order to safely embark on transvenous lead
placements. Simply reviewing previous surgical
notes (following cardiac surgery in earlier life)
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_14, © Springer-Verlag London 2012
14
or previous cardiac catheterization notes may
be useful in noting anatomical abnormalities.
In recent times with the advent of biventricular
pacing, it is relevant also to know the position of
the coronary sinus, for example in patients with
Ebstein anomaly who have already undergone
tricuspid valve replacement.
It goes without saying that many patients who
receive permanent pacemakers as children fol-
lowing surgery for their congenital heart disease
will require several further procedures in the
years to come. These range from generator
change (at EOL), lead problems requiring
replacement of a lead, resiting or replacement of
the whole system, and intervention for venous
thrombosis/occlusion.
Dextrocardia
This positional abnormality in which the cardiac
apex is located on the right side of the chest
should not pose a problem to pacemaker implan-
tation once the cardiologist is oriented as long as
no other cardiac structural defects are associated
with the dextrocardia. Providing the pre-paced
rhythm is not complete heart block with a wide
QRS complex, the 12-lead ECG should give the
diagnosis before the patient enters the pacing
theater. If not, fluoroscopy will suggest the
abnormality (Fig. 14.1).
315
316 14 Pacing in Patients with Structural Cardiac Abnormalities

Fig. 14.1 Active fixation leads are

placed in the right ventricular outflow
tract (arrow) and in the low right
atrium (twin arrows) via the left-sided
superior vena cava in this patient with
dextrocardia. A redundant right atrial
lead remains attached to the right atrial
myocardium

Persistent Left-Sided Superior

Vena Cava

0.3% of the general population has a persistent

left-sided SVC, and this anomaly may be present
in 4.3–11% of patients with congenital heart dis-
ease. In 90% of cases, the persistent left SVC
connects to the right atrium via the coronary sinus
(Fig. 14.2). In the other 10%, it connects to the
left atrium when most will have an associated
ASD or heterotaxy syndromes and a small right-
to-left shunt.
The anomaly is due to failure of regression of
the left anterior and common cardinal veins and
left sinus horn. The persistent left SVC starts at
the junction of the left subclavian vein and left
Fig. 14.2 This patient is shown to have bilateral SVCs hav-
internal jugular vein, passes lateral to the aortic ing had pacing leads introduced via the left-sided SVC and
arch, and receives the left superior intercostal coronary sinus. An active fixation lead is placed into the RA
vein. It then passes anterior to the left hilum, is appendage and a tined passive fixation lead into the RV apex
joined by the hemiazygous system, crosses the
posterior wall of the left atrium, and receives the Although it can be difficult to maneuver the
great cardiac vein to become the coronary sinus. atrial and ventricular leads into ideal positions in
In 65% of cases, the left brachiocephalic vein the RA and RV respectively as they course through
is absent or small (Fig. 14.2), and although the the coronary sinus, persistence and the use of active
majority of patients will have bilateral SVCs fixation leads usually proves successful (Fig. 14.5).
(Figs. 14.2 and 14.3), in 10–18% the right SVC is Left ventricular pacing via a cardiac venous tribu-
absent (Fig. 14.4). tary is usually not difficult to achieve but persis-
Ebstein’s Anomaly 317

LSVC

RA CS

Fig. 14.3 This patient has clear communication between

right and left-sided SVCs via the left brachiocephalic
vein. Previously placed RA and RV leads have been
placed via the right-sided SVC (green + orange arrows)
and a new RV lead (because of loss of capture of previous
RV lead) is shown to enter a left-sided SVC (blue arrow)
and coronary sinus (CS) en route to the RV apex

tence in placing a lead into the RV is often

worthwhile in pacemaker-dependent patients.
Thrombosis of a large coronary sinus following
pacemaker lead implantation has been reported.

Ebstein’s Anomaly

Ebstein’s anomaly is rare (1 in 20,000 live births;

0.5% of all congenital heart disease) and charac-
terized by downward displacement of the tricuspid
valve orifice so that the cusps originate from the
right ventricular wall rather than the tricuspid
annulus (Fig. 14.6). The displaced tricuspid valve
divides the RV into two parts – an atrialized por-

Fig. 14.4 This patient had a single chamber pacemaker

implantation inserted using the right subclavian vein for
lead insertion. However, the right-sided SVC is absent and
the lead passes across to a persistent left-sided SVC
(LSVC) which runs into the coronary sinus (CS). The RV
tined lead is manipulated into the right atrium (RA) and
across the tricuspid valve into the apex of the right ven-
tricle (RV) (black arrow)
318 14 Pacing in Patients with Structural Cardiac Abnormalities

Fig. 14.7 Chest X-ray in Ebstein’s anomaly shows

Fig. 14.5 It is probably preferable to use an active
fixation lead when placing leads via a left-sided SVC, as
in this case where a new RV lead actually enters a left-
sided SVC and enters RA/RV via the coronary sinus.
Clearly this patient also has a right-sided SVC down
which were placed the original RA and RV leads
marked cardiomegaly. This patient was being investigated
for recurrent palpitations and dizzy spells using an
implantable loop recorder. Significant tricuspid regurgita-
tion is not uncommon in Ebstein’s anomaly resulting in
marked dilatation of the RA. Active fixation leads should
probably be employed if there is a clinical indication for
permanent pacemaker implantation

tion lying between the tricuspid annulus and the

displaced tricuspid orifice and the remainder of
the true RV which lies beyond the tricuspid valve.
The relevance to pacemaker implanters is that
approximately 20–25% of such patients develop
arrhythmias and conduction abnormalities and
SVC
3–4% require pacing (Fig. 14.7). The commonest
indications for pacing include persistent atrial
standstill and AV block (de novo, post-AV node
Ao PA ablation, or post-surgery). The atrialized portion
LA
of the RV varies in size, muscularity, and thick-
ness but it has the electrophysiologic characteris-
Patent tics of the RV. Hence, the RV lead can be placed
foramen above the valve rather than through it. Active
ovale, fixation leads should be used in the atrium, the
or ASD Enlarged RA LV
atrialized portion of the RV, and in the RV apex or
RV outflow tract to avoid displacement in such
patients who often have significant tricuspid
IVC regurgitation. It is worth remembering that other
congenital cardiac defects may coexist with
Small RV TV Ebstein’s anomaly, for example, ASD and VSD.
When it is impossible to insert leads in the right
Fig. 14.6 Ebstein’s anomaly is characterized by down- atrium and ventricle, one may use the cardiac veins
ward displacement of the tricuspid valve orifice so that the
via the coronary sinus to achieve left ventricular
cusps originate from the right ventricular wall rather than
the tricuspid annulus. Other congenital cardiac defects pacing. However, in pacemaker-dependent patients,
may coexist with Ebstein’s anomaly, e.g., ASD and VSD epicardial pacing may be more appropriate.
Other Structural Defects Not Requiring Corrective Surgery 319

If surgery for tricuspid valve reconstruction/

replacement takes place, a pacing lead can still be
inserted. After annuloplasty, the lead can be
placed across the valve in the usual fashion. If
valve replacement is required, a lead can be
buried behind the sewing ring. The lead can be
tunneled to the anterior abdominal wall or pecto-
ral region and connected to a generator or capped
for future use. If a mechanical prosthesis is LA
Ao
implanted, then epicardial pacing should be the PA
method of choice, although even here endocar- RA
dial pacing is not impossible if the coronary sinus
TV
is positioned on the atrial side of the prosthesis.

MV RV
Atrial Septal Defect/Persistent
Foramen Ovale
LV

Generally, isolated foramen ovale and atrial sep-

tal defect do not hinder permanent pacemaker
implantation. It is possible to enter the LA and
the LV and if positioned there may inadvertently
result in systemic embolization – including Fig. 14.8 Congenitally corrected transposition of the
stroke. They should be removed or the patient great vessels
anticoagulated.
Fluoroscopy will suggest LV placement of a
lead. The lead will arch over the atrial septum at the RV apex or within the interventricular sep-
and the ECG will confirm LV pacing, that is, tum. A regurgitant tricuspid valve and enlarged/
RBBB complexes. scarred right atrium/ventricle can result in
When an ASD has been repaired by a patch or difficulty placing leads into stable, effective posi-
a closure device, atrial septal pacing may not be tions and generally active fixation leads should
possible because of fibrosis. Moreover, if the be used from the outset.
right-sided chambers are dilated as a result of a
long-standing defect, active fixation leads should
be preferred in order to try and prevent lead Other Structural Defects
displacement. Not Requiring Corrective Surgery

Congenitally Corrected L-Transposition

Ventricular Septal Defect of the Great Vessels

Patients with small VSDs that do not warrant clo-
sure may require pacemaker implantation. Care
should be taken to be sure that the lead does not
cross into the LV when systemic embolization
and stroke may be an associated risk.
Patients who have had surgical or device clo-
sure of a VSD may be difficult to pace endocardi-
ally due to scarring/fibrosis or synthetic material
In this condition, a morphologic RA drains into a
right-sided morphologic LV which gives rise to
the pulmonary artery. Pulmonary venous blood
enters the LA and then an LV with a right ven-
tricular morphology and then into the aorta
(Fig. 14.8). Although rare (<1% of all congenital
heart disease), 95% have associated anomalies,
for example, VSD with pulmonary stenosis.
320 14
Fig. 14.9 PA (left) and lateral (right) chest X-ray from a
26-year-old woman with corrected transposition of the
great vessels, ventricular septal defect and congenital
complete heart block who underwent permanent pace-
maker implantation at 4 years of age at the time of pulmo-
nary artery debanding and VSD closure. The surgeon
implanted a screw-in lead to the systemic ventricle and
sutured an epicardial lead to the surface of the RA –
implanting a dual-chamber pacemaker in the left subcos-
tal pouch. Four years later, failure to pace necessitated
implantation of a new endocardial pacing system
(Minuet™, Medtronic) via the left subclavian vein using
active fixation leads to the RA appendage (straight green
arrow) and anatomical RV apex with redundant loops
Congenital atrio-ventricular block (AVB) will
occur in 15–20% of patients, and AVB may be
precipitated by surgical repair of the VSD. When
pacing is necessary in early childhood, multiple
subsequent procedures that are likely to be
required can lead to access problems and redun-
dant leads requiring explantation.
The anatomy should be understood. The
ventricles lie side-by-side to each other rather
than the RV being anterior to the LV in a normal
heart. The septum is thus AP rather than left to
right. The atrial lead should position normally
but the ventricular lead may pass inferiorly
through the tricuspid valve to the RV apex (ana-
tomic LV) and the tip point vertically downwards
(Fig. 14.9). However, the lead tip may also point
Pacing in Patients with Structural Cardiac Abnormalities
(curved green arrows) to allow for somatic growth. Aged
17 years, insulation break resulted in intermittent loss of
sensing and pacing in the RV lead which was replaced. It
proved impossible to enter the left subclavian vein which
was now occluded and so the lead was inserted via the left
internal jugular vein and tunneled subcutaneously over
the left clavicle (red arrow) to the pre-pectoral pocket.
The tip of this active-fixation RV lead can be seen to point
vertically downwards (black arrow) – fairly typical of this
congenital abnormality. Seven years later, the Kappa™
DDD (Medtronic) was replaced by a Sensia™ DDD
device (Medtronic) but within 2 years – at the age of
26 years – further lead problems required a new endocar-
dial system from the right subclavian vein (see Chap. 15)
anteriorly or posteriorly and may even point to
the right on AP fluoroscopy. An intracardiac ECG
will confirm good endocardial contact but active
fixation leads should be preferred because of the
smaller trabeculae that are usually present.
After Corrective Surgery
for Congenital Cardiac Abnormalities
Tetralogy of Fallot
Tetralogy of Fallot is the commonest cyanotic
congenital heart defect occurring in 1 in 3,600
live births. Usually, patients with this anomaly
who require permanent pacing or ICD implanta-
After Corrective Surgery for Congenital Cardiac Abnormalities
PA
Ao
LA
RA
LV
RV
Fig. 14.10 Tetralogy of Fallot
tion will have had a previous surgical procedure.
This would usually have been a preliminary sys-
temic-pulmonary artery anastomosis as an infant
if significantly symptomatic. Waterston (ascending
aorta-right pulmonary artery), Cooley (ascending
aorta-right pulmonary artery), Potts (descending
aorta-left pulmonary artery), or Blalock-Taussig
(left subclavian artery-pulmonary artery) shunt
are the usual temporary procedures prior to a more
definitive intracardiac repair as the individual gets
older. In these situations if AVB occurs, these
procedures should not form a barrier to conven-
tional transvenous pacemaker implantation.
However, since the presence of a VSD and over-
lying aorta persists, the risk of stroke exists and
epicardial pacing should probably be preferred
(Fig. 14.10). Total corrective surgery usually
consists of patch closure of the VSD and infundib-
ular widening using a synthetic or pericardial
patch up to or across the pulmonary valve annu-
lus. Pulmonary regurgitation and a dilated RV,
prosthetic material, and myocardial fibrosis not
only make atrioventricular block a likely compli-
cation but also make endocardial lead placement
difficult and active fixation leads should be pre-
ferred (Fig. 14.11). A left SVC draining into a
321
Fig. 14.11 Following failure of the RV apical lead in this
patient with Fallot’s tetralogy, a second RV lead is actively
fixed to the interventricular septum. The proximal end of
the redundant lead is capped and then fixed with a suture
to the fascia over pectoralis major
large coronary sinus may coexist in 10% of
patients and the operator might consider imp-
lanting on the right side to avoid this potential
problem.
Tricuspid Atresia/Univentricular Heart
In this congenital abnormality, survival depends
on an effective atrial septal communication.
Surgery to separate and redirect venous blood
flow involves the Fontan repair or one of its
modifications. In the classic Fontan procedure,
the atrial septal defect is closed and a direct right
atrial-pulmonary artery anastomosis is created
and the connection between PA and RV/LV is
closed by sutures or banding (Fig. 14.12).
Frequently, the ultimately elevated atrial pres-
sures result in severe atrial dilatation and an
increase in wall thickening, sinus node dysfunc-
tion, and atrial arrhythmias. Variations on the
Fontan repair include a number of procedures
aimed at connecting the venous circulation to the
pulmonary artery either by directly connecting
the venae cavae to the pulmonary artery or by
using an extracardiac or intra-atrial tunnel/con-
duit. These procedures are known as total
cavopulmonary connections (Fig. 14.13). As with
322 14 Pacing in Patients with Structural Cardiac Abnormalities

the bidirectional Glenn shunt, when the SVC is D-Transposition of the Great Vessels
detached from the RA and anastomosed to the
PA, conventional transvenous pacing is not pos- Complete transposition of the great vessels (TGA)
sible in these cases. accounts for 5% of all congenital heart disease
cases. Without surgery soon after birth, infants
would not survive this situation where the pulmo-
nary artery arises from the LV and the aorta from
the RV (Fig. 14.14). Usually a coexisting commu-
nication such as a patent ductus arteriosus, ASD,
or VSD allow the infant to survive (40–50% will
have an associated VSD). Many infants will have
had an ASD created or a balloon atrial septostomy
Ao to allow mixing of venous and arterial blood.
Ideally, the arterial switch operation with reim-
plantation of the coronary arteries into the neo-
LA
aortic root should be performed. Alternatively,
RA
interatrial repair procedures may be preferred
PA depending on the clinical situation. The Senning
and Mustard procedures redirect venous blood by
removal of the atrial septum followed by the inser-
tion of an intra-atrial baffle which cleverly redis-
tributes the desaturated venous blood behind the
baffle to the mitral valve, LV, and to the transposed
PA (Fig. 14.15). Saturated pulmonary venous
blood is directed in front of the baffle to the RA,

Fig. 14.12 Fontan operation for tricuspid atresia

SVC
LA
PA
Ao
RA
PA

RA LV
Extra cardiac
conduit
RV

IVC Fig. 14.14 D-transposition of the great arteries. The pul-

monary artery arises from the LV and the aorta from the
RV. Usually a coexisting communication (not shown)
such as a patent ductus arteriosus, ASD or VSD allow the
Fig. 14.13 Total cavopulmonary connection surgery infant to survive (40–50% will have an associated VSD)
After Corrective Surgery for Congenital Cardiac Abnormalities 323

tricuspid valve, RV, and aorta. The Mustard proce-

dure uses atrial pericardium or synthetic material
as the baffle. Atrial tachyarrhythmias, junctional
rhythm, and complete heart block occur in these
patients and may require pacing (Fig. 14.16). In
the Senning procedure, flaps of the atrial septum
PVA and RA free wall are used to reroute systemic and
pulmonary venous return, and sinus node damage
Ao PA and atrial arrhythmias are not uncommon, presum-
ably as a result of the extensive atrial surgery.
SVA Although pacing in patients with
D-transposition may be a daunting task, surpris-
ingly it may be straightforward. The atrial lead
is advanced via the SVC and the stump of the
RA, behind the baffle and into the LA where it
LV
should be actively fixed to the roof of the LA
(Fig. 14.17). Lateral screening should show
RV posterior positions of both LA and LV leads
(Fig. 14.18). Preferably a curved or steerable sty-
let should be used to place the lead as medial as
possible in order to avoid phrenic nerve stimula-
tion (see Fig. 14.21). Steerable catheter delivery
Fig. 14.15 Senning operation for D-transposition of the
great arteries
systems may be useful for positioning the atrial
lead in optimum position. The ventricular lead is

Fig. 14.16 In D-transposition of the great arteries treated by the Mustard procedure, junctional bradycardia and com-
plete heart block may occur and require pacemaker implantation
324 14
advanced along the same route, across the mitral
valve and into the LV, where it should be actively
fixed. The ECG should confirm satisfactory dual-
chamber pacing (Figs. 14.19 and 14.20).
When baffles become obstructed as the patient
grows (>20% of patients), CT, MRI scans, or
Fig. 14.17 After a Mustard or Senning procedure, if
dual-chamber pacing is required, the atrial lead may be
passed behind the baffle into the LA and actively fixed to
the roof of the left atrium. The ventricular lead follows the
same route into the left atrium and then advanced across
the mitral valve into the LV where it is actively fixed
Fig. 14.18 This illustration shows a posterior position of both leads in the LA and LV in this patient who had under-
gone a Mustard procedure
Pacing in Patients with Structural Cardiac Abnormalities
venography might be helpful to show the anatomy
better prior to device implantation. Ventricular
leads must pass into the LA and into the LV before
being anchored actively. Figure 14.21 shows a
more medial position of the atrial lead in order to
try and prevent phrenic nerve stimulation. It is
worth remembering that chronic atrial arrhythmias
are not uncommon because of the extensive atrial
surgery, and if atrial fibrillation is present, then a
rate-adaptive (VVIR) pacemaker with a single
pacing lead is appropriate (Fig. 14.22).
If a Rastelli operation has been performed for
patients with TGA/VSD/ pulmonary stenosis and
AVB subsequently develops, leads can be placed
in the RA and RV by a conventional transvenous
approach rather than opting for epicardial pacing
(Fig. 14.23). The latter may be more appropriate
if the AVB occurs at the time of VSD closure.
Structural Defects Requiring
Epicardial Pacing
Occluded superior vena cava or subclavian veins,
mechanical tricuspid valves, and no access to
the venous ventricle, for example in tricuspid
atresia, make endocardial pacing impossible and
epicardial pacing is necessary.
After Corrective Surgery for Congenital Cardiac Abnormalities 325

Fig. 14.19 Complete heart block in a patient after a Mustard procedure

Fig. 14.20 ECG of same patient as in Fig. 14.19 after dual-chamber pacemaker implantation

After the Fontan procedure and its many vari-
ants and after patch closure of a VSD, when
atrial bradyarrhythmias and AV block occur,
pacing is indicated but endocardial pacing is or
may be impossible and epimyocardial pacing is
necessary (Fig. 14.24). If there is a venous route
to the right atrium, an atrial lead can be sutured
in the pectoral region and the epicardial ventric-
ular lead (usually from the LV) tunneled to the
pectoral pocket for pacemaker connection
(Fig. 14.25). Alternatively, the atrial lead can be
extended and tunneled to the anterior abdominal
326 14
wall and the pacemaker buried behind the rectus
sheath.
Figure 14.26 shows that a transvenous atrial
lead can be placed and actively fixed in the RA
which is often very dilated. In this situation,
Fig. 14.21 Following a Mustard procedure at the age of
19 months, a dual-chamber pacemaker was implanted in
this patient at the age of 16 years. An active fixation lead
was placed in the LA (venous atrium) but placed more
medially to try and avoid phrenic nerve stimulation. An
active fixation lead was placed in the apex of the LV and
an Elite DDDR generator (Medtronic) implanted. Ten
years later, the generator was changed to a Clarity DDDR
Pacing in Patients with Structural Cardiac Abnormalities
where the RA can be accessed via the SVC, a
subcutaneous pectoral pacing system can be
used. Clearly, if a total cavopulmonary anasto-
mosis is created, then epicardial pacing will be
necessary.
(Vitatron) because of reaching the ERT. A subsequent
procedure was required 4 years later to replace the mal-
functioning ventricular lead which was not extracted. The
lateral view shows the atrial lead positioned posteriorly
but pointing anteriorly and the two actively fixed ventricu-
lar leads posteriorly placed in the LV. The generator was
exchanged for a Sensia™ DDDR device (Medtronic) at
the same procedure
Fig. 14.22 After a Mustard procedure, if atrial fibrillation
and a slow ventricular rate are present or if atrial pacing is
not possible, a single active fixation lead can be passed
into the left ventricle (venous ventricle) and attached to a
rate-responsive pacemaker. This 19-year-old man had
transposition of the great vessels, had an atrial septostomy
at day 1 and a Mustard procedure at 15 months of age. At
the age of 12 years he developed complete heart block. No
acceptable pacing threshold could be obtained in the baffle
or LA and so the proposed dual-chamber procedure was
changed to a Thera SR rate-responsive pacemaker using a
single, actively fixed LV lead. Seven years later, the gen-
erator was replaced by an Identity™ SR (St Jude Medical)
and 6 years later by a Symphony SR device (Sorin) – both
as a result of battery depletion
After Corrective Surgery for Congenital Cardiac Abnormalities
PA
LA
RA
VC
LV
RV
Fig. 14.23 Rastelli operation. Here a valved conduit
(VC) is created between the RV and PA
Fig. 14.24 After closure of a perimembranous ventricular
septal defect with a Dacron patch atrioventricular block is
not uncommon. This patient developed complete heart block
5 years later and a Legend VVIR pacemaker was implanted
using a single ventricular lead. When SVC obstruction
developed as a result of lead adhesion/fibrosis accompanied
by a very low lead impedance, it was decided to remove the
lead and dilate the SVC obstruction and implant a DDDR
327
Fig. 14.25 Following a Fontan procedure, the large and
dilated RA can be accessed to allow transvenous implantation
of an atrial lead. If AV block is present, then epicardial dual-
chamber pacing may be more appropriate, although a hybrid
procedure of endocardial RA and epicardial RV pacing may
be possible. In this situation, tunneling of one or other leads to
the pectoral or abdominal sites will be necessary
device instead. However, it proved impossible to either
remove the adherent lead or dilate the stenosis. Surgical
treatment was performed to remove the lead and repair the
SVC obstruction, at which time an endocardial lead was
fixed in the RA and tunneled to the epigastrium. An epicar-
dial lead was attached to the surface of the RV and the lead
tunneled to the epigastrium where both leads are attached to
a DDDR generator and buried behind the rectus sheath
328 14
Fig. 14.26 Following a Fontan procedure, an active
fixation lead is placed in this dilated RA and connected to
a pectorally placed generator to function as an AAI
system
Fig. 14.27 When several procedures
have resulted in difficult or impossible
access to the RV transvenously (red
arrow shows remnant of old leads from
previous extractions), epicardial pacing
may be necessary. Here new epicardial
atrial and ventricular leads have been
tunneled to the abdominally placed
generator (green arrow)
Epicardial pacing may be necessary if access
to the atrium or ventricle cannot be achieved
transvenously (Fig. 14.27).
Superior Vena Cava Obstruction/
Occlusion
If the superior vena cava is severely stenosed or
occluded, an alternative to an epicardial system is
Pacing in Patients with Structural Cardiac Abnormalities
Fig. 14.28 An active fixation lead is placed in the RV
apex across a bioprosthetic tricuspid valve in this patient
with aortic (green arrow), mitral (blue arrow) and tricus-
pid valve prostheses (yellow arrow) undergoing dual-
chamber permanent pacemaker implantation
to use the femoral vein. After entering the femo-
ral vein using the standard Seldinger technique, a
guidewire and sheath are inserted to enable deliv-
ery of a ventricular lead to the right atrium.
Usually a long pacing lead is required and this
should be actively fixed in the right ventricle. The
lead can then be tunneled under the skin into the
lower abdominal wall where an incision can be
made and a pocket created for the generator to
which the lead can be attached (see Fig. 12.66).
After Corrective Surgery for Congenital Cardiac Abnormalities 329

An atrial lead can be similarly delivered if dual-
chamber pacing is desired.
Prosthetic Valves
Pacing leads cannot be placed across mechanical
valves. Generally, if a mechanical tricuspid valve is
present, epicardial RV lead placement will be
required if pacing is necessary. However, a perma-
nent lead can be placed across a bioprosthetic tri-
cuspid valve without too much difficulty (Fig. 14.28)
and an active fixation lead should be chosen espe-
cially if there is dilatation of the RA or RV.
An alternative approach is LV pacing via the
coronary sinus.
 Pacemaker and ICD Implantation in
Children
Introduction
The implantation and follow-up of pacemakers
and ICDs in children poses unique challenges.
Less than 1% of all pacemakers and ICDs are
implanted in children and the numbers of implants
taking place within individual centers are low. In
a recent US survey, the mean annual number of
new pacemaker implants per center was less than
25. A significant proportion of the pediatric pop-
ulation who require pacemaker and ICD implan-
tation are survivors of palliative surgical
procedures for complex congenital heart disease
(CHD). Physicians are thus faced with the
difficult situation of implanting few devices in
complex patients and as a result sometimes adult
cardiologists may be asked to implant devices in
children. This chapter focuses on the key differ-
ences between adults and children in terms of
pacemaker and ICD indications, implantation,
and follow-up.
Bradycardia Pacing Indications
There are no randomized trials of cardiac pacing
in children or patients with CHD; as a result
most recommendations are consensus-based.
The current indications for bradycardia pacing in
children are summarized in the latest ACC/AHA/
HRS guidelines published in 2008 and con-
densed in Table 15.1. Specific issues are dis-
cussed next.
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_15, © Springer-Verlag London 2012
15
Normal Heart Rates in Children
Resting heart rates in small children are consider-
ably higher than in adults. A resting heart rate of
50 bpm, while normal in an athletic 15-year-old
would represent profound bradycardia in an
infant (Fig. 15.1). Moreover, in the presence of
CHD, levels of bradycardia or loss of AV syn-
chrony may lead to symptoms which would not
occur in the presence of normal cardiovascular
physiology. It is important, therefore, to correlate
symptoms with age- and disease-specific rates of
bradycardia rather than absolute rates.
AV Block in Children
As in adults, pacing is mandatory for children with
symptomatic complete AV block. Although dra-
matic symptoms such as syncope are readily appar-
ent, children may find it difficult to describe more
subtle symptoms such as lethargy, breathlessness, or
dizziness and a high index of suspicion is required.
There is increasing evidence that asymptom-
atic patients with complete AV block have a risk
of developing left ventricular dysfunction if left
unpaced. There is also a small but definite risk of
sudden death. Permanent pacing is recommended
for neonates and infants (children aged less than
1 year) if the ventricular rate is less than 55 and in
children over 1 year if the heart rate is less than
50. In patients with structural CHD associated
with complete AV block, pacing is recommended
331
332 15 Pacemaker and ICD Implantation in Children

Table 15.1 Indications for permanent pacing in children, adolescents, and patients with CHD
Class I: Permanent pacing is indicated in the following groups of patients
1. Symptomatic third-degree AV block or high-grade second-degree AV block
2. Following cardiac surgery for CHD, postoperative third-degree AV block or high-grade second-degree AV
block which persists for at least 7 days
3. Asymptomatic congenital third-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy,
or evidence of ventricular dysfunction
4. Asymptomatic congenital third-degree AV block in infants with a ventricular rate <55 bpm in the absence of
CHD or <70 bpm in the presence of CHD.
5. Sinus node disease with correlation of symptoms with age-inappropriate bradycardia
Class IIa: Permanent pacing is reasonable in the following groups of patients
1. Asymptomatic congenital third-degree AV block over 1 year of age with an average heart rate <50 bpm or
pauses of 2–3 times the basic cycle length
2. Sinus bradycardia in the presence of complex CHD with a resting heart rate of less than 40 bpm or pauses of >3 s
3. Patients with CHD who have impaired hemodynamics as a result of sinus bradycardia or loss of AV synchrony
4. Unexplained syncope in the patient with prior surgery for CHD complicated by transient third-degree AV block
after evaluation to rule out other causes of syncope
5. CHD and sinus bradycardia for the prevention of recurrent episodes of atrial tachyarrhythmias
Class IIb: Permanent pacing can be considered in the following groups of patients
1. Patients who have undergone surgery for CHD who experienced transient postoperative third-degree AV block
and subsequently reverted to sinus rhythm with residual bifascicular block
2. Asymptomatic congenital third-degree AV block with an acceptable rate, a narrow QRS complex, and normal
ventricular function
3. Asymptomatic sinus bradycardia after biventricular repair of CHD with a resting HR of <40 bpm or pauses of >3 s
Class III: Permanent pacing is contraindicated in the following groups of patients
1. Asymptomatic Wenckebach
2. Asymptomatic sinus bradycardia with pauses of <3 s and a minimum HR of >40 bpm
3. Patients who have undergone surgery for CHD who experienced transient postoperative third-degree AV block
and subsequently reverted to sinus rhythm with normal AV conduction
4. Patients who have undergone surgery for CHD who did not experience transient postoperative third-degree AV
block but who develop asymptomatic first-degree AV block or bifascicular block
Adapted from Ref. [1]

if the resting heart rate is less than 70. Other fac-
tors such as chronotropic competence, the pres-
ence of pauses, and effort intolerance should be
taken into consideration.
Patients who develop complete AV block as a
result of surgery for CHD are at particularly high
risk of ventricular standstill, regardless of the rate
of the escape rhythm. If complete AV block per-
sists for more than 7 days after surgery, perma-
nent pacing is required. Mobitz Type II AV block
also warrants permanent pacemaker implantation
(Fig. 15.2). Even if AV nodal function recovers,
there is still a risk of late recurrence of AV block
years or decades after surgery. Syncope in this
group of patients should be considered to be due
to AV block until proven otherwise.
Permanent Pacing as Therapy
for Tachyarrhythmias Following
Surgery for Congenital Heart Disease
Some children who have undergone palliative
surgery for CHD develop recurrent atrial
arrhythmias (Fig. 15.3). Some cardiologists
advocate the implantation of pacing systems
which can be used to overdrive pace these
arrhythmias. With advances in mapping tech-
nology, radiofrequency ablation of these arrhyth-
mias is often possible, removing the need for
pacing. In most centers, pacing for the treatment
of atrial tachyarrhythmias is reserved for those
cases in whom ablation is not possible or
unsuccessful.
Introduction 333

Fig. 15.1 A normal ECG recorded from an infant in sinus rhythm, with a resting heart rate of 137 bpm

Vent. Rate 77 bpm Ref. MD: NM abnormality

PR interval 144 ms Technician: JG
QRS duration 58 ms System Evaluation:
QT/QTC 452/511 ms *** Pediatric ECG analysis ***
P-R-T axes 70/43/56˚ Sinus bradycardia
P duration 82 ms Left axis deviation
RR/PP interval 779/775 ms Possible Left ventricular hypertrophy
Borderline Prolonged QT, may be secondary to QRS

Fig. 15.2 2:1 AV block in an infant. The ventricular rate is well preserved and the QRS complexes narrow, in keeping
with an escape rhythm originating high-up in the His-Purkinje system
334
Fig. 15.3 Incessant atrial tachycardia following surgery for congenital heart disease
ICD Indications in Children
We have witnessed an evolution in ICD indica-
tions for children. Implants were initially
restricted to survivors of cardiac arrest. We now
implant routinely for hemodynamically unstable
VT and for primary prevention in patients per-
ceived to be a risk of sudden cardiac death (SCD).
ICDs are considered to be a safe and effective
way of preventing SCD in children as well as
adults, but the decision to implant will continue
to involve balancing the risks of SCD versus
those inherent with long-term ICD therapy.
Secondary Prevention ICDs
The current guidelines for secondary prevention
ICDs (survivors of cardiac arrest and patients with
documented ventricular arrhythmias) are very sim-
ilar to the adult guidelines (Table 15.2). Whereas
in the adult population the predominant cause of
ventricular dysfunction is ischemic heart disease,
in the pediatric population it is CHD with a small
contribution from dilated cardiomyopathy.
15 Pacemaker and ICD Implantation in Children
Table 15.2 Indications for ICD implant specifically in
pediatric patients and patients with CHD
Class I: ICD implant is indicated in the following
groups of patients
1. Survivors of cardiac arrest after evaluation to
exclude a reversible cause
2. Symptomatic sustained VT in association with CHD
after electrophysiological and hemodynamic
evaluation
Class IIa: ICD implant is reasonable in the following
groups of patients
1. CHD with recurrent syncope of uncertain origin
but with ventricular dysfunction or inducible
ventricular arrhythmias at EP study
Class IIb: ICD implant can be considered in the
following groups of patients
1. CHD with recurrent syncope of uncertain origin
with significant ventricular dysfunction where
thorough invasive and noninvasive investigations
have failed to determine the cause
Class III: ICD implant is contraindicated in the
following groups of patients
1. As per adult recommendations
Adapted from Ref. [1]
Primary Prevention ICDs
It is easy to make the case for ICD implant for
secondary prevention in young survivors of cardiac
ICD Indications in Children
arrest, who have a 30% 1-year risk and a 55%
3-year risk of recurrent arrhythmias. The decision
to implant an ICD on a primary prevention basis in
a child is much more difficult. Often the child will
have a family member who has died suddenly and
there is understandable anxiety about the diagno-
sis. This increases pressure on the physician to
implant a device.
In children, there is perhaps a greater need to
weigh the potential benefits of lifelong ICD ther-
apy against the undoubted drawbacks, with the
attendant risks of lead fracture, infection, and
inappropriate shock therapy. Most children who
receive a primary prevention ICD do so because
they have an inherited cardiac condition associ-
ated with an increased risk of arrhythmia
(Table 15.3). The estimated annual risk of sud-
den cardiac death in high-risk patients with long-
QT syndrome (Fig. 15.4) is of the order of 2%
and in hypertrophic cardiomyopathy 3%. This is
Fig. 15.4 Long QT syndrome in a 3-year-old girl who was resuscitated after a cardiac arrest. The corrected QT interval
is 532 ms
335
lower than the risk of SCD in adults with coronary
disease and advanced left ventricular dysfunction
who make up the majority of adult primary pre-
vention ICD recipients. As a result it is necessary
for the ICD to be in place for longer to obtain
comparable benefit. The longer life expectancy
of pediatric primary prevention ICD recipients
counterbalances their lower annual risk.
In contrast to the adult population, there is
little or no prospective data available to guide the
Table 15.3 Inherited conditions associated with sudden
cardiac death in children and adolescents
Long QT syndrome
Catecholaminergic polymorphic VT (CPVT)
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic right ventricular cardiomyopathy
(ARVC)
Dilated cardiomyopathy
336
Fig. 15.5 ECG of a patient with complex congenital heart disease. There is right bundle branch block
use of primary prevention ICDs specifically in
children. At the moment, pediatric indications for
these conditions are identical to adult indications
(Chap. 17). Children with advanced ventricular
dysfunction, often in the setting of CHD, are at
particularly high risk of ventricular arrhythmias.
The risks appear to be particularly high in patients
with repaired tetralogy of Fallot, d-transposition
of the great arteries and severe aortic stenosis.
Cardiac Resynchronization
Indications in Children
Biventricular pacing, or cardiac resynchroniza-
tion therapy (CRT), is a well-established therapy
in the adult population, particularly in heart fail-
ure patients with left bundle branch block (LBBB)
(Chap. 16). LBBB is quite rare in pediatric popu-
lations. Right bundle branch block (RBBB) is
much more common, especially in children with
CHD (Fig. 15.5).
There have been no randomized trials investi-
gating patient selection, lead site location or opti-
15 Pacemaker and ICD Implantation in Children
mization in the pediatric population. This may in
part be because heart failure etiology in children
is so heterogeneous. We do not know which of the
many substrates may be amenable to CRT. For
this reason, CRT is often reserved for those
patients in whom medical treatment is failing,
prior to cardiopulmonary transplantation. One
encouraging study found an average improve-
ment in left ventricular ejection fraction of 6%
and an 87% improvement in functional status in a
group of patients in whom 77% had CHD. Patients
with single ventricle physiology did particularly
well; it may be that CRT will be used earlier in the
disease process in CHD patients in the future.
In children with two ventricles and a systemic
left ventricle, established adult criteria are
applied. In more complex CHD (systemic right
ventricle and univentricular hearts), there is no
clear consensus.
The presence of multiple substrates for heart
failure may explain the observation that echo evi-
dence of mechanical dyssynchrony rather than
QRS duration seems to be the best predictor of
response.
Issues Unique to Device Implantation in Children
Fig. 15.6 Redundant loops of atrial
and ventricular leads (curved arrows)
are usually left to allow for somatic
growth in children in the hope of
preventing tension on the leads and
even lead displacement
Issues Unique to Device Implantation
in Children
Somatic Growth
Most children continue to grow after their pacing
systems have been implanted. Pacing leads need
to be implanted with large loops of redundant
lead (Fig. 15.6) in order to prevent leads from
tightening/stretching and possibly displacing as
the child grows (Fig. 15.7). Epicardial leads and
defibrillation patches can “strangulate” the heart
if insufficient slack is allowed.
Congenital Heart Disease
An increasing number of children are survivors of
surgery for complex CHD, which has palliated
rather than corrected the underlying circulatory
physiology. It is vital that the operator understands
the anatomy before embarking on any procedure.
Univentricular hearts and the presence of atrial
baffles placed to redirect bloodflow pose particu-
337
lar challenges. Patients who have undergone a
total cavopulmonary (Fontan) correction cannot
usually be paced endocardially. Up-to-date echo
and pre-procedural MR imaging and the use of
contrast radiology during the procedure improve
the chance of a successful outcome (Fig. 15.8).
The small number of device procedures per-
formed in children means that specifically
designed pediatric pacing systems are not avail-
able. Instead, adult equipment must be used. Adult
pacing leads are relatively large in diameter (6–9F)
in comparison to the small vessels found in small
children. Implanting such leads can lead to loss of
the vessel altogether, with resulting symptoms of
venous obstruction (Fig. 15.9). As a result, very
small children (less than 10–15 kg) are usually
paced epicardially in an attempt to preserve
venous structures for later in life (Fig. 15.10).
Most children receiving cardiac devices will
outlive not only their generators but also their
leads, and multiple surgeries will inevitably be
required for generator changes and the need for
replacement and extraction of malfunctioning
leads (Figs. 15.11 and 15.12).
338 15 Pacemaker and ICD Implantation in Children

Fig. 15.7 Chest X-ray showing a right

ventricular shock lead which has
become taut and partially dislodged
from the right ventricular apex as the
child has grown

Superior vena cava

Hemiazygous vein

Fig. 15.8 Three-dimensional

reconstruction of cardiac
anatomy in a patient being
considered for permanent
pacing. The image is Left atrium
projected in a left sagittal
view. The right atrium and
ventricle are rudimentary. A
left-sided superior vena cava,
the inferior vena cava, and a Right ventricle
hemiazygous vein empty into
Inferior vena cava
the left atrium (Image
courtesy of Dr. T. Bragadeesh
Right atrium
and Dr. D. Bardo)
Device Implantation 339

Fig. 15.9 Digital subtrac-

tion venogram in a patient
with a dual-chamber
pacemaker showing
obstruction of the innomi-
nate vein as it enters the
superior vena cava with
extensive collateralization

Anesthesia

Mobile While permanent pacing in adults is normally

performed under local anesthesia with or without
Supine
sedation, pacing all but the oldest children
requires a general anesthetic, even for simple
procedures such as generator changes and minor
wound revisions. The presence of CHD may
make safe anesthesia a challenge.

Side and Site

Most pacemakers are implanted in the left pecto-

Fig. 15.10 Epicardial pacing system with abdominal
generator in a child with dextrocardia and complex con-
genital heart disease
Device Implantation
Implanting an endocardial permanent pacemaker
or ICD in a child is procedurally similar to an
adult implant (Chaps. 7 and 17). The following
section highlights the important differences
between adult and pediatric pacing.
ral region, as this approach is easier for the opera-
tor and more comfortable for the right-handed
patient. CRT-P systems are considerably easier to
implant from the left side. Left-sided ICDs, where
the can forms part of the defibrillation circuit,
have lower defibrillation thresholds than right-
sided systems, although right-sided systems do
successfully defibrillate. The choice of site is not
infrequently limited by the site of previous pac-
ing systems, particularly if there has been infec-
tion and the need for extraction (Fig. 15.13).
Subpectoral implants are preferred for chil-
dren, largely for cosmetic reasons but also to
protect from manipulation, trauma, and possi-
bly infection. ICD generators almost always
need to be implanted subpectorally. Subpectoral
340
Fig. 15.11 Chest X-rays from a 26-year-old woman with
corrected transposition of the great vessels, ventricular sep-
tal defect, and congenital complete heart block who initially
underwent permanent pacemaker implantation at 4 years of
age at the time of pulmonary artery debanding and VSD clo-
sure. Left: The surgeon implanted a screw-in lead to the sys-
temic ventricle and sutured an epicardial lead to the surface
of the RA – implanting a dual-chamber pacemaker in the left
subcostal pouch. Four years later, failure to pace necessi-
tated implantation of a new endocardial pacing system
(Minuet™, Medtronic) via the left subclavian vein using
active fixation leads to the RA appendage (blue arrow) and
anatomical RV apex (red arrow) with redundant loops (black
arrows) to allow for somatic growth. Aged 17 years, insula-
tion break resulted in intermittent loss of sensing and pacing
implants pose a greater surgical challenge at
the time of generator change, with greater
scope to damage leads. Leads placed directly
below subpectoral generators may become
adherent to the ribs, making extraction extre-
mely difficult. Many operators prefer to coil
the leads superficial to the generator for this
reason.
Generators are implanted in the rectus sheath in
very small children, especially if the leads have
been placed epicardially, as the access point and
generator are close to one another (Fig. 15.14).
This provides good protection for the generator,
15 Pacemaker and ICD Implantation in Children
in the RV lead which was replaced. It proved impossible to
enter the left subclavian vein which was now occluded and
so the lead was inserted via the left internal jugular vein (yel-
low arrow) and tunneled subcutaneously over the left clavi-
cle to the pre-pectoral pocket. The tip of this active-fixation
RV lead can be seen to point vertically downwards (green
arrow) – fairly typical of this congenital abnormality. Seven
years later, the Kappa™ DDD (Medtronic) was replaced by
a Sensia™ DDD device (Medtronic) but within 2 years – at
the age of 26 years – further lead problems required a new
endocardial system from the right subclavian vein (right),
using a Medtronic 5592 lead to the RA appendage (orange
arrow), a Tendril® ST active-fixation lead (St. Jude Medical)
to the interventricular septum (pink arrow) and an Altrua™
50 DDDR pacemaker (Boston Scientific)
but the surgery involved is more complex and may
require the presence of a surgeon as well as a car-
diologist. There is a propensity for pacing and
ICD leads to fracture as they traverse the costal
margin due to repeated abdominal flexion
(Fig. 15.15).
Venous Access
In older children and adolescents, the cephalic
vein may be large enough to accept one or two
pacing leads. However, it is more usual to insert
Device Implantation 341

Fig. 15.12 Multiple leads in a patient.

This patient has catecholaminergic
polymorphic VT and underwent
implantation of an epicardial system
which has been extracted, leaving
behind the tips of the epicardial pace/
sense leads and a shocking coil in the
subcutaneous tissues. A new right-sided
ICD system has been implanted with an
endocardial shocking lead (green
arrow) and a stand-alone SVC coil in
the left subclavian vein (blue arrow)

Fig. 15.13 Infected pacing system

Fig. 15.14 Abdominal generator implanted in rectus

leads using a subclavian approach. Crushing of
the lead under the medial clavicle (Fig. 15.16) is
a not infrequent cause of lead failure and can
result in loss of pacing due to conductor fracture
(Fig. 15.17) or oversensing in bradycardia devices
and inappropriate shocks due to oversensing with
ICDs (Fig. 15.18). Many operators try and
sheath in an infant
perform subclavian puncture as laterally as pos-
sible. Using the extrathoracic subclavian or axil-
lary vein (Fig. 15.19) minimizes the risk of lead
crush and also eliminates the possibility of
pneumothorax.
342
Fig. 15.15 Atrial lead fracture immediately below the
left costal margin in abdominal system in a child several
years after the Fontan procedure. This lead fracture is at
the most common site, due to repetitive flexion movements
(Reproduced with kind permission of Silka et al. [2] and
the heart rhythm society)
Fig. 15.16 Subclavian “crush.” One of the pacing leads appears thinned as it passes below the clavicle due to damage
to the insulation (blue arrow)
15 Pacemaker and ICD Implantation in Children
Epicardial Pacing Systems
When reliable endocardial systems became
available in the 1970s and 1980s, adult pacing
moved away from epicardial systems to endo-
cardial systems. Initial enthusiasm for endocar-
dial systems in children was tempered by the
realization that vessel loss (due to implantation
of large leads in small veins with resulting
thrombosis and occlusion) had major implica-
tions in patients who had a lifetime of pacing
ahead of them. As a result, epicardial systems
are preferred if the patient weighs less than
10–15 kg in order to preserve the endocardial
approach for later in life.
Epicardial systems are also implanted in
children who require open heart surgery for
other reasons, in those in whom anatomy
prevents an endocardial approach (e.g., Fontan
circulation) and if the only ventricle which can
be paced is systemic and there is a perceived
high risk of systemic embolization despite
anticoagulation.
Epicardial lead implantation requires more
invasive surgery with sternotomy, thoracotomy, or
VAT-assisted surgery. Failure rates of epicardial
bradycardia pacing leads are slightly higher than
Device Implantation 343

for endocardial leads, although steroid-eluting

epicardial leads mean that the rate of exit block is
comparable. Many surgeons will implant two
ventricular leads so that there is a redundant lead
available in the event that the first lead fails.

Fig. 15.19 Axillary vein puncture

Fig. 15.17 Pacemaker lead fracture

Jan 25, 2010 15:01:06 Jan 25, 2010 15:01:09

9979 Software Version 7.0 9979 Software Version 7.0
ICD Model: Maximo VR 7232 ICD Model: Maximo VR 7232
Copyright Medtronic, Inc. 2003 Copyright Medtronic, Inc. 2003
Serial Number: PRN619862S Serial Number: PRN619862S
VT/VF Episode #81 Report Page 1 VT/VF Episode #81 Report Page 1

ID# Date/Time Type V. Cycle Last Rx Success Duration ID# Date/Time Type V. Cycle Last Rx Success Duration
81 Jan 24 07:44:07 VF 270 ms VF Rx 6 No 4.4 min 81 Jan 24 07:44:07 VF 270 ms VF Rx 6 No 4.4 min

• V-V VF = 320 ms FVT = 260 ms VT = 370 ms

V-V Interval (ms)
2,000 35.1 J 34.8 J 35.2 J No Match 10 % Match 91 % No Match 0 % No Match 10 %
1,700 35.2 J 35.1 J 35.1 J
1,400 4 mV
1,100
800 20 ms
QRS
600 Template
400

200 No Match 7 % No Match No Match 13 % No Match

−30 −20 −10 0 10 20 30 40 50 60 70

Time (s) [0 = Detection]

Fig. 15.18 Inappropriate ICD shock due to lead fracture causing noisy electrogram. The electrogram is interpreted as
VF and a shock is delivered
344
Fig. 15.20 PA and lateral chest X-rays of a ventricular pacing lead placed in the right ventricular outflow tract
Active versus Passive
Endocardial Leads
Active fixation leads are preferred by many oper-
ators, especially those who also extract leads.
Unless life expectancy is shortened due to coex-
isting cardiovascular or other disease, it is almost
inevitable that any implanted lead will fail within
the lifetime of the child. It is often very difficult
to implant new leads alongside old ones due to
venous occlusion. In such situations, one must
make a difficult choice between abandoning the
current site and moving elsewhere and extracting
the failed lead, leaving a channel for a new lead
on the same side. Extraction of active fixation
leads is possibly easier and lower in risk than
extraction of passive, tined leads.
Active fixation leads also have the advantage
of being able to be placed almost anywhere within
the heart, rather than relying on the presence of
trabeculated myocardium as is the case with pas-
sive leads. This has potential advantages if one is
trying to maintain physiological ventricular acti-
vation by pacing the interventricular septum
rather than the apex (Fig. 15.20) or faced with
unconventional pacing sites due to the presence
of CHD (Fig. 15.21).
One factor which limits a lead’s life expec-
tancy is the need for a lumen in which to pass the
15 Pacemaker and ICD Implantation in Children
stylet. This necessarily weakens the lead and also
increases the diameter. One manufacturer has
released a lumenless lead which is delivered
though a steerable outer catheter akin to an endo-
cardial LV lead (SelectSecure®, Medtronic, Ltd.).
The lead is only 4F and theoretically will have
significantly better longevity than a conventional
pacing lead, two factors of key importance in
children (Fig. 15.22). The lead is difficult to place
in patients with distorted anatomy due to the need
for a steerable catheter.
Right Ventricular Lead Placement
Conventionally the right ventricle is paced at
the apex as the trabeculated myocardium found
there provides good stability for passive fixation
leads. Right ventricular apical pacing causes the
resulting paced QRS to have a broad left bundle
branch block configuration. This leads to inter-
ventricular dyssynchrony and in adults has
been shown to increase the risk of developing
heart failure and atrial fibrillation. Pacing the
right ventricular outflow tract (RVOT) or mid-
interventricular septum is hemodynamically
superior to right ventricular apical pacing and
studies are ongoing in adults to see whether this
hemodynamic benefit translates to improvement
Device Implantation 345

Fig. 15.21 PA and lateral chest X-rays of a patient with transposition of the great arteries in whom a ventricular pacing
lead has been placed via an ASD into the left ventricle

Fig. 15.22 Left: Medtronic SelectSecure® pacing lead (4F fixed screw lumenless pacing lead). Right: Cut-away steer-
able introducer sheath (Image reproduced with permission of Medtronic, Inc.)

in clinical outcomes. There are no equivalent One Lead or Two?

studies in pediatric populations, although it has
been estimated that RV apical pacing contributes
to the development of heart failure in approxi-
mately 7% of pacemaker recipients. As a result,
it is common practice to apply active-fixation
ventricular leads to the mid-septum or RVOT
(Fig. 15.20).
When pacing small children with high-grade AV
block, there is a necessary compromise between
keeping a system simple and preserving AV syn-
chrony. The more leads that are present, the
greater potential problems exist and the higher the
risk of venous occlusion. However, there is clear
346 15 Pacemaker and ICD Implantation in Children

200 200
Heart rate ( 1 min Avg ) Aberrant beats per minute
HR max. = 183 bpm
180 HR mean = 123 bpm 180

160 160

140 140

120 120

100 100
HR max. = 94 bpm
80 80

60 60

40 40

20 20

0 0
11:00 17:00 23:00 +05:00 +11:00

Arrhythmia criteria :
Pause : ≥ 1.50 s Bradycardia : minimum of 4 beats at ≤ 60 bpm
Dropped beat : ≥ 180% of RR interval SVT : minimum of 5 beats at ≥ 160 bpm
VT : minimum of 5 beats at ≥ 130 bpm Premature aberrant : ≤ 90 % of RR interval
Salvo : minimum of 4 beats Premature normal : ≤ 66 % of RR interval

Fig. 15.23 Holter monitor of physiological heart rate in an 18-month-old patient. The heart rate varies between 94 and
183 bpm

evidence that preserving AV synchrony leads to
better left ventricular function in the long term.
In the past, VDD leads with an integrated atrial
sensing electrode have been implanted. Results
have been variable but overall seem disappointing.
Somatic growth leads to movement of the atrial
electrode relative to the right atrium and frequently
leads to issues with undersensing. Few of these
leads are implanted in current practice. Using very
low-profile leads, for example, Medtronic
SelectSecure® (Fig. 15.22), allows two leads to be
placed independently. Although such leads have
not been available for long enough for long-term
data to be available, it is hoped that smaller diam-
eter leads will reduce the risk of venous occlusion
compared to standard diameter leads. Children
who receive ICDs often benefit from the presence
of an atrial lead. Higher sinus rates in children
mean that there is frequently overlap in the rate of
sinus tachycardia and ventricular arrhythmias
(Fig. 15.23). Patients with CHD are at increased
risk of rapid atrial arrhythmias and an atrial lead
aids discrimination between supraventricular and
ventricular arrhythmias (Fig. 15.24). The few chil-
dren with sinus node disease may only require
atrial support pacing with a single atrial lead. The
function of the AV node is tested at the time of
implant by gradually increasing the pacing rate to
140 bpm and looking for the presence of
Wenckebach phenomenon. If this phenomenon is
present, it is usual to implant a ventricular lead and
a dual-chamber device. In patients with CHD and
sinus node disease, operators usually have a low
threshold for implanting a ventricular lead as there
is an increased risk of developing AV block later in
life (particularly if there has been cardiac surgery).
ICD Device and Lead Issues in Children
ICD system implantation in teenagers with struc-
turally normal cardiac anatomy is technically lit-
tle different than in adults. However, in younger
children and in those with CHD, it may be a
significant challenge and it is wise to have a strat-
egy or plan of action involving customized/hybrid
ICD Device and Lead Issues in Children 347

Fig. 15.24 Atrial lead aiding discrimination

between VT and SVT. Upper panel: From top to
bottom there is an atrial intracardiac bipolar
electrogram, a ventricular intracardiac bipolar
electrogram and marker channel. There is a
regular ventricular rhythm with more ventricular
than atrial events indicating VT. Lower panel:
From top to bottom there is a surface electrogram,
atrial intracardiac bipolar electrogram, ventricular
bipolar intracardiac electrogram, and marker VF Rx 1 Defib

channel. There is a slow, slightly irregular

ventricular rhythm. The atrial rate is rapid and 3−AUG−2004
5: 41
Lead− I
Atrial EGM
Vent EGM
(10 mm/mV)
GUIDANT
25
F11

slightly irregular and subsequent electrophysi-

ological study showed it to be an atrial tachycardia
arising from a pulmonary vein

AS (AS) (AS) AS (AS) (AS) AS (AS) AS AS (AS) AS AS

195 190 185 188 193 185 190 188 168 195 185 188 19
AS) (AS) AS (AS) (AS) AS (AS) (AS) (AS) (AS) (AS) (AS) (AS)
85 183 185 188 185 188 193 183 193 200 183 183 175
VS VS VS VS
5 VS 655 VS 623 VS 473 VS 468
423 468 750 620

techniques if necessary in order to achieve the

best outcome. The problems of body size, growth,
activity, and the need for future device and lead
insertion/replacement must be considered. An
important fact to remember is that defibrillator
pace/sense/shock leads are of a more complex
structure than bradycardia pacing leads and as a
result are more prone to damage at the time of
implant and subsequently.

Epicardial Patches and Leads

As ICD leads tend to be bulky, their size lim-

its their use to children over 15 kg. Children
under this weight require the placement of epi-
cardial patches and/or subcutaneous arrays for
defibrillation (Fig. 15.25), either alone or in com-
bination with an endocardial pace/sense lead.
Various ingenious alternatives to endocardial sys-
tems have been devised to preserve venous struc-
tures, including conventional leads placed in the
pericardium for pacing and sensing (Fig. 15.26)
or epicardial pacing/sense leads placed via vid-
eoscopic techniques via a small subxiphoid inci-
sion. Such lead placements are likely to have
lower defibrillation thresholds than subcutane-
ously placed leads. The placement of epicardial
patches requires a more prolonged, more invasive
Fig. 15.25 Subcutaneous ICD arrays in a child with long
QT syndrome. An epicardial pace/sense lead is in place
together with subcutaneous arrays for shocking. An endo-
cardial atrial lead has been placed at a later date to enable
atrial support pacing
procedure and for this reason epicardial systems
are almost exclusively used in secondary preven-
tion cases. Epicardial patches can in theory lead
to pericardial constrictive physiology, although
in practice this seems to be relatively rare.
348
Fig. 15.26 Pericardial ICD lead in a 3.5-year-old child
with CHD and dilated cardiomyopathy using a trans-
venous design ICD lead placed in the posterior pericar-
dium, DDD epicardial pacing leads, and subcutaneous
coil in the left lateral chest wall. The lead seen in the right
pleural space is the pace/sense portion of the ICD lead,
which is capped because the epicardial pacing leads are
used for sensing and pacing in this configuration
(Reproduced with kind permission of Berul [3] and the
Heart Rhythm Society)
Subclavian Crush
It is particularly important to avoid subclavian
crush, as in addition to the risk of failure to sense
or pace, there is a risk of inappropriate shocks.
Partial fracture of the pace/sense portion of the
lead results in repeated “make/ break” potentials
which are detected by the device and interpreted
as ventricular fibrillation (Fig. 15.16). Multiple
inappropriate shocks may lead to lasting psycho-
logical damage.
Coil Spacing
In smaller children, the shock coil portion of the
leads can extend into the right atrium, traversing
the tricuspid valve (Fig. 15.27). As the coil is much
stiffer than a conventional pacing lead, this can
lead to fouling of the tricuspid valve and significant
tricuspid regurgitation. If the shock coil overrides
15 Pacemaker and ICD Implantation in Children
Fig. 15.27 Endocardial single coil lead placed in a
3-year-old. The shock coil is within both right ventricle
and right atrium
into the right atrium, this can lead to shunting of
current away from the ventricular myocardium
and an increase in defibrillation threshold.
Choosing a lead with a shorter coil and short coil/
tip spacing can alleviate these difficulties.
Lead Diameter
Conventional ICD shock leads are 9F in diameter,
which poses significant problems in smaller chil-
dren, such as venous occlusion. Newer leads have
been developed which are smaller in diameter, for
example, 7F Durata (St Jude Medical) (Fig. 15.28).
Although initial enthusiasm has been tempered by
the realization that certain smaller diameter leads
may be more prone to early failure, for example,
Sprint Fidelis (Medtronic) and RiataTM (St. Jude
Medical), the perceived benefits of a lower profile
lead mean that many implanters prefer them.
T-Wave Oversensing
Many pediatric ICD recipients have long QT
syndrome. Significant QT prolongation can lead
to T-wave oversensing and double counting of
ICD Device and Lead Issues in Children
Fig. 15.28 St. Jude Medical
7F Durata® active-fixation
ICD shock lead (Image
provided courtesy of St. Jude
Medical, ©2008 St. Jude
Medical, Inc.)
ventricular sensed events (Fig. 15.29). It is
important to assess for the presence of this phe-
nomenon at implant as it is very difficult to pro-
gram around.
Potential Future Extraction
Complex ICD leads are more likely to fail than
conventional bradycardia leads. The coil tends to
become closely adherent to the myocardium
making extraction a challenge. The Gore™
expanded PTFE-coated leads, for example,
Endotak Reliance G/SG (Boston Scientific Ltd.),
prevent ingrowth of tissue into and around the
coils and theoretically make extraction easier
(Fig. 15.30).
Single Versus Dual Coil Leads
Somatic growth places more strain on ICD leads
than on bradycardia pacing leads, as the coil
moves as well as the pace/sense portion of the
lead. Single coil leads are usually chosen as the
spacing of the coils in adult-sized dual-coil leads
means that the SVC coil is usually in the neck or
pocket. Dual-coil leads are also much more
349
difficult to extract, as the SVC coil becomes
adherent to the SVC. Extraction has the potential
for tearing of the SVC with resulting massive
bleeding. If the defibrillation threshold is high
with a single coil lead, a stand-alone SVC coil can
be implanted.
Subcutaneous Defibrillators
Subcutaneous “leadless” ICDs have been devel-
oped, where there are no endocardial or epicardial
components; instead, a lead for sensing and
defibrillation is placed subcutaneously and con-
nected to a generator placed in the rectus sheath or
pectoral region. These devices have the advantage
that the venous system is preserved without the
need to perform sternotomy to place epicardial
patches. The energy required to defibrillate from a
subcutaneous array is higher than for endocardial
leads or epicardial patches. This makes the devices
larger than conventional ICDs and limits their use
in smaller children. In addition, they cannot pro-
vide permanent bradycardia pacing or antitachy-
cardia pacing, although they can provide
temporary post-shock pacing. These factors have
limited the take-up of subcutaneous devices in
children.
350
Fig. 15.29 T wave oversensing in an ICD. The patient is
in slow VT (the ventricular rate is faster than the atrial
rate) which self-terminates. The T waves are oversensed
(arrows), leading to double counting of the ventricular
Advantages and Disadvantages
of Lead Route Options
The advantages and disadvantages of the various
routes for ICD insertion are shown in Table 15.4.
Placing Endocardial Leads in Patients
with Congenital Heart Disease
Access to the right ventricle may be hampered by
the presence of congenital heart defects, for
example, tricuspid atresia, or by interventions
designed to palliate congenital lesions, for exam-
ple, Fontan procedure and atrial baffles. Although
15 Pacemaker and ICD Implantation in Children
rate and the ICD interpreting the rhythm as VF. The device
begins to charge but the oversensing terminates and the
shock is aborted
Fig. 15.30 Gore™-coated shock coils in the Endotak
Reliance® lead (Boston Scientific Ltd.) (©2010 Boston
Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)
a Fontan circulation effectively prevents access
to the right heart from the venous system, in other
situations it is often possible to pass a lead into a
Choice of Device
Table 15.4 Advantages and disadvantages of the various routes for ICD lead placement
Route Advantages
Transvenous Easy insertion, common use
Subcutaneous array Minimally invasive, no trans-
or coil venous coil, no epicardial patch
Pericardial lead Low DFT, no transvenous coil, no
epicardial patch
Epicardial patch Good DFT, long-term data
Subcutaneous No transvenous or epicardial
leadless ICD access required minimally invasive facility
chamber and secure it well enough to provide
permanent pacing. The use of active-fixation
leads, steerable stylets and introducers, venogra-
phy as well as a thorough prior understanding of
the anatomy helps ensure a successful outcome.
Placing a permanent pacing lead into a systemic
chamber (e.g., pacing the left ventricle via a septal
defect in a patient with tricuspid atresia) is often pos-
sible as an alternative to epicardial pacing. It is impor-
tant to weigh the perceived risks of thromboembolism
against the need for sternotomy. Lifelong anticoagu-
lation is mandatory in such situations.
Pacing unconventional sites increases the risk
of phrenic nerve stimulation and it is important to
test for this with high output pacing during the
implant procedure.
Chapter 14 discusses more extensively the
topic of device implantation in patients with car-
diac structural abnormalities.
Lead Placement in Pediatric
CRT Recipients
Placing left ventricular leads by the conventional
coronary sinus route may pose a significant chal-
lenge in pediatric patients, especially those with
CHD. Smaller hearts and guide catheters with
adult-sized curves make access to the coronary
sinus difficult. A steerable electrophysiology cath-
eter over a straight guide catheter may be helpful.
Siting the LV lead at the site of latest contrac-
tion appears to result in the best improvement in
left ventricular function. The site of latest con-
351
Disadvantages
Lead fractures, venous occlusion/obstruction, lead
insertions may be difficult in CHD, lead extractions
may be difficult
Higher DFT, little long-term data
Surgical procedure, adhesions may make visualization
with VAT system difficult, little long-term data
Surgical procedure, patch failure, possible constrictive
pericarditis may develop
Higher DFT, no pacing or antitachycardia pacing
traction can be identified using echocardiography
(speckle tracking) or by using the latest ventricu-
lar activation as a surrogate. Standard coronary
sinus sites are limited by venous anatomy and for
this reason many operators place epicardial leads
electively, particularly if surgery is being con-
templated for other reasons.
Choice of Device
Size
Most modern pacemakers are between 8 and
11 cc in volume. They provide sophisticated fea-
tures including automatic capture management,
rate response, rate drop response, and algorithms
to minimize ventricular pacing (see below).
Smaller pacemakers are available for very small
children, for example, Microny® (St Jude
Medical) (Fig. 15.31). Opting for a smaller pace-
maker usually requires some sacrifice in terms of
features, for example, single chamber only.
The different ICDs that are available tend to
be of a similar volume (around 30 cc) but vary in
shape, some being wide and flat, for example,
Teligen® (Boston Scientific Ltd.) (see Fig. 17.7)
and others shorter and wider, for example,
Secura™ DR/VR and Maximo DR/VR
(Medtronic Ltd.) (Fig. 15.32). The choice of
device will depend on the intended implantation
site. At the time of generator change it is often
helpful to replace like with like to save having to
refashion the pocket.
352
Pacing Modes
Pacing that restores or preserves AV synchrony is
preferable particularly in those with ventricular
dysfunction. Although single-lead VDDR sys-
tems have been widely used to provide effective
restoration of AV synchrony, problems of atrial
Fig. 15.31 Microny K® pacemaker weighs 12.8 g, is 6 mm
thin, and has a volume of 5.9 cc (Image provided courtesy of
St. Jude Medical, ©2008 St. Jude Medical, Inc.)
Fig. 15.32 Secura™ DR and Maximo™ DR ICDs (Image reproduced with permission of Medtronic, Inc.)
15 Pacemaker and ICD Implantation in Children
sensing in those with a scarred right atrium and
changing lead position as the child grows have
virtually confined this system to history. In con-
trast to adults, some young patients with isolated
SND (often due to cardiac surgery) do not require
dual-chamber pacing and AAI pacing can be
used if 1:1 AV conduction is maintained at heart
rates >140/min. AAIR pacing is also preferable
to DDD pacing in patients with ventricular
dysfunction.
Pacing Modes to Avoid RV Pacing
As well as avoiding right ventricular apical pac-
ing by pacing elsewhere in the right ventricle, it is
also possible to minimize right ventricular pacing
by the use of proprietary algorithms. Most mod-
ern pacemakers include an algorithm which either
progressively extends the AV delay, for example,
Search AV® (Medtronic Ltd.), or mode switches
between AAI and DDD mode, for example,
Managed Ventricular Pacing® (Medtronic Ltd.)
(Fig. 15.33). The more sophisticated algorithms
command a significant price premium, but work
very well in patients who have sinus node disease
alone or only intermittent AV block. Although
Choice of Device 353

AAI(R) Mode

Back up V pace in
the event of
Wenckebach

Switch to DDDR if
AV conduction
does not recover

Fig. 15.33 Managed ventricular pacing (MVP™) algorithm. This algorithm switches between AAI(R) and DDD(R)
pacing depending on intrinsic AV conduction (Image reproduced with permission of Medtronic, Inc.)

the majority of pediatric pacemaker recipients
have permanent complete AV block, many ICD
recipients do not and these algorithms are now
found integrated into most ICDs.
Longevity
There is little to choose between most modern
pacemakers in terms of longevity. Most have pro-
jected working life spans of 6–8 years. Epicardial
leads often have higher thresholds and this affects
device longevity. Many pacemakers automatically
measure pacing threshold and adjust the pacing
output to just above this. In this way, the life span
of the device can be increased by a few months.
Current ICD longevity is significantly shorter
than for bradycardia pacing systems (4–5 years).
Unlike the pacing population, many ICD recipi-
ents have structurally normal hearts and, apart
from their arrhythmia, should have a normal life
expectancy. However, multiple generator changes
are likely. When programming ICDs in children,
care must be taken to extend the longevity of the
device as much as possible, for example by mini-
mizing unnecessary bradycardia pacing.
MR Compatibility
Magnetic resonance imaging is rapidly emerging as
the investigation of choice for cardiac disease and
354
CHD as well as a huge number of noncardiac con-
ditions. Although there are theoretical issues with
movement, local heating, loss of pacing, and dam-
age to the generator, with appropriate precautions,
many modern pacemakers can enter an MR scanner
with only a very small risk of problems. Nevertheless,
there is often profound reluctance by radiology
departments to allow patients with pacemakers and
ICDs into the scanning room.
Medtronic Ltd. has developed an MR-safe
pacemaker (SureScan™ MRI) and MR-safe bra-
dycardia pacing leads. If a child is likely to need
MR scanning, one could reasonably make an
argument for implanting such a device. At the
time of writing, no MR-safe ICD had been
released.
Upper Rate
The upper rate (sensed and sensor driven) of most
pacemakers is 200 bpm. This is less than the max-
imum predicted heart rate of many young chil-
dren who receive pacemakers. At high levels of
exertion, upper rate behavior (pacemaker
Wenckebach) will occur. It is important to use a
pacemaker with a high upper rate and program
the upper rate as high as possible in small chil-
dren, as increases in cardiac output in young chil-
dren depend on increases in heart rate rather than
stroke volume.
Remote Follow-up Capability
Pediatric patients often receive their device in a ter-
tiary center many miles from their home. Pacemaker
follow-up may require long journeys. Some newer
pacemakers and most ICDs can be followed up
remotely via a remote telephone/internet link,
reducing the need to travel for very frequent fol-
low-up appointments. This is important if there are
concerns over lead integrity or arrhythmias.
Pacemaker Follow-Up
Problems identified during follow-up are
significantly more frequent in children than in
15 Pacemaker and ICD Implantation in Children
adults. Growth may lead to tension on leads and
eventual displacement.
Lead Fracture
Lead fractures are more common in the pediat-
ric pacing population than in the adult popula-
tion (see Fig. 15.17). One series suggests that
15% of bradycardia pacing leads in pediatric
cases failed over an average follow-up of
6.2 years. Twenty-eight percent of patients will
experience multiple lead failures. The factors
associated with lead fracture include age
<12 years at implant, a history of CHD, and an
epicardial lead.
Many pediatric pacemaker recipients, particu-
larly those with complete heart block, become
profoundly pacemaker-dependent. Syncope may
suggest incipient lead failure and requires prompt
evaluation.
Infection
System infection is not uncommon in the pediat-
ric pacing and ICD population. Infection affects
3–5% of those receiving new implants, com-
pared to 0.5–1% of adults. This may reflect more
invasive procedures, for example, epicardial sys-
tems, complex anatomy with long procedure
times or low-volume operators. Infection almost
always requires complete removal of a system
with reimplant at a later stage on the contralat-
eral side.
Adjuncts to Standard Follow-Up
Poorly functioning or inadequately programmed
pacing systems may produce symptoms which
children may find more difficult than adults to
describe. Prolonged monitoring or exercise test-
ing can often be helpful. Some pacemakers have
a Holter monitor feature which can be activated
by the application of an external magnet (magnet
application triggers electrogram storage rather
than fixed rate pacing) which can be useful to
diagnose the cause of infrequent symptoms.
Choice of Device
Fig. 15.34 Self-terminating ventricular tachycardia in a child with long-QT syndrome. The device detects ventricular
tachycardia and is charging when the episode spontaneously terminates
Ventricular Arrhythmias
Patients with CHD, especially those who have
undergone surgical repair for Fallot’s tetralogy,
may be prone to ventricular arrhythmias. Syncope
in such patients, if not due to device malfunction,
should prompt a thorough evaluation. Most pace-
makers can be programmed to automatically
store electrograms during ventricular high-rate
episodes. This feature should be programmed
“on” if possible.
ICD Programming and Follow-Up
All patients, but particularly children, find shock
therapy distressing. It is considered good practice to
program ICDs to prevent unnecessary shocks when-
ever possible. As in adults, programming anti-
tachycardia pacing results in a substantial reduction
in appropriate shock therapy with no observable
delay in shock delivery if ATP fails – even if the
ventricular arrhythmia is very rapid. Most ICDs
now permit the delivery of ATP during charging.
Detection Rate
The default rate for the VF zone in many ICDs is
188 bpm. Most teenagers and all younger chil-
dren regularly achieve sinus rates of over
190 bpm. It is usually necessary to program
higher detection zones in children than in adults.
If this is not possible, for example if there is a
ventricular arrhythmia which occurs at physio-
logical heart rates, ICDs can distinguish between
355
sinus tachycardia and ventricular tachycardia
using electrogram morphology and rate of onset.
The presence of an atrial lead also helps rhythm
discrimination. It may be necessary to prevent
sinus tachycardia pharmacologically, for exam-
ple, by beta blockade.
Supraventricular arrhythmias occur in 30% of
patients with CHD and should ideally be antici-
pated before inappropriate shocks are delivered.
Drugs and ablation should be considered as well
as device reprogramming.
Detection Duration
Monomorphic VT is a much less common indi-
cation for ICD in children than in adults.
Polymorphic VT, torsades de pointes VT and VF
are more frequently the indication. Very often
ventricular arrhythmias are self-terminating and
asymptomatic. Shock therapy in such situations
can and should be avoided by programming long
detection intervals (Fig. 15.34).
Failure Rate of ICD Leads
and Epicardial Patches
Perhaps due to their more complex construction,
ICD leads and patches appear to have a substan-
tially higher failure rate than bradycardia pacing
leads. In one study, system failure rates were 27%
at 1 year, 45% at 2 years, and 51% at 3 years.
Epicardial patches had three times the failure rate of
endocardial leads. In patients who receive such sys-
tems, regular and frequent follow-up is required.
356
In conclusion, from a pacing and device point
of view, children are not “small adults.” In the
pacing population, there is a high incidence of
congenital heart disease and there are significant
differences in cardiac physiology between chil-
dren and adults, even in normal hearts. Pacing
and ICD hardware has been designed principally
with adults in mind and this means that frequently
some ingenuity is required when implanting and
following up devices. There is still an unaccept-
ably high failure rate for systems, particularly
ICDs. This may improve with the introduction of
newer lead technology. It seems highly likely that
cardiologists will encounter increasing number
of adult patients who underwent device implanta-
15 Pacemaker and ICD Implantation in Children
tion as children. Many of these patients will pose
a considerable challenge in terms of lead compli-
cations and frequent surgical intervention.
References
1. Epstein AE et al. ACC/AHA/HRS 2008 Guidelines for
Device Based Therapy of Cardiac Rhythm abnormali-
ties. J Am Coll Cardiol 2008; 51:e l–62.
2. Silka MJ et al. Pacemakers and implantable cardioverter-
defibrillators in pediatric patients. Heart Rhythm.
2006;3:1360–6.
3. Berul C Defibrillator Indications and Implantation in
young children. Heart Rhythm. 2008;5:1755–7.
 Cardiac Resynchronization Therapy
Heart failure can potentially complicate all forms
of heart disease. Over the last 20 years, there has
been a significant increase in both its incidence
and prevalence due to the advancing age of the
population and improved survival from coronary
heart disease – the principal cause of heart failure.
Despite improvements in pharmacologic manage-
ment, many patients with heart failure have severe,
resistant symptoms and their prognosis remains
poor. Medical therapy consists of angiotensin con-
verting enzyme inhibitors (ACEI), aldosterone
antagonists, and b-blockers, all of which have been
shown to reduce morbidity and mortality. Digoxin
and loop diuretics provide symptomatic benefit
only. More recently, however, prospective random-
ized clinical trials have shown that cardiac resyn-
chronization therapy (CRT), also known as
biventricular pacing, results in improvements in
LV function, exercise capacity, quality of life and
mortality in selected patients with heart failure.
This chapter will describe the rationale for CRT,
the features that predict a potential benefit from
CRT, the technique of implantation and the equip-
ment required for the procedure, the complications
that may occur, the follow-up that is required, and
finally, the evidence that currently exists that sup-
ports its use.
Rationale for CRT
Many clinical and laboratory variables predict
mortality in patients with advanced heart failure
including severity of symptoms (NYHA class
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_16, © Springer-Verlag London 2012
16
III–IV), left ventricular ejection fraction (LVEF),
etiology, and wide QRS complex. The latter is
most commonly present in the form of left bundle
branch block (LBBB), which occurs in one quarter
to one third of patients with heart failure. It is usu-
ally associated with delayed depolarization and
contraction of the left ventricular free lateral wall,
whereas the interventricular septum contracts nor-
mally resulting in paradoxical septal motion.
Hence, patients with heart failure and altered elec-
trical depolarization manifest further mechanical
cardiac pump failure with a resultant deterioration
in symptoms and prognosis. Currently, four cate-
gories of electromechanical dyssynchrony are rec-
ognized in heart failure. These are prolonged AV
delay, interventricular delay, intraventricular delay,
and the most recently described intramural delay.
In its simplest form, the concept of CRT is to
simultaneously depolarize both right and left
ventricles, thereby correcting electromechanical
dyssynchrony, and in turn enhance ventricular
contraction.
Indications for CRT
CRT is indicated for patients with advanced cardiac
failure (NYHA Class III–IV despite medical treat-
ment) due to systolic dysfunction (LVEF £ 35%)
with intraventricular conduction delay (generally
LBBB, QRS duration >120 ms) and mechani-
cal LV dyssynchrony. These have been recom-
mended by the ACC/AHA in their Guidelines
for Heart Failure Treatment (2005). The recently
357
358 16 Cardiac Resynchronization Therapy

Sinus Rhythm Permanent AF Need for Pacing

NYHA III/IV(amb.) NYHA II NYHA III/IV(amb.) NYHA III/IV NYHA II

EF ≤ 35% EF ≤ 30% EF ≤ 35% EF ≤ 35% EF ≤ 35%

LBBB Non- LBBB Non- QRS ≥ 120ms any QRS any QRS
LBBB LBBB
Slow V rate or
QRS ≥ QRS ≥ QRS ≥ QRS ≥ Post AVN ablation or
120ms ≤ 60bpm at rest &
150ms 130ms 150ms ≤ 90bpm on ex.

Class Class Class Class Class Class Class

IA IIa A I A IIa A IIb C IIa C IIb C

CRT-P CRT-P Preferably Preferably CRT-P CRT-P CRT-P

CRT-D CRT-D CRT-D CRT-D CRT-D CRT-D CRT-D

Eur Heart J. 2012 All patients under Optimal Pharmacological Therapy & life expectancy > 1 year

Fig. 16.1 ESC HF Guidelines 2012: CRT Summary

released ESC Heart Failure Guidelines advocate
the use of CRT in less severe heart failure patients
(NYHA II) with a stress on LBBB morphology
rather than just QRS duration (figure 16.1). CRT
has been shown to restore synchrony within the
impaired LV, to equilibrate energy consumption
and improve LV performance and to reduce mitral
regurgitation, which in turn result in improved
long-term clinical outcomes.
In patients with sinus rhythm, simultaneous
ventricular depolarization can be triggered by
atrial sensing and the use of a short AV delay. In
such cases, CRT may correct AV, interventricu-
lar, and intraventricular conduction delays. The
resultant improvement in left ventricular systolic
contraction may then be associated with an
improvement in intramural delay.
Similar benefits may be achieved in patients
with atrial fibrillation, provided that the intrinsic
heart rate can be suppressed to a slower rate than
that programmed in the device. This usually
necessitates AV node ablation but can occasion-
ally be achieved with high-dose-rate-limiting
medication with drugs such as b-blockers or
digoxin. In order to achieve simultaneous ven-
tricular depolarization, pacing leads must be
positioned to pace both the right and left ventri-
cles. Right ventricular (and atrial) pacing can be
achieved as previously described in Chap. 7.
Although one might expect that LV pacing
would necessitate direct arterial access or a
trans-septal puncture and the resultant risk of
severe complications, it can be achieved by plac-
ing the lead in the coronary sinus (CS) via the
right atrium.
Selecting Cases for CRT
Currently, most device specialists use the current
guidelines for selecting suitable patients for
CRT, which include LV electrical dyssynchrony
Technique
based on a QRS duration of >120 ms. However,
approximately 30% of patients fail to show a
favorable response to CRT and much work has
been carried out to try and identify more specific
determinants of CRT response. Three major fac-
tors appear to be important. These are the pres-
ence and severity of LV dyssynchrony, the
position of the LV lead in relation to the area of
LV with the latest mechanical activation, and the
extent and location of LV scar tissue.
Echocardiography may be useful for evaluating
these three issues. Other imaging modalities
such as MRI have been used with some success
in scar mapping.
In heart failure patients, cardiac dyssyn-
chrony may be atrio-ventricular (between atria
and ventricles), inter-ventricular (between RV
and LV), or intra-ventricular (within LV). It is
of paramount importance to obtain A-V syn-
chrony to optimize LV filling and stroke vol-
ume but estimates of LV filling time using
pulse-wave Doppler transmitral flow record-
ings do not predict a favorable response follow-
ing CRT although may be of use for optimizing
CRT response during follow-up. In contrast,
estimates of inter-ventricular and intra-ventric-
ular dyssynchrony appear to be predictive of
response to CRT and likely long-term
outcome.
Estimates of inter-ventricular dyssynchrony
are based on the “inter-ventricular mechanical
dyssynchrony index.” The time-intervals between
the onset of the QRS complex to the onset of the
pulmonary and aortic ejection periods (pulmo-
nary and aortic pre-ejection times) are measured.
Significant inter-ventricular dyssynchrony is sug-
gested by a difference of >40 ms between the two
pre-ejection times and predicts favorable out-
come after CRT. Tissue Doppler imaging (TDI)
can provide other indices that are similarly
predictive.
Assessment of LV dyssynchrony may be the
best method for evaluating candidates who are
likely to benefit the most. These echocardio-
graphic parameters include the septal: posterior
wall motion delay (SPWMD) assessed by
M-mode echocardiography, TDI techniques, 2D
speckle tracking imaging, and real-time 3D
359
echocardiography (RT3DE). However, evidence
to support these claims is currently lacking.
Finally, it is useful to know the site and extent
of transmural myocardial scars in order to ensure
that the LV lead is not placed at these sites and
that an optimum outcome from CRT can be real-
ized. Techniques for assessing myocardial scar
include gadolinium contrast-enhanced MRI,
echocardiographically measured regional wall
end-diastolic wall thickness (<5 mm), integrated
backscatter imaging, myocardial contrast
echocardiography (areas of nonenhancement),
and low-dose dobutamine stress echocardiogra-
phy, which can all identify areas of the myocar-
dium to be avoided if at all possible.
Ideally, the presence of significant LV
mechanical dyssynchrony, an LV lead position
concordant with the latest mechanically acti-
vated segment and low amount of myocardial
scar, provides the highest likelihood of a favor-
able response to CRT. Studies suggest that a
QRS width of >150 ms seems to predict response
(with a heavy bias toward LBBB). More
recently, the presence of RBBB or indetermi-
nate bundle branch block rather than LBBB has
shown to be a predictor of “nonresponse” in
these patients. Unsurprisingly other adverse
clinical predictors in CRT include atrial
fibrillation, pulmonary hypertension, renal dys-
function, and diabetes mellitus. This has been
reflected in the recent ESC heart failure guide-
lines 2012.
Technique
Preparation of the patient for CRT pacemaker
implantation is as described in Chap. 7. However,
two or three leads need to be inserted. Three sub-
clavian vein punctures may be used (Fig. 16.2) or
two subclavian vein punctures and a cephalic
vein may be used (Fig. 16.3). A splittable safe-
sheath with a hemostatic valve is used for venous
access to the CS to prevent excessive blood loss
and air embolism (see below). If the patient is in
sinus rhythm, besides inserting leads into the RA
and RV, a third lead needs to be placed into the
CS usually in a posterolateral branch vein where
360 16 Cardiac Resynchronization Therapy

Fig. 16.2 Two or three

leads will need to be inserted
depending on whether the
patient is in sinus rhythm or
not. If three leads are
required, three subclavian/
axillary vein punctures can
be made

the activation delay is generally most pronounced

(Fig. 16.4). This has been shown to provide the
best hemodynamic result from CRT, although not
necessarily the best clinical response. In atrial
fibrillation, only a RV and LV lead are necessary.
Given the proximity of the CS os to the right bun-
dle, the possibility of “bumping” the right bundle
during catheter manipulation may result in com-
plete heart block in a patient with underlying
LBBB. It is thus generally sensible to place the
RV (and RA lead, if necessary) lead first before
placing the LV lead into the CS and one of its
branches, so that in an emergency the RV lead
can be used to pace the ventricle.

Cannulating the Coronary Sinus/

Positioning the LV Lead

Entering the CS may be easy and straightforward,

Fig. 16.3 Alternatively, two subclavian vein punctures
and a cephalic vein cut-down may be chosen
but can be impossible. The membranous Thebesian
valve close to the CS ostium may make it difficult
to enter the CS with a catheter and Vieussen’s
valve at the ostium of the primary posterolateral
vein at the junction of the CS and great cardiac
vein may make it difficult to advance the catheter
within the CS.
Technique
Fig. 16.4 Chest X-ray shows typical lead positions in the
RA, RV, and coronary sinus (LV) in a patient undergoing
CRT
The CS is initially cannulated usually with a
specially designed sheath or catheter and the CS
and coronary venous anatomy demonstrated by
contrast injection (Figs. 16.5 and 16.6). These
catheters are used in conjunction with a hemo-
static valve to facilitate safe manipulation of a
guidewire and enable injection of contrast agent
(see below). Various delivery sheaths are avail-
able of different diameters (5F–7F) and shapes
for accessing the CS (Fig. 16.7). Some implant-
ers use a coronary angiography catheter or
deflectable EP catheter to cannulate the CS and
the sheath is then advanced into the CS body
using the catheter as a railing system. Once the
CS is cannulated, a standard balloon occlusion
catheter (Fig. 16.8) may be inserted and retro-
grade venography performed using hand-injected
contrast agent to define the exact anatomy
(Figs. 16.9–16.11). It is preferable to perform a
prolonged injection for image acquisition in order
to fully define the anatomy as several branches
and, in particular, the middle cardiac vein may
fill late. The SafeSheath® CSG® Pressure
Products™ Inc. provides a comprehensive range
361
Fig. 16.5 A specially designed sheath or catheter is used
to enter the coronary sinus and demonstrate the coronary
venous anatomy using injection of contrast agent. (Single
arrow) Great cardiac vein; (Double arrow) posterolateral
cardiac vein; (Triple arrow) middle cardiac vein
of equipment for accessing the CS and then opti-
mal LV lead stimulation while avoiding blood
loss (Fig. 16.12). Steerable/selective catheters
are also available, for example, SafeSheath
Worley Telescopic Braided lateral vein intro-
ducer (LVI) (Fig. 16.13) and a wide variety of
catheters and telescopic systems are available
from the device companies (Figs. 16.14 and
16.15). Biotronik offer their Streamer, Selectra
and ScoutPro® series. The left ventricular lead
may then be inserted down the sheath and posi-
tioned in a suitable epicardial vein – if necessary
with the aid of a sub-selective catheter and con-
trast injection (Figs. 16.16 and 16.17). The
sheaths have different methods of removal (split-
ting, slitting, and over the lead removal)
(Figs. 16.18 and 16.19). The ultimate lead posi-
tion is accepted on the basis of obtaining adequate
pacing parameters and stability as with any other
pacing lead. Stability within the CS is best
secured by having as many points of contact with
the endothelial lining as possible and is aided by
362 16 Cardiac Resynchronization Therapy

Fig. 16.6 The top two images show placement of the arrow) (right). The bottom two figures show contrast filling
coronary sinus sheath (left) (arrow) and delineation of the of the posterolateral (left) vein (open arrow) and placement
coronary venous anatomy by contrast injection (blue of the LV lead into a distal position (right) (arrow)

Fig. 16.7 A range of different-shaped catheters/sheaths

are available for accessing and delineating the coronary
venous anatomy and for delivering LV leads
Technique 363

Fig. 16.8 Balloon occlusion catheter for use in the coro-

nary sinus while performing retrograde venography. (Top)
Balloon catheter – deflated balloon at tip (arrow); (Bottom)
Close-up of inflated balloon

Fig. 16.9 Coronary sinus (CS) balloon catheter placed

inside ostium of CS. Balloon (arrow) is inflated to occlude
the CS and enable contrast delineation of the great cardiac
vein and its branches and aid placement of the LV lead
into a stable position (curved arrow) with good sensing
and pacing characteristics
364 16 Cardiac Resynchronization Therapy

Fig. 16.10 Coronary sinus contrast injection shows the

main body of the CS (single arrow) and the middle car-
diac vein (twin arrows)

Fig. 16.11 The top two images show delivery of the LV bility was unacceptable. The bottom two images show
lead through the coronary sinus via the great cardiac vein repositioning of the LV lead into the posterolateral vein
and into an anterolateral vein. However, the electrical sta- with acceptable sensing and pacing
Technique
Fig. 16.12 SafeSheath® accessories reduce blood loss
during positioning of the LV lead and facilitate LV cathe-
ter manipulation without risk of air embolism. The safe
adaptor is used at the distal end of the LV catheter to facil-
itate use of contrast via the side port and manipulation of
the guidewire within the catheter itself
Fig. 16.14 A variety of different shaped sheaths available
for accessing the coronary sinus and its branches for LV lead
delivery from St. Jude Medical. (Top left) CPS Aim™ Slittable
Inner Catheter Subselector enhances access to first vein
choice through Direct-to-Target™ placement. (Top right)
CPS Direct ™ SL Slittable Outer Guide Catheter designed for
coronary sinus access and left heart lead delivery. (Bottom
365
Fig. 16.13 SafeSheath® Worley superselective/steerable
introducer system for accessing distal branches of the
coronary venous system
left) CPS Venture™ Wire Control Catheter has a deflectable
tip for steering guidewires during left heart vein subselection.
(Bottom right) CPS Luminary™ Cannulator is a bideflectable
catheter with a lumen for cannulation of the coronary sinus
and subselection of target vein (Images provided courtesy of
St. Jude Medical, ©2008 St. Jude Medical, Inc.)
366
Fig. 16.15 (Top left) Medtronic’s equipment include the
range of Attain Command™ coronary sinus cannulation
catheters; (top middle) Attain® deflectable catheter deliv-
ery system for changing tip shapes of a single guide cath-
eter; (top right) Attain Select™ guide catheters for aiding
utilizing leads with pre-shaped curves
(Fig. 16.20), spiral formations (Figs. 16.21 and
16.22), and other fixation mechanisms.
Unfortunately pre-shaped leads have reduced
tracking ability within the coronary sinus and
this can make delivery to the desired target
difficult. To overcome this, the tips of CS leads
have valve-like structures permitting a guidewire
to be placed through the central lumen of the
lead, producing an “over the wire” lead to aid
delivery in a manner akin to a coronary artery
stent or angioplasty balloon (Fig. 16.23).
Occasionally it is necessary for an operator to
negotiate tortuous CS anatomy or even venous
stenosis (Fig. 16.24). Hence, skills and tech-
niques acquired in the catheter laboratory can be
put to good use in the pacing theater. The use of
balloon venoplasty to dilate stenosed target
branches has been described (Fig. 16.25).
Leads can either be placed using the stylet or
by the “over the wire” (OTW) technique. Some
16 Cardiac Resynchronization Therapy
vessel subselection; (bottom left) Attain Prevail™ steer-
able catheter for delivery of LV leads; (bottom right)
Attain Select® II Left Heart delivery system (Image repro-
duced with permission of Medtronic, Inc.)
leads may be deployed using both techniques
applied sequentially. With the stylet in the distal
tip of the lead, the lead is stiff and straight, but as
the stylet is withdrawn, the lead assumes its shape
with a curve on the end. After the lead is placed
into the proximal vein segment using the stylet, it
is then advanced into the target branch by the
OTW technique. Using a conventional 0.014″
angioplasty guidewire, the OTW technique is
particularly useful in tortuous veins and veins
with a sharp-angled course. Leads may have
“tines” to aid stability but the absence of trabecu-
lae within the coronary venous system limits
their value. Although most “fixation” is achieved
by simply wedging the tip of the lead in the distal
segment of the branch vein or by anchoring the
lead against the wall of the vein using a fixed
“spiral” or “J” shape of the distal end of the lead,
the StarFix® LV lead has a unique mechanism for
helping it to fix itself against the vein’s wall
which is useful for veins of larger diameter
Technique 367

Fig. 16.17 Coronary sinus venogram enables careful

Fig. 16.16 (Top left) X-ray showing the telescopic coro- placement of the LV lead (arrow) into the anterior inter-
nary sinus catheter system (green arrow) used to reach ventricular vein
and delineate the distal anterior interventricular vein (3
arrows) (middle left) and enable placement of the LV lead
(open arrows) (bottom left)
368 16 Cardiac Resynchronization Therapy

Fig. 16.18 Slitting of

LV sheath. Note
stabilization of LV lead in
order to prevent
displacement

Fig. 16.19 Slitting tool

Fig. 16.20 Medtronic’s over-the-wire LV leads. (Top)

Bipolar Model 4194; (Bottom) Unipolar Model 4193.
These have steroid-eluting tips to minimize threshold
peak, angled distal ends for steerability and stable fixation,
a tip seal for allowing guidewire reinsertion without blood
ingress, guidewire or stylet delivery and availability in
three lengths – 78, 88 and 103 cm (Image reproduced with
permission of Medtronic, Inc.)
Technique
Fig. 16.21 (Left) The Acuity® Spiral LV lead uses the
spiral shape to help fix the lead once it has been placed in
the desired branch coronary vein by delivering it over a
guidewire. (Right) the Acuity® Steerable IS-1 LV lead has
a J-shaped tip to aid positioning and enhance stability. The
tip is deflectable with the aid of a stylet but can be deliv-
ered over-the-wire (©2010 Boston Scientific Corporation/
affiliates. All rights reserved. Used with permission of
Boston Scientific Corporation)
Fig. 16.22 Easytrak® LV leads from Boston Scientific
Ltd. have an over-the-wire design, steroid-eluting tips,
uni- or bi-polar configurations and tines to reduce lead
displacement (©2010 Boston Scientific Corporation/
affiliates. All rights reserved. Used with permission of
Boston Scientific Corporation)
(Fig. 16.26). Boston Scientific offers a steerable
LV lead with a deflectable “J-shaped” tip
(Acuity®Steerable), a spiral LV lead for extra sta-
bility (Acuity®Spiral LV lead), a bipolar lead
with silicone tine fixation and over-the-wire
delivery (Easytrak®2 LV lead), and a 3-D helical
369
Fig. 16.23 Fluoroscopic image showing an LV lead
placed in the anterior vein with leads in the RA and RV
apex
bias fixation lead for stability in larger veins
(Easytrak®3 LV lead) (Fig. 16.27).
The caliber of the target vein relative to the
diameter of the lead is another important aspect
of lead selection. Stiff, thick leads (>1.5 mm) can
be placed safely in large straight veins with a
diameter of more than 3.5 mm, whereas thin dis-
tally pre-bent leads may not be stable in these
vessels and lead displacement with loss of cap-
ture may occur. These leads are more suited for
narrow or kinked and tortuous veins. Thick leads
might also traumatize the venous endothelium
with resulting vessel occlusion due to thrombosis
or dissection.
The success rate of the transvenous approach
has improved during the last decade from 90% to
95%. This represents greater operator experience
over a steep learning curve and the availability of
superior implanting equipment. The most com-
mon reasons for unsuccessful left ventricular
implants include the inability to access the CS,
acute dislodgment or unstable lead position, and
electrical issues with lead threshold and phrenic
nerve stimulation. What can be done in these sit-
uations is discussed below.
370
Fig. 16.24 (Upper left) This image shows the coronary
sinus sheath entering the small cardiac vein (arrow) in this
patient with a dual chamber ICD already in situ. (Upper
middle) This shows the sheath (arrow) in the CS after con-
trast injection. (Upper right and lower left) A balloon cath-
eter (green arrow) occludes the CS and demonstrates the
Testing After Lead Positioning
and Completing the Procedure
Once the lead position is acceptable, the R wave
amplitude, the lead’s pacing threshold, and its
impedance should be measured. Before anchor-
ing the lead using the suture collar and a nonab-
sorbable suture, the lead’s stability should be
checked by ensuring pacing is steady at 1 V out-
put during deep breathing/coughing. Occasionally
higher thresholds than this have to be accepted.
Moreover, because the posterolateral vein is in
close proximity to the phrenic nerve, lead stimu-
lation can result in diaphragmatic stimulation and
uncomfortable twitching for the patient. The
16 Cardiac Resynchronization Therapy
distal venous anatomy. The lateral vein is shown to have a
severe stenosis (red arrow). (Lower middle) The telescopic
inner sheath (green arrow) is used to select the branch with
the aid of a guidewire (arrow). (Lower right) Once the
branch is selected the guidewire can be removed and the LV
lead inserted. The arrows show local dissection of the CS
twitch threshold should always be measured
during CRT implantation, and unless there is a
considerable margin over the pacing threshold in
case of lead microdisplacement, the risk of dia-
phragmatic stimulation postoperatively is a real
possibility. Diaphragmatic stimulation should not
occur when pacing at 10 V. When all leads have
been secured using nonabsorbable sutures (such
as Ethilon™) around the collars provided on the
leads, the biventricular device can be attached to
the leads using the screwdriver provided, and the
device and leads buried in the pre-pectoral pocket.
The wound can then be closed in layers, with
absorbable, nonbraided sutures such as
Monocryl™ to the subcutaneous tissue and
Technique
Fig. 16.25 (Left) A severe stenosis is found in the target
branch of the coronary sinus (arrow); (right) a 2.0 mm
Sprinter balloon over a 0.014″ BMW guidewire is used
Fig. 16.26 Attain StarFix® (Medtronic) is the first active
fixation LV lead with exclusive deployable lobes allowing
for customized lead placement in a wide variety of vein
sizes and locations (Image reproduced with permission of
Medtronic, Inc.)
371
to dilate the stenosis (arrow). The subselective guide
catheter is clearly visible in the coronary sinus (open
arrow)
Fig. 16.27 LV leads from Boston Scientific. From left to
right: Acuity® Steerable IS-1, Easytrak® 3 and Easytrak®
2 and Acuity® Spiral (©2010 Boston Scientific
Corporation/affiliates. All rights reserved. Used with per-
mission of Boston Scientific Corporation)
372 16 Cardiac Resynchronization Therapy

Fig. 16.28 Chest X-ray

shows leads placed in the RA,
RV septum and an LV lead
placed in the postero-lateral
vein

Fig. 16.29 PA and lateral chest X-rays showing typical positions of actively-fixed RA and RV outflow tract leads and
a LV lead passively placed in posterior branch of the coronary sinus

subcuticular layer and Dermabond® glue to the
skin edges.
Before discharge from hospital, a PA and lateral
chest X-ray should be performed to confirm sat-
isfactory positions for the implanted leads and no
evidence of pneumothorax (Figs. 16.28–16.30).
A 12-lead ECG should be recorded and this
shows characteristic features of biventricular
pacing with a shortish AV delay and predomi-
nantly positive complexes in lead V1 and/or neg-
ative complexes in lead 1 (Figs. 16.31 and
16.32).
CRT Devices and LV Leads
CRT Devices and LV Leads
CRT Devices
A range of devices for CRT are now available
from several manufacturers. They are generally
divided into those devices which offer CRT pac-
ing only (CRT-P) (Figs. 16.33–16.36) and those
Fig. 16.30 Lateral chest X-ray shows the anterior place-
ment of the RA and RV leads and the posterior placement
of the coronary sinus lead
Fig. 16.31 ECG in a patient pre CRT-P implantation shows sinus rhythm but a wide QRS complex of LBBB
373
that offer both CRT pacing and defibrillation
(CRT-D) (Figs. 16.37–16.42). Some of these
devices are listed in Table 16.1. CRT systems
consist of a pulse generator plus two or three leads
– RV/LV or RA/RV/LV. The RV lead is typically
placed about midway on the RV septum, and the
LV lead into a coronary vein via the coronary
sinus. The RA lead is as for a conventional pace-
maker. A CRT-D device uses a RV defibrillation
lead. The LV lead is unique to CRT systems and
does not usually have a fixation mechanism (see
below). It is anchored in place because of its dis-
tal geometry or a spiral shape of its distal end.
These modern devices have extensive and
sophisticated programmability (Fig. 16.43), for
example, independent channel programmability,
possess patient-centric diagnostics, for example,
activity log, heart rate variability monitor (Figs. 16.44
and 16.45), and have the ability to be interrogated
remotely, for example, using the Latitude® home
monitoring system (Boston Scientific Ltd.).
LV Leads
A range of LV leads for implanting into the
cardiac venous system via the coronary sinus
are available from the various pacemaker
374 16 Cardiac Resynchronization Therapy

Fig. 16.32 ECG after CRT-P implantation shows ventricular pacing with a narrow QRS complex

Fig. 16.33 Contak® Renewal™ TR CRT-P device

(Guidant Ltd.) (©2010 Boston Scientific Corporation/
affiliates. All rights reserved. Used with permission of
Boston Scientific Corporation)

Fig. 16.34 InSync® III CRT-P device (Image reproduced

with permission of Medtronic, Inc.)
CRT Devices and LV Leads 375

Fig. 16.35 The Frontier™ II and Anthem™ RF CRT-P

devices (Images provided courtesy of St. Jude Medical,
©2008 St. Jude Medical, Inc.)

Fig. 16.36 Stratos LV-T CRT-P device (Courtesy of

Biotronik)

Fig. 16.37 InSync Maximo™, InSync Marquis™ and

InSync II Marquis™ CRT-D devices (Image reproduced
with permission of Medtronic, Inc.)
376 16 Cardiac Resynchronization Therapy

Fig. 16.39 The Concerto™ CRT-D device (Image repro-

duced with permission of Medtronic, Inc.)

Fig. 16.38 Cognis™ 100-D CRT-D device is small and

thin and can deliver 41 J shocks. The stored data is easily
printed out on interrogation (©2010 Boston Scientific
Corporation/affiliates. All rights reserved. Used with per-
mission of Boston Scientific Corporation) Fig. 16.40 The Livian® CRT-D device (©2010 Boston
Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)
CRT Devices and LV Leads
Fig. 16.41 The Lumax 340 HF-T CRT device (Courtesy
of Biotronik)
Fig. 16.42 The Promote™ + CRT-D device seen next to
the Current™ + ICD device (Images provided courtesy
of St. Jude Medical, ©2008 St. Jude Medical, Inc.)
manufacturers. These are listed in Table 16.2.
Recently, quadripolar leads have been produced,
for example, Quartet™ (St. Jude Medical), with a
low-profile IS-4 connector pin for use with new
devices such as the Promote Quadra™ CRT-D
(St. Jude Medical) (Fig. 16.46). These leads
377
provide more pacing vectors, allowing more
options and greater control in minimizing implant
complications such as diaphragmatic stimulation
and high pacing thresholds.
Complications
The complications of biventricular pacemaker
implantation (Table 16.3) include those associ-
ated with conventional pacing (see Chap. 12) and
those specifically related to the positioning of the
LV lead. The latter include failure to deploy the
LV lead, phrenic nerve stimulation, CS dissection
or perforation, and embolic phenomena.
The coronary venous anatomy precludes suc-
cessful LV lead placement in up to 15% of cases.
This may be due to absence of an appropriate
lateral branch, anomalous drainage into the left
atrium, stenosis or a vessel of insufficient caliber
obstructing passage of the lead. However, the
major technical problem encountered is the
inability to locate and enter the CS with the guid-
ing catheter. The anatomy may be distorted in
dilated hearts increasing the difficulty. Although
once the guide catheter has engaged the CS, it is
rare, with the newer technologies available, not
to be able to enter the target branch vessel.
However, occasionally it proves impossible to
advance a guidewire because of acute angulation
or stenosis. Early displacement may occur – par-
ticularly during guide catheter removal. The lead
displacement risk is dependent upon several
factors including the position and type of lead
used, the angle of the opening of the CS, and the
experience of the operator. Lead dislodgement
results in late failure of LV capture in 5–10% of
cases.
The more serious procedural complications
relate largely to the use and manipulation of the
guiding catheters within the heart. Serious
arrhythmias occur in up to 5% of all implanta-
tions. For example, guide catheter manipulation
may cause right bundle branch block, and in those
patients with existing left bundle branch block,
may result in ventricular standstill. For this rea-
son, it is best practice to position the right ven-
tricular lead first.
Table 16.1 Currently available CRT devices
378

CRT-P
Dimensions A and RV pace/ LV pace/sense
Manufacturer/device Type Weight (g) (H × W × D) mm Volume (cc) sense lead ports lead port
Boston Scientific
Contak Renewal TR H140 DR 26 54 × 45 × 8.5 14 IS-1 IS-1/LV-1
Medtronic
Syncra™ DR 26 57 × 59 × 6 15 IS-1 IS-1
Consulta™ DR 26 57 × 59 × 6 15 IS-1 IS-1
*InSync® III no longer available
St. Jude Medical
Anthem™ RF PM3212 DR 25 52 × 52 × 6 13.7 IS-1 IS-1
Frontier™ II 5596 DR 25 49 × 52 × 6 11.5 IS-1 IS-1
Sorin
None available
Biotronik
Stratos LV-Ta DR 30 55 × 50 × 6 14 IS-1 IS-1
CRT-D
Dimensions Defib A and RV pace/ LV pace/sense
Manufacturer/device Type Weight (g) (H × W × D) mm Volume (cc) lead ports sense lead ports lead port
Boston Scientific
Cognis® 106b DR 72 79 × 62 × 9.9 32.5 DF-1 IS-1 LV-1
16

Cognis® P107b DR 72 79 × 62 × 9.9 32.5 DF-1 IS-1 IS-1

Cognis® P108b,c DR 72 79 × 62 × 9.9 32 DF-4 IS-1 IS-1
Livian™H240 DR 79.5 77 × 63.5 × 14.5 40 DF-1 IS-1 IS-1
Livian™H245 DR 79.5 77 × 63.5 × 14.5 40 DF-1 IS-1 LV-1
Livian™H247HEd,e DR 87.5 82.5 × 67 × 14.5 44 DF-1 IS-1 IS-1
Livian™H249HEd,e DR 87.5 82.5 × 67 × 14.5 44 DF-1 IS-1 LV-1
Contak Renewal® 4 H190 DR 89 78 × 59 × 11.5 37 DF-1 IS-1 IS-1
Contak Renewal® 4 H195 DR 89 78 × 59 × 11.5 37 DF-1 IS-1 LV-1
Contak Renewal® 4 H197HEc DR 89 83 × 63 × 11.5 40 DF-1 IS-1 IS-1
Contak Renewal® 4 H199HEc DR 89 83 × 63 × 11.5 40 DF-1 IS-1 LV-1
Contak Renewal® 4 M170AVT DR 89 78 × 59 × 11.5 37 DF-1 IS-1 IS-1
Cardiac Resynchronization Therapy
 Contak Renewal® 4 M175AVT DR 89 78 × 59 × 11.5 37 DF-1 IS-1 LV-1
Contak Renewal® 4 M177AVTHEc DR 89 83 × 63 × 11.5 40 DF-1 IS-1 IS-1
Contak Renewal® 4 M179AVTHEc DR 89 83 × 63 × 11.5 40 DF-1 IS-1 LV-1
Contak Renewal® 4M235RFe DR 82 78 × 62 × 14 39 DF-1 IS-1 LV-1
Contak Renewal® 4 M239HEcRFe DR 90 83 × 66 × 14 43 DF-1 IS-1 IS-1
Medtronic
Maximo™ II DR 68 69 × 51 × 15 38 DF-1 IS-1 IS-1
CRT Devices and LV Leads

Consulta™ DR 68 69 × 51 × 15 38 DF-1 IS-1 IS-1

Protecta D364TRG DR 68 69 × 51 × 15 38 DF-1 IS-1 IS-1
Protecta D364TRM DR 73 66 × 51 × 15 40 DF-4 (RV pace/sense + high IS-1
voltage)
Protecta XT D354TRG DR 68 69 × 51 × 15 38 DF-1 IS-1 IS-1
Protecta XT D354TRM DR 73 66 × 51 × 15 40 DF-4 (RV pace/sense + high IS-1
voltage)
*InSync Sentry™, InSync Maximo™, InSync Marquis™, InSync® II Marquis and Concerto™II are no longer available
St. Jude Medical
Promote Accel CD3215-36Q DR 82 75 × 50 × 14 42 DF-4 IS-1 (A) IS-1
Promote Accel™ CD3215-30 DR 76 80 × 50 × 13 39 DF-1 IS-1 IS-1
Promote Accel™ CD3215-36 DR 82 81 × 50 × 14 43 DF-1 IS-1 IS-1
Promote™ RF 3213-36 DR 82 81 × 50 × 14 43 DF-1 IS-1 IS-1
Promote® + 3211-36 DR 82 81 × 50 × 14 43 DF-1 IS-1 IS-1
Promote® + 3211-36Q DR 82 75 × 50 × 14 42 DF-4 IS-1 (A) IS-1
Promote Quadra CD3239-40 DR 88 81 × 51 × 14 46 DF-1 IS-1 IS-4
Promote Quadra CD3239-40Q DR 87 74 × 51 × 14 44 DF-4 IS-1 (A) IS-4
Unify™ CD3235-40f DR 78 79 × 40 × 14 36 DF-1 IS-1 IS-1
Unify™ CD3235-40Qf DR 77 73 × 40 × 14 36 DF-4 IS-1 (A) IS-1
Unify™ Quadra CD3251-40 DR 83 83 × 41 × 14 40 DF-1 IS-1 IS-4
Unify™ Quadra CD3251-40Q DR 81 76 × 41 × 14 38 DF-4 IS-1 IS-4
*Atlas Plus HF, Atlas II HF, Epic HF, Epic II HF, Epic Plus HF are no longer available
(continued)
379
Table 16.1 (continued)
380

CRT-D
Dimensions
Defib A and RV pace/ LV pace/sense
Manufacturer/device Type Weight (g) (H × W × D) mm Volume (cc) lead ports sense lead ports lead port
Sorin
Paradym CRT-D 8750 DR 94 62 × 73 × 11 34
Paradym RF CRT-D 9750 DR 95 69 × 73 × 11 38.6 DF-1 IS-1
Paradym RF SonR CRT-D 9770 DR 95 69 × 73 × 11 38.6 DF-1 IS-1
NB: Ovatio™ is no longer available
Biotronik
Lumax 340 HF-T DR 94 66 × 59 × 13 39.8 DF-1 IS-1
Lumax 540 HF-T DR 94 66 × 59 × 13 39.8 DF-1 IS-1
*Kronos LV-T and Tupos LV/A-Tx no longer available
a
Compatible with Home Monitoring
b
High energy device, extended battery life, self-correcting software and improved programming e.g., BiV trigger for managing frequent atrial arrhythmias in pts with cardiac
failure, electronic repositioning, LV-only pacing
c
4site lead (DF4)
d
HE – High energy
e
RF – wireless telemetry
f
Has CorVue™ monitors intrathoracic impedance as a marker for increasing heart failure
16
Cardiac Resynchronization Therapy
CRT Devices and LV Leads 381

Fig. 16.43 Programmable parameters for the Paradym CRT 8750 biventricular device (Courtesy of Sorin Group)

Fig. 16.44 Interrogation of modern devices such as the Boston Scientific Corporation/affiliates. All rights
Contak® Renewal™ produces information on current pro- reserved. Used with permission of Boston Scientific
gram, activity, heart rate variability, and ABM (©2010 Corporation)
382
Fig. 16.45 Pacing and sensing data from each lead can
be retrieved in the Contak® Renewal™ TR device
(©2010 Boston Scientific Corporation/affiliates. All
As with any pacing electrode placement, car-
diac perforation is an uncommon but serious com-
plication during CRT implantation (Figs. 16.47
and 16.48), although this in itself may not pre-
clude successful left ventricular pacing.
Dissection or even perforation of the CS may
occur due to manipulation of the guide catheter, a
diagnostic catheter, occlusion balloon, or the pac-
ing lead (Figs. 16.24 and 16.49). Most often this
produces minor asymptomatic staining of the cor-
onary sinus but rarely can cause pericardial effu-
sion and tamponade. Dissection in the low-pressure
venous system is generally well-tolerated and
does not usually cause permanent disruption of
the anatomy. Thrombus formation within the
lumen of the guiding catheter or on the guidewires
used to deliver some leads may result in emboli.
These are rarely serious. The guide catheter also
increases the risk of air embolus.
Once the lead has successfully been delivered
to the target vein, problems may still occur with
sensing and stimulation. Poor R wave amplitude
16 Cardiac Resynchronization Therapy
rights reserved. Used with permission of Boston
Scientific Corporation)
is less of an issue than with right-sided leads but
far-field sensing of right ventricular or left atrial
activity may occur (particularly in the older gen-
eration devices). It is vanishingly rare these days.
Despite good lead positioning, high thresholds
are often obtained on the left ventricular lead.
Pacing thresholds up to 2 V are generally con-
sidered acceptable considering that the patients
are generally not pacemaker-dependent, have
back-up pacing from the right ventricular lead
and have a poor prognosis.
In inadequately positioned left ventricular
leads, inadvertent stimulation of the left atrium or
the right ventricle may occur. More commonly it
is stimulation of the phrenic nerve that causes
difficulties and, indeed, is a major cause for fail-
ure at a given position. This is most commonly
seen with leads in the posterior and posterolateral
branches of the CS. It is very variable with posture
and respiration, and therefore may only become
evident once the patient is off the table. It is rarely
seen in the branches of the great cardiac vein. In
Table 16.2 Characteristics of LV pacing leads
Manufacturer/device Polarity Lead Lead diameter Length (cm) Steroid elution
Biotronik
Corox OTW BP 75/85 Bi Helix 5.4F 77/87 Yes
Corox OTW-S BP 75/85 Bi Thread 5.4F 77/87 Yes
Corox OTW-L BP 75/85 Bi S-shaped curve 5.4F 77/87 Yes
Corox OTW UP Uni Helix 4.8F 77/87 Yes
CRT Devices and LV Leads

Boston Scientific
Acuity™ Spiral LV OTW lead 4591/2/3 Uni IS-1 2.6–4.1/4.5F 80/90/100 Yes
Acuity™ Steerable IS-1 LV OTW lead 4554/5 Bi IS-1 5.3/6F 80/90 Yes
Easytrak® 2 OTW 4517/18/20 Bi LV-1 5.2/5.3F 80/90/100 Yes
Easytrak® 2 IS-1 OTW 4542/3/4a Bi IS-1 5.2/5.7F 80/90/100 Yes
Easytrak® 3 OTW 4524/5/7b Bi LV-1 3.4–5.3/6F 80/90/100 Yes
Easytrak® 3 IS-1 OTW 4548/9/50b Bi IS-1 3.4–5.3/6F 80/90/100 Yes
Medtronic
Attain® OTW 4193 Uni IS-1 LV lead 5/5.4F 78,88,103 Yes
Attain® OTW 4194 Bi IS-1 LV lead 5.4/6.0F 78,88,103 Yes
Attain® OTW 4195 Uni IS-1 LV lead 5/5.3F 78,88,103 Yes
Attain® Ability® OTW 4196 MP-dual cathode IS-1 LV lead 4/5.1F 78,88 Yes
Attain Ability® + OTW 4296 Dual cathode IS-1 LV lead 5.3F 78,88 Yes
Attain Ability® Straight OTW 4396 Dual cathode IS-1 LV lead 4F 78,88 Yes

Sorin Group
Situs™ BW28D OTW-silicone screw Bi IS-1LV lead 6Fc 80 Yes
Situs™ OTW UW28D Uni IS-1 LV lead 6Fc 80 Yes
Situs™ LV UC28D/UL28D Uni IS-1 LV lead 6Fc 75 Yes
Situs™ BW28D MV Bi IS-1 LV lead 6Fc 80 Yes
Celerity Pilot Bi IS-1 LV lead 5.4F 77/87 Yes
Celerity 2D Bi IS-1 LV lead 5.4F 77/87 Yes
Celerity 3D Bi IS-1 LV lead 5.4F 77/87 Yes
SonR Tip P555Dd Tri IS-1 A lead 9F 52 Yes
(continued)
383
Table 16.2 (continued)
384

Manufacturer/device Polarity Lead Lead diameter Length (cm) Steroid elution

St. Jude Medical
Quickflex™ 1156T Bi LV lead 6Ff 75,86 Yes
Quickflex™ 1158Te Bi LV lead 6Ff 75,86 Yes
QuickFlex™ m Optim®-insulation 1258Tg Bi LV lead 4.3F 75,86,92 Yes
Quartet™ 1458Qg Quad LV lead 4.7F 75,86,92 Yes
a
Straight distal tip
b
3D spiral fixation mechanism
c
Needs 7F introducer
d
Contractility sensor A lead for SonR CRTD Auto optimizing device
e
S-shaped for stability
f
Minimum 7F introducer
g
Optim insulation; minimum introducer size = 5F ID
16
Cardiac Resynchronization Therapy
CRT Devices and LV Leads
Fig. 16.46 (Right) The Quartet™ quadripolar LV pacing
lead (arrow) features four pacing electrodes and ten pac-
ing vectors to provide more options and greater control to
minimize implant complications such as diaphragmatic
some circumstances, the presence of phrenic nerve
stimulation may be acceptable provided there is
an adequate margin between cardiac and phrenic
nerve threshold (generally threefold difference).
More commonly it is necessary to reposition the
lead more proximally within the vessel, in a
different distal sub-branch or in a different vessel
altogether. The newer, small-caliber leads may
reduce the likelihood of this complication devel-
oping because of their lower pacing thresholds.
The technological developments facilitating “elec-
tronic repositioning” within the existing lead may
help avoid having to physically reposition the lead
in some instances. This design enables one to alter
the cathode and anode and involve the RV lead as
well, giving various options for LV stimulation
and avoidance of phrenic nerve stimulation.
As with any pacemaker implantation involv-
ing subclavian vein puncture, pneumothorax and
hemothorax are realistic potential and serious
complications (Figs. 16.50 and 16.51).
385
stimulation and high pacing thresholds. Its low-profile
IS-4 connector pin is suitable for use with the Promote
Quadra™ (Left) (Image provided courtesy of St. Jude
Medical, ©2008 St. Jude Medical, Inc.)
Table 16.3 Complications of device implantation for
CRT
Complications of pacemaker implantation
Infection, hematoma, pneumothorax, hemothorax,
lead displacement, etc. (see Chap. 12)
Specific complications related to LV lead placement
Failure to enter coronary sinus or suitable branch
vessel
Failure to obtain stable LV lead position
Coronary sinus dissection/perforation/thrombosis
Embolization of thrombus/air from guiding catheter
Serious bradyarrhythmia, for example, ventricular
standstill
LV lead displacement
Phrenic nerve stimulation
Contrast agent toxicity
With the use of angioplasty guidewire-aided
LV lead positioning, guidewire fracture resulting
in retained intracardiac fragments is an unusual
complication. Such intracardiac fragments can
386 16 Cardiac Resynchronization Therapy

Fig. 16.47 The RV lead tip

appears on the very outer
border of the cardiac
silhouette (arrow) – suggest-
ing possible cardiac
perforation

Fig. 16.48 The lead tip

appears to have moved
further forward and now
points upwards as it is now
within the pericardial space
(arrow)
CRT Devices and LV Leads 387

Fig. 16.49 (Left panel) Coronary sinus dissection (arrow) is evident by contrast staining proximal to the occlusive
balloon. (Right panel) Despite the complication, an LV lead is placed distally in the posterior vein (open arrow)

Fig. 16.50 Following CRT

implantation, a post-operative
chest X-ray shows a small
pneumothorax to account for
the patient’s pleuritic chest
pain. However, the pain
persisted and he became
dyspneic. A further chest
X-ray was done the next
morning and is shown in
Fig. 16.51
388
Fig. 16.51 The chest X-ray
showed a left basal pleural
effusion – shown to be a
hemothorax
be retrieved using a variety of devices such as
loop and “goose-neck” snares and Dotter basket
kits usually inserted from the femoral vein
(Fig. 16.52).
What to do if deployment
in the Coronary Sinus fails
Even in the most experienced hands, occasionally
the procedure is technically impossible. In such cir-
cumstances, one may have to resort to a surgical
approach, with a limited thoracotomy or video-
assisted thoracoscopy and epicardial pacing
(Fig. 16.53). These procedures have additional
risks which must be weighed against the potential
benefits of CRT. Endocardial pacing of the LV via
a transeptal approach is not currently recom-
mended, although there is emerging evidence that
this may be an alternative strategy in failed tradi-
tional coronary sinus lead positioning. Systemic
anticoagulation is probably necessary in these
cases.
A left-lateral mini-thoracotomy has the advan-
tages of predictable procedure time and success
16 Cardiac Resynchronization Therapy
rate, and direct visualization should avoid phrenic
nerve stimulation. The disadvantages are that it
is invasive, often involves a hybrid approach and
a prolonged hospital stay. It may also be difficult
to position the lead sufficiently posterior for
effective therapy and complications are not
uncommon. Thoracoscopy is less invasive, but is
not readily available. Again it is usually a hybrid
procedure and sometimes it is necessary to revert
to open surgery. Moreover, these procedures only
provide access to the anterior and lateral LV wall
for LV lead placement.
Recent small studies have achieved ventricu-
lar resynchronization in a minimally invasive
fashion using the da Vinci robotically assisted
left ventricular epicardial approach (Intuitive
Surgical Inc., Sunnyvale, CA) via four “access
ports” (Fig. 16.54). It is claimed that the best
hemodynamic position can be obtained fairly
easily with this approach, including posterior
lead placement, and this is ideal for patients who
have previously undergone cardiac surgery and
for those with failed percutaneously placed LV
leads. The device is composed of the surgeon-
control console and the surgical arm unit that
What to do if deployment in the Coronary Sinus fails
Fig. 16.52 Retrieval of fractured angioplasty guidewire.
(Top left) 0.014″ BMW guidewire (black arrow) retained
within the CS. The proximal end of the guidewire lies in
the upper RA. The orange arrow points to a CS guiding
catheter in situ. (Center left) Needle eye snare (blue arrow)
is advanced out of its sheath in the RA to try and capture
the free end of the guidewire. (Center right) The guidewire
(black arrow) is captured by the snares and withdrawn
389
into the sheath (green open arrow) and removed from the
femoral vein. The radiopaque tip of the guidewire can be
seen to have been removed from the CS and is seen to be
in the upper RA. (Bottom left) Combination of “needle-
eye” and “Goose-neck” snares exiting the femoral sheath.
(Bottom right) Once caught within the snare(s), retracting
the snares back into the femoral sheath tightens its grip on
the wire to allow all to be removed from the femoral vein
390
Fig. 16.53 Chest X-ray
showing an endocardial lead
placed in the RV apex and an
epicardial lead attached to the
LV in this patient undergoing
CRT
positions and directs the microinstruments.
Computer interfacing allows for scaled motion,
and the optics viewed in the surgeon console for
high-definition, magnified, real 3-D vision. All
operations are performed under GA with selec-
tive right lung ventilation. With the patient in the
posterolateral thoracotomy position and a TOE in
situ, a camera port is placed in the seventh inter-
costal space in the posterior axillary line. The
right and left arms are positioned in the fifth and
ninth intercostal space, respectively (see Chap.
20). A pacing lead is then introduced into the
chest through the working port. A good position
is often midway between the base and apex of the
LV, between the first and second obtuse marginal
(OM) arteries (Fig. 16.55). The robotic arms are
used to fix the lead to the LV surface either by
screw-in active fixation or by a suture technique.
This lead is capped and delivered into the chest.
A second lead is then delivered through the work-
ing port and again fixed to the LV surface near the
second OM artery. If the lead measurements are
satisfactory, the pericardium is closed over the
16 Cardiac Resynchronization Therapy
leads to aid permanent fixation. The two leads are
tunneled to the axilla and the lead with the best
parameters used as the LV lead. If right-sided
pacing leads or an ICD lead are required, these
can then be inserted and attached to the device in
the axillary pocket.
CRT Optimization
In order to get the most out of CRT, it is recom-
mended that a routine series of steps should be
followed by the cardiologist/technician. It is first
important to assess the patient’s symptoms, their
physical activity, and the medication that they
are taking. Particular attention should include a
review of the standard program, especially the
lower and upper rate limits, the rate response
program, the requirement for Mode Switch and
the MTR. Research has shown that compared to
nominal AV delay settings, AV delay optimiza-
tion improves heart failure symptoms, quality of
life, LV ejection fraction, and a 6-min walk test.
CRT Optimization
Fig. 16.54 The Da Vinci Robotic SiHD system can be used to
attach an LV epicardial lead when access to a coronary vein
is impossible and CRT felt to be worthwhile. (Top left) The
surgeon sits at the console several feet away from the operat-
ing table. The surgeon has his head tilted forwards and his
hands inside the system’s master interface. The surgeon sits
viewing a magnified 3D image of the surgical field with a
VV optimization does not appear to offer any
additional clinical benefit over simultaneous BiV
pacing. Although there is no consensus among
cardiologists regarding optimization strategies
or methods, dP/dtmax (measurement of the maxi-
mal rise in LV pressure during systole) is per-
haps the most reliable. Echocardiography may
be used to estimate myocardial performance
index (MPI), aortic velocity time integral (VTI),
mitral inflow (E and A waves), and mitral inflow
VTI as a measure of LV function. Algorithms
391
real-time progression of the instruments as he operates. (Top
right) The patient side-cart contains the robotic arms that
directly contact the patient. It consists of two or three instru-
ment arms and one endoscope arm. (Bottom left) Equipment
set-up in operating theater. (Bottom right) Close-up of endow-
rist instrument control (Photo courtesy of Dr. J DeRose Jr.
and Intuitive Surgical®, Inc., Sunnyvale, CA, USA, 2009)
within some CRT devices use the IECG obtained
from the implanted device to calculate optimal
AV delay values and optimal VV timing. The
algorithm runs semi-automatically and takes
approximately 1 min to determine optimal tim-
ing values. Such a facility is easier and quicker
than echocardiographic methods of assessment.
The recently introduced SonR® system (Sorin
Group) includes the SonR® hemodynamic sensor
embedded in the SonRtipTM atrial pacing lead
and the ParadymTM RF SonR® CRT-D device and
392
Fig. 16.55 Screw-in lead
inserted into surface of LV
between two obtuse marginal
arteries (Photo courtesy of
Dr. J DeRose Jr. and Intuitive
Surgical®, Inc., Sunnyvale,
CA, USA, 2009)
provides weekly automatic optimization during
the patient’s real-life activities as an alternative
to in-clinic manual echocardiography-based
device optimization for improved CRT response.
SonR® measurements correspond to LVdP/dtmax,
the gold standard for assessing left ventricular
(LV) contractility, a key indicator of cardiac
performance.
Basic Programming
Following implantation of the CRT device, initial
programming includes the choice of pacing
mode, lower and upper rate limits, and AV delay
after atrial sensing and pacing. Particular atten-
tion needs to be paid to upper rate programming
which may depend on the VT zone in a CRT-D
device (Fig. 16.56). Special features may include
rate response and mode switching, although the
role of rate response in advanced heart failure
remains unclear. All leads in a CRT system should
have their capture threshold measured and output
settings programmed appropriately to ensure reli-
able capture. A new algorithm with automatic
capture management (ACM) with Medtronic
devices may help optimize output settings without
16 Cardiac Resynchronization Therapy
compromising pacing. Sensitivity settings should
be programmed after appropriate sensitivity
threshold testing on each lead.
Usually the AVD is initially programmed
empirically with a range of 80–120 ms during
atrial sensing with an additional offset of
30–50 ms during atrial pacing. The upper rate
limit (URL) should reflect the patient’s predicted
activity level and age. Optimization of the AVD
should be done predischarge and should provide
complete BiV pacing. The goal of CRT is to pace
LV/RV as much of the time as possible (unlike
pacemakers). Atrial pacing is not a key objective
of CRT, and native atrial activity should be
encouraged where possible by programming the
base rate to 40 bpm unless there is evidence of
chronotropic incompetence. This should increase
the likelihood of ventricular pacing at the intrin-
sic atrial rate. Patients with chronic AF should be
programmed to VVI, whereas those with more
intermittent atrial arrhythmias might benefit from
DDI (without atrial tracking).
Diagnostic facilities may be programmed
“on” to help evaluate the device function. For
example, an event histogram may show how
much sensed and paced activity is happening in
the ventricles. Stored intracardiac electrograms
More Advanced Programming
Fig. 16.56 “Therapy guide”
page on the Medtronic
programmer interrogating the
Protecta CRT-D device
(Image reproduced with
permission of Medtronic,
Inc.)
can help in troubleshooting. Automatic mode
switching is aimed at preventing atrial tracking at
high rates for patients with paroxysmal atrial
arrhythmias. Although the MTR is useful for
avoiding high tracked atrial rates, when this
happens the device may be made to function in
“upper-rate behavior” mode, which includes a
pacemaker-induced Wenckebach or AV block.
Mode-switching will change the function to a
nontracking mode (DDD to DDI) or to a nona-
trial sensing mode (VVI) until the atrial rate falls
within the normal range.
More Advanced Programming
CRT programming is intended to encourage 100%
ventricular pacing. Negative AV hysteresis (com-
pletely the opposite to hysteresis in pacemakers)
encourages this by automatically shortening the AV
delay in the presence of a sensed ventricular event.
“Rate-responsive or Rate-adaptive AV delay”
(nothing to do with activity sensors) automatically
shortens the AV delay when the patient’s atrial
rate increases. The post-ventricular atrial blank-
ing period (PVAB) allows the atrial channel to be
blanked for a very brief period immediately after
393
a ventricular output pulse is delivered. Along with
PVARP, the PVAB helps prevent far-field R-wave
sensing which CRT systems used to be susceptible
to. Clearly too short a PVARP might make PMT
more likely to occur. The maximum sensor rate
is the highest rate at which the device will pace
the ventricles in response to activity sensor input.
It is programmable and independent of the MTR.
In the diagnostic facilities, AV interval histograms
and sensor-indicated rate histograms can be use-
ful for optimizing performance and observing
what the settings produce during a patient’s daily
activities. In addition to battery status, program
settings and lead system data, device diagnostics
show heart failure/bradycardia counters and dis-
play histograms showing cardiac events and the
percentage of time ventricular pacing. Continuous
details of sensing amplitudes from each lead as
well as lead impedance values are also available.
Details on any arrhythmia that has been detected
can also be retrieved for further analysis in many
of the modern devices (Figs. 16.57–16.60).
CRT-D devices also require detailed interro-
gation at follow-up concerning the frequency of
use of therapy for ventricular arrhythmias, the
current anti-tachyarrhythmia program set-up,
lead thresholds, sensitivities and impedance,
394 16 Cardiac Resynchronization Therapy

Fig. 16.57 Screenshot: the Paradym™ 8750 CRT-D ventricular arrhythmias requiring treatment and current
device offers swift interrogation, a detailed “overview set-up parameters for this aspect of the device.
screen,” including detailed data on lead function, battery Programming of LV pacing output is also very flexible
longevity and statistical information on the frequency of (Courtesy of Sorin Group)
More Advanced Programming 395

Fig. 16.58 Print-out from a Contak Renewal TR 2 CRT-P the amount of bi-ventricular pacing that the device is
device (Boston Scientific) shows data on battery status achieving (red circle)
and device longevity, current settings and information on

Fig. 16.59 Print-out from the same device as in Fig. 16.57 lead configuration. Details on arrhythmia Logbook, trend-
shows data on tachycardia response settings, rate enhance- ing and daily measurement set up (e.g., intrinsic ampli-
ments, AV delay, refractory periods, noise response and tude and lead impedance data) are also available
396
Fig. 16.60 Print-out from the same device as in Fig. 16.58 shows trend data on lead intrinsic amplitude and impedance
measurements as well as histogram displays showing the amount of biventricular pacing taking place
Fig. 16.61 Interrogation
display screenshot of the
Paradym™ CRT-D device:
“Overview” screen
(Courtesy of Sorin Group)
battery life, etc., and these should be obtainable
with ease by the technical staff in clinic. The
Paradym™ 8750 CRT-D (Sorin Group) can be
interrogated and reprogrammed swiftly by use of
the “overview screen” which has a simplified
interface, automatic file storage to hard drive, and
an interrogation time of 5s (Fig. 16.61). Other
screens display a range of information from
details concerning the device’s programmed set-
tings such as bradycardia A and V sensing param-
eters as well as its anti-tachycardia program
(Figs. 16.62 and 16.63).
16 Cardiac Resynchronization Therapy
Troubleshooting
It has been estimated that CRT is interrupted in
over one third of patients after successful implan-
tation. The most common reasons are the devel-
opment of atrial tachyarrhythmias (18%), loss of
LV capture (10%) (Figs. 16.64 and 16.65), and
sensed ventricular events (ventricular ectopics
and rapid ventricular rates with atrial tachycar-
dias). Less common causes include diaphragmatic
or phrenic nerve stimulation, loss of RV capture,
loss of atrial sensing, infection requiring device
Troubleshooting 397

Fig. 16.62 Bradycardia A

and V settings are shown in
this interrogation screenshot
of the Paradym™ CRT-D
device (Courtesy of Sorin
Group)

Fig. 16.63 Anti-tachycardia

settings are shown in this
screenshot of the Paradym™
CRT-D device (Courtesy of
Sorin Group)

removal, intolerance of CRT, and ventricular over-
sensing. However, in a high proportion of patients,
CRT can be re-established and only about 5% of
patients will have permanent loss of CRT.
A systematic approach should be adopted
when trying to diagnose and treat nonresponders.
Firstly, the problem should be identified; sec-
ondly, possible causes considered; and finally,
each possible cause should be investigated. The
majority of issues have some typical causes and
these should clearly be considered first. The most
likely problems are the ones that occur most
often! One should establish that the device is pac-
ing in both ventricles since CRT is only provided
when the device paces the ventricles. AV or VV
timing should be optimized and the leads should
be checked for displacement, conductor, or insu-
lation fracture. If lead impedance values vary by
>200 W in a short time, this suggests lead damage
or a loose lead connection and a chest X-ray may
be helpful. Generally, a good AV delay for a CRT
patient is approximately 75% of the intrinsic PR
398 16 Cardiac Resynchronization Therapy

Fig. 16.64 Loss of LV capture is evidenced by the posi-
tive complex in lead I and ‘qs’ complex in V1 on this 12
lead ECG. Multiple sites in the coronary venous circula-
tion were tested for stability at implantation of this
InSync® III device. The most stable position in an infero-
lateral vein had a pacing threshold of 2.5 V and resulted in
satisfactory biventricular pacing initially with significant
symptomatic improvement. However, 9 months later exer-
tional dyspnea returned and the above ECG suggested
loss of capture of the LV lead

Fig. 16.65 Twin ventricular pacing spikes (circled). The first spike represents failed LV capture followed by a second
spike and RV capture in an InSync® III CRT DR device (Medtronic, Inc.)
What Evidence Exists to Support CRT Use?
interval and helps to ensure continuous ventricu-
lar pacing. Too long an AV delay encourages
mitral regurgitation and too short an AV delay
shortens effective diastole, undermines CRT
stimulation, and may make symptoms worse. VV
optimization defines how the RV and LV contract
in relation to each other. The severity of mitral
regurgitation can be assessed by echocardiography.
Moreover, an echocardiographic assessment of
mechanical dyssynchrony can be helpful. Two
parameters of use are the interventricular mechan-
ical delay (IVMD) and the septal: posterior wall
motion delay (SPWD). IVMD defines the time it
takes from the onset of electrical stimulation of
RV/LV until blood is ejected out of the heart into
the aorta (aortic outflow) or pulmonary artery
(pulmonary outflow) and should be <40 ms. The
SPWD value should be <130 ms. Unfortunately
if these values are exceeded, improvement is only
likely with lead revision.
Oversensing, for example of far-field P-waves,
may inhibit ventricular pacing and this can affect
RV or LV pacing. Sensing and pacing problems
can often be sorted out by studying combined
EGMs and annotated tracings (marker chan-
nels). Arrhythmias, such as atrial fibrillation,
may cause nonresponse, and if not evident on
the resting ECG, should be sought for in the
device’s diagnostics memory. Episodes of AF,
duration of episodes, and number of mode
switches are usually available, for example,
Cardiac Compass Report (Medtronic) (see Figs.
17.48 and 21.21).
A not infrequent reason of loss of BiV capture
is related to sensing atrial rate close to the pro-
grammed maximal tracking rate (MTR). Upper
rate behavior of BiV pacemakers may be like a
traditional pacemaker Wenckebach response or
the equivalent of fixed-ratio block as occurs in
standard pacemakers defined by the programmed
MTR and the total atrial refractory period
(TARP). For example, when the atrial rate exceeds
the programmed URL but the P-P interval remains
longer than the TARP, the device produces a
Wenckebach response. If the P-P interval becomes
shorter than the TARP (AVD + PVARP), 2:1
block occurs when every other atrial event falls in
the PVARP.
399
If the problem cannot be figured out, one
should not hesitate to call on the manufacturer’s
technical support.
What Evidence Exists to Support
CRT Use? (Table 16.4)
Several studies in the mid-1990s reported acute
hemodynamic benefits from biventricular pac-
ing. These included a reduction in left ventricu-
lar filling pressures and the severity of mitral
regurgitation, as well as an improvement in
ejection fraction and cardiac index [1, 2]. These
benefits prompted several other studies to
examine the short-term effects in patients with
severe heart failure (NYHA III/IV) and electrical
dyssynchrony (QRS ³ 120 ms) [3, 4]. These stud-
ies demonstrated improved quality of life (QOL),
6-min walk test (6MWT), peak VO2 (respiratory
oxygen uptake), and clinical status. However,
they were not randomized, controlled, or blinded
with the exception of The Pacing Therapy for
Congestive Heart Failure (PATH-CHF) Trial,
which was a blinded crossover study [5].
Nevertheless, large randomized clinical trials
have subsequently confirmed both morbidity and
mortality benefits of CRT.
The MUSTIC trial [6] (Multisite Stimulation
in Cardiomyopathy) was the first randomized
trial of CRT. This was a single blind cross-over
study in 75 patients with NYHA class III heart
failure, LVEF < 35%, LV end-diastolic diameter
>60 mm, and in either sinus rhythm (SR) or atrial
fibrillation (AF) with QRS >150 ms. Patients
were randomized to a 3-month period of CRT or
back-up pacing at 40 bpm. The investigators
demonstrated that CRT was associated with sta-
tistically significant (20%) increase in 6MWT in
the SR group and 17% increase in the AF group.
QOL score and NYHA class also improved
significantly in both SR and AF groups with CRT.
Eighty-five percent of the patients preferred to be
in the active pacing CRT arm.
The MIRACLE study [7] (Multicenter In
Sync Randomized Clinical Evaluation) was a
multicenter, double-blind, randomized, par-
allel study examining the 6-month effective-
400 16 Cardiac Resynchronization Therapy

Table 16.4 Evidence in the literature for benefit of CRT

Authors Publication Journal reference
Saxon LA, et al. [1] Acute effects of intraoperative multisite LV pacing J Cardiovasc Electrophysiol.
on LV function. 1998;9:13–21.
Kass DA, et al. [2] Improved LV mechanics from acute VDD pacing. Circulation. 1999;99:1567–73.
Gras D, et al. [3] Preliminary results of the Medtronic Inc, InSync Pacing Clin Electrophysiol.
study. 1998;6:171–84.
Bakker PF, et al. [4] BiV pacing in end-stage heart failure improves J Interv Card Electrophysiol.
functional capacity. 2000;4:395–404.
Auricchio A, et al. [5] Long-term benefit as a result of pacing resynchro- Circulation. 2000;102:II-693A.
nization in congestive heart failure: results of the
PATH-CHF trial.
Linde C, et al. [6] Long-term benefit of biventricular pacing in J Am Coll Cardiol. 2002;40:111–8.
congestive heart failure: Results from the Multisite
Stimulation in Cardiomyopathy (MUSTIC) Study.
Abraham WT, et al. [7] MIRACLE study Group. Cardiac resynchronization N Engl J Med.
in chronic heart failure. 2002;346(24):1845–53.
Higgins SL, et al. [8] Cardiac resynchronization therapy for the treatment J Am Coll Cardiol. 2003;42:1454–9.
of heart failure in patients with intraventricular
conduction delay and malignant ventricular
tachyarrhythmias.
Young JB, et al. [9] Combined cardiac resynchronization and implant- JAMA. 2003;289:2685–94.
able cardioversion defibrillation in advanced
chronic heart failure: the MIRACLE ICD Trial.
Bristow MR, et al. [10] Cardiac-resynchronization therapy with or without N Engl J Med. 2004;350:2140–50.
an implantable defibrillator in advanced chronic
heart failure.
Cleland JGF, et al. [11] Cardic resynchronization in heart failure study N Engl J Med. 2005;352:1539–49.
(CARE-HF) study investigators. The effect of
cardiac resynchronization on morbidity and
mortality in heart failure.
Linde C. [12] Cardiac resynchronization therapy in mild heart Europace. 2009;11(Suppl 5):v72-6.
failure.
Moss AJ, et al. [13] Cardiac resynchronization therapy for the N Engl J Med 2009;361:1329–1338.
prevention of heart failure events.

ness and safety of CRT on NYHA class, QOL
(Minnesota Living with Heart Failure question-
naire) and 6MWT. The investigators recruited
453 patients with advanced heart failure
(NYHA functional class III/IV), left ventricular
ejection fraction (LVEF) £ 35%, left ventricular
end diastolic diameter (LVEDD) ³ 55 mm, and
a QRS ³ 130 ms. The CRT patients showed sta-
tistically significant improvements in NYHA
class, 6MWT (increased by 29 m), and QOL
(improved by 9 points). Ejection fraction also
increased by 4.8% with a reduction in LV diam-
eter and MR severity. Treadmill time increased
by 62 s and peak VO2 by 0.9 ml/kg/min with
fewer hospitalizations in the CRT arm (8%
vs. 15%).
The CONTAK CD study [8] was a randomized,
double-blind trial examining the safety and effec-
tiveness of CRT when combined with an implant-
able cardioverter defibrillator (ICD). In total, 490
patients were implanted with a device capable of
providing both CRT and ICD therapy. Inclusion
criteria were NYHA II–IV, LVEF £ 35%,
QRS ³ 120 ms and a conventional indication for
an ICD implantation (VT/VF). Patients were ran-
domized to have CRT turned on or off for a 3- to
6-month period. The study was designed to show
a 25% reduction in a composite outcome reflecting
heart failure progression defined as all-cause mor-
tality, hospitalization for HF, and VT/VF requir-
ing device intervention. Although this study
showed a nonsignificant (P = 0.35) 15% reduction
What Evidence Exists to Support CRT Use?
in the composite primary endpoint in the CRT
patients, it showed statistically significant
improvements in peak VO2 (0.8 ml/kg/min vs.
0.0 ml/kg/min, P = 0.030) and 6MWT (P = 0.043).
The MIRACLE-ICD trial [9] examined the
effect of CRT-ICD (CRT with Implantable
Cardioverter-Defibrillator) in NYHA functional
class III–IV heart failure patients with
LVEF £ 35%, QRS ³ 130 ms, and LVEDD ³ 55 mm.
The CRT significantly improved the functional
capacity (P = 0.007) and increased peak VO2 by
1.1 ml/kg/min (P = 0.04) as well as improving the
QOL by 17.5 points compared with an improve-
ment of 11 points in the control group (P = 0.02).
The COMPANION Trial [10] (Comparison of
Medical Therapy, Pacing and Defibrillation in
Heart Failure) was a randomized controlled study
in which patients with NYHA functional class III
or IV heart failure, LVEF £ 35%, and QRS dura-
tion ³ 120 ms were randomly allocated to receive
optimal medical therapy alone or in combination
with CRT pacing or with CRT and ICD. The risk
of the combined end point of death from or hos-
pitalization for heart failure was reduced by 34% in
the pacemaker group (P < 0.002) and by 40% in
the pacemaker–defibrillator group (P < 0.001)
in comparison with the pharmacologic-therapy
group. CRT reduced the risk of the secondary
endpoint of death from any cause by 24%
(P = 0.059), while CRT-ICD significantly reduced
this risk by 36% (P = 0.003). Equal benefits were
noted both in ischemic and nonischemic etiolo-
gies of heart failure.
In the CARE-HF study [11] (Cardiac
Resynchronization in Heart Failure), 813 heart
failure patients with predominantly NYHA func-
tional class III symptoms despite optimal medi-
cal therapy were randomized to receive optimal
medical therapy alone or with CRT. Patients were
eligible if they had a LVEF £ 35%, QRS dura-
tion > 150 ms, or QRS duration between 120 and
150 ms and two of three echocardiography crite-
ria for dyssynchrony (an aortic pre-ejection delay
of >140 ms, an interventricular mechanical delay
of >40 ms, and delayed activation of the postero-
lateral LV wall). The primary endpoint was the
time to death or unplanned hospitalization for a
major cardiovascular event. After a mean follow-
401
up of 29.4 months, the primary endpoint was
reached in 39% of patients in CRT group com-
pared with 55% on control medical therapy.
Several important firsts were achieved in this
study, including being the first to show benefit for
CRT pacing alone with respect to survival as a
single endpoint, the first study to show benefit for
CRT pacing for up to 18 months, and continued
improvement over time, the first study to show
that neurohormonal measures (e.g., N-terminal
pro-brain natriuretic peptide (NT-BNP)) improve
dramatically with CRT and the first study to use
direct measures of dyssynchrony in the inclusion
criteria.
The last two large, long-term studies
(COMPANION and CARE-HF) provide good
evidence that CRT, with or without ICD, reduced
mortality and hospitalization in heart failure
patients. The benefit of CRT-ICD therapy was
further highlighted by the observation that in
the COMPANION trial, 36% of the deaths in the
CRT pacing arm were sudden, very similar to the
35% in CARE-HF. The absence of ICD back-up
in both studies showed that despite the evident
benefits of CRT pacing therapy, one third of the
fatalities were due to sudden death. The CRT-
ICD arm of COMPANION reduced the sudden
cardiac death incidence to 16%. In terms of abso-
lute mortality, 7% of patients in the CRT limb of
CARE-HF died suddenly, compared with only
2.9% in the CRT-ICD limb of COMPANION.
A recent study (MADIT-CRT) reported at the
European Society of Cardiology in 2009 found
that CRT combined with ICD decreased the risk of
heart failure events even in relatively asymptom-
atic patients, with a 34% reduction in the risk of
all-cause mortality or heart failure. Both the
REVERSE [12] and MADIT-CRT [13] trials sug-
gested that such treatment also reduces morbidity
and mortality in patients with NYHA class II heart
failure – reducing the risk for heart failure hospital-
izations or death by 62% and 34%, respectively.
Although the use of CRT implants has risen
substantially from 46 per million in 2004 to 99
per million in 2008 in Europe – an increase of
115% – it is estimated that only a very small per-
centage of those who would benefit from CRT
actually receive the treatment.
402
In summary, trials with a total of more than
4,000 patients have shown unequivocal benefit
for CRT in the treatment of patients with end-
stage, drug-refractory heart failure with wide
QRS as an indicator of dyssynchrony. CRT
improves NYHA functional class, QOL, and
peak VO2; it also improves left ventricular ejec-
tion fraction, reduces left ventricular end-dia-
stolic diameter and mitral regurgitation, reduces
hospitalization, and, most importantly, reduces
mortality.
References
1. Saxon LA, et al. Acute effects of intraoperative multi-
site LV pacing on LV function. J Cardiovasc
Electrophysiol. 1998;9:13–21.
2. Kass DA, et al. Improved LV mechanics from acute
VDD pacing. Circulation. 1999;99:1567–73.
3. Gras D, et al. Preliminary results of the Medtronic Inc.,
InSync study. Pacing Clin Electrophysiol. 1998;
6:171–84.
4. Bakker PF, et al. BiV pacing in end-stage heart failure
improves functional capacity. J Interv Card
Electrophysiol. 2000;4:395–404.
5. Auricchio A, et al. Long-term benefit as a result of
pacing resynchronization in congestive heart failure:
16 Cardiac Resynchronization Therapy
results of the PATH-CHF trial. Circulation.
2000;102:II–693A.
6. Linde C, et al. Long-term benefit of biventricular pac-
ing in congestive heart failure: Results from the
Multisite Stimulation in Cardiomyopathy (MUSTIC)
Study. J Am Coll Cardiol. 2002;40:111–8.
7. Abraham WT, MIRACLE Study Group, et al. Cardiac
resynchronization in chronic heart failure. N Engl
J Med. 2002;346(24):1845–53.
8. Higgins SL, et al. Cardiac resynchronization therapy
for the treatment of heart failure in patients with intra-
ventricular conduction delay and malignant ventricu-
lar tachyarrhythmias. J Am Coll Cardiol.
2003;42:1454–9.
9. Young JB, et al. Combined cardiac resynchronization
and implantable cardioversion defibrillation in
advanced chronic heart failure: the MIRACLE ICD
Trial. JAMA. 2003;289:2685–94.
10. Bristow MR, et al. Cardiac-resynchronization therapy
with or without an implantable defibrillator in
advanced chronic heart failure. N Engl J Med. 2004;
350:2140–50.
11. Cleland JGF, Cardiac Resynchronization in Heart
Failure Study (CARE-HF) Study Investigators, et al.
The effect of cardiac resynchronization on morbidity
and mortality in heart failure. N Engl J Med. 2005;
352:1539–49.
12. Linde C. Cardiac resynchronization therapy in mild
heart failure. Europace. 2009;11 Suppl 5:v72–6.
13. Moss AJ, et al. Cardiac Resynchronization Therapy
for the Prevention of Heart Failure Events. N Engl J
Med 2009;361:1329–1338.
 Implantable Cardioverter
Defibrillators 17

Sudden cardiac death (SCD) is defined as death
from a cardiac cause occurring unexpectedly
within a short time of onset of symptoms (usu-
ally within 1 h). It accounts for 325,000 deaths
per year in the USA – an incidence of 0.1–0.2%
per year in the adult population. SCD represents
the largest proportion of the deaths attributable
to coronary artery disease. Several risk factors
have been identified for SCD and include pre-
vious myocardial infarction and myocardial
scars, active coronary lesions, for example,
ulcerated atheromatous plaques with subtotal
or total thrombotic occlusion, and compro-
mised left ventricular systolic function. In addi-
tion, there are familial cardiac conditions that
may increase the risk of SCD such as Long QT
syndrome (Fig. 17.1) and Brugada Syndrome
(Fig. 17.2).
About 80% of SCDs are due to ventricu-
lar tachyarrhythmias (VT or VF). It typically
involves a trigger (such as a crucially timed
ectopic) (Fig. 17.3) for the arrhythmia to start
and a substrate for it to be sustained. Typical
substrates are anatomical (scars within the myo-
cardium) (Fig. 17.4) but may be functional,
for example, electrolyte imbalance. Moreover,

Fig. 17.1 12-lead ECG showing long-QT syndrome

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 403

DOI 10.1007/978-1-4471-2939-4_17, © Springer-Verlag London 2012
404 17 Implantable Cardioverter Defibrillators

Fig. 17.2 12-lead ECG in Brugada syndrome

Fig. 17.3 R-on-T ectopic (red arrow) causing VF

Evolution of ICD Therapy
Fig. 17.4 (a) Chest X-ray showing LV aneurysm which
may be associated with ventricular arrhythmias. (b)
Delayed gadolinium-enhanced magnetic resonance image
showing presence of myocardial scar from which the gad-
olinium is released more slowly compared to the sur-
rounding viable myocardium (arrows)
those who survive an episode of life-threatening
arrhythmia are at high risk of further episodes.
Half of such patients will be re-hospitalized
within 1 year and about 40% will die within
2 years.
Prevention of sudden cardiac death is either
primary, defined as prevention of the first
life-threatening consequences of an arrhythmic
event, or secondary, which refers to the preven-
tion of a future life-threatening event in survivors
of sudden cardiac death or patients with recurrent
405
unstable arrhythmias. Treatment options include
drugs and implantable cardioverter defibrillators
(ICD).
Evolution of ICD Therapy
The inventor of the implantable cardio-
defibrillator is held to be Michel Mirowski. He
was born in Poland in 1924 and attended medical
school in Lyon, France. He completed his resi-
dency in Israel and Cardiology fellowships at the
John Hopkins Hospital in Baltimore and Institute
of Cardiology in Mexico City. He returned to
Israel in 1962 to become the Chief of Cardiology
at Asaf Horofeh Hospital. The death of a friend
and colleague from recurrent VT in 1966 inspired
Mirowski’s idea of implanting an automatic
defibrillator.
The first ICD patient was a 57-year-old lady
with significant coronary artery disease, a history
of acute MI, and recurrent syncope with docu-
mented VF. She had failed extensive drug therapy
and agreed to try device therapy. The device was
implanted successfully under general anesthetic
in 1980. ICDs were approved for commercial use
in 1985.
Over the last three decades ICDs have under-
gone a remarkable transformation in both size
and capability (Fig. 17.5). The early devices
were large (11 × 7 × 2.5 cm and 290 g) and
were implanted in the abdomen under general
anesthetic. The original defibrillation leads were
epicardial patches (Fig. 17.6), large mesh conduc-
tors that were sutured to the outside of the heart
via a thoracotomy. This highly invasive surgery
conferred significant risk to patients (especially
for patients with poor LV function), necessitat-
ing long hospital stays of almost 1 week after
implantation.
The initial pulse generators had longevity of
less than 2 years, had almost no diagnostic capa-
bilities, and had pacing capabilities limited to
only back-up ventricular pacing. The current
“tiered-therapy” ICD devices are capable of
delivering anti-tachycardia pacing, low-energy
cardioversion, and high-energy defibrillation
406
Fig. 17.5 Change in size of ICD cans over the last two decades
Fig. 17.6 Epicardial patch with the large mesh conductor
to be sutured to the outside of the heart
therapy. They also have the capability to store the
morphology and rates of arrhythmias before,
during, and after therapy, and have a longevity
exceeding 6 years.
In a recent analysis of 15 European countries,
the number of ICD implantations was shown to
have increased substantially from 80 per million
population in 2004 to 140 per million in 2008.
The highest rate of ICD implants was in Germany
(264 per million in 2008), followed by Denmark
and the Netherlands. The lowest number of
implants was observed in Spain (63 per million),
Portugal (68 per million), and the UK (74 per
million). It has been estimated that some 200,000
17 Implantable Cardioverter Defibrillators
ICD implants occur annually worldwide and the
number is expected to increase.
Indications for ICD Implantation
The indications for ICD implantation have ex-
panded considerably since the mid-1980s. Tables 17.1
and 17.2 summarize the primary and secondary
prevention trials that have provided the evidence
on which guidelines are based.
The joint bodies of the American College of
Cardiology, American Heart Association and Heart
Rhythm Society (ACC/AHA/HRS) 2008 guide-
lines recommend primary prevention ICD therapy
(class I indication) for one of the following:
1. Left ventricular ejection fraction (LVEF) <40%,
nonsustained ventricular tachycardia, prior
MI, and inducible VF or VT on electrophysi-
ology study
2. LVEF <35%, NYHA class II or III, and prior
MI >40 days post event
3. LVEF <35%, NYHA class II or III and nonis-
chemic dilated cardiomyopathy
4. LVEF <30%, NYHA class 1 and prior MI
>40 days post event
Secondary prevention ICD implantation is
indicated in patients with a history of sudden car-
diac arrest, VF, hemodynamically unstable VT,
or unexplained syncope with LV dysfunction and
inducible VT.
Table 17.1 Clinical trials of ICD therapy for spontaneous or inducible ventricular arrhythmias
Primary Number needed to
Trial (year) Inclusion criteria N Comparison endpoint Main finding treat (36 months)
Indications for ICD Implantation

Antiarrhythmics Versus
Implantable Defibrillators
(AVID) (1999)
Canadian Implantable
Defibrillator Study (CIDS)
(2000)
Cardiac Arrest Study Hamburg
(CASH) (2000)
Multi-center Automatic
Defibrillator Implantation Trial
(MADIT) (1996)
Multi-center Unsustained
Tachycardia Trial (MUSTT)
(1999)
CABG coronary artery bypass graft, EF ejection fraction, ICD implantable cardioverter-defibrillator, MI myocardial infarction, NSVT nonsustained ventricular tachycardia,
NYHA New York Heart Association functional class, VF ventricular fibrillation, VT ventricular tachycardia
Resuscitated VF, sustained VT and syncope, 1,016 ICD vs. All-cause 31% relative reduction 9
or sustained VT with EF £ 40% and severe antiarrhythmic drugs mortality in primary endpoint
symptoms: no reversible cause. (amiodarone) (P < 0.02) with ICD
Resuscitated VF, sustained VT and syncope, 659 ICD vs. amiodarone All-cause 20% relative reduction 23
sustained VT with EF £ 35%, or unmonitored mortality in primary endpoint
syncope with subsequent spontaneous or (P = 0.1) with ICD
inducible VT; no reversible cause.
Cardiac arrest secondary to VF or VT; no 228 ICD vs. drug therapy All-cause 23% relative reduction 20
reversible cause. – amiodarone, mortality in primary endpoint
metoprolol (P = 0.2) with ICD
Age 25–80 year, NYHA I–III, EF £ 35%, 196 ICD vs. best medical All-cause 56% risk reduction 3
nonrecent MI (>3 weeks) or CABG therapy that could mortality in primary endpoint
(>3 months), Spontaneous NSVT, include amiodarone (P = 0.009) with ICD
and inducible VT.
Age < 80 year, NYHA I–III, EF £ 40%, 704 ICD vs. Cardiac 76% relative reduction 5
nonrecent MI (>4 days), spontaneous NSVT, antiarrhythmic arrest or in primary endpoint
and inducible VT. Nonrandomized ICD use. therapy – amiodarone death from (P < 0.001) with ICD
and class I agents arrhythmia
407
 408

Table 17.2 Clinical trials of ICD therapy for heart failure or left ventricular dysfunction alone
Trial (year) Inclusion criteria N Comparison Primary endpoint Main finding Number needed to
treat (36 months)
Second Multicenter Automatic NYHA I–III, EF £ 30%, remote 1,232 ICD vs. best All-cause 31% relative reduction in 10
Defibrillator Implantation Trial MI (>1 month) medical therapy mortality primary endpoint (P = 0.02)
(MADIT-II) (2002) with ICD
Amiodarone Versus Implantable NYHA I–IV, EF £ 35%, dilated 103 ICD vs. best All-cause No significant alteration 39
Cardioverter- Defibrillator Trial cardiomyopathy, NSVT medical therapy mortality (P = 0.8) with ICD
(AMIOVIRT) (2003)
Cardiomyopathy Trial (CAT) NYHA II–III, EF £ 30%, dilated 104 ICD vs. best All-cause No significant alteration 12
(2002) cardiomyopathy, recent onset medical therapy mortality (P = 0.6 with ICD)
heart failure (£ 9 months)
Comparison of Medical Therapy, NYHA III–IV, EF £ 35%, 903 Resynchronization All-cause 20% relative risk reduction 5
Pacing, and Defibrillation in Heart nonrecent MI or CABG, ICD vs. best mortality or in primary endpoint
failure (COMPANION) (2004) QRS ³ 120 ms, PR ³ 150 ms, medical therapy hospitalization (P = 0.01) with resynchroni-
recent heart failure hospitaliza- zation ICD
tion (<12 months), and nonrecent
onset of heart failure (>6 months)
17

Sudden Cardiac Death Heart NYHA II–III, EF £ 35%, 1,676 ICD vs. placebo All-cause 23% relative reduction in 23
Failure Trial (SCD-HeFT) (2005) nonrecent MI or revascularization mortality primary endpoint (P < 0.01)
(>30 days), nonrecent heart with ICD
failure onset (>3 months)
Defibrillators in Nonischemic NYHA I–III, EF £ 35%, dilated 458 ICD vs. best All-cause 35% relative reduction in 24
Cardiomyopathy Treatment cardiomyopathy, NSVT, or ³ 10 medical therapy mortality primary endpoint (P = 0.08)
Evaluation (DEFINITE) (2005) PVCs/h with ICD
CABG coronary artery bypass graft, EF ejection fraction, ICD implantable cardioverter-defibrillator, MI myocardial infarction, NSVT nonsustained ventricular tachycardia,
NYHA New York Heart Association functional class, PVC premature ventricular complex
Implantable Cardioverter Defibrillators
The ICD System
These guidelines differ between countries, and
in the UK, ICD implantation is recommended by
the National Institute of Clinical Excellence for
patients in the following categories:
Primary Prevention
1. History of previous MI (>4 weeks) and
either:
• LVEF of less than 35%, nonsustained VT
on Holter monitoring and inducible VT on
EP testing or
• LVEF of <30% and QRS duration >120 ms.
2. Familial cardiac condition with a high risk of
sudden death, including long-QT syndrome,
hypertrophic cardiomyopathy, Brugada syn-
drome or arrhythmogenic right ventricular
dysplasia (ARVD), or patients who have
undergone surgical repair of congenital heart
disease.
Secondary Prevention
This is for patients who present, in the absence of
a treatable cause, with one of the following:
1. Having survived a cardiac arrest due to either
VT or VF.
2. Spontaneous sustained VT causing syncope or
significant hemodynamic compromise.
3. Sustained VT without syncope or cardiac
arrest, and who have an associated reduction
in LVEF <35%.
The ICD System
ICDs consist of electronic components and a bat-
tery housed in a hermetically sealed titanium case
or “can.” A clear, epoxy header on the top of the
device is connected to the internal battery through
metal “feed-throughs.” The leads plug into the
header with set screws and allow device energy to
travel through the feed-throughs into the leads
and onto the heart. Similar to a pacemaker, the
409
ICD has to be a self-contained, battery-powered
device. Lithium-silver vanadium oxide batteries
have emerged as the ideal battery (as against the
lithium-iodine batteries used in pacemakers).
Lithium is a very light metal with a very high
energy density. It serves as the positive pole
(anode) and Vanadium (a trace element) acts as
the cathode in these cells. These cells are power-
ful, long-life batteries with reliable discharge
curves.
ICDs are now implanted in a similar fashion
to a permanent pacemaker system, usually as a
day-case procedure. A significant problem for
ICDs is the size of the battery. Pacemakers typ-
ically pace at 1–2 V. Lithium-iodine cells in
use produce around 2.4 V, and so these batter-
ies work well in pacemakers. Components
called voltage multipliers take the voltage pro-
duced and ramp it up, allowing outputs of up to
10 V. The defibrillating energy delivered by an
ICD is hundreds of times that amount (500–
700 V) and this feature is responsible for the
increased size of the ICD. Capacitors were
added to hold a charge and deliver it all at once.
However, the sizes of ICDs have progressively
diminished from 700 g originally to about 70 g
today. Today’s capacitors, such as MicroTech
capacitors (Medtronic), are thin and contoured,
which allows the entire ICD to be made much
smaller. Figure 17.7 shows the Teligen® 100
ICD (Boston Scientific Ltd.) – until recently,
the smallest, thinnest high-energy ICD in the
world. It is 9.9 mm thick, 31.5 cc in volume
and weighs 72 g. It can deliver high-energy
shocks and has an estimated longevity of
7 years. It has a wide range of programmable
features including bradycardia pacing parame-
ters, ventricular anti-tachycardia pacing param-
eters (2-3 zones), ventricular shock parameters
(energy levels, polarity, shock vector), atrial
arrhythmia management options, electrophysi-
ology test functions (including VF and shock-
on-T induction), and Zip™ telemetry. The
Virtuoso™ VR/DR ICDs (Medtronic) have
similar outstanding features, 37 cc in volume,
68 g in weight, 6.9–8.0 years longevity, and
can deliver 35 J shock (Fig. 17.8). The
410
Fig. 17.7 Teligen® 100 ICD (©2010 Boston Scientific
Corporation/affiliates. All rights reserved. Used with per-
mission of Boston Scientific Corporation)
Fig. 17.8 Virtuoso™ ICD (Image reproduced with per-
mission of Medtronic, Inc.)
Paradym™ DR 8550 (Sorin Group) has a vol-
ume of 33 cc but weighs 90 g.
In addition to innovative therapies and
advanced diagnostics, Virtuoso™ ICDs provide
remote patient monitoring (using Conexus™
17 Implantable Cardioverter Defibrillators
Wireless Telemetry and the Medtronic CareLink
Network) and CareAlert™ notification when
problems arise. In a similar fashion, LATITUDE™
remote monitoring is available for the Teligen®
and Cognis® devices (Boston Scientific) and
MERLIN™ is available for the St. Jude Medical
devices. A range of currently available ICDs is
shown in Table 17.3.
In order to deliver high-voltage output to the
heart, a special type of lead is needed to transmit
voltage from the ICD to the myocardium. The
first generation devices relied on epicardial leads,
which were titanium mesh made with Dacron
reinforced rubber (see Fig. 17.6). The develop-
ment of the transvenous defibrillation lead was
one of the greatest innovations in ICD technology
and revolutionized the implant procedure and
improved patient acceptance. A defibrillation lead
can pace and sense (like a pacemaker lead) but
also deliver a large amount of electrical energy in
a single output. To facilitate this, the electrical cir-
cuit must be capable of withstanding a large bolus
of electricity. This is achieved with a special “coil”
of wire. A defibrillation lead typically contains
two coils (Fig. 17.9), one at the distal end (the
right ventricular or RV coil) and a proximal coil
(the superior vena cava or SVC coil). The “shock
energy” travels along the circuit formed by SVC
and RV coils. There are thus three proximal con-
nectors. A single coil lead was designed with only
two proximal connectors instead of three (Fig.
17.10) but in the newer single coil, DF4 leads, the
circuit is formed between the RV coil and the
device can. The defibrillation (coil) and pacing
components are integrated into that single lead,
resulting in a more streamlined lead and device
without the presence of the “yoke” on the lead.
This also means one connection into the header
instead of three for the RV lead (see Fig. 17.12).
The leads may be active or passive fixation leads
(Fig. 17.11). The Endotak Reliance G lead (Boston
Scientific) is coated with GORE ePTFE to pre-
vent tissue ingrowth and makes it simpler to
remove if necessary (Fig. 17.12). The ICD leads
currently available are shown in Table 17.4.
The ICD System 411

Table 17.3 Currently available ICDs

Dimensions
Manufacturer/device Weight (g) H × W × D (mm) Volume (cc)
Biotronika
Lumax™ 340 VR-T 92 66 × 55 × 13 37.2
Lumax™ 340 VR-T XL 92 66 × 55 × 13 37.2
Lumax™ 540 VR-T 92 66 × 55 × 13 37.2
Lumax™ 340 DR-T 92 66 × 55 × 13 37.2
Lumax™ 540 DR-T 92 66 × 56 × 13 37.2
Lumax™ 540 VR-T DXb 92 66 × 56 × 13 37.2
*Lumos™DRT/VRT, Xelos™DRT, Lexos™DR/DRT/VR/VRT and Belos™DR/DRT/VR/VRT are no longer
available
Boston Scientific
Teligen® 102 VR(IS-1/DF1)c 72 74 × 62 × 9.9 31.5
Teligen® 103 VR(IS-1/DF4)c,d 72 69 × 62 × 9.9 30.5
Teligen® 110 DR(IS-1/DF1)c 72 74 × 62 × 9.9 31.5
Teligen® 111 DR(IS-1/DF4)c,d 72 74 × 62 × 9.9 31.5
Confient®RF DR HE F030 (IS-1/DF1)c 87.5 82 × 67 × 14.5 44
Vitality® 2 AVT DR A155 (IS-1/DF1) 82 65 × 59 × 11 30
Vitality® 2 VR T175 (IS-1/DF1) 82 65 × 69 × 11 30
Vitality® 2 DR T165 (IS-1/DF1) 82 65 × 69 × 11 30
Vitality® 2 DR EL T167 (IS-1/DF1) 90 71 × 63 × 11 35
Vitality® 2 DR EL T177 (IS-1/DF1) 90 71 × 63 × 11 35
Medtronic
Secura™ VR/DR 68 64 × 51 × 15 37
Maximo™ II VR/DR 68 64 × 51 × 15 37
Protecta™ VR/DR 68 64 × 51 × 15 37
Protecta™ VR/DR M 73 66 × 51 × 15 41
Protecta™ XT VR/DR 68 64 × 51 × 15 37
Protecta™ XT VR/DR M 73 66 × 51 × 15 41
*Maximo™ VR/DR, Entrust™ VR/DR, Intrinsic™ DR, Marquis VR/DR, Gem™ VR/DR, Gem™ II VR/DR,
Gem™ IIIVR/DR and Virtuoso™ VR/DR are no longer available
Sorin
Paradym VR 8250 90 58 × 73 × 11 33
Paradym DR 8550 91 58 × 73 × 11 33
Paradym™ DR/VR – 32.8
Paradym™ VR 9250 95 69 × 73 × 11 38.6
Paradym™ DR 9550 95 69 × 73 × 11 38.6
*Ovatio™ VR and Ovatio™ DR are no longer available
St. Jude Medical
Analyst Accel™ DR CD 2219-36Qd 80 74 × 50 × 14 41
Analyst Accel™ VR CD 1219-30 73 75 × 50 × 13 37
Analyst Accel™ VR CD 1219-36 79 76 × 50 × 14 41
Analyst Accel™ VR CD 1219-36Qd 79 74 × 50 × 14 41
Current™ VR RF 1207-30 73 75 × 50 × 13 37
Current™ VR RF 1207-36 79 76 × 50 × 14 41
Current™ DR RF 2207-30 74 76 × 50 × 13 38
Current™ DR RF 2207-36 80 77 × 50 × 14 42
Current® + VR CD1211-36 79 76 × 50 × 14 42
(continued)
412 17 Implantable Cardioverter Defibrillators

Table 17.3 (continued)

Dimensions
Manufacturer/device Weight (g) H × W × D (mm) Volume (cc)
Current® + VR CD1211-36Qd 79 74 × 50 × 14 41
Current® + DR CD2211-36 80 77 × 50 × 14 42
Current® + DR CD2211-36Qd 80 74 × 50 × 14 41
Current Accel™ VR CD1215-30 73 75 × 50 × 13 37
Current Accel™ VR CD1215-36 79 76 × 50 × 14 41
Current Accel™ VR CD1215-36Qd 79 74 × 50 × 14 41
Current Accel™ DR CD2215-30 74 76 × 50 × 13 38
Current Accel™ DR CD2215-36 80 77 × 50 × 14 42
Current Accel™ DR CD2215-36Qd 80 74 × 50 × 14 41
Fortify™ ST VR CD1235-40e 76 73 × 40 × 14 35
Fortify™ ST VR CD1235-40Qd,e 75 71 × 40 × 14 35
Fortify™ VR CD1233-40f 76 74 × 40 × 14 35
Fortify™ VR CD1233-40Qd,f 75 71 × 40 × 14 35
Fortify™ ST DR CD2235-40e 76 74 × 40 × 14 35
Fortify™ ST DR CD2235-40Qd,e 75 71 × 40 × 14 35
Fortify™ DR CD2233-40 (DF-1)f 76 74 × 40 × 14 35
Fortify™ DR CD2233-40Q (DF4)d,f 75 71 × 40 × 14 35
*Atlas and Epic models are no longer available
a
Life expectancy 6.1–9.8 years
b
VR ICD with dual chamber sensing and arrhythmia discrimination
c
Enhanced AV Search Hysteresis to reduce unnecessary RV pacing; wireless capability for faster interrogation, small
device, extended battery life, self-correcting software.
d
4-Site lead
e
Offers ST Monitoring and CorVue™ Congestion Monitoring
f
Offers CorVue™ Congestion Monitoring

Fig. 17.9 Dual • DF-1 Connector (SVC)

coil active lead • IS-1 Connector (Tip & Ring)
• DF-1 Connector (RV)

RV & SVC* Cables

Defib Electrodes

Tip Electrode
Pacing Coil Conductor

Sensing Ring
Sense Cable
The ICD System 413

Tip electrode
12 mm 8 mm Surface area: 2.5 mm2
Ring electrode
Surface area: 20.2 mm2
RV coil electrode
Length : 62 mm
Surface area: 513 mm2
Electrical shadow
area: 430 mm2

Anchoring sleeve
Note: Leads 85 cm or
longer have two
anchoring sleeves

Fig. 17.11 Fixation mechanism of lead. (a) Tined lead;

(b) retractable spiral screws (This is an atrial tined lead)
DF-1 connector
(red band)
Note: Connector
pin is common to RV
coil electrode IS-1 BI connector
Note: Connector pin is
common to tip electrode:
connector ring is common to
ring electrode

Fig. 17.10 Single coil lead

One, two, or three leads plug into the clear
epoxy header on top of the device depending on
the type of device (single-chamber, dual-cham-
ber, or biventricular device).
A single-chamber ICD (Fig. 17.13) has just an
RV lead which can sense and pace the RV in
addition to delivering shocks. The Lumax
340VR-T XL is a single-chamber ICD specifically
designed for primary prevention of sudden car-
diac death providing extended longevity of nearly
10 years and featuring the advanced Biotronik
Home Monitoring technology for continuous and
remote monitoring of the device and therapy
status (Fig. 17.14). It also offers anti-tachycardia
pacing, a 40 J shock energy delivery, the clinically
proven biphasic two shock form, and alternating
shock polarity.
Fig. 17.12 The Endotak Reliance G lead is coated with
GORE ePTFE to prevent tissue ingrowth and makes it
easier to remove if necessary (©2010 Boston Scientific
Corporation/affiliates. All rights reserved. Used with per-
mission of Boston Scientific Corporation)
A dual-chamber ICD (Fig. 17.15) has both RA
and RV leads and can sense and pace both the
atrium and ventricle in addition to defibrillation.
Newer generation devices offer various algo-
rithms to avoid unnecessary ventricular pacing,
for example the Intrinsic™ dual-chamber ICD
(Medtronic) offers MVP (Managed Ventricular
Pacing) which minimizes right ventricular pacing
by providing AAI(R) pacing with the safety of
dual-chamber ventricular support in the presence
of transient or persistent loss of AV conduction.
Table 17.4 ICD leads currently available
414

Manufacturer/lead Fixation Polarity Shock config. Sens config. Fr Lengths (cm)

Biotronik
Linox S 65 Active Tripolar True Bi 7.8F 65
Linox S 75 Active Tripolar True Bi 7.8F 75
Linox SD 65/16 Active Quadripolar True Bi 7.8F 65
Linox SD 65/18 Active Quadripolar True Bi 7.8F 65
Linox SD 75/16 Active Quadripolar True Bi 7.8F 75
Linox SD 75/18 Active Quadripolar True Bi 7.8F 75
Linox T 65 Passive Tripolar True Bi 7.8F 65
Linox T75 Passive Tripolar True Bi 7.8F 75
Linox TD 65/16 Passive Quadripolar True Bi 7.8F 65
Linox TD 65/18 Passive Quadripolar True Bi 7.8F 65
Linox TD 75/16 Passive Quadripolar True Bi 7.8F 75
Linox TD 75/18 Passive Quadripolar True Bi 7.8F 75
Linox smart SD 60/16 Active Quadripolar True Bi 7.8F 60
Linox smart SD 65/16 Active Quadripolar True Bi 7.8F 65
Linox smart SD 65/18 Active Quadripolar True Bi 7.8F 65
Linox smart SD 75/18 Active Quadripolar True Bi 7.8F 75
Linox smart TD 65/16 Passive Quadripolar True Bi 7.8F 65
Linox smart TD 65/18 Passive Quadripolar True Bi 7.8F 65
Linox smart TD 75/18 Passive Quadripolar True Bi 7.8F 75
Linox smart S DXa Active Pentapolar True Bi 7.8F 65/15;65/17
17

Boston Scientific
Endotak Reliance® 4-site 0265/66 Tines Bi Dual coil/4-site 8.1F 59/64
Endotak Reliance® 4-site 0275/76 Ext/retr screw Bi Dual coil/4-site 8.1F 59/64
Endotak Reliance® G 0174/75/76/77 Tines Bi Dual coil 8.1F 59/64/70/90
Endotak Reliance® G 0184/85/86/87 Active Bi Dual coil 8.1F 59/64/70/90
Endotak Reliance® G 4-site 0285/86 Tines Bi Dual coil/4-site 8.1F 59/64
Endotak Reliance® G 4-site 0295/96 Ext/retr screw Bi Dual coil/4-site 8.1F 59/64
Endotak Reliance® SG 0170/71/72/73 Tines Bi Single coil 8.1F 59/64/70/90
Endotak Reliance® SG 0180/81/82/83 Active Bi Single coil 8.1F 59/64/70/90
Endotak Reliance® SG 4-site 0282/83 Tines Bi Single coil/4-site 8.1F 59/64
Endotak Reliance® SG 4-site 0292/93 Ext/retr screw Bi Single coil/4-site 8.1F 59/64
Medtronic
Sprint Quattro Secure 6947 (DF-1/IS-1) Helix/active Quad, dual coil 8.6F 58/65/75/100
Sprint Quattro Secure S 6935(DF-1/IS-1) Helix/active Tri, 1 coil 8.6F 52/58/65/75/100
Implantable Cardioverter Defibrillators
 Sprint Quattro 6944 (DF-1/IS-1) Passive/tines Quad, dual coil 8.2F 58/65/75/100
Sprint Quattro Secure 6947M (DF-4) Helix/active Quad, dual coil 8.6F 55/62/72/97
Transatrial lead
Transvene 6937A Uni 7.5F 35/58/65
Epicardial patch
The ICD System

Transvene epicardial patch 6721S Suture 3 coils 7.5F 50 Electrode SA-370 mm2
Transvene epicardial patch 6721M Suture 4 coils 7.5F 50 Electrode SA-660 mm2
Transvene epicardial patch 6721L Suture 5 coils 7.5F 50 Electrode SA-840 mm2
Subcutaneous lead
6996SQ Suture Uni 7.5F 41/58
Sorin Group
Isoline™ 2CR-6 Active Dual coil Integ 7.8F 65Si
Isoline™ 2CT-6 Passive Dual coil Integ 7.8F 65Si
Vigila 1CR 65/18 Active Single coil True Bi 7.8F 65Si
Vigila 2CR 65/18 Active Dual coil True Bi 7.8F 65Si
Vigila 1CT Passive Single coil True Bi 7.8F 65Si
Vigila 2CT Passive Dual coil True Bi 7.8F 65Si
St. Jude Medical
Durata™ 7120b Active Dual-coil True bipolar 6.8F 60/65
Durata™ 7121b Active Dual-coil True bipolar 6.8F 60/65/75
Durata™ 7122b Active Single-coil True bipolar 6.8F 60/65
Durata™ 7170/71b Passive/tines Dual-coil True bipolar 6.8F 60/65/65/75
Durata™ 7172Q Passive/tines Single coil True bipolar 6.8F 52/58/65
Riata™ (not available in UK) 1570/71c Passive/tines Dual-coil True bipolar 6.7F 65
Riata™ (not available in UK) 1572c Passive/tines Single-coil True bipolar 6.7F 65
Riata™ (not available in UK) 1580/81c Active Dual-coil True bipolar 6.7F 60/65/75
Riata™ (not available in UK) 1582c Active Single-coil True bipolar 7.6F 60/65
Riata™ ST Optim™ 7020/21 Active Dual-coil True bipolar 6.8F 60/65/75
Riata™ ST Optim™ 7022 Active Single-coil True bipolar 6.8F 60/65/75
Riata™ ST Optim™ 7070/71 Passive/tines Dual-coil True bipolar 6.8F 60/65/75
a
Single coil ICD lead with atrial sensing electrodes
b
Durata™ 7120Q, Durata™ 7121Q, Durata™ 7122Q, Durata™ 7170Q and Durata™ 7171Q leads are also available. These are like the non-Q versions but available in 52, 58 and 65 cm lengths. Their connector
is DF4
c
Silicone insulation, endocardial, steroid-eluting
415
416
Fig. 17.13 Chest X-ray
showing a single chamber
device and RV lead (red
arrow)
Fig. 17.14 Lumax 340 VR-T XL is a single-chamber
ICD with extended battery life (Courtesy of Biotronik)
It also provides 35 J shocks and a battery life of
approximately 8 years (Fig. 17.16).
A Cardiac Resynchronization Therapy ICD
(CRT-D) (Fig. 17.17) requires a coronary sinus
17 Implantable Cardioverter Defibrillators
lead for pacing the left ventricle in addition to
RA and RV leads (see Chap. 16). It is designed to
synchronize the contraction of the RV and LV
and improve symptoms in heart failure in addi-
tion to delivering shocks for a life-threatening
arrhythmia. The major device companies offer
CRT-Ds in addition to single- and dual-chamber
devices. For example, St. Jude Medical have the
Promote Accel™ II CRT-D and the Promote™
RF CRT-D devices which are ICDs and which
can also provide CRT to patients with advanced
heart failure (Fig. 17.18).
Occasionally, a stand-alone SVC coil
(Fig. 17.19) is used in conjunction with a single
coil lead to improve the shocking vector and
provide appropriate defibrillation. This may also
be used when faced with a dilated heart and the
proximal coil of a dual coil lead does not stay in
the SVC but ends up in the RA.
The ICD System 417

Fig. 17.15 Chest X-ray

showing a dual-chamber ICD
with atrial and ventricular
leads

Fig. 17.16 Intrinsic™ DR is a

dual-chamber ICD with MVP™
(Image reproduced with
permission of Medtronic, Inc.)
418 17 Implantable Cardioverter Defibrillators

Fig. 17.17 Chest X-ray

showing a biventricular ICD
with RA, RV and coronary
sinus leads (red arrow) in situ

DF-4 draft standard lead, for example, the SJ4/

Fig. 17.18 St. Jude Medical have the Promote Accel™
CRT-D and the Promote™ RF CRT-D ICDs which can also
deliver CRT to patients with severe heart failure (Image pro-
vided courtesy of St. Jude Medical, ©2008 St. Jude Medical,
Inc.)
DF-4 ICD Lead Connector System
A new introduction that probably represents the
next standard in ICD lead technology is the
Durata lead (St. Jude Medical) and the Endotak
Reliance 4-site lead system (Boston Scientific)
(Fig. 17.20), which are designed to simplify the
implant procedure by combining three terminals
into one integrated connector (Fig. 17.21),
reducing the required implant area within the
pocket. The Endotak Reliance 4-site lead is
usable with the Teligen® ICD and the Cognis®
CRT-D devices. The connector reduces the vol-
ume of the Teligen® and Cognis® to 32 cc and
30 cc, respectively, while maintaining a thick-
ness of <10 mm. Some models of this lead also
feature the proprietary GORE™ covering to
prevent tissue ingrowth into the defibrillation
coils, without compromising the electrical
performance of the lead.
The new design incorporates four conductors
into a quadpole connection replacing the
defibrillation coil DF-1 and pace-sense IS-1
connections with the DF-4 connection. The IS-4
draft standard is similarly a quadpole connection
for low-voltage applications (LV lead). The result
DF-4 ICD Lead Connector System
Fig. 17.19 Stand-alone
SVC coil (red arrow) in
addition to a single coil lead.
Note that this patient also has
a pacing lead in the
mid-septum (blue arrow)
following an unsuccessful
attempt at a coronary sinus
lead, this lead was left there
and plugged into the LV port
Fig. 17.20 Endotak Reliance 4-site lead system and
Teligen® 100 ICD (Boston Scientific). This IS4 lead with
integrated pace sense and defibrillation components is
compatible with this device which has a much smaller
header than the earlier devices (©2010 Boston Scientific
Corporation/affiliates. All rights reserved. Used with per-
mission of Boston Scientific Corporation)
is that the three ports previously required for a
defibrillation lead are now combined into a single
port and connection (Fig. 17.22). The new DF-4
419
lead moves the sealing rings from the lead to the
device header where they are less likely to be
damaged at generator change. The novel design
simplifies the initial implant process as well as
generator replacement procedures by reducing
the total ports and set-screw connections and
eliminating the possibility of inadvertently revers-
ing the high-voltage pins when connecting the
lead.
Dual-chamber devices utilize the DF-4 draft
standard for the ventricular lead and the smaller
IS-1 for pace-sense lead in the atrium, eliminat-
ing inadvertent pace-sense lead reversal, for
example, Current® + DR (St. Jude Medical)
(Fig. 17.23).
Biventricular devices will use IS-1 connec-
tions for atrial and left ventricular pace-sense
leads, and the RV lead uses the DF-4 design. With
the advent of quadpole left ventricular leads,
devices will use an IS-1 connection for the atrial
lead, IS-4 connection for the LV lead, and DF-4
for the RV pace-sense and coils, for example,
Promote Quadra™ CRT-D (St. Jude Medical)
(Fig. 17.24).
420 17 Implantable Cardioverter Defibrillators

Fig. 17.21 Endotak Reliance

4-site lead connector (©2010
Boston Scientific Corporation/
affiliates. All rights reserved.
Used with permission of
Boston Scientific Corporation)

Fig. 17.22 The Durata SJ4

lead version of the DF-4
standard lead incorporates
four conductors into a
quadpole connector. The
lead is shown next to the
alternative which has three
lead components and a yoke
to bring them together. This
low-profile lead is compat-
ible with the FortifyTM VR
VVIR ICD (Image provided
courtesy of St. Jude Medical,
©2008 St. Jude Medical,
Inc.)

Among the benefits of the new design is a

reduction in lead length due to absence of yoke
on the high-energy lead (reducing lead-on-can
abrasion), smaller pocket volume (for lead as
well as reduced pulse generator size owing to a
smaller header design), possibly reduced implant
time, and reduced risk of port mismatch.
The Durata™ defibrillation lead with SJ4 con-
nector pin is suitable for use with St. Jude Medical
ICDs and CRT-Ds with the SJ4 connector system
and is shown in Fig. 17.22.
ICD Implantation Procedure
Preimplant
Informed written consent is obtained prior to
the procedure. A full explanation of the risks
and benefits is discussed with the patient
including the implications of having an ICD
on driving and work. It is recommended that
ICD “switch off” at end of life be discussed
ICD Implantation Procedure
Fig. 17.23 The Current® DR dual-chamber ICD has a
low-profile header and two ports. One port takes the DF-4
(SJ4-LLHH) quadripole connector (RV/SVC on can) and
the second port takes the IS-1 bipolar connector pin of the
atrial lead (A on can) (Image provided courtesy of St. Jude
Medical, ©2008 St. Jude Medical, Inc.)
Fig. 17.24 The Promote Quadra™ CRT-D uses the
Quartet™ quadripolar LV pacing lead featuring 4 pacing
electrodes and 10 pacing vectors to provide more options
and greater control to minimize implant complications
such as diaphragmatic stimulation and high pacing thresh-
olds. The device also offers triggered pacing with BiV
Trigger mode to maintain a high percentage of BiV pac-
ing, negative AV hysteresis and the Corvue™ congestion
monitoring feature for monitoring intrathoracic imped-
ance and pulmonary venous congestion. The dual DF-4
header option for the defibrillation lead (DF4-LLHH) and
LV pacing lead (SJ4-LLLL) reduces pocket bulk (Image
provided courtesy of St. Jude Medical, ©2008 St. Jude
Medical, Inc.)
pre implant. The possibility of inappropriate
shocks due to device or lead malfunction must
also be mentioned. A specialist “ICD nurse”
talks to the patient and his/her family and pro-
421
vides psychological support to help individuals
cope with the stress of potentially experiencing
a life-threatening arrhythmia and its termina-
tion by the ICD. Support groups are a popular
adjunctive treatment for ICD patients by pro-
viding a conduit for education, focusing on
patient concerns, and sharing effective strate-
gies to address them. Excellent patient book-
lets are available from the manufacturers, and
patients should be asked to carefully read the
information provided.
Patients should understand that shocks from
their ICD may be unpleasant. They may feel as
if they have been hit in the chest and they may
even be knocked to the ground. Patients should
be told to report single shocks to their GP and
the device implantation center but to call para-
medics if shocks occur in quick succession or
if they have been rendered unconscious. The
use of additional antiarrhythmic therapy may
be necessary in some individuals and this
should be explained to them.
Preparation for Implant
ICDs are now implanted in a similar fashion
to a permanent pacemaker system, usually as a
day-case procedure. Light sedation may be pre-
ferred and if the device is being tested under short
GA, then the patient is usually asked to refrain
from eating for 6 h (or as per local sedation
guidelines).
The patient is prepared for implantation and
monitored by ECG and pulse oximetry as well as
noninvasive blood pressure measurement –
recorded throughout the procedure. A stat dose of
prophylactic intravenous antibiotics is given prior
to beginning the procedure. In our center, 1.5 g of
IV Cefuroxime is given as a stat dose. 80–160 mg
IV of gentamycin is added if the patient is deemed
to be at high risk of infection or has a prosthetic
heart valve.
Defibrillation pads are attached and the patient
is connected to an external defibrillator prior to
draping (Fig. 17.25). Emergency equipment should
be available throughout the procedure. For older
generation devices, a programmer with a wand
placed in a sterile plastic pouch should be avail-
able for use during the procedure (Fig. 17.26).
422
Fig. 17.25 Defibrillator
pads are in situ and the left
pectoral area is cleaned with
1% Chlorhexidine
Fig. 17.26 Programmer wand within sterile sleeve
This is done by RF telemetry in the modern
devices.
The device should be “prepared” for implant.
The device is interrogated while it is still in its
sterile box to confirm that it is switched off and
that the battery voltage is appropriate for a new
device. The next test is a capacitor-maintenance
charge test during which the “charge-time” is
confirmed – usually less than about 15 s. Some
initial bradycardia parameters for the device
17 Implantable Cardioverter Defibrillators
may be programmed at this stage. It is crucial
that the tachycardia parameters are not pro-
grammed “on” at this stage as implanting a
“live” device exposes the implanter to the risk of
a shock!
The implanting physician is usually a cardiol-
ogist (either electrophysiologist or device thera-
pist). The team includes a nurse, radiographer
and a cardiac physiologist. An anesthetist should
be present during testing of the device.
Implantation
The chest wall is cleaned with 1% chlorhexidine
solution thrice and allowed to dry. The area is
then draped with sterile surgical drapes as previ-
ously described in Chap. 7. The left side is pre-
ferred for an ICD implant due to the direction of
the shock vector involving the can.
A subclavicular or a delto-pectoral incision
is made and a pre-pectoral pocket fashioned
medially (Fig. 17.27). It is worth noting that
different ICDs have different shapes (Fig. 17.28)
and it is well worth making a device-specific
pocket. Moreover, it is important that the plane of
the pocket is correct; otherwise, the device is
likely to erode or at least cause discomfort.
Venous access for introduction of leads may be
ICD Implantation Procedure 423

cephalic, subclavian or axillary, or a combination

of these depending on the number of leads to be
introduced. The defibrillation lead is usually
positioned in the RV apex and the lead may have
passive (tined) or active (screw-in) fixation mech-
anisms. For devices that have dual-chamber pac-
ing capabilities, an atrial lead is also inserted into
the RA appendage and a third lead may also be
inserted into a lateral vein of the coronary sinus
to allow biventricular pacing or CRT for the man-
agement of patients with advanced heart failure
and a wide QRS complex to improve their symp-
toms. Transvenous defibrillation leads are either
dual-coil (distal and proximal) with one lying in
the RV and the other in the superior vena cava, or
single coil with only a distal coil lying in the RV.
The shocking coils for single-shock and dual-
shock leads are ideally placed as shown in
Fig. 17.29.
Fig. 17.27 A deep medial pocket appropriate to device
size and shape

Fig. 17.28 Varying device shapes and sizes of modern day ICDs. The Confient® (Boston Scientific), the Intrinsic™
(Medtronic) and the Current DR RF (St. Jude Medical) are shown (with permission)
424
Proximal coil
electrode
Distal coil
electrode
Fig. 17.29 The shocking coils for single-coil (left) and dual-coil (right) leads are ideally placed in the RV and SVC as
shown
Lead Testing
Once the leads are positioned they must be tested.
It is useful to screen the lead during inspiration and
expiration to ensure that some slack exists in the
relevant lead, so as not to place undue tension on
the lead tip and risk displacement (Fig. 17.30).
Sensing
The first test involves assessing the P wave
(intrinsic atrial signal) and R wave (intrinsic ven-
tricular signal). R wave should be >5 mV and P
>2 mV. It is worth bearing in mind that some-
times one can measure an injury current as an R
wave, and as this settles, the R wave amplitude
may fall. As sensing is very important in an ICD,
we recommend testing the R wave again prior to
closure after the other leads have been positioned
and secured.
Pacing
Next, it is important to confirm that pacing leads
can capture or consistently and reliably depolarize
the heart. The pacing threshold should be assessed
for all chambers to obtain suitable values.
Leads are then anchored with the suture
collar using a nonabsorbable suture onto the
17 Implantable Cardioverter Defibrillators
Distal coil
electrode
muscle – with at least two sutures per lead. The
leads are connected to the header of the device
taking care to ensure that the connector pins are
inserted into the appropriate headers (the pace/
sense lead have a lumen and are IS1 connectors
and the shock leads are DF1 connectors)
(Fig. 17.31). The device is then inserted into the
previously fashioned pre-pectoral pocket
(Fig. 17.32).
Device-Based Testing (DBT)
This refers to the capacity of the ICD to self-test
the defibrillation circuit. During DBT, imped-
ance values of the defibrillation lead are obtained.
This is also known as the high-voltage lead
integrity check (HVLIC). If the impedance is out
of range (normal: 30–100 Ω), it indicates a prob-
lem with the lead or connections in the header.
Defibrillation Threshold Testing
Acute defibrillation testing, after induction of VF
in the pacing theater, is performed to ensure that
appropriate detection of ventricular arrhythmias
occurs and that the device can defibrillate effec-
tively with an adequate safety margin. The
ICD Implantation Procedure
Fig. 17.30 Actively fixed ICD lead placed in the apex of
the right ventricle showing an acceptable amount of slack
in the electrode before (top) and on inspiration (bottom)
defibrillation threshold (DFT) is defined as the
lowest energy that can successfully and consis-
tently terminate VF.
The goal of any DFT test is first to induce an
arrhythmia and then allow the device to sense it,
deliver an appropriate shock, and terminate the
arrhythmia. The device will deliver a shock –
according to how the device is programmed prior
to induction; this is usually 10–15 J below maxi-
mum output.
425
Fig. 17.31 Connection of leads into the transparent
header
Inducing the arrhythmia can be done through
the device using a direct current shock, a
“shock-on-T” (Fig. 17.33), or through “burst
stimulation.” The method of induction largely
depends on personal preference. One might
need to employ various methods to induce VF in
some patients. Once VF is induced, the device
senses the arrhythmia and delivers high-energy
therapy, with the patient being monitored to
verify successful defibrillation. One must be
prepared to deliver an external rescue shock in
the event of unsuccessful therapy. After the
shock is delivered, the intra-cardiac electrogram
(IEGM) is monitored to verify there was ade-
quate sensing, appropriate detection, shocking
impedance was within range, and that the charge
time was acceptable.
More recently, there is a trend to avoid DFTs
unless essential, particularly in patients having an
ICD implanted for primary prevention. This is
because of the increasing reliability of the new
generation devices and the small but significant
risk of DFT. Implanting physicians may opt to
forgo DFT testing because of the risk of a stroke
in a patient with AF (off anticoagulation),
significant triple vessel coronary artery disease,
severe aortic stenosis, severely impaired LV func-
tion, or general frailty of a patient. In any case,
patients must not be allowed to stay in the arrhyth-
mia for any longer than absolutely necessary and
426 17 Implantable Cardioverter Defibrillators

Fig. 17.32 Insertion of the

device and leads into the
pre-fashioned pocket

T-shock 20-J
SR V-Pace VF SR

Surface
ECG

Markers

IEGM

2000 ms

Fig. 17.33 Defibrillation testing. VF induction with eight paced beats and a T wave shock, followed by detection and
appropriate therapy

a prompt external rescue shock must be adminis-
tered if internal cardioversion via the device fails.
High DFTs
High DFTs are any DFT which are within 10 J
of the device’s maximum delivered energy out-
put. A few strategies can be undertaken to make
defibrillation therapy more effective. It is worth
first trying a different lead position, such as
changing the lead from a septal to an apical
position or vice versa. If a single-coil
defibrillation lead was initially used, one might
add a separate SVC coil or in the case of a dual-
coil lead a more elaborate lead such as a subcu-
taneous array to increase the surface area over
which defibrillation may occur. However, this
involves subcutaneous tunneling of leads to alter
the shock vector.
ICD Implantation Procedure
Fig. 17.34 Post-closure
and application of glue as a
barrier instead of a dressing
The ICD device itself serves as part of the
defibrillation circuit and is referred to as the
“active” can. Initially, studies of transvenous sys-
tems used the RV coil as the cathode for the
shocks. Subsequently, however, a lower defi-
brillation threshold was found with “reverse
polarity” or anodal shocks. Shock polarity has a
much less effect on bi-phasic defibrillation than
on mono-phasic defibrillation. Depending on the
device, the shock may be delivered from the dis-
tal coil (RV), that is, anode, to the proximal, neg-
ative coil (SVC) coupled with the “active” can.
Reversing polarity makes the RV coil negative
and the SVC coil or “can” positive.
Another option is to change the “Tilt value.”
Tilt is defined as the percentage drop in voltage
on the capacitor from the beginning to the end
of each phase over the course of one entire
pulse. Based on the waveform, the formula for
Tilt is (V1–V2)/V1 × 100%, where V1 is the
leading edge and V2 is the trailing edge. This
feature is only available on devices from specific
manufacturers.
Waveforms
Current ICDs deliver energy utilizing a biphasic
waveform which achieves more effective defibrillation
than previous monophasic defibrillation pulses.
427
Closure
Once the implanter is satisfied that the connec-
tions are satisfactory and the therapy output
parameters are appropriate, the wound is
closed in layers with a nonbraided absorbable
suture. We recommend closure in two layers
with 2.0 Monocryl for subcutaneous layer and
3.0 Monocryl or Dexon® for the subcuticular
layer. Surgical glue such as Dermabond may
be used instead of a dressing to provide a
waterproof barrier for the wound (Figs. 17.34
and 17.35).
Postoperative Care
After implantation, an ECG should be obtained
to document appropriate pacing behavior. This,
however, is less useful in single- and dual-cham-
ber ICDs as they are frequently programmed to
VVI 40 bpm or DDI 40 bpm to minimize ven-
tricular pacing. One should be able to document
biventricular pacing in a biventricular ICD with
evidence of LV pacing on the 12-lead ECG (see
Chap. 16).
A chest X-ray (PA and lateral) will demon-
strate lead position and exclude a pneumotho-
rax (especially if the subclavian vein was
accessed).
428
Fig. 17.35 After glue
application to skin edges
A full device check must be performed
by the cardiac physiologist prior to discharge
to ensure that the device is programmed
appropriately and that anti-tachycardia therapy
is switched on.
Appropriate discharge instructions would
include driving advice and advice on what to do
in the event of a shock. Patients are usually told
to present to the local ICD clinic as soon as fea-
sible, to confirm that the shock was appropriate.
They are also given the contact details of a spe-
cialist ICD nurse to help answer their queries
after discharge. A device-specific card is issued
to the patient and they are advised to carry it with
them at all times (Fig. 17.36).
Complications
The complications that occur following ICD
implantation are similar to those that arise after
pacemaker implantation such as pneumothorax,
cardiac perforation, and lead displacement. They
are presented in Chap. 12. However, besides sens-
ing and/or pacing problems, other complications
are specific to ICD devices. These include inap-
propriate shocks and ineffective cardioversion/
defibrillation. Failure of the device to cardiovert
ventricular tachycardia may simply be due to the
rate being lower than the programmed threshold
(i.e., arrhythmia rate being under the set detection
17 Implantable Cardioverter Defibrillators
rate). Inappropriate shocks may occur in fast atrial
fibrillation or be due to T-wave oversensing, lead
fracture or insulation breaks, electrocautery or
electromagnetic interference. Failure to deliver a
shock may be caused by failure to sense, lead frac-
ture, electromagnetic interference, and inadvertent
ICD deactivation, for example, with magnet appli-
cation. Ineffective cardioversion may be due to
inadequate energy output, a rise in defibrillation
threshold (due to antiarrhythmic agents), myocar-
dial infarction, lead fracture and insulation breaks,
lead displacement and exit block. Some of these
problems are illustrated in Chap. 21.
Driving and ICDs
With regards to driving (Group I entitlement), at
present in the UK, the DVLA recommends
1 month driving restriction after ICD implanta-
tion for primary prevention and 6 months after a
device implanted for secondary prevention.
Subsequent symptomatic therapy from the device
(ATP or shocks) incurs a further 6-month driving
restriction but this is extended to 2 years if any
therapy following device implantation has been
accompanied by incapacity. This may be reduced
to 6 months in the absence of further symptom-
atic therapy if further steps have been taken to
prevent a recurrence, for example, antiarrhyth-
mic agents or ablative therapy. A 1-week driving
ICD Implantation Procedure
restriction applies after an ICD “box change”
and 1-month restriction after lead revision or
alteration of antiarrhythmic medication. Further
Fig. 17.36 Patient identification card with details of the
device and lead
Fig. 17.37 Under-sensing on device leading to inappropriate pacing and failure to detect the ventricular arrhythmia
429
details are available from the DVLA web site
http://www.dft.gov.uk/dvla/medical/ataglance.
aspx.
Patients with an ICD are barred from holding
a Group II licence.
ICD-Arrhythmia Detection
Sensing
Sensing in ICDs refers to the device’s ability to
pick up intrinsic signals from the heart and
interpret them properly, in such a way that
allows the device to respond appropriately. This
is a challenge because there is a wide variation
in the size of the signals in a given patient –
while signals during normal ventricular activity
may be stable and large, ventricular arrhyth-
mias, particularly ventricular fibrillation (VF),
may be small and variable in amplitude. The
ICD sensing has to be sensitive enough to pick
this up, but not sense other low-amplitude sig-
nals such as T waves and far-field signals. If the
device is not sensitive enough, signals will be
missed (i.e., under-sensing) and may result in
over-pacing or failure to detect an arrhythmia
(Fig. 17.37). If the device is too sensitive, it will
pick up noise as well (i.e., over-sensing), result-
ing in under-pacing or worse, inappropriate
therapy due to interpreting noise as VF
(Fig. 17.38). To prevent these problems, ICDs
have sophisticated sensing algorithms which
allow for automatic dynamic sensitivity-setting
adjustments. Signal amplitudes are processed
430
Fig. 17.38 Inappropriate ICD shock (green arrow) due to “over-sensing” (noise) on the ventricular intra-cardiac EGM
(red arrow). This was due to a lead fracture
Fig. 17.39 Tiered therapy. The device has been repro-
grammed from a single zone device (VF detection at
214 bpm) (red arrow) to a 2-zone device with a VT zone
at 154 bpm and a VF zone at 214 bpm
and the sensitivity-setting is based on the most
recently sensed amplitudes. The ICD uses the
intracardiac EGM (IEGM) to gather informa-
tion it will use to categorize rhythm.
Programming
Most ICDs have detection zones with tiered ther-
apy – categorized by rates. In current devices, 1–3
zones may be programmed for tachyarrhythmia
detection usually along the lines of VT and VF
zones (Figs. 17.39 and 16.63). These rhythms are
defined by rate and the device looks at the corre-
17 Implantable Cardioverter Defibrillators
sponding cycle length in milliseconds to decide the
rhythm. The VF zone is always programmed “on”
typically with a detection rate of at least 180 bpm.
If the patient’s only known arrhythmia is VF or
a very rapid, hemodynamically unstable VT, the
ICD may be programmed as a single-zone device,
with only one rate cut-off for arrhythmia detec-
tion. If a patient has monomorphic VT, the device
may be programmed to include other zones. This
will allow programming of other therapy options
in the “VT zones,” such as antitachycardia pacing
(ATP). This may enable termination of a tachyar-
rhythmia with pacing therapy, avoiding uncom-
fortable defibrillator shocks (see below).
Discrimination between supraventricular and
ventricular arrhythmias may be programmed “on”
to avoid inappropriate therapy. These additional
features include “stability,” “onset,” and “mor-
phology” criteria. Stability refers to the degree
of regularity of the arrhythmia and is useful in
patients who have atrial fibrillation (AF) with a
rapid ventricular response, which may fall within
the programmed detection rates of VT or even
VF. The setting may vary from 20 to 80 ms, that
is, if the R-R interval changes by more than the
set value over a number of intervals, the rhythm is
deemed to be irregular. This leads to a diagnosis of
AF and therapy is withheld. Sudden Onset refers
to the degree of prematurity of the first beat of the
Antitachycardia Pacing (ATP)
Fig. 17.40 Stored intra-cardiac atrial (top tracing) and ventricular (bottom tracing) electrograms can aid in arrhythmia
diagnosis. The presence of AV dissociation with V > A is seen in this stored event, confirming the diagnosis of VT
tachycardia compared to previous beats. Sinus
tachycardia is characterized by gradual onset,
while ventricular and supraventricular arrhyth-
mias are often sudden in onset. Morphology cri-
teria help identify IEGMs during a tachycardia
that are very different from the underlying sinus
rhythm, suggesting that the rhythm may be ven-
tricular in origin. In patients with dual-chamber
ICDs, separate sensing of atrial and ventricular
activity is possible. This allows therapy to be
withheld if atrial rate > ventricular rate (atrial
fibrillation or flutter) or indeed confirm VT if the
ventricular rate is greater than the atrial rate sug-
gesting AV dissociation (Fig. 17.40).
Antitachycardia Pacing (ATP)
Overdrive pacing is used as a method of termi-
nating ventricular tachycardia in ICDs as an
effective adjunct to shock therapy. It has the
advantage of being painless with negligible
431
battery drain. ATP can be effective in terminat-
ing over 90% of spontaneous VT with cycle
lengths >300 ms. The pacing rate is usually
programmed as a percentage of the tachycardia
cycle length (ms) of each episode. It may be
programmed to a “Burst” with a constant cycle
length in the drive train or a “Ramp” with dec-
remental cycle lengths in the train. In general,
5–10 capture beats may be sufficient to termi-
nate an arrhythmia. For example, a VT at a rate
of 200 bpm has a cycle length of 300 ms. ATP
programmed as a “burst” at 81% would deliver
pacing at a cycle length of 81% of 300 ms, that
is, 243 ms – which is about 247 bpm for 8–10
beats (depending upon programming). A com-
bination of these ATPs may be programmed to
be delivered prior to shocks to terminate VT
and prevent unnecessary shock therapy. The
rate required for termination of the VT varies
depending on the VT – too slow and it is inef-
fective, too fast and it can result in acceleration
of the tachycardia from an organized rhythm to
432
Fig. 17.41 Chest X-ray showing lead and device positions in a SICD. Note the absence (red arrow) of a transvenous
lead via the subclavian vessel
disorganized chaotic rhythm, that is, ventricu-
lar fibrillation.
Subcutaneous ICDs
A subcutaneous implantable defibrillator (S-ICD)
has been developed by Cameron Healthcare,
which does not require leads to be implanted
within the heart transvenously (Fig. 17.41). The
SQ-RX™ pulse generator is about 69 cc (as
against 35 cc for a conventional ICD), weighs
145 g (Fig. 17.42), and has a longevity of about
5 years. The device is capable of delivering
80 J with some post-shock pacing. The S-ICD
is placed by anatomical landmarks and does not
require fluoroscopy for placement (Fig. 17.43).
The Q-Trak™ subcutaneous electrode is first
tunneled from the xiphoid incision to a lateral
incision (Fig. 17.44) and then subcutaneously
along the sternum via a xiphoid incision to a
superior sternal incision. The lead is then fixed
in situ with a suture sleeve. The generator is con-
nected to the lead and the wound closed. Clinical
studies have confirmed reliable detection of VF
17 Implantable Cardioverter Defibrillators
and VF-conversion efficacy comparable to that
of conventional ICDs (Fig. 17.45). The greatest
advantages are that the implant procedure is sim-
ple, low risk, and does not involve fluoroscopy.
The possible disadvantages include limited pac-
ing capabilities, although post-shock pacing is
possible with these devices. The Q-TECH™
programmer communicates wirelessly with the
SQ-RX™ device to enable adjustment of pro-
grammable settings and data collection.
ICD Follow up
Most patients who undergo secondary preven-
tion ICD implantation will receive therapy from
their ICD appropriately due to ventricular
arrhythmias. It has been estimated that the chance
of receiving any shock is 57–81% during an
average follow-up of 2.5–5 years. Primary pre-
vention patients have an approximate 16% annual
incidence. Inappropriate shocks may occur, most
commonly for AF or SVT. Other causes of inap-
propriate shocks include nonsustained ventricu-
lar arrhythmias, oversensing secondary to lead
Subcutaneous ICDs 433

Fig. 17.42 The Q-Tech™

programmer communicates
wirelessly with the SQ-RX™
pulse generator to enable
adjustment of programmable
settings and data collection.
The Q-TRAK™ subcutane-
ous electrode is also shown
(Image courtesy of Cameron
Health Inc.)

Fig. 17.43 Possible sensing

vectors in the SICD (Image
courtesy of Cameron Health
Inc.)
434
disruption, or sensing of extracardiac signals.
Review of real-time electrograms can help in
identifying lead problems, with reproduction of
Fig. 17.44 Tunneling of leads subcutaneously using ana-
tomical landmarks for implant of SICD (Image courtesy
of Cameron Health Inc.)
Fig. 17.45 VF detection, appropriate shock (orange arrow) resulting in cardioversion and post-shock pacing (green
arrow) in a subcutaneous ICD
17 Implantable Cardioverter Defibrillators
artifact during body motion or palpation over the
device or area of lead insertion under the clavi-
cle. Oversensing of the T-wave may also be seen
which may be corrected by reprogramming.
Patients are first reviewed in the local ICD
clinic at 4 weeks post-implant. A full wound and
device check is performed at this stage and the
pacing outputs may be reduced if appropriate.
Regular ICD visits are recommended every
3–6 months and this may include remote follow-
up. The follow-up sessions are designed to
ensure that the device is functioning appropri-
ately and the patient is coping with the device.
Most modern day ICDs have automated follow-
up protocols that can easily be accessed by the
programmer (Fig. 17.46). However, at each fol-
low-up visit, the history should include questions
regarding the awareness of shocks, symptoms of
palpitations, presyncope, or syncope. The defibril-
lator site should be examined to exclude infec-
tion, hematoma and erosion. Arm swelling on
the side of the implantation or development of
excessive superficial chest wall collaterals could
indicate deep venous thrombosis.
Interrogation
The programmer wand is placed over the
implanted device and the “interrogate button” is
pressed. In case of “remote monitoring” just
Subcutaneous ICDs
Fig. 17.46 The Paradym™ 8750 CRT-D device offers swift
interrogation, a detailed “overview screen” (shown here),
including detailed data on lead function, battery longevity
proximity of the device to the programmer can
facilitate this. The device then reports basic
information to the programmer (Fig. 17.47).
These measurements include lead impedance
measurements and battery voltage indicators (to
435
and statistical information on the frequency of ventricular
arrhythmias requiring treatment and current set-up parame-
ters for this aspect of the device (Courtesy of Sorin Group)
estimate longevity of device), charge time, pac-
ing threshold, and sensing. Real-time measure-
ments provide information at the time of testing.
Intrinsic atrial “P” waves and ventricular “R”
waves are measured and reflect what the ICD is
436
Fig. 17.47 ICD interrogation data printouts from the
Medtronic Virtuoso™ DR (left panel) and Maximo II™
VR (right panels). Left panel shows an overview of the
current “set-up” program and therapy delivery for the
“seeing.” A capture threshold is performed and
confirmed by review of the real-time EGM to
observe the pacing function of the device. This is
performed by decreasing the pacing output in
small steps till capture is lost. Knowing the
threshold enables one to program an adequate
safety margin without wasting the battery. Real-
time impedance measures are documented and
should remain fairly steady. Various automatic
capture management algorithms exist and could
be used effectively for efficient programming of
outputs on the lead. Depending on the manufac-
turer, the device may check threshold beat to beat
and vary outputs accordingly or may do so at pro-
grammed intervals during the day and vary out-
put accordingly.
17 Implantable Cardioverter Defibrillators
Virtuoso™ DR device. Right upper panel details lead
parameters and right lower panel details the episode sum-
mary for the Maximo II™ VR device
New-episode data, for example, shocks,
aborted shocks, or ATP, since the last visit may
be present on the screen, prompting one to look
in more detail and ensure the episodes and ther-
apy are appropriate for the device.
In addition to routine follow-up, interrogation
of the ICD should be performed in all patients
who receive shocks or experience loss of
consciousness.
Device reprogramming or additional therapy
may also be indicated. Exercise testing may be
considered in young or active patients to evaluate
the peak sinus rate, especially when the device is
programmed to a relatively low rate cut-off for
VT detection. Beta-blockers may also be useful
to prevent delivery of inappropriate therapy for
Subcutaneous ICDs
sinus tachycardia when these rates overlap with
the lower limit of the VT zone.
The occurrence of multiple shocks should
prompt more urgent evaluation. Multiple shocks
may be due to recurrent ventricular arrhythmias,
inappropriate shocks due to SVT or lead mal-
function. In the event of recurrent defibrillator
shocks from ICD malfunction or AF with a rapid
ventricular response, a magnet can be temporar-
ily placed on top of the device to inhibit sensing.
In this regard, patients who have ICDs and are
undergoing other surgical procedures should be
given specific recommendations regarding pro-
gramming of the device or use of a magnet in the
operating theater to prevent inappropriate device
therapy during surgery.
Unnecessary defibrillator therapy may also
occur for certain ventricular arrhythmias such as
nonsustained VT. Programming “on” ATP will
help to minimize ICD shock therapy in patients
who have monomorphic VT. However, many
patients will require concomitant antiarrhyth-
mic drug therapy for management of frequent
shocks delivered for rapid VT or aborted shocks
for frequent episodes of long, nonsustained VT.
Frequent aborted shocks, although painless,
may lead to premature battery depletion. For
many patients, catheter ablation for the treat-
ment of recurrent, sustained monomorphic VT
may be the best option to reduce the frequency
of appropriate ICD therapy and improve quality
of life. Nevertheless, between 40% and 70% of
cases with ICDs may require concomitant anti-
arrhythmic drug therapy. Because class I agents
and amiodarone can significantly slow the VT
rate, reprogramming the ICD rate “cut-off”
is often necessary. Moreover, antiarrhythmic
drugs may alter the quality of the sensed elec-
trogram and may result in undersensing of ven-
tricular arrhythmias and some agents can have a
significant effect on the defibrillation threshold.
For patients with significant LV dysfunction, b-
blockers are the mainstay of treatment of VT,
but amiodarone is the most powerful antiar-
rhythmic agent for the prevention of both atrial
437
and ventricular arrhythmias. Sotalol may also be
useful.
Remote Monitoring
If the device has the capability for remote moni-
toring, then the patient is counseled about the
option, consented for it, and provided with a
remote monitor to facilitate transmissions to a
secure website. The feasibility of remote moni-
toring of ICDs was first demonstrated in a multi-
center study evaluating an internet-based system
[1]. The network is comprised of a patient moni-
tor, a secure server, and clinician and patient
websites. Clinician review of data transmissions
may reveal several clinically significant findings
including silent AF discovery, assessment of anti-
arrhythmic drug efficacy in a previously diag-
nosed AF patient, previously unobserved atrial
under-sensing and ventricular tachycardia.
Wireless Telemetry offers automatic data
transmissions and customizable alert notifications
including AF or concerns about lead integrity or
battery life. Comprehensive device data are cap-
tured by the monitor, transmitted and available for
access and review at the clinician’s convenience.
This includes stored episodes, parameters, diag-
nostics including stored IEGMs and real-time
electrograms (Fig. 17.48). With wireless device
interrogation, routine follow-ups can occur auto-
matically while the patient sleeps, alleviating
patient compliance issues. At present, the major
manufacturers have remote monitoring avail-
able for their new generation devices. Medtronic
has CareLink® (see Fig. 6.38), Boston Scientific
has LATITUDE® (see Figs. 11.40 and 11.41),
St. Jude Medical has Merlin@home™ (see Fig.
1.86), and Biotronik have CardioMessenger II®/
Biotronik Home Monitoring Service (see Figs.
11.36–11.39).
Precautions After ICD Implantation
To minimize the chance of interference or dam-
age to the ICD, patients are advised to avoid
438
Fig. 17.48 Comprehensive remote follow-up data transmission on the secure server
exposure to sources of high-energy electrical and
magnetic fields. Possible sources of interference/
damage are similar to those described in Chap.
10 in relation to pacemakers.
Internal and external defibrillation with pad-
dles can damage the ICD and paddles should be
positioned as far as possible from the device. The
device should be checked afterwards to ensure
that the ICD is functioning normally and that the
program settings have not been altered. External
pacing and temporary transvenous pacing can
interfere with ICD sensing.
Most household electrical items (including
microwave ovens) and car engines do not affect
ICDs. Cellular phones should not be turned on or
carried near an ICD since emitted signals may be
sensed as cardiac activity by the device. Mobile
telephones should be held to the ear on the oppo-
17 Implantable Cardioverter Defibrillators
site side to the ICD. Security detection devices
and electronic theft detection devices should not
pose a problem to ICDs when the patient is sim-
ply passing through the device.
Fluoroscopy, standard X-ray, CT imaging, and
ultrasound procedures will not interfere with ICD
function but MRI scanning is currently contraindi-
cated in patients with an ICD. Electroconvulsive
therapy should not affect ICD function but ECG
monitoring is recommended. Lithotripsy is likely
only to damage an ICD if it is at the focal point of
the shock wave. Diathermy can both damage the
components within an ICD as well as interfere with
its diagnostic functions. During general surgery in
patients with an ICD, it is often advisable to inacti-
vate the device for the duration of the procedure
and then reactivate it at completion and help should
be sought from a cardiologist or knowledgeable
Reference
pacing technician. This is in order to avoid inap-
propriate ICD function as a result of signals from
electrocautery or other spurious electrical signals
in the theater. Suffice to say that ECG monitoring
is mandatory in such cases and an external
defibrillator must be immediately available.
439
Reference
1. Schoenfeld MH, Compton SJ, Mead RH, Weiss DN,
Sherfesee L, Englund J, et al. Remote monitoring of
implantable cardioverter defibrillators: prospective
analysis. Pacing Clin Electrophysiol. 2004;27:
757–63.
 Elective Generator Change
After permanent pacemaker or device implanta-
tion, regular follow-up in a pacemaker clinic or
transtelephonic follow-up is mandatory. The tests
that should be performed include an assessment
of battery life and time to elective replacement.
The latter is assessed by the elective replacement
indicator (ERI) for each device. The latter usually
allows 6 months or more to arrange device
replacement before end-of-life (EOL) parameters
are reached when imminent replacement must
take place in order to avoid loss of output and
potentially serious clinical events.
As the number of pacemakers implanted
around the world has progressively increased, so
has the number of procedures to replace battery-
depleted generators. In 2001, almost 52,000
generator replacement procedures were performed
in the USA (Fig. 18.1).
Preoperative Checks
It is usual to see the patient prior to generator
replacement or “box change” to gain written con-
sent, identify whether the patient is pacemaker-
dependent, identify any relevant clinical issues,
including significant comorbidities, for example,
renal impairment, cardiac failure, etc., and to
ensure that any anticoagulant therapy is stopped
prior to admission for the procedure. In our prac-
tice, anticoagulant therapy is discontinued for
4 days preoperatively and an INR checked on the
day of the procedure. Anti-platelet agents are
also stopped preoperatively but discretion is
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_18, © Springer-Verlag London 2012
18
required depending on the clinical need for the
medication.
It is important to establish prior to the proce-
dure whether or not the patient is pacemaker-
dependent. This can be done prior to admission,
on the ward or in the operating theater before the
procedure itself begins. It is also useful to deter-
mine the percentage of ventricular pacing, espe-
cially in patients with symptomatic heart failure
as one may consider the merits of upgrading the
device to a CRT device instead of simply replac-
ing the pacemaker “like-for-like.”
In case of an ICD, the anti-tachycardia features
of the device should be switched off prior to any
intervention. The absence of a therapeutic INR in
patients with atrial fibrillation may prevent the per-
formance of a defibrillation test post-box change.
This may be particularly relevant in patients in
whom lead revisions are deemed necessary at the
time of the box change and the issue should be fac-
tored in when taking consent for the procedure.
It is important to be confident that the operating
room possesses an array of screwdrivers appropri-
ate for the generators that are to be replaced.
Accessories such as lead extensions and attachable
“pins” should be available in case the insulation is
damaged by the operator or if the lead’s connector
pin is “non IS-1” and incompatible with the new
device to be implanted. This latter situation is
becoming exceedingly rare with the almost univer-
sal use of IS-1 leads for many years. Oscor® have a
range of universal, unipolar and bipolar adaptors as
well as bifurcated multipolar adaptors to help man-
age every conceivable situation (Fig. 6.58). Some
441
442
PACEMAKER REPLACEMENTS – WORLDWIDE SURVEY 2001
12000
10000
8000
6000
4000
2000
0
Ecuador Indonesia Pakistan
New Zealand South Africa Norway
China Denmark Argentina
Belgium UK France
Fig. 18.1 Numbers of pacemaker generator replacements per country (From World Survey 2001)
units keep a stock of pacemakers with 5/6 mm lead
connections for box replacement procedures in
patients with 5/6 mm connector pins on their old
leads. With regard to CRT-Ds, it is worth being
aware of the LV1 generation of LV leads that require
either an adaptor, for example, LV1- IS1, or a spe-
cial LV1 device at the time of the box change. In the
future, IS-4 devices will be in more widespread use
and this will be particularly relevant when swap-
ping devices at “box change procedures.”
Procedure
The patient should be fasted for 6 h pre-procedure
but clear fluids should be allowed by mouth prior to
the procedure depending on local sedation policy.
Antibiotic therapy should be given as per local pro-
tocols and the pacemaker site cleaned with antisep-
tic solution prior to transfer to the operating room.
An intravenous cannula should be placed in case IV
fluids or drugs need to be administered. If the patient
has a reasonable underlying intrinsic cardiac rhythm
that will allow the device to be disconnected for a
minute or so, then it should be possible to proceed
without inserting a temporary pacemaker. Otherwise
a temporary pacing lead needs to be inserted
18 Elective Generator Change
Hong Kong Panama Slovenia Ireland Taiwan
South Korea Uruguay India Israel Switzerland
Canada Austria Sweden Australia Netherlands
Brazil Japan USA 51,616 – NOT SHOWN
electively before the generator-replacement proce-
dure begins. A temporary lead may be inserted from
the contralateral subclavian, jugular or basilic vein,
but the femoral vein is usually easier and more con-
venient (see Chap. 13). The latter should take no
more than a few moments to complete and the tem-
porary pacing lead can be withdrawn immediately
after the new generator is connected.
Prepectorally Placed Generator
of an Endocardial System
Once in the pacing theater, the skin is initially
cleansed with antiseptic and cleaned and draped
as indicated in Chap. 7 as for primary device
implantation (Fig. 18.2). 30–40 mls of 1% ligno-
caine is infiltrated around the generator pocket
and around the area of the proposed incision. It is
ideal to make an incision along the previous scar
for cosmetic reasons, although the subcutaneous
tissue here is frequently tough and fibrotic and
requires careful blunt dissection (Fig. 18.3). Once
this has been done, the box itself should be pushed
upwards toward the area of incision and a scalpel
used to cut down onto the box itself – avoiding
Procedure
Fig. 18.2 After cleaning the skin with antiseptic solu-
tion, the patient is covered with a sterile drape. Some
purpose-designed drapes are available
Fig. 18.3 Blunt dissection is necessary down onto the
generator, avoiding damage to the leads en route
the leads at all costs. A thoughtful pacemaker
implanter will have placed the leads behind the
generator in order to avoid lead damage during a
subsequent replacement procedure. Once the
fibrous pocket has been opened, a large pair of
443
Fig. 18.4 An incision onto the generator will open the
fibrous sac surrounding it. This can be opened further
using a large pair of scissors
Fig. 18.5 Widening the wound with a pair of self-retain-
ing retractors will help visualization
blunt-tip scissors should be used to split the inci-
sion further in order to allow access to the device
and its easy removal (Fig. 18.4). Widening the
wound with a pair of self-retaining retractors may
help visualization (Fig. 18.5). Not infrequently,
444
Fig. 18.6 Careful dissection
around the leads/header unit
will help mobilization of the
pacing system
the leads themselves will be tethered by fibrotic
tissue around the coils and blunt dissection will
be necessary to free them sufficiently to allow
free mobilization of the system and ease the
device exchange (Fig. 18.6). Diathermy (prefer-
ably bipolar) can be useful for this situation but
care must be taken not to damage the leads.
Forceps may be used to grip the “can” and help
extraction (Fig. 18.7). Once the generator is free
and sufficiently mobile, it can be removed fully
from the pocket (Fig. 18.8). The leads should
then be unscrewed from the header using the
appropriate screwdriver (Fig. 18.9). If necessary,
the temporary pacemaker can be used to take
over the patient’s cardiac rhythm during the short
18 Elective Generator Change
period required for lead testing and new genera-
tor attachment.
The electrode(s) can be connected to a single
ECG lead to record an intracardiac EGM signal
(Fig. 18.10) if desired. The ventricular (Fig. 18.11)
and atrial (Fig. 18.12) leads should then, in turn,
be connected to the pacemaker analyzer using the
leads provided in order to test the pacing and
sensing thresholds and the lead impedance (black/
negative to tip pin; red/positive to ring electrode
on connector pin). Generally a chronic RV thresh-
old of <2 V, R-wave amplitude of >3 mV, and a
chronic RA threshold of <3 V and P-wave ampli-
tude of >1 mV would be acceptable, although
even measurements less favorable than these may
Procedure
Fig. 18.7 A pair of forceps may be used to aid removal
of the generator from its pocket
Fig. 18.8 Generator removed from pocket
Fig. 18.9 Unscrewing the connector pins from the gen-
erator allows the leads to be pulled out from the header
be acceptable depending on the clinical situation
and the risks associated with performing an
explant/implant procedure. Much higher chronic
LV lead threshold measurements may be
acceptable.
445
Fig. 18.10 An intracardiac electrogram can be obtained
from each lead by connecting a single ECG lead to the
distal pole of the lead
Fig. 18.11 The black negative ECG analyzer lead is con-
nected to the distal pin and the red positive ECG analyzer
lead is connected to the proximal ring electrode of this
bipolar ventricular lead in order for the ECG technician to
measure the lead parameters (sensing and pacing thresh-
old, R wave amplitude and lead impedance) using a
Pacemaker System Analyser (PSA)
The programmability available on most mod-
ern pacing devices will allow continued normal
function despite significantly elevated chronic
thresholds and suboptimal sensitivity measure-
ments. It is important to ensure that the new
446
Fig. 18.12 The black negative ECG analyzer lead is then
connected to the distal pin and the red positive ECG ana-
lyzer lead is connected to the proximal ring electrode of
this bipolar atrial lead in order for the ECG technician to
measure the lead parameters (sensing and pacing thresh-
old, P wave amplitude and lead impedance) using a
Pacemaker System Analyser (PSA)
Fig. 18.13 The new generator is smaller in volume than
the older pacemaker
device has similar capabilities to the one being
replaced, especially as regards electronic repro-
gramming of pacing vectors in CRT devices (see
Chap. 16 for details). If a single-coil ICD lead is
in situ, then the SVC port on the new device
needs to be plugged prior to connecting the lead.
18 Elective Generator Change
Fig. 18.14 The new generator is thinner than the older
pacemaker
Fig. 18.15 Inserting the leads into the new device’s
header unit
Figures 18.13 and 18.14 show the significant
reduction in volume and thickness of the old and
new generators.
Once the connector pins of the leads have been
inserted into the new device (Figs. 18.15 and 18.16)
and have been secured with the appropriate screw-
driver (Fig. 18.17), the device can usually be placed
back into the fibrous pocket (Fig. 18.18) and the
wound closed in layers using an absorbable suture
material (Figs. 18.19–18.22). Occasionally, the
pocket has to be extended to accommodate a new
pacemaker with a different shape. Any temporary
pacing lead can then be removed prior to closure.
Some operators will spray antibiotic powder or an
antiseptic powder into the pocket with the inten-
tion of minimizing the chance of pocket infection.
It is essential to ensure that all bleeding points are
Procedure 447

Fig. 18.16 When inserting the leads into the new device’s Fig. 18.19 Subcutaneous tissues are closed with an
header unit, it is important to see that the connector pin absorbable suture on a curved needle
has passed beyond the fixing screw(s) in the header unit

Fig. 18.17 Each lead is fixed securely into the header

unit by tightening the screws with the appropriate
screwdriver

Fig. 18.20 Wound closure

Fig. 18.18 The new generator is placed back into the

previous fibrous pocket
448
Fig. 18.21 Wound closure
Fig. 18.22 Effective wound closure brings the skin edges
close together
Fig. 18.23 Subcuticular suturing using Dexon on a
straight needle closes the wound in a cosmetically satis-
factory manner
cauterized or sutured before closing the wound in
layers. A nonbraided, absorbable suture to the sub-
cuticular layer will usually produce a good cos-
metic result (Figs. 18.23 and 18.24) but skin
adhesive/glue will usually be just as pleasing. Glue
18 Elective Generator Change
Fig. 18.24 Result of subcuticular Dexon suture
Fig. 18.25 The skin edges can be closed with Dermabond
glue
Fig. 18.26 Result after application of glue
may also be used after placing a subcuticular suture
(Figs. 18.25 and 18.26).
Before or after implantation, the device should
be interrogated and programmed to the desired
settings while in the theater and a printout of the
Procedure
Fig. 18.27 This patient’s fading scar from her first epi-
cardial pacemaker implantation is indicated by the arrow
Fig. 18.28 After cleaning the skin with antiseptic solu-
tion, the patient is covered with a sterile drape
current program placed in the case records at the
time of implantation.
Discharge from hospital should be the same day
unless the procedure has been complicated or devel-
oped into an explant/implant procedure or if medi-
cal or social circumstances are such as to indicate
an overnight stay. The patient should be provided
with or sent a new “pacemaker card” with the details
of the new device and the latest program settings.
Four weeks after discharge, the pacemaker
wound should be checked and a 12-month appoint-
ment arranged for a generator check at the pace-
maker clinic.
Patients can drive after 1 week following
generator replacement but drivers of passenger
carrying vehicles (PCV) and larger goods vehi-
cles (LGV) must refrain from driving for
6 weeks.
449
Fig. 18.29 The operation area is covered with an adhe-
sive Ioban™ drape
Fig. 18.30 The incision is made through the previous
scar if possible
Replacement of Abdominally Placed
Generator of an Epicardial System
These procedures are best done in a sterile operating
theater by a cardiac surgeon or cardiologist who is
experienced in this type of surgery. A general anes-
thetic is preferable to local anesthetic especially
for removing generators placed deep in the abdo-
men and behind the rectus sheath.
Once the patient is anesthetized, the chest and
abdomen are cleansed with antiseptic solution
(Fig. 18.27). After drying the skin, the patient is
then draped (Fig. 18.28) and the exposed area
over the generator covered with an adhesive
Ioban™ transparent, sterile drape (3M Health
Care) (Fig. 18.29). The skin is then incised over
the original scar – if possible (Fig. 18.30) and
hemostasis secured with diathermy. The wound
450 18 Elective Generator Change

Fig. 18.31 Blunt dissection is performed down onto the Fig. 18.34 Once the pacemaker and leads are mobile, the
generator generator is ready to be removed from the pocket

Fig. 18.32 Exposing the wound with a pair of self- Fig. 18.35 Forceps delivery of the old generator
retaining retractors reveals the generator

Fig. 18.33 Careful dissection is required to free the Fig. 18.36 Extraction of the old generator from the
lead(s) and the pacemaker itself pocket

is dissected carefully down onto the generator Once the generator and lead(s) have been care-
using blunt dissection and the fibrous pocket fully mobilized (Figs. 18.33 and 18.34), the gen-
opened with a scalpel or scissors in order to erator can be lifted out of the pocket (Figs. 18.35
expose the generator (Figs. 18.31 and 18.32). and 18.36). If the patient is pacemaker-dependent,
Procedure
Fig. 18.37 Unscrewing the atrial lead from the old gen-
erator’s header unit
Fig. 18.38 Unscrewing the ventricular lead from the old
generator’s header unit
Fig. 18.39 Generator being detached from the leads
temporary pacing should be commenced prior to
this. The lead(s) can then be unscrewed from the
generator (Figs. 18.37 and 18.38) and pulled out
of the header unit and the generator removed
(Fig. 18.39). The leads can then be tested (as
above) for signal amplitude, pacing threshold,
451
Fig. 18.40 Lead measurements being tested by ECG
technician
Fig. 18.41 In this case, the DDD system is being replaced
with a VVIR single-chamber device following the develop-
ment of permanent atrial fibrillation. The atrial connector
pin is being “capped off” and the cap tied with a silk suture
and impedance (Fig. 18.40), and if changing
from a dual-chamber system to a single-chamber
rate-responsive system, the redundant lead can
be capped and tied (Fig. 18.41). The new genera-
tor can then be attached to the leads (Fig. 18.42)
and the connector pins secured in place using the
appropriate screwdriver (Fig. 18.43). The new
device can then be placed carefully into the old
pocket (Figs. 18.44 and 18.45). The generator
can then be programmed and tested by the pacing
technician by placing the wand (inside a sterile
plastic bag) over the pacemaker (Figs. 18.46 and
18.47). Once satisfied that the device is function-
ing appropriately, the wound is then closed in
layers with absorbable sutures to the pocket and
subcutaneous fat (Fig. 18.48) and subcuticular
dexon to the skin edges (Figs. 18.49 and 18.50).
The skin incision (Fig. 18.51) may then be
452
Fig. 18.42 The ventricular lead is inserted into the new
pacemaker
Fig. 18.43 The connector pin is secured to the generator
by tightening the screw in the header unit
Fig. 18.44 New generator is placed back into the origi-
nal pocket
18 Elective Generator Change
Fig. 18.45 The generator is deep below the subcutane-
ous fat in the abdomen
Fig. 18.46 A programming/analyzing “wand” is inserted
into a sterile plastic bag and placed over the site to enable
testing and programming of the new system
covered with Dermabond glue or simply covered
with a sterile dressing (Fig. 18.52).
Patients undergoing a general anesthetic are
generally kept in hospital overnight. The next
morning, the patient is provided with a new pace-
maker identification card and an appointment for
the follow-up pacing clinic in 1 month. Some
simple analgesia should be offered to the patient
for postoperative pain which should settle quickly.
If a dressing has been applied, it should be
changed daily for approximately 5–6 days. Glued
wounds do not require this.
Procedure 453

Fig. 18.50 Subcuticular Dexon suture nearly completed

with skin edges being perfectly aligned

Fig. 18.47 ECG technician analyzes the performance

and sets up the required program for this patient before
leaving theater

Fig. 18.48 The subcutaneous layer is closed with absorb- Fig. 18.51 End result. The skin edges may be glued
able suture material together

Fig. 18.49 A subcuticular Dexon suture brings the skin

edges securely together
Fig. 18.52 An alternative to gluing the skin edges is to
simply cover the wound with a sterile dressing
454
Replacement of ICDs
After disconnecting the ICD, the operator should
ensure that the in situ leads are functioning satis-
factorily and that the proximal connections are
compatible with the header of the new device to
be implanted. Adaptors may be required and
plugs may be required to close unused ports.
When the new device is significantly smaller
than the device being removed, care must be
taken to reduce the size of the pocket in order to
avoid free movement of the device within the
pocket.
18 Elective Generator Change
Once the wound has been closed, the anti-
tachycardia features of the ICD should be turned on.
Major complications, such as serious infection
and hematoma formation, may occur more com-
monly after ICD replacement than after pace-
maker replacement (7.4% vs. 2.7% in the
REPLACE Registry). This is probably related to
the increased size of ICDs compared to pacemak-
ers, the more dissection that is required and the
fact that ICD patients are more likely to be on
antiplatelet agents or require anticoagulant
therapy.
 Explant Procedures
Indications
The important indications for removal of a
pacemaker, CRT device, or ICD are shown in
Table 19.1. The most frequent reason is infection
of the pacing system (see Figs. 12.31 and 12.32).
Erosion of leads (see Fig. 12.69) or pacemakers
(Fig. 12.71) through the skin and associated sep-
sis has become less of a problem as the devices
have become smaller and more ovoid and the
leads softer. The techniques of careful asepsis
and burying the generator deep in a prepectoral
or subpectoral pocket away from the skin have
resulted in lowering the incidence of infection
and erosion. However, ICDs are still large and
infection/erosion will more commonly occur
with these devices unless care is taken to avoid
Table 19.1 Indications for device/lead removal
Infection of device – pocket infection/infective
endocarditis
Erosion of the device or lead(s)
Lead fracture
Insulation break in lead
Potential lead failure/company alert/advisory
Chronic pain from the pacemaker/lead which is not
manageable medically
Thrombosis of great veins/significant thromboembolic
events associated with thrombosis on a lead or lead
fragment
Location of device in a therapy field, e.g., radiotherapy
for lung cancer
Replacement of device for MRI-safe device
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_19, © Springer-Verlag London 2012
19
the causal factors. Elderly, frail and thin patients
are more at risk of infection and erosion, as
are those who develop hematoma in the pocket
necessitating drainage.
When infection/erosion is the indication for
removal of the pacemaker, it is mandatory to
remove the lead as well. In other situations, the
decision to extract the lead when removing the
pacemaker may be influenced by other factors
and is discussed briefly below.
Although perhaps a moot point, the term
“explant” is used where the lead has been in situ
for <1 year and removed with manual traction
and “extraction” when in situ for >1 year and
removed using specialized tools.
Preoperative Considerations
Careful follow-up of patients in a dedicated pac-
ing clinic should alert the cardiologist to signs of
pre-erosion such as pain, redness, swelling, and
tenderness over the generator or lead. Adherence
of either lead or generator to the skin’s dermis
is an indicator of risk of subsequent erosion
(Fig. 12.68). Patients should be aware to inform
the pacing center in the event of any of the above
features developing following device implanta-
tion and they should be seen by the cardiologist
without delay.
If any components of the pacing system have
eroded through the skin, it is important to swab
the wound and commence appropriate IV anti-
biotic therapy prior to removal of the system.
455
456
When there is no erosion but clear evidence of
pocket infection, blood cultures should be col-
lected and unless explantation is going to take
place imminently, antistaphylococcal antibiot-
ics should be commenced intravenously without
delay. High-dose IV flucloxacillin (3G qds) is a
reasonable regimen and needs to be continued
for 2–4 weeks – and perhaps 6 weeks if there is
evidence of infective endocarditis. Arrangements
should be made to explant the device – generator
and lead – as soon as practically possible. If the
patient is septicemic, it is worth considering
planning to remove the system and continue IV
antibiotics for 4–7 days prior to implanting a new
system from the contralateral side. A temporary
pacemaker may be necessary to cover this period
if the patient is pacemaker dependent and con-
sideration as to the best site for temporary pac-
ing is important. The site should not compromise
placement of the new pacing system.
For all cases, it is important to establish the
original indication for pacing, the type of pace-
maker and its mode of operation and whether the
patient is pacemaker dependent. If there is evi-
dence of dependency (or any doubt exists), then
a temporary pacemaker should be inserted prior
to the explant procedure. It is also important to
establish how many leads are present, how long
the lead(s) has been in situ, the type of lead(s),
whether the leads were active- or passive-fixation
electrodes, and whether the lead(s) were placed
via the subclavian or cephalic vein. A chest X-ray
is useful for identifying undocumented hardware.
If infection is the reason for removal, echocar-
diography should be performed to look for vege-
tations on the leads as surgical lead removal may
then be preferred if large mobile vegetations are
evident. Routine blood tests should include full
blood count, ESR, CRP, renal, and liver function
tests.
Leads that have been in place for >12 months
(particularly passively fixed “tined” leads) may
be difficult to remove by simple traction or by
a combination of “unscrewing and traction” (in
the case of active-fixation leads). It has been esti-
mated that leads implanted for <4 years have a
95% successful extraction rate compared to 80%
for those implanted >10 years. Actively fixed
19 Explant Procedures
Table 19.2 Indications for lead extraction
Mandatory Septicemia
Pocket infection
Infective endocarditis
Superior vena caval syndrome
Pacemaker/lead erosion
Lead migration into the RV or PA
causing life-threatening arrhythmias
Clinically significant thromboembolic
event caused by redundant lead or
fragment
Lead that interferes with a new device
Lead fracture
Lead insulation break
Retention wire fracture, e.g., Accufix J
lead
Discretionary Redundant leads thought to be
potentially obstructive to great veins
Interference with function of new
lead(s)
Nonfunctional lead in young patient
Lead migration
Potential lead failure – company alert/
advisory
atrial leads that have been in place for a long
period of time may be hazardous to remove and
the risk of perforation by avulsion of the myo-
cardium is real and potentially devastating (see
Chap. 12). Stretching of leads by prolonged trac-
tion may lead to disruption of the lead which then
makes it impossible to remove percutaneously.
Moreover, leads may become fibrotically adher-
ent to the tricuspid valve, the superior vena cava,
or to the wall of the great veins and the degree
of tethering varies markedly. Traction alone will
then not free the lead and again increases the risk
of rupture of the adherent structure. If anything,
the speed and degree of tethering may be greater
in younger patients.
Generally, there are mandatory and discretion-
ary indications for lead extraction and these are
shown in Table 19.2. However, there are other
factors that may influence the decision to embark
on a lead removal procedure. These include the
age of the patient and coexisting comorbidities
such as the presence of a terminal illness, bleed-
ing diatheses, or unfitness for general anesthesia.
The duration of lead implantation and the type of
Procedure
lead and its fixation may influence the decision
to attempt lead removal but even these are now
relative with the availability of the laser extrac-
tion device.
Knowledge about lead construction and design
is of value. Unipolar leads consist of a single heli-
cal conductor which links the lead connector pin
to the tip electrode. The coil has a central lumen
and is surrounded by a layer of insulation made
either of silicone rubber or polyurethane. Bipolar
pacing electrodes have an additional coaxial outer
coil connected to the proximal ring electrode.
In this situation, there are layers of insulation
between the inner and outer coils and surrounding
the outer coil. Defibrillator leads are constructed
differently, although all have a tip electrode
for sensing and pacing. Whatever the lead, it is
important when considering extraction to identify
and expose the coil that leads to the tip electrode.
Contraindications
If epicardial systems require removal, surgery is
required.
Relative contraindications for percutane-
ous pacemaker/lead extraction include lead
calcification (seen on X-ray) involving the SVC
or RA, unavailability of necessary equipment,
no surgical cover for emergency thoracotomy,
inexperienced operators, and severe comorbidity
which precludes emergency thoracotomy.
Procedure
The procedure, its risks and benefits, and alterna-
tive treatments need to be carefully explained to
the patient prior to the procedure. For all patients
undergoing an explant (± new implant) procedure
under local anesthetic, an anesthetist should be
present or at least available to provide sedation
or a general anesthetic if necessary. Indeed, seri-
ous consideration to elective general anesthesia
should be given for each patient requiring an
explant procedure. Procedures may be prolonged
especially if done in a single-stage rather than
a two-staged procedure and special equipment
457
(e.g., laser-extraction device and other extraction
tools) may be required in order to remove adher-
ent leads.
Such procedures should only be done in a car-
diothoracic center with a cardiac surgeon fully
informed about the case and prepared to help as
an emergency in the event of a disastrous com-
plication such as atrial, ventricular, or great vein
rupture. It has been suggested that extraction
procedures should only be performed within cen-
ters performing at least 20 procedures per year.
Facilities for emergency pericardiocentesis are
essential and blood should be grouped and saved
for crossmatching in case blood transfusion is
urgently required.
Two experienced cardiologists make these
difficult procedures less daunting, although of
course two are not absolutely essential. One may
be responsible for inserting a temporary pace-
maker from a femoral vein puncture and then
removal of the infected/eroded or redundant
system, while the second cardiologist concen-
trates on inserting the new pacing system from
the opposite side. Both pectoral regions and the
temporary site require cleaning and draping in
an aseptic manner (as described in Chap. 7) and
two coordinated operators will make the whole
procedure easier. When laser or other mechani-
cal extraction devices are required to remove old
and firmly adherent electrodes, two operators are
ideal. In these circumstances, it is usually easier
to have the image intensifier on the side of the
“implanter” until the leads have been extracted
(Fig. 19.1) and then moved by the radiographer
to the “explanter’s” side for the new implant
procedure.
Insertion of Temporary Pacemaker
This is usually best placed from the femoral vein
under local anesthetic (Figs. 19.2 and 19.3). A 7F
venous sheath with side arm and a 6F temporary
pacing electrode is generally quick and easy to
insert and allows administration of drugs and large
volumes of fluid if necessary. The operator should
regown prior to moving to the “explant side” of
the patient for that part of the procedure.
458 19 Explant Procedures

Fig. 19.1 Explantation of

an old pacing system and
implantation of a new
pacemaker and lead is best
performed by two experi-
enced operators working
together

Fig. 19.2 This patient was

having an infected ICD
removed under general
anesthesia. As he was also
pacemaker-dependent, not
only was a temporary
pacemaker placed from the
right femoral vein but
defibrillation pads were
placed on his back and
anterior chest wall in case of
intraprocedural ventricular
tachycardia or fibrillation

Explant of Infected/Eroded/Redundant wound should be opened (preferably along the

Pacemaker System
Local anesthetic should be infiltrated around
the pacemaker and lead in the direction of the
subclavicular puncture site, although this is
not essential if the patient is receiving a gen-
eral anesthetic (Figs. 19.4 and 19.5). Indeed, if
there is clear pocket infection with evidence of
redness and swelling, effective local anesthe-
sia may be impossible and a general anesthetic
should be administered from the outset. The
line of the previous incision) and swabbed for
microbiology (Fig. 19.6). This may be altered to
include the point of erosion if present. The inci-
sion should be extended down onto the generator
and the fibrous pocket opened and the generator
removed once the temporary pacemaker is turned
on and functioning (Fig. 19.7). The leads can
then be unscrewed and removed from the gen-
erator and the old device discarded. The leads
are next freed by local dissection of fibrous tissue
(if necessary with diathermy) and any anchoring
Procedure 459

Fig. 19.3 Temporary

pacing box connected to
temporary electrode inserted
via right femoral vein

Fig. 19.4 Local anesthetic is given around the device Fig. 19.6 The pocket is drained of pus and the generator
unless a general anesthetic is being administered for a and leads exposed
difficult procedure, e.g., excimer laser lead extraction, where
it is anticipated that simple traction will not be successful

Fig. 19.5 Local anesthetic being administered leads to Fig. 19.7 Generator and leads are removed from pocket
discharge of pus from this infected pocket
460 19 Explant Procedures

sutures removed (Fig. 19.8). At this point, a
locking stylet should be inserted into the first
lead to be removed, if necessary after cutting
off the lead connector. If the lead was passively
fixed, firm traction should be applied to them
both. Steady traction may tug the lead away from
the myocardium and allow the stylet/lead to be
removed. For leads that have been actively fixed,
it is worth trying to unscrew the helix in order to
retract it back into the distal tip of the lead before
applying steady, firm traction. This is especially
important in atrial leads. For leads without a
retractable helix, rotating the entire lead coun-
terclockwise might help to unscrew the tip from
the myocardium. Experienced operators come to
know whether the tip of the lead will come free
with traction and when to stop and use a more
active way of freeing the tip. Care must be taken
not to damage the lead during this maneuver.

Extraction of Fixed Leads

Although occasionally it may be necessary to

Fig. 19.8 Generator is unscrewed from the leads and the
leads’ anchoring sutures cut and removed
Fig. 19.9 The connector pins are cut off with special wire cutters
remove leads from the femoral vein after cut-
ting the lead proximally and detaching the pace-
maker and lead connector, most leads can be
removed from the subclavian vein. In order to
improve success of lead extraction, several tech-
niques are currently available using a locking
stylet, dilator sheaths, diathermy, or laser outer
sheath to free adhesions which are preventing
extraction.
Once the lead’s connector is cut-off with a
lead cutter (Fig. 19.9), the inner coil is exposed
in order to introduce a locking stylet (Cook)
(Figs. 19.10 and 19.11). A special “coil-expander
tool” might be helpful for introduction of the
locking stylet (Figs. 19.12–19.14). The locking
stylet is advanced to the tip of the inner con-
ductor coil (Figs. 19.15–19.18) when a locking

Fig. 19.10 Unless the lead

has only been implanted for
a few days or weeks (when
inserting a stylet into the
lead may be good enough for
applying traction to the lead
tip during attempted
removal), a special lead
locking device (shown here)
is necessary
Procedure 461

Fig. 19.11 Lead locking device (LLD) in its unlocked

form is placed inside the pacing lead’s inner lumen Fig. 19.15 Distal end of lead locking device

Fig. 19.12 Exposing the lumen of the severed lead

Fig. 19.16 Inserting LLD into lead (I)

Fig. 19.13 A special “coil-expander tool” can help to dilate

the end of the cut-off lead to allow introduction of the LLD

Fig. 19.17 Inserting LLD into lead (II)

Fig. 19.14 Using the “coil-expander tool”

462
Fig. 19.18 Advancing LLD down the lead to be
removed
Fig. 19.19 Preparing to lock the LLD within the
electrode
Fig. 19.20 When the LLD is released or activated, the
steel wire “bunches-up” inside the lead’s lumen and jams
within it. This prevents traction on the lead itself from
simply unwinding the coils of the lead
mechanism is activated that fixes the stylet to
the conductor coil (Figs. 19.19 and 19.20). This
allows traction to be delivered along the length
of the lead and its tip and prevents the lead from
uncoiling as it is being retrieved. The outer lead
19 Explant Procedures
Fig. 19.21 LLD in situ, a suture is used to fix the lead
and insulation to the LLD
Fig. 19.22 Tension can be put on the LLD
Fig. 19.23 Traction is placed on the lead/LLD to try and
free the lead
insulation should then be secured with a suture
(Figs. 19.21 and 19.22). It is worth an attempt
to remove the lead again by applying traction
to the lead/stylet combination (Fig. 19.23).
Figures 19.24 and 19.25 show the stylet and
Procedure
Fig. 19.24 The LLD is
stretched out over a sterile
table
Fig. 19.25 LLD ready to be inserted inside outer sheath
Fig. 19.26 Stiff outer sheath to be placed over LLD
locking mechanism in place. If this maneu-
ver fails, a stiff dilator sheath with a beveled
distal end is then advanced over the lead/lock-
ing stylet (Figs. 19.26 and 19.27). Controlled
traction is applied to the lead via the locking
stylet while the dilator sheath is advanced and
rotated under fluoroscopic guidance to deter-
mine progress (see below). Counterpressure is
463
Fig. 19.27 The stiff outer sheath has a beveled distal tip
applied at the site of fibrous adhesions in order
to shear the tissue away from the vessel wall.
The dilator is advanced to the lead’s tip which
is adherent to the myocardium and countert-
raction applied to the lead via the locking
stylet. The dilator sheath prevents invagination
of the myocardium as tension tears the tip from
its fibrous anchor point (Fig. 19.28). Spectrane-
tics have recently released the VisiSheath®
whose gold-coated steel marker bands at its
distal beveled end enhance fluoroscopic vis-
ibility. It also has a more robust tip design
and orientation marker, a range of sizes, and
an advanced multi-layer construction for high
performance.
If the use of the dilator sheath alone is unsuc-
cessful, three other options are available –
the Electrosurgical Dissection Sheath system
(EDS) (Cook Vascular Inc.), the Evolution sys-
tem (Cook Medical), and the Spectranetics Laser
Sheath (SLS II) (Spectranetics CVX-300).
The EDS has a pair of bipolar electrodes at the
beveled tip of the inner sheath and uses radiof-
requency (RF) energy to allow adhesions to be
freed during advancement.
464
a b
Tension
c d
Fig. 19.28 (a) Close-up of pacing lead tip embedded in
fibrous tissue adherent to the myocardium. The locking
stylet filament wire is seen at the distal end of the lead’s
lumen. (b) The stylet is locked inside the lead’s lumen and
the outer sheath is advanced to the myocardium. (c) Firm
traction is placed on the locking stylet, while the sheath
The Evolution system is a mechanical rotat-
ing device which is hand-operated by the cardi-
ologist using a trigger mechanism that rotates the
threaded tip of the inner sheath that then pulls
itself slowly down the lead (Fig. 19.29). The han-
dle and trigger are designed in such a way that the
operator performing the procedure can actually
“feel” the ease or difficulty of movement of the
sheath through the trigger, providing the tactile
indication of the device’s progress down the lead
or through lesions. The sheaths are single-use
and disposable.
Wide experience has been gained with the
Spectranetics Laser Sheath (SLS II) (Spectranetics
CVX-300) which delivers excimer laser energy
19 Explant Procedures
Locking stylet
Lead coil
Locking
filament wire
Lead lumen
Lead insulation
Outer sheath
Scar tissue
provides countertraction, preventing invagination of the
heart and confining the force within the circumference of
the sheath. (d) When the lead tip is freed from the scar
tissue, it is removed through the sheath. The outer sheath
may be used to introduce a new lead
in a ring at the tip of the sheath. Laser energy
vaporizes fibrous tissue adhesions without pen-
etrating adjacent structures and has been shown
to be more successful than dilator sheaths alone.
However, this is an expensive procedure and less
effective against calcification, which may be a
problem in older leads. The laser sheaths/acces-
sories cost approximately £3,000 each, and the
Laser CVX-300 generator costs £150,000. The
laser extraction procedure is discussed in detail
below.
If a femoral approach is preferred, the
femoral vein opposite to the one being used
for temporary pacing should be used. First,
the lead’s connector is removed and a stylet
Procedure
Fig. 19.29 Evolution™ (Cook Medical) mechanical rotational cutting device for freeing the lead from adherent fibrous
tissue
Fig. 19.30 Lead which had been cut-off in the pectoral
pocket because it could not be removed by traction alone
has prolapsed into the RA and RV
Fig. 19.31 Dotter basket is introduced through its sheath
from the right femoral vein. Retraction of the retaining
sheath releases the coils into its open helical state
465
Fig. 19.32 A loop of the redundant lead is captured within
the helix and the helix closed trapping the lead (arrow)
introduced down the inner coil so that the lead
can be advanced as far as possible into the right
atrium. After grabbing the cut-proximal end
of the lead with a Dotter Basket or some other
snare inserted via the femoral vein, it can then
be brought into the inferior vena cava. Once
snared, the outer sheath can then be advanced
over the lead up to 1–2 cm from the electrode’s
tip. The lead is then pulled into the sheath using
countertraction. It may be possible to simply tug
the lead away from the myocardium by pulling
the Dotter basket and its outer sheath once the
lead has been well ensnared inside the basket
(Figs. 19.30–19.39).
The Dotter basket can also be used for
removing other remnants of permanent pac-
ing leads such as “tined tips” (Fig. 19.40) and
even severed/embolized temporary pacing leads
466 19 Explant Procedures

Fig. 19.33 Loop of lead is pulled down into the RA and Fig. 19.35 The “free-end” is pulled down into the IVC
IVC

Fig. 19.34 A second retrieval device (alligator jaw Fig. 19.36 The “free-end” is then grabbed by the Dotter
device) is used to grab the “free-end” of the lead basket which enables firm traction on the lead tip
Procedure
Fig. 19.37 Firm, steady traction on the Dotter basket/
electrode frees the lead from the RV apex and pulls it into
the IVC
Fig. 19.38 Dotter basket with ensnared lead is now in
the right common iliac vein, and removed by pulling
Dotter/sheath/lead combination out of the femoral vein
467
Fig. 19.39 Dotter/sheath/lead combination removed
from the femoral vein
(Fig. 19.41) can be removed using similar snares
or devices with a “jaw mechanism” at its distal
tip.
Leads placed in the coronary sinus can
be removed by traction using locking sty-
lets but sheaths may damage the delicate vein
and should not be advanced beyond the first
centimeter or so.
If all else fails and it is felt necessary to remove
a lead, surgical removal by a limited thoracotomy
should be performed.
468
Fig. 19.40 The Dotter basket can be used to remove other
pacemaker lead fragments such as this tined lead tip
Excimer (Excited Dimer) Laser
Extraction of Retained Pacing Leads
This technique demands training and expertise
and requires expensive equipment. Laser safety
regulations must be adhered to when these
devices are in use. Personal protective equipment
must always be used by all personnel within the
room.
If traction on the leads and traction/counter-
traction with the locking stylet and outer sheath
in situ fail to free a tethered lead, Excimer Laser
extraction may be worthwhile. The Spectranetics
CVX-300® Excimer Laser generator is a Class
IV laser and produces a pulsed ultraviolet laser
beam at a wavelength of 308 nm for the removal
of intravascular tissue by photoablation. The gen-
erator weighs 295 kg, is 125 cm long, 89 cm high,
19 Explant Procedures
Fig. 19.41 Bioptome device can be used to removed sev-
ered/embolized temporary pacing wires
and 61 cm wide. It is a compact and mobile unit.
The active medium is XeCl. The system is user
friendly. It automatically recognizes the cath-
eter when connected, calibration is automated
and energy management is also automatic. The
catheter output fluence is 30–60 mJ/mm2 and
the maximum repetition rate is 40 pulses/s. The
penetration depth is low (50 m), making the
lasers suitable for efficient tissue ablation. The
device takes 5 min for the system to warm up.
The control panel is prominent and easy to use
(Fig. 19.42).
The Spectranetics Laser Sheath II (SLS® II)
kit (Fig. 19.43) and lead locking devices (LLD®,
LLD® E and LLD EZ™) (Fig. 19.44) are avail-
able from Spectranetics.
If a locking stylet has not already been inserted,
an LLD EZ™ should be inserted into the lead’s
Procedure 469

Fig. 19.42 The Spectranetics CVX-300® Excimer Laser generator and its console

Fig. 19.44 LLD EZ™ lead locking device (Spectranetics

Ltd.) has an improved locking mechanism that extends
Fig. 19.43 Spectranetics laser and sheath (SLS II) system over a length inside the lead to be removed
470 19 Explant Procedures

lumen (Figs. 19.45 and 19.46). The LLD EZ™ The SLS II is then prepared for use
should then be locked into the lead by removing (Fig. 19.48). The flexible distal segment has a
the proximal connector from the crimped section 15° bevel tip for advancement over acute angles
of the Mandrel (Fig. 19.47). (Fig. 19.49). The laser energy will be emitted

Fig. 19.45 LLD is inserted into the lead Fig. 19.46 Proximal connector being removed in order
to lock the LLD in place

EZ Tracking Radiopaque Marker

EZ Viewing

Unlocked

EZ Sizing
Locked

To lock, release
Proximal Connector
from Crimped Section
EZ Locking and of Mandrel
Unlocking

Proximal Connector

Crimped Section
Proximal of Mandrel
Mandrel Connector

Proximal Loop

EZ Loading

Distal Loop

Fig. 19.47 Anatomy of LLD

showing component parts and
mechanism of locking
Procedure
Fig. 19.48 Spectranetics
laser sheath (SLS II)
Fig. 19.49 Distal end of laser sheath showing its
beveled edge
from the outer ring seen in Fig. 19.50. The Teflon
coated outer sheath and SLS II are flushed with
heparinized saline (Fig. 19.51). The SLS II is
then inserted into the outer sheath (Fig. 19.52).
The laser device is then connected to the gen-
471
Fig. 19.50 Ring of laser fibers at distal end of device
erator and calibrated by holding it close to the
grid on the generator (Figs. 19.53 and 19.54).
Both are then advanced over the locking stylet
(Figs. 19.55–19.58). Two operators are neces-
sary. The second operator keeps tension on the
472 19 Explant Procedures

Fig. 19.51 Laser sheath

and outer sheath are flushed
with heparinized saline

Fig. 19.52 Outer sheath is

placed over laser sheath

Fig. 19.53 Laser and outer

sheaths combined
Procedure 473

Fig. 19.54 Laser is

calibrated by holding it
close to the grid (arrow) on
the generator

Fig. 19.55 Laser/outer

sheaths are passed over the
LLD

Fig. 19.56 Laser/outer

sheaths being advanced over
LLD
474 19 Explant Procedures

Fig. 19.57 Laser/outer sheath about to enter left subcla- Fig. 19.59 Advancement continues with two hands,
vian vein lasering when resistance is felt and seen on fluoroscopy

Outer Sheath
The SLS II
Radiopaque Band
15° Tapered Tip
Fig. 19.58 With a firm grip on the laser/outer sheath and 3
Cardiac Lead
slight rotational movement, the device is advanced over 4 Fibrosis
the LLD/lead and into the venous system 5

LLD EZ™/lead while the first operator advances
the SLS II/outer sheath combination into the
subclavian vein (Figs. 19.59–19.62). The tip of
the laser sheath is radio-opaque, which can be
seen on fluoroscopy (Figs. 19.63 and 19.64).
Each time resistance is felt during advance-
ment, the laser device can be activated and
the laser and outer sheath advanced forwards
6
Fig. 19.60 Illustration of SLS II system showing the
laser catheter inside the outer sheath being advanced over
the adherent pacing lead (cardiac lead) ablating the fibrosis
as it advances (Illustration courtesy of Spectranetics Co.,
CO, USA)
Procedure 475

Fig. 19.61 Firm tension is

placed on the LLD/lead as the
laser/outer sheath is railed
along it, lasering at points of
resistance

Fig. 19.62 Typical view of

the 4-handed technique
required for removing
adherent leads with laser
using fluoroscopy

Fig. 19.63 Tip of laser is radio-opaque (arrow). Twin

arrows show ICD lead to be removed
476 19 Explant Procedures

a b

c d

Fig. 19.64 Fluoroscopic images showing advancement of laser/outer sheaths and retraction of lead (a–d). Tip of laser
is radio-opaque (Open arrow). Twin arrows show ICD lead to be removed
Procedure 477

Fig. 19.65 Continued

advancement of laser/outer
sheath while maintaining
tension on LLD

Fig. 19.66 Further advancement of laser catheter Fig. 19.67 Laser sheath/outer sheath being advanced

(Fig. 19.65) while maintaining tension on the
LLD EZ™ (Figs. 19.66, and 19.67). Further
advancement of the SLS II and lasering should
lead to release of the lead back into the sheath
(Fig. 19.68). The sheath, SLS II, and LLD EZ™
can then be removed from the subclavian vein
in their entirety (Fig. 19.69). The extracted lead
and fibrous tissue are shown in (Figs. 19.70 and
19.71). Other lead(s) can then be addressed in
the same manner (Fig. 19.72).
An excellent animated video presentation of
this lead extraction technique is presented on the
Spectranetics website http://spectranetics.com.
Closing the Old Pocket
After removing the leads, it is important to
confirm by visualization and by fluoroscopy
that the leads have been removed intact and
478
Fig. 19.68 Upper left: Laser sheath advanced into the
SVC (green arrow); upper right: Further advancement
into the upper RA; lower left: Further advancement into
upper RA – purple arrow shows distal electrode of this
ICD lead; bottom right: Lead has now been retracted into
that no part of the lead has fractured and been
retained. If this has happened, then an alterna-
tive strategy to retrieve the retained parts must
be considered, especially if it is an infected sys-
tem. If all has been retrieved, then the opera-
tor should ensure that hemostasis has been
achieved and the pocket closed in layers. A fine
tube drain may be left in situ if there is much
pus in the pocket (Fig. 19.73), but otherwise
19 Explant Procedures
the sheath (red arrow). Second lead attached to the RA
(yellow arrow) is subsequently easily removed by trac-
tion. Blue arrow marks tip of laser sheath and black
arrowhead marks the tip of the outer sheath
it is reasonable to close the wound with inter-
rupted silk sutures rather than a continuous sub-
cuticular suture and glue. The wound should
be cleaned and dressed on a daily basis until
signs of inflammation have settled and healing
is advanced.
Eroded skin perforations may be repaired with
simple sutures to obtain closure and as good an
esthetic result as possible.
Procedure
Fig. 19.69 Lead removed from inside of laser sheath
Fig. 19.70 ICD lead after removal
Fig. 19.71 Extracted lead with adherent fibrous tissue
Insertion of New Pacing System
If appropriate, once the old system has been
removed, the second operator can proceed with
implantation of the new pacemaker and leads as
described in Chap. 7. The latter approach of a com-
bined explant/implant procedure is usually reserved
for cases with noninfected systems, for example,
479
Fig. 19.72 Adherent tined lead removed by the SLS II in
a patient with an infected system
Fig. 19.73 Vacuum drain can be placed in an infected
pocket after generator and leads have been removed
lead fractures, pre-erosions, etc. For infected pac-
ing systems, implantation of the new system is usu-
ally planned for 4–7 days after explantation of the
infected system and treatment with IV antibiotics. It
is usual to await evidence that the infection is under
control such as reduction of signs of inflammation,
absence of discharge, normalization of tempera-
ture, reduction of leucocytosis, ESR, and CRP.
If a non-infected lead has been extracted to
create space for a new lead, a guidewire may be
inserted at the time of extraction which can then
be used to gain access for lead replacement.
Lead Abandonment
Nonfunctioning or fractured leads may be left
in situ rather than be extracted by a prolonged
difficult and expensive procedure as long as the
pacing system is not infected. This may be suit-
able for frail, elderly patients, for those not fit
enough for a general anesthetic, and for those
480
Fig. 19.74 An attempt was made to remove the RA and
RV leads in a patient with an eroded/infected 15-year-old
pacing system. Neither could be removed by traction
alone and no other extraction technique was used. The RA
lead was cut-off and left in the pacemaker pocket (black
arrow) (right). An attempt was made to remove the RV
lead by manual traction alone. This failed and the dis-
rupted RV lead (blue arrow) and bare filaments (yellow
arrow) were allowed to recoil into the RV (left). A further
attempt was then made to remove the prolapsed RV lead
with a terminal illness who require a revision of
their nonfunctioning system in order to prevent a
recurrence of symptoms.
In this situation, after opening the pocket and
detaching the generator, the lead may be capped,
tied and secured with nonabsorbable sutures to
the fascia overlying pectoralis major. This is
necessary to prevent possible retraction of the
lead’s “free-end” back into the great veins, right
atrium, right ventricle, and even the pulmonary
artery (see Fig. 19.30). A new pacing system can
then be implanted from the opposite side or on
the same side if venous access can be gained.
Active-fixation leads that are being left in situ
rather than removed should not be cut since this
will preclude retraction of the helix of the lead if
extraction should ever be needed.
Surgical Removal
Infected endocardial pacing systems must be
removed unless it is deemed that the patient is
19 Explant Procedures
by traction on the severed proximal end using a Dotter
basket inserted via the right femoral vein. This proved
impossible and both leads had to be removed surgically.
Note that an active fixation lead has been screwed into the
interventricular septum and a new VVIR pacemaker
placed in the right pectoral region. The patient had previ-
ously undergone coronary artery bypass graft surgery and
the surgeon wanted to establish the patency and position
of the grafts within the chest prior to sternotomy, atri-
otomy, and surgical lead extraction
too frail or is in the final phase of a terminal ill-
ness that is deemed untreatable. If percutaneous
retrieval by traction, diathermy, or laser extrac-
tion techniques proves impossible, then surgi-
cal removal should be performed. Thoracotomy
and right atriotomy will be necessary to visu-
alize and excise the adherent leads from the
right ventricular apex, right atrial appendage, or
tricuspid valve apparatus. Adherence of leads
to the superior vena cava may require further
dissection.
Large vegetations on pacing leads usually neces-
sitate surgical rather than percutaneous removal.
Other situations that probably require sur-
gical removal of leads include the presence of
multiple redundant endocardial leads associated
with superior vena caval obstruction or cardiac
arrhythmias or where the lead structure has been
destroyed by prolonged and severe traction and
then allowed to recoil into the right-sided cham-
bers or pulmonary artery (Fig. 19.74) with the
intention of preventing arrhythmias and pulmo-
nary thromboembolism.
Complications During Lead Extraction 481

Infected epicardial pacing systems will require Table 19.3 Complications of pacemaker/lead extraction
a surgical procedure if the entire system is to be Death
removed. However, not infrequently, the decision Myocardial avulsion Hemopericardium, cardiac
is made to remove the pacemaker and as much of tamponade requiring
the lead as possible without resorting to thoraco- emergency pericardiocentesis
and thoracotomy
tomy to dissect the lead tip from the epicardial
SVC/great vessel tear As above
surface. Hemothorax
Pneumothorax
Pulmonary embolism
Complications During Lead Extraction Air embolism
Respiratory arrest
The most serious complication of lead extrac- Cardiac arrhythmias Supraventricular, ventricular
tion is tearing/perforation of the great veins SVC/great vein SVC obstruction, arm
or myocardium leading to severe and uncon- thrombosis swelling
trolled intrapleural or pericardial hemorrhage. Pocket hematoma
Pulmonary embolism of large vegetations, lead Sepsis Septicemia, pocket infection
material, or air can occur. Other complications
during lead extraction include arrhythmias –
such as atrial flutter/fibrillation and ventricular low extraction volume centers. Procedural failure
tachycardia/fibrillation, myocardial and tricus- was higher in leads implanted for >10 years and
pid valve trauma from the equipment used dur- when performed in low-volume centers. Major
ing lead removal and late thrombosis of the great adverse events (in 20 patients) were procedure-
veins from which the lead(s) has been extracted related in 1.4% including four deaths (0.28%).
(Table 19.3). Overall in-hospital mortality was 1.86%. The
An observational retrospective study of con- presence of endocarditis increased overall in-hos-
secutive laser lead extractions of 2,405 leads in pital mortality to 4.3%, endocarditis and diabetes
1,449 patients (the LExICon study) reported to 7.9%, and endocarditis and renal impairment to
successful complete lead removal 96.5% of the 12.4%. Pocket infection also increased in-hospital
time with a 97.7% clinical success rate. Failure mortality especially when associated with device-
to achieve clinical success was associated with related endocarditis, diabetes, renal insufficiency,
patients with a body mass index of <25 kg/m2 and or a low body mass index.
 Epicardial/Epimyocardial Pacing
Indications
Epicardial/epimyocardial pacing is generally
used only when the transvenous endocardial route
is contraindicated or likely to be very difficult.
Recurrent infections in endocardial systems may
be an indication for epicardial pacing. The indi-
cations are shown in Table 20.1.
Table 20.1 Indications for epicardial pacing
No access to venous atrium/ventricle
Occluded superior vena cava
Occluded subclavian veins
Tricuspid atresia/post Fontan procedure
Mechanical tricuspid valve prosthesisa
Risk of further infection
Recent infective endocarditis on tricuspid valve
IV drug abuse
Recurrently infected endocardial systems
Difficult/failed endocardial procedure
Failure to achieve a stable, functioning lead despite
use of active fixation leads, e.g., recurrent displace-
ment; as may occur with giant RA or grossly dilated
RV
Impossible to place LV leads in coronary sinus
a
LV pacing via the coronary sinus might be considered an
alternative when the need for pacemaker implantation
arises some time after tricuspid valve replacement has
taken place – but the risk of lead displacement in a pace-
maker-dependent patient has to be taken into account
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_20, © Springer-Verlag London 2012
20
Procedure
Epicardial pacing is usually performed by a
cardiac/cardiothoracic surgeon in a cardiac/car-
diothoracic operating theater under general anes-
thesia and strict aseptic conditions. A trained
cardiac technician and a range of pacemakers,
leads, and accessories must be readily available.
Agreement with the cardiologist over the pace-
maker prescription should be reached before the
procedure and full informed consent should be
obtained after an explanation of the risks and
benefits of the procedure. Antibiotic prophy-
laxis to cover gram-positive and gram-nega-
tive organisms should be given preoperatively.
Anticoagulants should be stopped for 3–5 days
and antiplatelet agents for 5–7 days before the
procedure unless clinically contraindicated.
The patient’s chest and abdomen should be
shaved. The patient should be prepared and
draped so that they are exposed from above the
umbilicus to the suprasternal notch, in case the
incision has to be extended into a median sterno-
tomy to control bleeding (Fig. 20.1).
Anterior Thoracotomy Approach
This approach is usually reserved for patients who
have previously undergone cardiac surgery. Access
483
484 20 Epicardial/Epimyocardial Pacing

Fig. 20.1 After cleaning the skin with antiseptic, the Fig. 20.3 Following the skin incision with a scalpel, dia-
patient is covered with a sterile drape and the operating thermy is used to incise the subcutaneous tissue
field covered with an Ioban™ drape prior to epicardial
pacing via a mini-thoracotomy

Fig. 20.2 Skin marked for submammary incision for left Fig. 20.4 Diathermy being used to incise the subcutane-
mini-thoracotomy ous tissue

is usually via the left 5th intercostal space when

the RV or anterolateral surface of the LV is
exposed. Prior to draping the patient, it is worth
marking the site of the proposed incision
(Fig. 20.2). The skin incision is made with a scal-
pel and the subcutaneous tissue with diathermy
(Figs. 20.3 – 20.5). A self-retaining retractor can
help during deeper dissection down to the inter-
costal space (Fig. 20.6). A heavier retractor is used
to spread the intercostal space (most commonly
the 5th) and expose the pericardium (Fig. 20.7).
The pericardial sac is then opened using cutting
diathermy (Figs. 20.8 and 20.9). A pericardial Fig. 20.5 Incision of subcutaneous tissue plane
Procedure 485

Fig. 20.6 Self-retaining retractor is used to explore deep Fig. 20.9 Opening the pericardium with cutting dia-
layer and intercostal space thermy to expose the heart

Fig. 20.7 Retractor being used to spread intercostal Fig. 20.10 Pericardial window exposes the epicardial
space (usually 5th intercostal space) and expose the surface of the left ventricle
pericardium

Fig. 20.8 Opening the pericardium to expose the heart Fig. 20.11 Mobilizing the pericardium from the heart
due to adhesions from previous cardiac surgery

window exposes the epicardial surface of the LV (Figs. 20.10 and 20.11). After freeing and expos-
and adhesions (commoner after previous cardiac ing the anterior wall of the LV (Figs. 20.12 and
surgery) can then be carefully dissected off it 20.13), the LV is retracted to expose the left atrial
486
Fig. 20.12 Exposed left ventricular anterior wall (1)
Fig. 20.13 Exposed left ventricular anterior wall (2)
Fig. 20.14 Retraction of left ventricular free wall to
expose the left atrial appendage (1)
appendage (Figs. 20.14 and 20.15). The atrial lead
is attached to the left atrium (LA) and the sensing,
pacing, and impedance measurements made by
connecting the lead to the analyzer with the long
connecting leads (Fig. 20.16). The LV lead is then
20 Epicardial/Epimyocardial Pacing
Fig. 20.15 Retraction of left ventricular free wall to
expose the left atrial appendage (2)
Fig. 20.16 Testing epicardial pacing lead inserted on the
left atrial appendage
Fig. 20.17 Implantation of left ventricular pacing lead
(using a MyoDex™ epicardial pacing lead with insertion
tool) with left atrial pacing lead in situ (1)
fixed to the epicardial surface of the LV using an
introducer tool such as the FasTac® introducer
(Figs. 20.17–20.19). Figures 20.20 and 20.21 show
the MyoDex™ steroid-eluting, bipolar, screw-in
lead mounted onto the FasTac® introducer tool.
Procedure
Fig. 20.18 Implantation of left ventricular pacing lead
(using a MyoDex™ epicardial pacing lead with insertion
tool) with left atrial pacing lead in situ (2)
Fig. 20.20 Top left: MyoDex™ 1084T steroid-eluting,
bipolar, “screw-in”, sutureless myocardial pacing lead
with Titanium Nitride electrode loaded onto the FasTac™
Introducer (EnPath Medical). The plastic Tunneler, bidi-
rectional Tunneler Tip and a suture sleeve are also shown.
Figures 20.22 and 20.23 show the LV and LA
leads in situ. A new device, the FasTac® Flex, has
a deflectable tip which is ideal for placing a suture-
less, screw-in lead onto the heart’s epicardial sur-
487
Fig. 20.19 Implantation of left ventricular pacing lead
(using a MyoDex™ epicardial pacing lead with insertion
tool) with left atrial pacing lead in situ (3)
Bottom left: MyoDex™ lead loaded onto the FasTac™
Introducer. The release button is shown. Top and bottom
right: MyoDex™ helical-screw tip shown mounted on the
distal tip of the FasTac™ Introducer
face using a mini-thoracotomy and thoracoscopic
approach (Fig. 20.24). It is used in conjunction
with the MyoPore® line of epicardial leads from
Greatbatch Medical.
488 20 Epicardial/Epimyocardial Pacing

Fig. 20.21 Top: FasTac™

Introducer’s simple locking/
unlocking mechanism in its
unlocked position. Center
and bottom: Close-up of the
“screw-in” electrode tip
Procedure 489

Fig. 20.22 Left ventricular and left atrial pacing leads Fig. 20.23 Left ventricular and left atrial pacing leads in
in situ (1) situ (2)

Fig. 20.24 FasTac® Flex tool

works in conjunction with the
Greatbatch MyoPore® line of
sutureless leads to provide
remote distal deflection
capabilities, remote lead
rotation for insertion of the
helix into the myocardium,
remote lead release and the
possibility of regrasping the
lead button

After fixing the lead(s), the latter are tunneled

subcutaneously to the pulse generator, which
may be placed in the left upper quadrant of the
abdomen behind the rectus sheath or in the left
pectoral region, subcutaneously or subpectorally.
It is possible to use the right side and atrial and
ventricular leads can be placed and tunneled to
the generator. Figures 20.25 and 20.26 show a
midline subxiphoid incision being made in order
to expose the rectus sheath by careful dissection.
The rectus muscle is mobilized and a pocket is Fig. 20.25 Midline, subxiphoid skin incision to expose
created behind the muscle in which to place the rectus sheath (1)
490 20 Epicardial/Epimyocardial Pacing

Fig. 20.26 Midline, subxiphoid skin incision to expose Fig. 20.29 Pocket created behind left rectus muscle
rectus sheath (2) sheath to house the permanent pacemaker

Fig. 20.27 Incision and exposure of rectus muscle Fig. 20.30 Preparation for tunneling of epicardial pacing
sheath leads from left mini-thoracotomy wound to abdominal pocket

Fig. 20.28 Mobilization of rectus muscle to create an Fig. 20.31 Creation of the track
abdominal pocket behind the muscle sheath

pacemaker (Figs. 20.27–20.29). A track is then the pacemaker pocket (Figs. 20.30 and 20.31).
created in which to tunnel the lead(s) from the The tunneling tool provided may be used or a
intercostal space to the subxiphoid wound toward track may be created by blunt dissection using a
Procedure
Fig. 20.32 A connector pin is protected with a silicone
cap, grasped by forceps and pulled into the pocket
Fig. 20.33 After tunneling, the epicardial pacing lead is
passed through to the abdominal pocket behind the rectus
sheath (arrow)
pair of forceps. The connector end of the lead is
connected to the tunneler and the tunneler passed
to the pocket. Alternatively, the connector pin of
the lead should be protected by a silicone cap if
being gripped by forceps and pulled into the
pacemaker pocket (Figs. 20.32–20.34). Once the
lead(s) measurements have been shown to be sat-
isfactory, the leads are then attached to the pace-
maker when it is important to ensure that the tip
of the connector pins pass the screws in the header
unit (Figs. 20.35–20.37). Once the leads are
firmly attached into the pacemaker, the leads are
wound behind the generator and both are placed
into the pocket behind the rectus muscle
(Figs. 20.38 and 20.39). If the pleural cavity has
491
Fig. 20.34 Both atrial and ventricular leads have been
tunneled into the abdominal pocket and are ready to be
connected to the generator
been entered, an intercostal drain must be
inserted. The wounds are then closed in layers
using nonabsorbable sutures. Subcuticular sutures
to the skin edges will produce a good cosmetic
result and glue to the incision is preferable to
external dressings. Local anesthetic may be
infiltrated to improve pain relief further.
Subxiphoid Approach
This approach is preferred for those patients who
have not undergone previous cardiac surgery.
A 10 cm longitudinal incision is made from
1 cm above the xiphoid toward the umbilicus.
Diathermy is used to dissect down to the xiphis-
ternum, controlling the vein that runs across the
sternum at the level of the sterno-xiphisternal
junction. The incision is deepened to the rectus
muscle and a pocket made by blunt dissection
behind the rectus and anterior to the rectus
sheath – as indicated above. The xiphisternum
is divided with scissors after widening the inci-
sion with a self-retaining retractor. A finger is
used to develop the plane between the sternum
and the pericardium while staying close to the
underside of the xiphisternum. The RV pulsa-
tion should be palpable. The pericardium is
then opened with McIndoe scissors and the
opening extended in order to visualize the RA
and RV. Stay sutures should be fixed to help the
exposure.
492 20 Epicardial/Epimyocardial Pacing

Fig. 20.35 The epicardial

leads are connected to the
pacemaker

Fig. 20.36 The connector

pin on the ventricular lead is
inserted into the pacemaker’s
header unit. It is important to
see that the distal end of the
pin passes the most distal
screw (arrow)

Fig. 20.37 Both left atrial and left ventricular epicardial Fig. 20.38 The pacemaker and leads are placed into the
leads are connected to this Altrua™ 50 DDDR pacemaker pocket behind the rectus muscle
Procedure
If an atrial lead is required, this should be
placed first by retracting the RV gently to the
left. The easiest lead to insert comes with a long
handled applicator and is inserted with a simple
punch and twist action. The RV lead is placed in
similar fashion taking great care to avoid the pos-
terior descending artery and the great cardiac vein.
Each lead is then tested in turn for electrogram,
pacing threshold, and lead impedance before the
Fig. 20.39 The pacemaker and leads should be away from
the wound edges and then the pocket closed in layers
Fig. 20.40 Chest X-ray showing abdominally placed DDDR permanent pacemaker with epicardial pacing leads
attached to the RA and RV outflow tract
493
connector pins are inserted into the pacemaker.
Recommended electrical measurements (at pulse
duration of 0.5 ms) at implantation might be atrial
and ventricular sensed amplitudes 2.0 and 4.0 mV,
respectively, and acute stimulation/pacing thresh-
olds of 1.5 V in both atrium and ventricle.
Any spare lead is carefully placed behind the
pacemaker and the unit then placed behind the
rectus muscle and the wound closed in layers
after ensuring hemostasis. Again the skin may be
closed with interrupted sutures or preferably with
a subcuticular absorbable suture and the edges
sealed with Dermabond glue. The wound should
be dry before closing and drains are to be avoided
if at all possible. Local anesthetic may be
infiltrated for further pain relief.
A chest X-ray should be performed after the pro-
cedure and pneumothorax excluded. Figure 20.40
shows epicardial RA and RV outflow tract pacing
and an abdominally placed pacemaker. Figure 20.41
shows a single-chamber VVIR epicardial system,
and Fig. 20.42 shows a DDDR epicardial system
with leads attached to the LA and LV.
494
Lead Fixation
The epicardial lead may be attached to the epicar-
dium with sutures and does not penetrate the myo-
cardium (Fig. 20.43). Alternatively, leads may be
screwed into the epimyocardium.
Fig. 20.41 Chest X-ray showing abdominally placed
VVIR permanent pacemaker with an epicardial pacing
lead attached to the LV
Fig. 20.42 Chest X-ray
showing abdominally placed
DDDR permanent pacemaker
with epicardial pacing leads
attached to the left atrium and
left ventricle
20 Epicardial/Epimyocardial Pacing
Epicardial lead placement involves careful
placement of the electrode onto the surface of the
epicardium and fixation by direct suturing. The
attachment site should be an avascular area free
of infarcts, fat, or fibrosis. If bipolar pacing is
indicated, a separate electrode may be placed
adjacent to the first with a minimum of 1.0 cm
space between them. Before fixation, the epicar-
dial lead can be used as a mapping probe by rest-
ing the electrode against the epicardium and
recording stimulation and sensing signal ampli-
tudes (Fig. 20.44). Once an optimal electrode
position is confirmed for atrium/ventricle, stable
fixation through proper suturing of the electrode
is critical for maintaining good chronic lead per-
formance. Suture holes and grooves are provided
as guides and allow for a variety of suturing
options. The recommended technique is illustrated
in Fig. 20.44. When using the left thoracotomy
approach, a moderate amount of the lead should
be left on both sides of the thoracic exit point to
prevent stretching of the lead body. Leaving the
lead body deep in the abdominal musculature, the
lead should exit the thorax through the subxi-
phoid space – preferably at an angle rather than
parallel to the midsagittal plane to reduce acute
bending of the lead at the subcostal border and
Lead Fixation
Fig. 20.43 Capsure® EPI 4965 steroid eluting, unipolar,
epicardial lead has a silicone suture pad for suture attach-
ment to the epicardium. Top left: The lead, a plastic tun-
neler and a lead end cap are presented in a transparent
sterile package. Bottom left: The 110 cm long lead has an
IS-1 unipolar connector pin, a platinum alloy electrode
and silicone rubber insulation and a tip electrode. Top
subsequent coil fracture (Fig. 20.44). Platinized,
porous, button-shaped, steroid-eluting lead tips
such as the CapSure Epi models 4965/4968 (Uni/
Bi-polar) (Medtronic Inc) give excellent long-
term pacing/sensing thresholds (Fig. 20.43).
The epimyocardial leads penetrate the myo-
cardium by means of a helical or barb design
(Fig. 20.45). These leads permit adequate elec-
trode–tissue interface when there is significant
epicardial fat or fibrosis. The St. Jude Medical
MyoDex™ silicone-insulated, sutureless, steroid-
eluting, bipolar lead (Model 1084T) on the
FasTac® Introducer tool (Figs. 20.20 and 20.21)
and Greatbatch Myopore® lead on the FasTac®
Flex tool are currently available. The MyoDex™
lead has a titanium nitride (TiN) fractal coating
on the helix and ring electrodes which is designed
to provide precise sensing and improved contact
with the myocardium. A full 3.5 mm helix
penetration is designed for stable fixation.
Titanium with TiN coating on the anode electrode
(surface area 62 mm) and platinum-iridium with
TiN coating on the cathode electrode (surface
495
right: Close-up view of the platinized, porous, steroid-
eluting electrode tip with a surface area of 14 mm2. The
suture holes and grooves on the silicone suture pad allow
attachment of the electrode tip to the epicardium. Bottom
right: Close-up of upper surface of electrode tip showing
the suture holes and grooves
area 10 mm) create a textured surface, designed
to facilitate tissue ingrowth and better contact.
A low-profile electrode head construction is
designed to provide excellent retention and a
multifilar inner conductor is designed to offer
safety and durability. The unique design of the
FasTac™ allows a quick, one-handed motion for
releasing the lead once it is attached to the heart.
The distal end provides simple, fast regrasping,
reloading and repositioning of the lead if necessary.
The lead is available in 35 and 54 cm length. The
Myopore® sutureless bipolar lead has a platinized
10 mm2 electrode and is available in 25, 35, and
54 cm lengths whereas the unipolar lead is avail-
able in 35 and 54 cm lengths. Medtronic market a
malleable Epicardial Lead Implant Tool (Model
no.10626) which is made of stainless steel but
which can be shaped to maneuver and position a
lead optimally on the posterior surface of the RV
or LV. It has distal gripping tongs for the epicar-
dial lead and proximally a thumbwheel and actu-
ator button allow active fixation and release of
the lead on the myocardium. The tool allows for
496
Xiphoid
Costal and subcostal
areas to avoid
during tunneling
Approximate lower
costal margin
Fig. 20.44 Top left: Sub-xiphoid approach, showing
exposure of the epicardial surface and (top right) using
the lead as a mapping probe; center right: Suturing the
Capsure EPI 4965 electrode to the epicardium using the
perpendicular alignment to the heart from differ-
ent angles of approach. Perpendicular access to
the heart is therefore no longer needed to place
the Medtronic 5071 lead. It allows the lead to be
placed through an anterolateral mini-thoraco-
tomy or thoracoscopic approach.
Table 20.2. shows the currently available epi-
cardial pacemaker leads. Figure 20.46 shows a
20 Epicardial/Epimyocardial Pacing
Heart outline
Suture
Gently grasp the lead directly
over the suture groove
Base of the heart
suture holes and the proximal grooves; Center left: A left
thoracotomy approach; bottom: Tunneling the lead (Image
reproduced with permission of Medtronic, Inc.)
Kappa® DDDR device with a bipolar epicardial
ventricular lead and a unipolar screw-in atrial
lead.
Any lead being reserved for pacemaker con-
nection at a future date or being abandoned
should have its connector pin/sealing ring cov-
ered with a lead end cap which should be sutured
in place with a nonabsorbable suture.
Video-Assisted Thoracoscopic and Robotic Epicardial Lead Placement
Fig. 20.45 Unipolar
epicardial pacing leads. Top:
Screw-on type. Bottom:
Fish-hook type
Video-Assisted Thoracoscopic and
Robotic Epicardial Lead Placement
Recent small studies have achieved ventricular
resynchronization in a minimally invasive fash-
ion using the da Vinci® SiHD™ robotically assisted
left ventricular epicardial approach (Intuitive
Surgical Inc, Sunnyvale, CA) via four “access
ports” (Fig. 20.47). It is claimed that the best
hemodynamic position can be obtained fairly
easily with this approach, including posterior
lead placement, and this is ideal for patients who
have previously undergone cardiac surgery and
for those with failed percutaneously placed
497
(transvenous) LV leads. The device is composed
of the surgeon-control console and the surgical
arm unit that positions and directs the micro-
instruments (see Figs. 16.54 and 20.48). Computer
interfacing allows for scaled motion, and the
optics viewed in the surgeon console for enhanced,
high-definition, magnified (up to ×10), real 3-D
vision. All operations are performed under GA
with selective right lung ventilation. With the
patient in the posterolateral thoracotomy position
and a TOE in situ, a camera port is placed in the
7th intercostal space in the posterior axillary line.
The right and left arms are positioned in the 5th
and 9th intercostal space, respectively. A pacing
498 20 Epicardial/Epimyocardial Pacing

Table 20.2 Pacemaker electrode Polarity Length/Insulation (cm) Fixation Steroid-eluting

Permanent
Boston Scientific
pacemaker
epicardial leads 4316 Uni 54Si Screw-in yes
4046 Bi 35Si Screw-in yes
4047 Bi 54Si Screw-in yes
Medtronic
5071-25/35/53 Uni 25/35/53 Si Turn Screw-In No
4951M-20/35/53 Uni 20/35/53 PU Hook-In No
4965-25/35/50 Uni 25/35/50 Si Suture On yes
4968-25/35/60 Bi 25/35/60 Si Suture On yes
St. Jude Medical
MyoDex 1084T Bi 35/54 Si Screw-in yes
Greatbatch Medical
MyoPore® Uni 35/54 Si Screw-in No
511111/511112
MyoPore® Bi 25/35/54 Si Screw-in No
511210/511211/511212

Right arm port Working

Robot port
Left arm port Camera
port
Fig. 20.46 Kappa® DDDR permanent pacemaker with
unipolar screw-on type epicardial lead to be attached to
the right atrium and bipolar epicardial lead for “suture-
Fig. 20.47 Port access points for performing epicardial
attachment” to the right or left ventricle (Image repro-
pacemaker lead placement using the Da Vinci® Surgical
duced with permission of Medtronic, Inc.)
System
Video-Assisted Thoracoscopic and Robotic Epicardial Lead Placement
Fig. 20.48 Left: da Vinci® Surgical System and robotic
arms. Upper right: Surgeon with head inside the console.
Middle right: Hands on the Endowrist instruments which
allow the operator to make fine movements with the
robotic arms and the attached instruments. The camera
Fig. 20.49 The da Vinci® Robotic system being used to
suture an LV epicardial lead in place (Photo courtesy of
Dr. J DeRose Jr. and Intuitive Surgical®, Inc., Sunnyvale,
CA, USA, 2009)
499
unit or endoscope arm provides enhanced, high-resolu-
tion, real-time, magnified three-dimensional images.
Lower right: Close-up of instrument (Photo courtesy of
Dr. J DeRose Jr. and Intuitive Surgical® Inc., Sunnyvale,
CA, USA, 2009)
lead is then introduced into the chest through the
working port. A good position is often midway
between the base and apex of the LV, between the
first and second obtuse marginal (OM) arteries
(see Fig. 16.55). The robotic arms are used to fix
the lead to the LV surface either by screw-in active
fixation or by a suture technique Fig. 20.49. This
lead is capped and delivered into the chest. A sec-
ond lead is then delivered through the working
port and again fixed to the LV surface near the sec-
ond OM artery. If the lead measurements are satis-
factory, the pericardium is closed over the leads to
aid permanent fixation. The two leads are tunneled
to the axilla and the lead with the best parameters
used as the LV lead. If right-side pacing leads or an
500
ICD lead are required, these can then be done and
attached to the device in the axillary pocket.
Temporary Epicardial Pacing
At the time of cardiac surgery, temporary atrial
and ventricular epicardial pacing wires may be
attached when indicated. They are passed
superficially through the epicardial surface and
20 Epicardial/Epimyocardial Pacing
sutured in place with fine prolene sutures. The
distal ends are connected to a temporary pacing
box (see Fig. 13.2). The thresholds are usually
higher than endocardial leads and the duration of
capture varies. The majority will become unreli-
able after 7–10 days. When they are no longer
required, they are extracted by traction of the
exposed wires. The wires can be cut while under
traction which then recoil. Usually, no harm
results and the remnants can be left in situ.
 Troubleshooting After Device
Implantation
Troubleshooting after pacemaker implantation
is the task of both the cardiac physiologist and
the cardiologist. It is a process which begins at
the time of implantation and should be read-
dressed not only if the patient re-presents with
ongoing or new symptoms post-implant, but
also at every routine follow-up appointment.
Adherence to these rules not only promotes safe
and effective pacemaker function, but also serves
to increase device longevity and reduce the
adverse effects of unnecessary or inappropriate
cardiac pacing.
Where once understanding and diagnosing
faults in a minimally programmable, single-
chamber system was relatively simple, with the
advent of two- and three-lead systems with mul-
tiple, advanced and infinitely programmable fea-
tures, troubleshooting has become potentially
much more complex. In addition, pacemakers
with defibrillation and anti-tachycardia pacing
facilities pose further challenges to the cardiolo-
gist. Thankfully, however, alongside advances in
pacemaker functionality and programmability
has come an increase in “user-friendliness” of the
programming software. This, in its different
forms from different manufacturers, allows more
rapid and comprehensive understanding of the
interaction between pacemaker and intrinsic car-
diac rhythm. A sound understanding of basic
pacemaker timing cycles is a necessity when
undertaking troubleshooting.
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_21, © Springer-Verlag London 2012
21
Patient and Device Familiarization
Before troubleshooting any system one must
endeavor to familiarize oneself with the patient’s
underlying cardiac diagnoses, principally the rea-
son for device implantation, the implantation
details, pacemaker details (e.g., model/manufac-
turer, alerts/recalls), and the current settings,
especially any special programming features par-
ticular to the model or patient (Table 21.1) as
well as information on the lead (e.g., model/man-
ufacturer, polarity and fixation mechanism, pin
type and insulation material). A 12-lead ECG and
rhythm strip are essential. This information is
invaluable in understanding the way the device is
Table 21.1 Features of implanted device that should be
known prior to troubleshooting
Lead configuration Bipolar or unipolar
Mode of function Especially in dual-chamber
devices
Sensor Turned ON or OFF
Intervals Base rate, upper rate limit,
AV delay, PVARP,
sensor-based rates/
sensitivity
Back-up rate/mode/lead configuration
Are marker channels available for interrogation?
Mode switching ON or OFF
Automatic capture ON or OFF or not available
control
ERI/EOL parameters
501
502
Fig. 21.1 “Automatic AV hysteresis” available in Sorin’s ESPRIT™ DR pacemaker automatically extends the AVD to
maximize intrinsic conduction and minimize ventricular pacing (Courtesy of Sorin Group)
interacting with the intrinsic cardiac rhythm. An
example would be to compare the patient with
sinus node disease to a patient with complete
heart block, both of whom might receive a dual-
chamber pacemaker. One might assume that the
patient with sinus node disease would not pace
the ventricle often, if at all, whereas the patient
with complete heart block will pace the ventricle
most of the time. Where both patients might have
been rendered asymptomatic and thankful for
their device implantation, the cardiologist is
doing the patient with sinus node disease a
disservice if an attempt is not made to reduce the
amount of time they spend ventricularly paced.
This might be achieved by simply automatically
extending the AV delay of the device to encour-
age intrinsic AV conduction (automatic AV hys-
teresis – Dplus™) as in the ESPRIT™ DR and
SYMPHONY® DR 2550 (Sorin Group)
(Fig. 21.1) or by switching to the AAI SafeR™
mode setting if available, for example, REPLY™
DR (Sorin Group) (Fig. 21.2). The latter program
21 Troubleshooting After Device Implantation
provides AAI pacing while continuously moni-
toring AV conduction and ensures DDD pacing
when needed for all types of AV block. SafeR™
is more effective than automatic AV hysteresis
for minimizing ventricular pacing.
When familiarizing oneself with the device, it
is necessary to realize that not only are there a
wide variety of companies with different inter-
faces between device and cardiologist (Fig. 21.3),
but that there are also a large number of devices
available from each manufacturer. As generator
longevity ranges 5–10 years, there will also be a
historical variety of pacemakers and program-
mers, each with differing capabilities and limita-
tions. This makes understanding the finer points
of each and every device a difficult task for a
single individual. Therefore, when attempting to
troubleshoot problems fails to produce appropri-
ate results, one must always consider involving
the specialized expertise of the manufacturer’s
technical services department before re-operation
and replacement is considered. An example of
Patient and Device Familiarization 503

Fig. 21.2 Safe R™ pacing algorithm in the REPLY™ DR device minimizes ventricular pacing by allowing AAI pac-
ing until certain criteria are met when the device switches to DDD mode (Courtesy of Sorin Group)

Fig. 21.3 Manufacturer-specific pacemaker programmers from (left to right) Guidant/Boston Scientific, Medtronic
and Sorin Group
504
Fig. 21.4 Interrogation of Reply™ DR pacemaker. First screen on the Orchestra™ programmer displays all essential
basic programmed data (Courtesy of Sorin Group)
the way devices display information is shown in
Fig. 21.4.
It goes without saying that knowledge of any
manufacturer alerts or recalls on pacemaker sys-
tems might raise suspicion of a particular malfunc-
tion which should be excluded in a certain device.
After collecting and analyzing all the data, the
simplest explanation that covers all the facts is prob-
ably the true explanation for the “abnormality” –
whether the “abnormality” is real or apparent.
21 Troubleshooting After Device Implantation
Pacemaker Diagnostics
Pacemaker manufacturers include aids within
their pacemakers to help the cardiologist/techni-
cian evaluate the pacemaker’s function. It may be
invaluable to use the real-time diagnostic aids
during troubleshooting. These aids include mea-
sured data, event markers, and endocardial elec-
trograms. For establishing a diagnosis, initially at
least, one should aim to establish the atrial and
Pacemaker Diagnostics
Fig. 21.5 Parameters settings and programming screen for the Reply™ DR pacemaker – taken from the Orchestra™
programmer (Courtesy of Sorin Group)
ventricular rhythms, whether there is proper A
and V sensing and capture, what other informa-
tion would be useful, and what further tests might
be helpful.
Measured data may include measurements of
battery voltage, current drain and internal imped-
ance, pulse voltage, charge, current and stimula-
tion impedance (Fig. 21.4). Regular measurements
of lead impedance and pacing thresholds, for
example, allow for early detection of lead insula-
tion break, fracture, displacement, or other prob-
505
lems. Trends plotted by device diagnostics are
particularly useful to track sudden or unexpected
changes in these parameters. For each case, one
should know the programmed pacing mode, the
upper and lower rate limits, the AVD and the
PVARP settings and data on battery longevity,
ERT and predicted EOL are usually available
(Figs. 21.5 and 21.6) (Table 21.2).
Event Markers represent timing information
telemetred from the device to the programmer,
displayed on a screen or printed and reflect what
506 21 Troubleshooting After Device Implantation

Fig. 21.6 Interrogation of Vitatron Clarity DDDR device reveals details of the current program parameters, the rate
response details, and some diagnostic data, for example, lead impedance

Table 21.2 Basic parameters checked during device the pacemaker is doing. Markers of sensed and
interrogation paced events and the duration of the refractory
Battery impedance period are useful when taken in conjunction with
Magnet rate the ECG, especially if pacing spikes are small in
Longevity estimation bipolar systems (Fig. 21.7).
Device modes The intracardiac electrogram (EGM) is useful in
Lead threshold values identifying false signals that are being sensed and
Intrinsic activity and lead sensing values in confirming the nature of signals that are difficult
Lead impedance to see on the surface ECG. An analysis of stored
Upper and lower rate limits EGMs alerts the cardiologist to oversensing and
AVD setting undersensing problems, which may manifest as
PVARP setting abnormal device function, inappropriate arrhythmia
Rate histograms and high rate episodes
detection, or inappropriate therapy. Simultaneous
Pacemaker Diagnostics 507

Fig. 21.7 (Top–bottom) Lead II ECG, intracardiac atrial electrogram, ventricular electrogram, and annotated event
markers (AS atrial sense, VP ventricular pace) suggests initially Mobitz Type I followed by 2:1 AV block in this case

Fig. 21.8 Intracardiac atrial and ventricular electrograms (second and third rows) confirm Wenckebach phenomenon

dual-chamber EGMs and event markers help the
clinician diagnose the electrophysiological mecha-
nism of atrial and ventricular tachyarrhythmias
and help to distinguish between true and pseudo-
malfunction of the device (Fig. 21.8).
Other features which provide information
about the pacing system over time include event
counters, which may give an overview of the
pacemaker’s general behavior with respect to
time, its behavior with respect to specific
events, and its activation of various algorithms.
Manufacturers have their own names for event
counters but generally will provide total sys-
tem performance counters which, for example,
may be useful for seeing the chronotropic
response in a rate responsive system, subsys-
tem performance counters such as the number
of automatic mode switches or the peak atrial
508 21 Troubleshooting After Device Implantation

Fig. 21.9 Automatic Interpretation for Diagnosis Assistance (AIDA) showing 7 day Holter ECG recording illustrating
frequency of rate response from this Reply™ DR system (Courtesy of Sorin Group)

rates that triggered the switch and time-based Patient Symptoms

system performance counters or “event record”
(Figs. 21.9–21.14).
Troubleshooting
The troubleshooting process should begin only
after the device type and implant indications are
reviewed. Problems will generally arise in two
forms – patient symptoms such as dizziness/pre-
syncope, syncope, fatigue, shortness of breath or
palpitations, or abnormalities picked up at device
interrogation such as loss of capture, loss of out-
put, oversensing, undersensing, impedance
changes, or pseudomalfunction.
Dizziness/Presyncope and Syncope
This is probably the most common symptom
manifest prior to pacemaker implant and one
would expect that the majority of these symptoms
might abate following a successful device implant.
In the patient with persisting or returning symp-
toms, the technician must be mindful of a number
of potential problems with basic system malfunc-
tion. Appropriate chamber pacing must be
confirmed looking specifically for loss of capture,
rising thresholds, and evidence of inappropriate
pacing inhibition by oversensing. Sometimes
provocative movements such as arm movements
or rolling the patient might uncover subtle
Troubleshooting 509

Date of Last Reset 26-JAN-2007

100%
Atrial

Paced
Sensed

0%
30 50 70 90 110 130 150 170 190
Rates (min−1)

100%
Ventricular

Paced
Sensed
0%
30 50 70 90 110 130 150 170 190
Rates (min−1)

Fig. 21.10 Rate histograms from dual-chamber pace-
maker in a young active patient with advanced complete
heart block. The patient complained of a lack of energy
and exercise intolerance. Observe the top graph showing
the amount of atrial pacing and sensing. Intrinsic sinus
rate is rarely above 80 bpm and paced atrial rates never
above 60 bpm (lower rate). The lower graph demonstrates
that the ventricle is paced at 60 bpm over 80% of the time.
This patient had not had rate response programmed on due
to the assumption of preserved chronotropic competence.
Rate responsive programming quickly fixed this issue

Ventricular Long Term Histogram

Paced

% of Beats

50

40

30

20

10

< 40 60 80 100 120 140 160 180 >

Rate (bpm)

Fig. 21.11 Adequate rate response demonstrated by this long-term histogram retrieved from the device interrogation
510 21 Troubleshooting After Device Implantation

Fig. 21.12 (Right) The Altrua™ pacemaker (Boston
Scientific) can show events expressed as histograms. A-V
histograms (left) show the type of ventricular events
(paced or sensed) that follow atrial activity. Pace/sense
histograms show atrial paced and sensed events and
ventricular paced and sensed events. Counters and
Arrhythmia Logbook can also be selected (©2010 Boston
Scientific Corporation/affiliates. All rights reserved. Used
with permission of Boston Scientific Corporation)

Fig. 21.13 Sophisticated pacemakers such as the Symphony D 2450 (Sorin Group) can show program data and diag-
nostic data. The latter may be expressed numerically, graphically, or in histogram format
Troubleshooting
Fig. 21.14 A “diagnosis” on pacemaker function, A/V
arrhythmia, and AV conduction may be helpful when
troubleshooting
intermittent problems, particularly if the patient
has previously had a good symptom response
from the pacemaker implant for many years.
Patients in whom a device implant has not
affected their symptoms should have their under-
lying diagnosis reviewed. While the pacemaker
should be appropriately treating bradycardia,
other conditions such as tachyarrhythmias and/or
vasodepressor hypotension are not affected. In
the patient with neurocardiogenic syncope, in
whom bradycardia and hypotension feature
equally, hypotension may be the predominant
cause for syncope and programming the “rate-
drop response” feature to increase cardiac output
during presyncope might alleviate some symp-
toms (see below).
511
Tachycardia may also present with syncope or
presyncope, even in the absence of symptoms of
palpitations. Rate histograms, high rate episode
markers, mode-switch episodes, and, where avail-
able, stored EGMs should be analyzed (see
above). Finally, in the chronotropically incompe-
tent patient, failure to increase cardiac output
through increasing heart rates may cause exer-
cise-induced presyncope and appropriate rate
response should be sought (see above). When all
of the above have been excluded, then noncardiac
causes of presyncope must be considered.
Fatigue and Shortness of Breath
Fatigue and dyspnea are very common symp-
toms in patients attending the pacemaker clinic
and the symptoms have a diverse range of etiol-
ogies. Once basic programming parameters have
been assessed, one must concentrate on specific
pacemaker entities which may be contributing.
Patients with a lack of chronotropic competence
(e.g., sinus node disease) will often feel exer-
tional fatigue and the pacing rate response
should be assessed. This is best done by exam-
ining the rate histograms and looking for a good
rate variation. Excessive amounts of time spent
pacing >90 bpm is suggestive of a too aggres-
sive response, whereas a flat heart rate histo-
gram suggests an inadequate rate response
(Fig. 21.10).
Tachycardias can also cause shortness of
breath, with the commonest being atrial
fibrillation. Assessing the atrial EGM for atrial
tachycardia and fibrillation (Fig. 21.15), atrial
high rate markers, mode-switch episodes, and the
ventricular-sensed histograms for unexplained
tachycardia helps in the evaluation of symptoms.
The development of systolic heart failure as a
result of continuous RV apical pacing is a phe-
nomenon which has gained recognition recently,
and patients in whom this is suspected should
have the appropriate imaging investigations.
512
Fig. 21.15 Atrial tachycardia. Marker channels show normal atrial (AS) and ventricular (VS) sensing
Attempts should be made to minimize the amount
of time the RV is paced, especially in patients
with intermittent AV block. Appropriate use of
programmed algorithms and AV delay should be
made to achieve this. In patients who are RV
paced for long periods, upgrade to a biventricular
device should be considered, – especially those
with symptomatic LV dysfunction.
Rarer causes of acute dyspnea in the pace-
maker patient are pericardial effusion, pneu-
mothorax, and hemothorax – these are generally
confined to the peri-implant period and usually
require intervention. Clues to diagnosing pneu-
mothorax are the use of subclavian puncture for
venous access and an unexplained rise in thoracic
impedance at the post-implant check. Pericardial
effusion and tamponade might be suggested by
the use of active fixation leads and multiple lead-
siting attempts at implant. Apart from physical
signs on examination, clues during system inter-
rogation include a rise in pacing threshold, loss
of capture (Figs. 21.16 and 21.17), marked
21 Troubleshooting After Device Implantation
change in lead impedance, and loss of the ST
elevation pattern on the EGM. Biphasic or
inverted EGM T waves are sometimes seen. A
chest X-ray and echocardiography should be used
to clarify the situation (see Fig. 12.10).
Management of shortness of breath and fatigue
in the biventricular pacemaker patient is a more
complex issue. Dyspnea is the primary reason
why these devices are used and therefore failure
to improve after pacing needs targeted assess-
ment. Common reasons for lack of improvement
are inadequate LV pacing due to failure of LV
capture, high intrinsic ventricular rates leading to
RV-triggered LV pacing or no ventricular pacing
at all, atrial tachyarrhythmias with high rate ven-
tricular sensed events and frequent ventricular
ectopics – not uncommon in this population.
Assessment of ventricular thresholds should eas-
ily evaluate LV-capture problems but more
detailed assessment of sensing histograms may
be necessary to ensure adequate amounts of
biventricular pacing. Interrogation of the device
Troubleshooting 513

Fig. 21.16 Loss of ventricular output. The marker channels indicate emission of a ventricular pacing output from the
generator (VP) but no pacing spike on the ECG lead II. The atrial and ventricular EGMs are shown

Fig. 21.17 Failure to capture on this V lead at 4.5 V out- the chest X-ray looked normal and the lead positions were
put at 1.0 ms pulse width was accompanied by a significant satisfactory and unchanged, transthoracic echocardiogra-
fall in lead impedance shortly after implantation. Although phy confirmed myocardial perforation of the V lead
514
Fig. 21.18 Screenshot from Biotronik programmer dur-
ing interrogation of a Lumax 540 HF-T CRT device shows
the percent of time spent Bi-V pacing as well as an indica-
will quickly provide an estimate of RV/LV pac-
ing and if detected details of any ventricular
arrhythmias (Figs. 21.18 and 21.19). This whole
process may be simplified by the use of automatic
capture management algorithms available in
some devices.
In those patients who do not have an obvious
cause for lack of response, more detailed echocar-
diography-guided A-V and V-V offset analyses
may be needed. Only when patients have under-
gone this extensive assessment are they deemed
true “nonresponders” (Fig. 21.20).
Palpitations, Chest Pain and Twitching
This third common symptom group lends itself
well to evaluation by interrogation of the
implanted pacemaker. Inappropriate pacing can
21 Troubleshooting After Device Implantation
tion of the periods when not Bi-V pacing (Courtesy of
Biotronik)
cause symptoms of palpitations and undersensing
must be sought. Most paced patients are not
aware of the times they are paced; however,
abnormal “pounding” or pain particularly when
witnessed during programmed pacing must raise
the suspicion of diaphragmatic stimulation from
RV lead perforation with tip migration into the
pericardial space or from too high an output.
Phrenic nerve stimulation from atrial or ventricu-
lar lead displacement can also cause extracardiac
stimulation/hiccoughs. Lead insulation breaks
might also initiate a pectoral muscle twitch and
should also be actively sought (see Fig. 12.49).
Inappropriately set rate drop response, rate
response, or hysteresis might also present with
palpitations due to sudden and unnecessary
increases in heart rate. Pacemakers are useful
Troubleshooting
Fig. 21.19 Print-out from the Contak Renewal CRT-P
device (Boston Scientific) showing data on battery status
and heart failure/bradycardia parameters (left and central
panels). The right panel shows the lead system data and the
Fig. 21.20 After CRT it is sometimes necessary to care-
fully evaluate the optimal A-V delay and the RV-LV delay
settings to maximize LV systolic function. (Left) Optimization
of AV delay after CRT by pulsed Doppler mitral inflow pat-
tern. At programmed AV delay of 180 ms (left panel) the
closure of mitral valve occurs before the onset of ECG QRS.
Optimizing AV delay at 120 ms (right panel), the diastolic
filling time is much longer and the duration of atrial filling is
515
heart failure/bradycardia event counters. This indicates vir-
tually 100% Bi-V pacing and one episode of VT (red circle).
In the “arrhythmia detail” section, the VT can be seen in
more detail using stored EGMs and annotations (bottom)
preserved. (Right) Calculation of interventricular mechani-
cal delay by standard Doppler method. The time from ECG
Q wave to onset of left ventricular outflow tract flow
(=211 ms) (left panel) is longer than the time occurring from
Q to onset of right ventricular outflow tract flow (=122 ms)
(right panel). The resulting inter-ventricular mechanical
delay (IVMD) is 89 ms, thus indicating a significant inter-
ventricular dyssynchrony (From Galderesi et al. [1])
516
Fig. 21.21 Diagnostic interface detailing the amount of AF and the intrinsic and paced rhythm response to arrhythmia.
Medtronic® Cardiac Compass user interface
monitoring tools for identifying new arrhythmias,
either ventricular or atrial in origin (Fig. 21.21).
Stored EGMs or “dot plots” during episodes
are very helpful in diagnosing the specific dys-
rhythmia but are luxuries generally confined to
defibrillation devices or “high-end” pacemakers
(Figs. 21.22– 21.24). However, most modern
pacemakers have high rate markers and episode
counters (Fig. 21.25). Before symptoms of palpi-
tations are discounted due to absence of incrimi-
nating data, sensing parameters and high rate
21 Troubleshooting After Device Implantation
detection zones must be adjusted to incorporate
the speed and amplitude of the clinical tachycar-
dia. A Holter monitor is often useful to identify
the problem, especially when one gets symptom
correlation with episodes on the Holter
recordings.
Pacemaker-mediated tachycardia (PMT)
arises in dual-chamber systems where retrograde
atrial activation (outside the PVARP) becomes a
sensed atrial event and initiates a new A-V delay
with resultant ventricular activation and further
Troubleshooting 517

Fig. 21.22 Intracardiac EGM showing atrial tachyar- lower rate limit ventricular pacing implying a lack of AV
rhythmia. The rapid atrial EGM with a cycle length of nodal conduction
200 ms likely represents an atrial flutter. Note the regular

Fig. 21.23 Stored EGM found during routine interroga- shows a 15 beat run of nonsustained VT. Markers interpret
tion of dual-chamber pacemaker. Note the atrial EGM (top) the tachycardia as frequent PVCs, although with a cycle
shows sinus rhythm while the ventricular EGM (bottom) length of approximately 300 ms, the likely diagnosis is VT

Fig. 21.24 Ventricular high

rate episode. An episode of
VHR shown in a “dot-plot”
with interrogation showing
the detection rate threshold
(180 bpm) and beat duration
threshold (5 beats)
518
Fig. 21.25 Arrhythmia
summary in dual-chamber
pacemaker. Observe the
wealth of information
recorded for each event. In
this set-up, EGMs were not
stored but this feature can be
easily programmed
Fig. 21.26 Telemetered ECG tracing with surface lead II
(top), intracardiac electrograms (atrial electrogram – cen-
ter and ventricular electrogram – lower) and marker chan-
nel (bottom) showing pacemaker-mediated tachycardia
(PMT). The intracardiac markers indicate that the retro-
grade P waves, labeled AS for atrial-sensed event, occur
retrograde atrial activation – so-called “endless-
loop tachycardia” (Figs. 21.26–21.28). It is com-
monly initiated by a PVC, but PMT can also be
started by failure to capture the atrium with a
paced beat followed by a ventricular paced beat.
When this occurs the atrium may be amenable to
depolarization by the impulse conducted retro-
21 Troubleshooting After Device Implantation
280 ms after the ventricular-paced beats, labeled VP
(Published with permission of Prof. Brian Olshansky
M.D., University of Iowa College of Medicine and
WebMD Professional) (Image reprinted with permission
from eMedicine.com, 2010. Available at: http://emedi-
cine.medscape.com/article/159645-overview)
gradely from the ventricle. Adjustments in the
PVARP should serve to combat this phenomenon.
Use should be made of rhythm monitoring
devices such as Holter monitoring devices or
loop recorders to try and identify the problem
(Fig. 21.29). Other causes of PMT include maxi-
mum tracking rate during atrial arrhythmias,
Troubleshooting
Fig. 21.27 Telemetered ECG tracing showing atrioven-
tricular (AV) – paced rhythm at 60 per min after termina-
tion of the pacemaker-mediated tachycardia (PMT). The
tracing, from top to bottom, shows lead II, atrial electro-
gram, ventricular electrogram, and marker channels. The
intracardiac markers indicate the rhythm is atrial paced
Fig. 21.28 This is a typical example of PMT with ven-
tricular pacing at maximum tracking rate (VP-MT) and
then termination of the tachycardia as the atrial sensing
(AS) is in the PVARP. This is due to PVARP extension,
which is a feature of this particular pacemaker. The solid
line indicates where PMT is detected and this is the point
at which PVARP extension occurs. As this electrogram
was detected, but not sensed to be acted upon, the ven-
519
(AP) and ventricular paced (VP) with AVD of 200–220 ms.
Note that the VP beats are ventricular pseudofusion beats
(Image reprinted with permission from eMedicine.com,
2010. Available at: http://emedicine.medscape.com/
article/159645-overview)
tricular tracking stopped and the tachycardia terminated.
In some cases, pacemakers have a program to lengthen the
PVARP after PMT detection to potentially stop the tachy-
cardia. Alternatively, prevention of one ventricular paced
beat can also stop the tachycardia. Some pacemakers use
this algorithm (Image reprinted with permission from
eMedicine.com, 2010. Available at: http://emedicine.
medscape.com/article/159645-overview)
520
Fig. 21.29 The 24 h ECG Holter monitoring confirms
that this patient’s palpitations were due to PMT initiated
by ectopic beats – single (top) or couplets (bottom). In the
sensor-driven tachycardia, myopotential track-
ing, and runaway pacemaker. Most modern
devices have PMT termination algorithms to
facilitate this automatically.
Other devices such as CRT and ICD should be
interrogated in the event of symptoms. Cardiac
arrhythmias may be revealed during interrogation
and the nature of the arrhythmia and the device’s
response should be evident (Fig. 21.30).
Pain or Prominence
Pain and prominence of devices is a common
complaint in the follow-up clinic. Excessive
weight loss, ICD implantation in the wrong plane,
inappropriately positioned devices, and multiple
procedures increase the likelihood of a prominent
or painful device. While the prominent device
may just appear unsightly to the patient, it does
21 Troubleshooting After Device Implantation
top ECG, loss of atrial capture followed by a ventricular
fusion beat with retrograde VA conduction may be an
alternative explanation
carry a risk of trauma and/or erosion (see Fig.
12.69). Submuscular reburial of the painful or
prominent device is the treatment of choice if con-
servative measures do not alleviate symptoms.
Pacemaker Syndrome
The pacemaker syndrome (see Chap. 12) has a
diverse clinical spectrum, but generally incorpo-
rates one or more of the above symptoms. It is
widely believed to occur as a result of a loss of
A-V synchrony and rapid changes in cardiac
output. Although less common than in former
years, when single-chamber pacing was the
norm, certain scenarios should heighten clinical
suspicion: single-chamber systems (VVI), inap-
propriate rate response and long AV delays.
Sensing and capture problems must always be
sought.
Troubleshooting
Fig. 21.30 Interrogation of this Paradym™ CRT-D
revealed slow VT which was terminated by anti-tachycardia
pacing (ATP). Brady-Tachy-Overlap (BTO) facility avail-
Abnormalities Detected During Device
Interrogation
Device interrogation usually follows a center or
manufacturer-specific protocol and should always
incorporate a number of basic parameters. The
parameters are shown in Table 21.2.
Further interrogation is guided by the out-
come. The commonest issues to be raised at inter-
rogation are loss of capture, loss of output,
oversensing, undersensing, impedance changes,
and pseudomalfunction.
Loss of Capture
Increase in the voltage threshold at which the
myocardium is captured is seen during the matu-
ration phase of most new leads. Loss of capture
describes the phenomenon where the pacing out-
put is insufficient to meet the lead threshold and is
recognized by the presence of pacing artifact but
no ECG complexes (P or QRS) (Figs. 21.31 and
521
able in this model 8750 ensures CRT at high pacing rate
while offering unmatched accuracy for rhythm discrimina-
tion from slow VTs to VF (Courtesy of Sorin Group)
21.32). Assuming only minimal rises in threshold,
this can usually be overcome by reprogramming
the device to an increased pacing output and/or
pulse duration but may in certain cases require fur-
ther investigation and reoperation. Loss of capture
can be caused by a number of conditions and these
are shown in Table 21.3. Lead displacement (hours
or days after implantation), exit block (weeks –
months after implantation), conductor fracture
(many months – years after implantation) (Fig. 21.33),
and impending battery failure may give rise to
both loss of capture and eventually loss of output
(see Fig. 12.73). In pacemaker-dependent patients,
loss of capture (whether intermittent or perma-
nent) can have serious consequences and the prob-
lem must be rectified promptly.
A simple guide to consider when loss of cap-
ture is apparent is shown in Table 21.4.
Loss of LV lead capture in a CRT device may
be evident on the 12-lead ECG (see Figs. 16.64
and 16.65).
522 21 Troubleshooting After Device Implantation

Fig. 21.31 Loss of capture. VVI pacing in an elderly den increase in pacing spike amplitude in the last two
patient with complete heart block. Loss of capture after beats as the technician returns pacing outputs to normal to
the 13th pacing spike with only underlying P waves is restore cardiac output
seen during a ventricular lead threshold test. Note the sud-

Fig. 21.32 Recording from

AAI pacemaker showing loss
of capture. Observe
intracardiac atrial EGM
(upper), surface ECG
(middle), and marker channel
(lower). Intermittent loss of
capture is noted on the fifth,
eighth and ninth markers with
clear pacing artifact on the
EGM, clear pacing markers
(AP) but a notable lack of P
wave on the surface ECG
corresponding to these times.
Increasing the atrial lead
output rendered atrial capture
more reliable (AP atrial pace,
AS atrial sense)
Troubleshooting
Table 21.3 Causes of loss of capture
Myocardium is refractory, e.g., prior depolarization
Generator output problems, e.g., battery depletion and
erroneous programming to too low an output setting
Drug induced alterations in refractoriness/ pacing
threshold, e.g., flecainide
Lead displacement (evident on X-ray, frequently
accompanied by undersensing)
Lead tip fibrosis – exit block
Conductor damage (impedance high)
Insulator failure (impedance low, increase in battery
current drain, possible extracardiac muscle stimulation)
Malconnection at header (impedance high)
Myocardial conduction problems, e.g., myocardial
infarction/scar, myocardial perforation
Metabolic disturbance
Air in pocket in unipolar system
Component failure within pacemaker
Fig. 21.33 Chest X-ray showing (arrow) break in the
conductor in the ventricular shocking lead of a secondary
prevention dual-chamber defibrillator. The patient pre-
sented with lead impedances >2,000 Ω, lead noise and loss
of capture in the ventricular lead despite maximal output
programming. The therapy functions of the device were
initially programmed “off” due to the risk of oversensing
“make or break” potentials in the broken conductor caus-
ing inappropriate shocks. The patient underwent urgent
lead replacement
Loss of Output
This is a rare problem which results in failure of
the pacemaker to pace. The key to identifying loss
of output comes with the presence of pacing event
523
Table 21.4 Simple guide on how to approach loss of
capture
Recently implanted Consider lead displacement
device
Old device Consider battery depletion, exit
block
High impedance Consider lead conductor fracture
Consider loose connection at
header
Low impedance Consider insulation break
New drugs, e.g. Consider rise in threshold
flecainide
markers without the appearance of a pacing arti-
fact on the ECG or chamber capture (Fig. 21.34).
It is imperative to ensure pacing outputs are appro-
priately programmed, and if necessary to pace in
unipolar configuration in order to obtain the best
chance of visualizing the pacing artifact. Instances
of this malfunction are rare and are usually based
around the production of a pacing output but with
failure to conduct down the lead. Oversensing, an
open circuit due to complete lead transection and
loose connectors and internal insulation failure
are possible causes (Table 21.5).
Magnet application will not produce any pac-
ing output when an open circuit or insulation
failure exists in contrast to an oversensing situa-
tion. When the circuit is incomplete, lead imped-
ance will be high, whereas in insulation failure
the impedance will be low. A chest X-ray
(in more than one view) should help to confirm a
fractured lead (see Fig. 21.33) or a connector pin
that “falls short” of the set screw (see Fig. 12.29).
It may also demonstrate insulation breaks.
Generator Failure
In the rare event of total battery failure, there will
be no pacing event markers and no pacing artifact
on the ECG. Whatever cardiac rhythm the patient
possesses should be evident on the ECG (see Fig.
12.73).
Oversensing
Oversensing (sometimes known as underpacing)
means that the pacemaker is sensing some activity
that it should not be sensing and that the device is
inhibited when it should be pacing. It may be
524
Fig. 21.34 Loss of atrial output. Although at first site
this ECG appears to show VVI pacing, the marker chan-
nel shows that atrial pacing was supposed to occur but
there is an absence of atrial artifacts on the ECG. However,
at the second complex there is an atrial sensed event.
Table 21.5 Causes of loss of output (no pacer artifact/no
QRS)
Oversensing P wave, R wave and T wave
Myopotentials
Pacing afterpotentials
Crosstalk
Make/break potentials
Incomplete Lead conductor fracture (high lead
circuit- impedance)
Loose set-screw
Lead connector pin-header mismatch
Air around generator in pocket (e.g.,
subcutaneous emphysema) in unipolar
system
Lead insulation failure (low lead impedance)
Component failure within pacemaker
Battery at end-of-life
intermittent or a permanent situation. Causes of
oversensing are shown in Table 21.6.
It is worth remembering that a “low sensitivity”
setting decreases the pacemaker’s sensing ability
and is toward higher mV (10 mV), whereas a “high
sensitivity” setting increases the pacemaker’s
sensing ability and is toward lower mV (1 mV).
21 Troubleshooting After Device Implantation
Loose connections, lead fractures, or component failure
are the likely causes. The sensed atrial event probably
rules out complete continuous lead fractures or discon-
nected leads (Courtesy of Medtronic Connect)
Table 21.6 Oversensing causes of loss of output
Too high P wave, R wave, T wave
sensitivity setting Pacing afterpotential
Skeletal Pectoral, diaphragm, seizure/shiver
myopotentials
EMI Electrocautery, MRI, cardiover-
sion, electrotherapy, implanted
neuromuscular stimulators,
transcutaneous nerve stimulation,
lithotripsy
Lead fracture producing “make-break potentials”
Crosstalka Atrial lead displacement into RV
V lead displacement into RA
High atrial output current
High ventricular sensitivity
Short blanking period
a
Crosstalk-inhibition is also known as “far-field sensing”
or “self-inhibition” occurs when a pacemaker-generated
electrical event in one chamber is sensed by the lead in
another chamber, which then results in inappropriate inhi-
bition of pacing artifact in the second chamber. It occurs
in dual chamber or biventricular devices but rarely in cur-
rent dual-chamber systems due to the “ventricular blank-
ing period” which coincides with the atrial stimulus to
prevent V-channel oversensing of A output, bipolar leads
with smaller pacing spike and with steroid-eluting leads
with lower pacing thresholds. It is perhaps commoner in
unipolar systems due to larger pacing spikes and can occur
in the pacemaker circuit itself
Troubleshooting
Fig. 21.35 Intracardiac tracings from dual-chamber
defibrillator showing noise oversensing. Note the atrial
EGM (top) showing larger, sharp atrial signal followed by
low-voltage far-field ventricular signal from sinus rhythm.
Ventricular EGM (bottom) shows regular sharp signals cor-
responding with intrinsic R wave. Repeated erratic signals
Fig. 21.36 Ventricular oversensing. Here the pacemaker
records a ventricular sense on the marker channel but no
activity is demonstrated on the ECG strip. Pauses or inter-
vals longer than the programmed lower rate will occur in
Oversensing results from the device falsely
interpreting an electrical voltage as a P or R wave
and may be simply due to an inappropriate (too
sensitive) sensitivity setting. The key to
recognizing oversensing is observing markers
corresponding to signals other than the specific
intra-cardiac signal that is being sensed
(Figs. 21.35 and 21.36). A sensing threshold test
should be performed. Diagnostic counters may
also provide evidence of oversensing by revealing
525
with very short cycle length are seen in the latter half of the
tracing and represent “noise” from an insulation break. The
device interprets the signals as R waves (R) and triggers the
ventricular fibrillation zone of the device (F). The imped-
ance was found to be <200 Ω consistent with insulator fail-
ure and the patient underwent lead replacement
single chamber systems. The oversensing may be attrib-
uted to lead insulation failure (a decrease in lead imped-
ance will be seen), make-and-break fracture or a lead
connection problem
an unexpectedly low percentage of paced beats
or cardiac activity at below the programmed base
rate. The result of oversensing depends on the
programmed activity in case of a sensed event
(e.g., false inhibition on V lead, noise tracking or
mode switching on A lead). In cases where the
oversensed signals are “far-field” signals from
other cardiac chambers (e.g., V sensing in the
atrial lead – so-called “crosstalk”) or are QRS
double counting due to sensing of the T wave
526
Fig. 21.37 Intracardiac tracing from a dual-chamber
defibrillator showing oversensing. Observe the top tracing
which is the atrial EGM and the bottom tracing which is a
simulated surface ECG taken from RV lead tip to genera-
tor. In the first half of the trace appropriate P wave and R
wave sensing occurs as evidenced by the appropriate ven-
Fig. 21.38 Intracardiac EGM of paced T wave oversensing. Note the V sense (VS) events that occur at the nadir of the
T wave following only the V paced (VP) beats. The T waves of subsequent true VS events are not oversensed
(Figs. 21.37 and 21.38), then alterations to the
PVARP, PVAB, VRP, and lead sensitivity can
usually facilitate safe and effective pacemaker
function. Magnet application (a very temporary
measure) will eliminate pauses as should reduc-
ing sensitivity.
To remedy the problem of simple oversensing,
the sensitivity setting should be reprogrammed to
a less sensitive setting, that is, increase the mV
setting. This should be done with extreme caution
in ICDs as reducing sensitivity may affect the
ability to sense fine VF and deliver appropriate
therapy. For oversensing of polarization poten-
tials, extending the appropriate blanking period
might help the device not “to respond” to them.
Crosstalk is another unusual cause of over-
sensing. This results when a pacemaker-gener-
ated event in one chamber is sensed by the lead in
21 Troubleshooting After Device Implantation
tricular markers (R) and the correctly timed cycle lengths.
Despite steady atrial and ventricular rhythms, the device
starts to double count the R waves (presumably due to T
wave counting) dramatically halving the cycle length and
falling into the fibrillation zone (F)
the other chamber resulting in inappropriate inhi-
bition in the second chamber. Thankfully, it is
unusual because the ventricular blanking period
coincides with the atrial stimulus to prevent ven-
tricular sensing of atrial output. The most com-
mon causes of crosstalk include lead dislodgement,
high atrial outputs, high ventricular sensitivity
programming, and short ventricular blanking
period.
Many cases of oversensing however result
from sensing of extracardiac myopotentials
(Fig. 21.39). If unipolar sensing is “programmed
on,” then sometimes myopotentials can be reduced
by switching to bipolar sensing. In the setting of a
bipolar-sensing circuit, myopotential oversensing
is likely to signify insulation failure and imped-
ance trends should be scrutinized together with
radiological imaging of the lead (Fig. 21.40).
Troubleshooting 527

Fig. 21.39 Electromy-

opotential inhibition. Skeletal
myopotentials (arrow) are
sensed by the pacemaker and
cause inhibition of pacing
output. This phenomenon is
commoner in unipolar
systems than bipolar devices

Fig. 21.40 X-ray showing a

biventricular pacemaker with a
clear break (arrow) in the
insulation of the right
ventricular lead. The X-ray
demonstrates one of the
commonest sites for lead
damage at its point of
articulation with the clavicle.
The patient presented with low
lead impedances and lead
“noise”

Intermittent conductor or circuit failure can chronous pacing or avoidance of diathermy.

produce sharp potentials, referred to as “make or
break” potentials, and can occur as a result of
lead fracture or poor connection at the header
(see above). Sometimes provocative movements
(e.g., circling arms, gentle arm traction) are
needed to reproduce the features.
Extra-corporeal signals can sometimes cause
oversensing. Intra-operative diathermy is prob-
ably the most common in-hospital source and
usually necessitates either switching to asyn-
Other strong electromagnetic sources (e.g.,
MRI, industry production lines) are recognized
causes of oversensing, together with more
benign devices such as power drills and toys for
sexual pleasure! In the cases where industrial
interference is suspected, site-specific field test-
ing can be arranged for clarification. Oversensing
might be reported in the diagnostic data/stored
EGMs but not be evident during an ECG at the
follow-up visit.
528
Fig. 21.41 Surface ECG showing atrial undersensing (in beats 1–4). The third and fourth beats also demonstrate func-
tional ventricular undersensing as ventricular pacing stimuli fall early in the ST segment
Undersensing
Undersensing (sometimes known as overpacing)
is the reverse phenomenon to oversensing. Here
the device does not “see” the intrinsic cardiac
signal. The resultant action is often an attempt to
pace the specific chamber, as the device recog-
nizes no intrinsic activity. Occasionally this stim-
ulus will fall in the refractory period of the
chamber in question, thereby also giving the
appearance of loss of capture (Figs. 21.41 and
21.42). Causes of undersensing are shown in
Table 21.7.
Ensuring good intrinsic P and R wave ampli-
tudes and slew rates at implant helps prevent
problems with undersensing. Increasing lead sen-
sitivity to a lower mV value should deal with
undersensing problems but can often result in
oversensing issues as the leads are made more
sensitive. The key to recognizing undersensing
lies in the absence of appropriate markers when
intracardiac signals (P or QRS waves) are clearly
visible (Fig. 21.43).
As well as inappropriately programmed sensi-
tivity, causes of undersensing include lead dis-
placement (see Figs. 12.18–12.20), fracture or
insulation break, and lead tip fibrosis. Under-
sensing also arises when the intrinsic cardiac
activation changes (e.g., sinus rhythm to atrial
fibrillation). In this setting, the amplitude of the
21 Troubleshooting After Device Implantation
fibrillation wave is often variable and lower than
that of the intrinsic P wave. Undersensed
fibrillation signals may lead to problems with
mode switching and intermittent atrial fibrillation
tracking.
Fusion and pseudofusion are problems which
simulate undersensing. Here it is not the lack of
an appropriate sensitivity margin in the lead that
causes the problem, but a timing issue. Usually
seen in the ventricular lead of dual chamber pac-
ing systems, fusion occurs when the pacemaker
commits to a V pacing stimulus at the end of the
AV delay just at or following the moment that the
intrinsic QRS is activated. The result is a slightly
altered QRS morphology (fusion) or a native
QRS with superimposed pacing artifact if the
stimulus timing allowed no intrusion into the ven-
tricular depolarization (pseudofusion) (Fig. 21.44).
Extending the AV delay either manually or as
part of an automated algorithm is the best way to
deal with fusion – although this is not strictly
necessary.
Miscalculated blanking periods are a cause of
physiological undersensing. As the function of
blanking periods is to avoid repeated sensing
of the pacing artifact, true intrinsic signals which
arise during this period will not be sensed. Simi-
larly programmed refractory periods (PVARP,
VRP) are present to avoid oversensing.
Troubleshooting 529

Fig. 21.42 Surface ECG

showing ventricular
undersensing. Ventricular
pacing spikes are clearly
seen in the T wave. Although
the spikes do not capture
(due to pacing in the
refractory period), the
primary problem is one of
undersensing the preceding
QRS complexes.
Reprogramming the
ventricular sensitivity in this
patient resolved the issue

Table 21.7 Causes of undersensing Impedance Changes

Inappropriate program- Too low (not sensitive
ming of sensitivity enough)
Intracardiac signal occurs in pacemaker refractory
period
Lead displacement Macro or micro
Insulation failure (fall in impedance occurs)
Loose connection of electrode’s connector pin into
header
Conductor fracture
Low amplitude EGM Poor lead position/small
EGM at implant
“Entrance block” due to lead
tip fibrosis/lead maturation
Ectopic activation, e.g.,
PAC/PVC/AF
Drugs, e.g., flecainide
Electrolyte abnormalities,
e.g., hyperkalemia
Myocardial infarction
Pacing lead impedance is checked routinely at
each visit. It is an invaluable indicator of the
physical state of the leads’ conductors and
insulation. In many systems, a rise or fall in
impedance is the first sign of lead failure, occur-
ring before any physiological signs of failure are
present.
Rises in impedance suggest a restriction to the
flow of current and hence conductor failure
(Figs. 21.33 and 21.45). Signs of noise, sensing,
or capture issues should be sought, together with
radiological evidence of lead state, connection,
and position.
A fall in impedance in the circuit is suggestive
of a leak of current through an insulation break
(see Fig. 12.49) when local muscle twitching may
occur. In bipolar leads, this break can be localized
530
Fig. 21.43 Atrial undersensing
Fig. 21.44 Surface ECG showing A pacing and V
pseudofusion. Observe the large unipolar A pacing arti-
fact best seen in lead III followed by what initially looks
like an intrinsic QRS complex. Closer scrutiny of the
nadir of the QRS complexes reveals a small bipolar pac-
ing artifact. The pacemaker has committed to this output
by normalizing impedances through unipolar
pacing. This removes the outer conductor and
insulation from the equation and hence normal-
ization of impedances is highly suggestive of a
defect in this part of the circuit.
Pseudomalfunction
In this category, apparent pacemaker malfunction
is actually a function of normal pacemaker activ-
ity. It is partially due to new algorithms within the
device to preserve intrinsic conduction and physi-
ologic pacing. Adjustments in programming are
21 Troubleshooting After Device Implantation
just as the intrinsic QRS has activated. Comparing the
morphology of these QRS complexes with ones unhin-
dered by any pacing artifacts would be unlikely to show
any difference. This suggests the lack of intrusion into the
ventricular depolarization by the pacing output
usually not needed when one understands how
the device is programmed to work. Causes of
pseudomalfunction are shown in Table 21.8.
Upper Rate Behavior
Dual-chamber pacemakers try to maintain 1:1 AV
synchrony but this is not always possible. In the
presence of high intrinsic atrial rates, pacemakers
may revert to upper rate responses. These include
fixed-ratio block (e.g., 2:1 block), Wenckebach
behavior, fallback, rate smoothing, CVTL/
SMARTracking (Conditional Verticular Tracking
Troubleshooting 531

Fig. 21.45 Lead performance trends from an ICD inter- impedance suggest an intermittent break in the circuit.
rogation showing rise in impedance. Note the relatively This patient was found to have a loose connection between
stable impedance (~400 Ω) seen from implant up to the pin and header and required reoperation to secure the
marker “last session.” Subsequent marked fluctuations in connection

Table 21.8 Causes of pseudomalfunction Limit), or automatic mode switching. Thus, upper
Triggered mode rate behavior can be programmed on certain devices
Fusion/pseudofusion beats to simulate normal physiological AV nodal function
Functional oversensing with short ventricular blanking by simulating Wenckebach or 2:1 heart block
period (Fig. 21.46). This can give the appearance of inter-
Upper-rate behavior mittent atrial undersensing unless the function of
Inappropriate rate with rate hysteresis, rate drop the feature is fully realized (Figs. 21.47 and 21.48).
response, rate responsive mode, rate smoothing,
programmed rest/sleep rate function, rate smoothing
algorithms, mode switch Rate Drop Response
Algorithms to reduce ventricular pacing Rate drop response is a feature of many “high-end”
Auto capture algorithms pacemakers and is invaluable in the treatment of
Battery depletion the sudden bradycardia and hypotension found in
Magnet operation neurocardiogenic syncope. Inappropriate use or
Noise reversion aggressive parameters can lead to unnecessary
Ventricular safety pacing tachycardia (Fig. 21.49).
PVC responses
Sensor adaptive refractory periods Rate Response
Rate adaptive AV delays Rate response can give the appearance of a pace-
maker-mediated tachycardia if not appropriately
532 21 Troubleshooting After Device Implantation

Fig. 21.46 Upper rate

behavior may be character-
ized by 2:1 block, character-
ized by atrial rates that occur
at intervals less than the
TARP. Every other P wave
falls into the refractory period
and is thus not proceeded by
a paced ventricular event

Fig. 21.47 Rhythm strip of a dual-chamber pacemaker, lar tracking suggests functional atrial undersensing
A sensing and V pacing. P waves are buried within the with atrial events likely falling within the preceding
peak of each T wave. Intermittent absence of ventricu- PVARP

Fig. 21.48 Intracardiac analysis of this pacing response channel appears to not recognize every third P wave as a
is shown. The top EGM shows clearly a constant atrial result of upper rate Wenckebach behavior. Further evi-
rate which is sensed appropriately as evidenced by the dence of this is seen with increasing AV delays simulating
uppermost timing channel (430–440 ms). The marker the Wenckebach phenomenon (third timing channel)
Troubleshooting 533

Fig. 21.49 The 24 h tachogram showing inappropriate rate has caused repeated activation of the RDR feature of
rate drop response (RDR) behavior. The patient was expe- this dual-chamber system, giving nocturnal rates between
riencing nocturnal palpitations and underwent holter mon- 70 and 100 bpm. Programming a sleep mode on and less
itoring. During night time hours a fall in the resting heart aggressive RDR alleviated this pseudomalfunction
534
Table 21.9 Causes of rapid paced ventricular rates
Normal tracking of rapid atrial rates
Sinus tachycardia
Atrial fibrillation
Atrial flutter
Automatic atrial tachycardia
DDD pacemakers
Pacemaker-mediated tachycardia (PMT)
Myopotential triggering
With/without subsequent PMT
Electromagnetic triggering
Electrocautery
Environmental
Chest wall stimulation
Rate - adaptive pacing
Activation of sensor in rate-adaptive pacemakers may cause
tachycardia for as long as the sensor remains activated
programmed. Guiding the aggressiveness of the
programming (sensor setting, maximum sensor
rate) is best done by assessing patient’s perceived
level of activity, rate histograms, and symptoms.
Other functions can result in rate variations
which require explanation. Sleep rate and hyster-
esis are discussed below. AF suppression over-
drives the atrium at above its intrinsic rate and
allows for ventricular tracking in response. It is
sensible to establish whether these functions are
“on” and to what they are set.
Other causes of rapid ventricular pacing are
shown in Table 21.9.
Algorithms to Reduce Ventricular Pacing
Manufacturer-specific algorithms are in place in
most high-end pacemakers to reduce the inci-
dence of RV pacing in patients with intermittent
heart block. The so-called AV search hysteresis,
AAI safeR™ and MVP® programs allow increasing
degrees of AV block to encourage intrinsic ven-
tricular activity and can give the appearance of
dropped beats. It is perhaps worth discussing this
product development in more detail since a clear
understanding will help explain apparent “abnor-
malities” which require troubleshooting.
In 2003, ELA Medical (now Sorin Group)
introduced a dual-chamber device where the
ventricular lead tests for AV block instead of AV
conduction. When the intrinsic AV conduction is
21 Troubleshooting After Device Implantation
normal, the pacemaker paces in AAI. If the test
criteria for AV block are met, the device switches
to DDD to preserve cardiac output. Sorin named
its version of ADI pacing AAI SafeR™. In 2004,
Medtronic introduced its own version for both
pacemakers and ICDs – Managed Ventricular
Pacing (MVP®).
Sorin’s algorithm uses five criteria to test for
either blocked P waves or long PR intervals: First,
3° AV block: 2 consecutive blocked P waves.
Second, 2° AV block: 3 blocked P waves within
12 atrial cycles. Third, 1° AV block: 7 consecu-
tive atrial cycles, where the PR interval exceeds a
programmed value. Fourth, a ventricular pause
(programmable up to 4 s). Fifth, ventricular safety
pacing: if ventricular sensing occurs within the
ventricular safety pacing window after two con-
secutive atrial events, the device switches to DDD
(Figs. 21.50–21.52).
Medtronic’s MVP® mode uses a single crite-
rion. When a P wave is blocked, the pacemaker
synchronizes a ventricular pace with the next P
wave. It then looks for one conducted beat after the
next two P waves (Figs. 21.53–21.55).
The two companies differ in how they check
for a return of intact conduction. The Sorin algo-
rithm paces for 100 cycles in DDD, then switches
to AAI and uses the 5 AV block criteria to search
for intact conduction. Medtronic paces for 60 s,
then switches to AAI for one atrial cycle to look
for intact conduction (Fig. 21.56). If conduction
is not evident, both manufacturers’ devices revert
to DDD. The Sorin device then retests for con-
duction after 100 cycles, and the Medtronic pace-
maker retests after 2 min.
Auto Capture Algorithms
Some devices will automatically adjust the out-
put in order to obtain appropriate capture. Unless
one is aware of this feature, changed pacing out-
put values can cause concern.
Back-up Pacing Mode
Back-up pacing mode – usually asynchronous
pacing – is most often initiated after prolonged
exposure to EMI. It may result in symptoms of
pacemaker syndrome and usually needs a repro-
gram to exit the mode.
Troubleshooting 535

Fig. 21.50 Screenshot from interrogation of this Reply™ DR device showing a mode switch from AAI to DDD on
AVB I criteria (Courtesy of Sorin Group)

Fig. 21.51 Screenshot from interrogation of this Reply™ DR device showing a mode switch from AAI to DDD on
pause and AVB II criteria (Courtesy of Sorin Group)
536
Fig. 21.52 Screenshot from interrogation of this Reply™ DR device showing a mode switch from AAI to DDD on
AVB III criteria (Courtesy of Sorin Group)
Fig. 21.53 MVP mode from Medtronic. The system
allows the paced AV interval to prolong without V pacing
but will revert from AAI (R) to DDD if there is no following
Battery Depletion
Certain devices will revert to a safety mode or an
asynchronous output mode on severe battery
depletion. When attempts are made to interrogate
the device, warnings will often highlight the severe
state of battery depletion and not uncommonly
21 Troubleshooting After Device Implantation
QRS complex. The device will allow prolonged AV inter-
vals and occasional, single, nonconducted normal P waves
(Image reproduced with permission of Medtronic, Inc.)
will prevent further device interrogation or pro-
gramming in order to conserve power.
Magnet Operation
Most devices will revert to an asynchronous pac-
ing mode at a manufacturer specified magnet rate
Troubleshooting 537

Fig. 21.54 MVP mode from Medtronic. Following a looks for normal AV conduction after the next 2 P waves
nonconducted P wave, the system delivers a synchronized (Image reproduced with permission of Medtronic, Inc.)
ventricular pace after the next atrial paced beat. It then

Fig. 21.55 MVP mode from Medtronic. In the event of a conducted beat after the next two P waves (Image repro-
further blocked P wave, the system switches from AAI to duced with permission of Medtronic, Inc.)
DDD(R) after back-up VP. After 1 min, it then looks for a

Fig. 21.56 MVP mode from Medtronic. If a conducted P wave is seen, then the system switches back to AAI(R)
(Image reproduced with permission of Medtronic, Inc.)
538 21 Troubleshooting After Device Implantation

Fig. 21.57 Magnet

rate. (Top) Application
of a magnet to this
dual-chamber
pacemaker caused
reversion to DOO
pacing with a shorter
AV delay than DDD
pacing. This is normal
function. (Bottom)
Marker channels show
atrial pacing (AP)
followed by ventricular
pacing (VP) during this
magnet application
Troubleshooting
when challenged in this way (Fig. 21.57). Some
devices can also be programmed to perform
specific functions on challenge with a magnet
(e.g., EGM storage) (Table 21.10).
Hysteresis and Sleep Function
These modes will allow pacing/sensing at rates
below the lower rates and can often create cause
Table 21.10 Uses of magnet
To assess capture by fixed-rate pacing
To determine ERT/EOL of pacemaker
To terminate PMT
To treat crosstalk inhibition
For immediate treatment of oversensing
Fig. 21.58 ECG strip showing ventricular pacing at
70 ppm. Following a sinus beat and a pause, ventricular
pacing is reestablished at 70 ppm, although the first paced
Fig. 21.59 Example of rate
hysteresis in nonadaptive
rate mode
539
for concern when the devices appear to be set at
one lower rate yet do not appear to be functional
when that rate is reached. When evaluating a
rhythm strip, one should know whether hysteresis
is switched on and at what rate (Fig. 21.58). For
example, when Rate Hysteresis is enabled in the
nonadaptive-rate modes DDD or DDI or in sin-
gle-chamber atrial modes, a single nonrefractory
sensed atrial event will activate rate hysteresis
(Fig. 21.59). Rate Hysteresis will be deactivated
by a single atrial pace at the hysteresis rate. In
DDD and DDI mode, Rate Hysteresis will also
be deactivated by a single atrial pace during a
cardiac cycle when a ventricular pace is sched-
uled at the hysteresis LRL, or, in DDD mode,
whenever the atrial rate rises above the MTR. In
beat occurs after 1,200 ms because the hysteresis rate is
set at 50 ppm
540
30
min
Lower
Rate
Rate
Sleep
Rate
Bed Time
Time
Fig. 21.60 How the sleep function works
Fig. 21.61 Noise reversion
in a Thera™ SR pacemaker
(Medtronic)
the VVI mode, a single nonrefractory sensed
ventricular event will activate Rate Hysteresis. A
single ventricular pace at the hysteresis rate will
deactivate it.
The Sleep Function suspends the programmed
Lower Rate and replaces it with a Sleep Rate
(slower than the Lower Rate) during a specified
sleep period. The slower pacing rate during the
sleep period is intended to reduce the paced rhythm
during sleep. The Sleep Function is controlled by
three programmable parameters: Bed Time, Wake
Time, and Sleep Rate. The Sleep Function works
as follows: During the 30 min following the pro-
grammed Bed Time, the pacemaker gradually
reduces the operating rest rate from the Lower
21 Troubleshooting After Device Implantation
30
min
Wake Time
Rate to the Sleep Rate. The Sleep Rate remains in
effect as the operating rest rate until the pro-
grammed Wake Time. During the 30 min follow-
ing the programmed Wake Time, the pacemaker
gradually raises the operating rest rate from the
Sleep Rate to the Lower Rate (Fig. 21.60). Of
course, any sensed activity above sleep rate or sen-
sor-driven activity will deactivate sleep function.
Noise Reversion
If sensing occurs during the predefined refractory
periods, then the refractory periods are reset.
With continual reset of the refractory periods the
pacemaker will revert to the sensor or lower pac-
ing rate (Fig. 21.61).
Helpful Tests When Troubleshooting
Fig. 21.62 Ventricular
safety pacing is aimed at
preventing “crosstalk”
Ventricular Safety Pacing (VSP)
In order to prevent crosstalk inhibition, VSP
delivers short-coupled ventricular stimuli after
atrial pacing when sensing any activation in the
ventricular lead after the end of the ventricular
blanking period (Fig. 21.62).
PVC Responses
Premature ventriclar complexes (PVCs) can often
upset timing cycles by causing retrograde P
waves and potentially setting up pacemaker-
mediated tachycardia circuits (see Fig. 21.29). A
number of different mechanisms, such as extended
PVARPs to ignore retrograde atrial conduction
and post PVC atrial stimulation, are used to try
and combat this and can give unusual appear-
ances on the surface ECG.
Helpful Tests When Troubleshooting
12-Lead ECG
A 12-lead ECG is useful to diagnose undersens-
ing, oversensing, and loss of capture.
Pacemaker Interrogation
Evaluation of pacing and sensing thresholds and
lead impedance on all leads, battery voltage, stored
electrograms with visible marker channels, together
with a review of stored histograms and the details
of mode switching episodes, will be helpful.
541
Magnet Application
Putting the device into an asynchronous pacing
mode will help in the diagnosis of loss of capture
and battery life depletion.
Chest X-Ray
An overpenetrated PA and lateral chest X-ray can
show lead position/displacement, lead fracture,
insulation fracture, set-screw position, and
specific markers/codes on the pacemaker for
identification purposes.
Fluoroscopy
This can be useful for identifying possible sites
of lead fracture and real-time imaging can be
used while applying traction on the lead.
Echocardiography
Echocardiography can be used to identify peri-
cardial effusion/tamponade and lead perforation.
Telemetry
Early after implantation, telemetry can show
loss of sensing/capture as a result of lead
displacement.
542 21 Troubleshooting After Device Implantation

Holter Monitoring Transtelephonic Monitoring

Atrial and ventricular arrhythmias and abnormal Periodic transtelephonic monitoring is helpful for
sensing or capture may be picked up on 24–48 h early recognition of battery depletion.
ambulatory monitoring.

Reference
Event/External Loop Recorder
1. Galderesi M, Cattaneo F, Mondillo S. Doppler echocar-
diography and myocardial dyssynchrony: a practical
More useful for diagnosing intermittent pace-
update of old and new ultrasound technologies.
maker dysfunction. Cardiovasc Ultrasound. 2007;5:28.
 Training in Pacing
Over the past 15 years, training to be a competent
implanter of cardiac electrical implantable devices
(CEID) and expert in post-implant clinical and
technical management has taken a more structured
format than previously. However, there are still
significant variations on the degree of formality
from country to country! Perhaps the most formal-
ized regulations on training come from the USA
and these will be presented first. Although the
European Society of Cardiology has published
guidelines for pacing and cardiac resynchroniza-
tion therapy, there are none specific to training in
pacing. In the UK, most large specialist or tertiary
referral centers which boast a large and advanced
pacing/device implant and monitoring service will
be responsible for teaching specialist fellows or
registrars all aspects of cardiac electrophysiology,
arrhythmias, pacemaker, and other device implan-
tation as well as the basic techniques for interroga-
tion, programming, and surveillance of pacemakers
and ICDs. The Joint Royal Colleges of Physicians
Training Board (JRCPTB) in the UK has produced
a detailed document on the training requirements
for those pursuing a specialist career in pacing.
Elsewhere in the world, for example, Australasia,
less detailed guidelines have been published by a
Specialist Advisory Committee.
Training in the USA
In the USA, training in pacing forms part of the
Core Cardiac Arrhythmia and Electrophysiology
Curriculum Training and extends over a 2–3 year
D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy,
DOI 10.1007/978-1-4471-2939-4_22, © Springer-Verlag London 2012
22
period across 3 levels. In order to sit the Clinical
Cardiac Electrophysiology (CCEP) examination
and achieve certification for such added skills by
the American Board of Internal Medicine (ABIM),
a trainee must be trained in an accredited unit –
running an approved training programme.
Level 1
Level 1, within the cardiology “core training pro-
gram,” comprises at least 2 months of CCEP
rotation designed for cardiology trainees to
acquire knowledge and experience in the diagno-
sis and management of brady/tachyarrhythmias.
They should learn the indications for and limita-
tions of electrophysiology (EP) studies, the abil-
ity to interpret intracardiac recordings such as
AH, HV intervals, and basic activation sequences
during tachycardia, differentiation of a supraven-
tricular and ventricular tachycardia, and the use
of antitachycardia pacing to terminate tachyar-
rhythmias. They should also learn about the
proper use of antiarrhythmic agents, including
drug interactions and proarrhythmic potential as
well as the indications for catheter ablation pro-
cedures. Within Level 1, the trainee should be
exposed to noninvasive and invasive techniques
related to the diagnosis and management of
patients with cardiac arrhythmias including con-
tinuous ambulatory ECG monitoring, event
recorders, external and implantable ECG loop
recorders, exercise testing for arrhythmia assess-
ment, tilt-table testing, invasive EP studies, and
543
544
implantation of cardiac arrhythmia control
devices. Formal teaching on the ECG manifesta-
tion of arrhythmias should be supplemented by
participation in the on-call rota responsible for
arrhythmia interpretation. Arrhythmias associ-
ated with congenital heart disease and with car-
diac and noncardiac surgical procedures are
important aspects of core training. Specifically,
they should learn the fundamentals of cardiac
pacing, recognize normal and abnormal pace-
maker function, indications for temporary and
permanent pacing and the implantation of ICDs,
and the indications and limitations of biventricu-
lar pacing in patients with congestive cardiac
failure.
The cardiology trainee should be formally
instructed in and gain experience with the inser-
tion, management, and follow-up of temporary
pacemakers, measurement of pacing and sensing
thresholds and recording of intracardiac electro-
grams, and the indications and techniques for
elective and emergency cardioversions. Insertion
of a minimum of ten temporary pacemakers and
performance of ten elective cardioversions are
required. They should be instructed in and gain
experience with the application and use of trans-
cutaneous pacing systems, although these may be
accumulated during the whole of the cardiovas-
cular training period.
Level 2
Level 2 allows trainees to obtain advanced train-
ing in normal and abnormal cardiac electrophysi-
ology and mechanisms of arrhythmias. It consists
of 6 months (minimum) of training in noninva-
sive arrhythmia management techniques designed
to develop advanced competence and proficiency
in the diagnosis, treatment, and longitudinal care
of patients with complex arrhythmias. They
should have a thorough knowledge of the basic
and clinical pharmacology of antiarrhythmic
agents and demonstrate proficiency in their use.
Of particular importance is the acquisition of
skills and experience for managing patients with
complex cardiac arrhythmias, including program-
ming and follow-up management of all types of
22 Training in Pacing
bradycardia pacing, biventricular pacing and ICD
systems. The trainee is expected to function as
the primary programming operator who interro-
gates, interprets, prescribes, and reprograms devices
in at least 100 patients. He/she should acquire
advanced competency in temporary pacing, car-
dioversion, interpretation of invasive EP study
data and complex arrhythmia ECG interpretation.
Although the Level 2 trainee must have significant
exposure to invasive EP, ICDs and the surgical
aspects of arrhythmia control device implanta-
tion, Level 2 training by itself does not qualify
the trainee to perform these invasive procedures.
The Level 2 trainee has the option of obtaining
additional training in pacemaker implantation or
may choose the additional training required for
invasive cardiac EP, or both, as described under
Level 3.
Level 3
Level 3 is designed for the individual who wishes
to specialize in invasive diagnostic and therapeu-
tic EP. Prior procedure volume during Level 1
and 2 training is cumulative and counts toward
the overall numbers to reach Level 3 training.
Clinical cardiac EP training includes a mini-
mum of 4 years of clinical cardiology and EP.
Current ACGME (Accreditation Council for
Graduate Medical Education) requirements spec-
ify a 3-year training program in general cardiol-
ogy, which consists of a core 2-year clinical
program and an additional 12 months, which may
involve research and/or elective time in EP.
A dedicated fourth year of training in CCEP is
required. The appropriate use, safe performance,
and judicious interpretation of these complex
procedures require highly specialized training
and competence. Although CEID and invasive
cardiac EP training including ablation is usually
done concomitantly, sequential training is also
acceptable. To complete Level 3, trainees should
perform at least 150 EP procedures and be a pri-
mary operator and analyze 100–150 initial diag-
nostic studies. At least 50–75 of these should
involve patients with supraventricular arrhyth-
mias. Because therapy with antiarrhythmic
Training in the USA
devices forms a major part of current EP practice,
the trainee should also have been a primary oper-
ator during >25 EP evaluations of implantable
antiarrhythmic devices.
EP procedures should cover supraventricular
and ventricular arrhythmias and bradyarrhyth-
mias. Given the complexity of the specialty and
the growing amount of information and new pro-
cedures, it is common for trainees to extend train-
ing for an additional year or more to gain advanced
expertise in specific procedures, such as ischemic
ventricular tachycardia, ablation in patients with
congenital heart disease, atrial fibrillation proce-
dures, and lead extractions. This type of training
can also be achieved during a post-training men-
tored practice. Expertise in catheter placement,
programmed electrical stimulation, endocardial
mapping, catheter ablation, and interpretation of
data is essential. The endocardial mapping expe-
rience should include some exposure to left heart
mapping by the retrograde aortic approach.
Experience with ³10 trans-septal catheterization
procedures should be a minimal training require-
ment. Participation in a minimum of 75 catheter
ablations, including AVN ablation, AV accessory
pathways, atrial flutter, and atrial and ventricular
tachycardia, is required. Given the rapid evolu-
tion of new mapping technologies, it is unlikely
that the trainee will gain exposure to all mapping
technologies during their training. Trainees
should be exposed to intravascular ultrasound for
defining intracardiac anatomy, cardiovascular
MRI, and CAT scanning. It is anticipated that the
Level 3 trainee should participate in 30–50 men-
tored AF ablations.
Level 3 training in EP requires ICD experi-
ence that includes assisting with the primary
device implantation, with EP testing at the time of
implantation, with follow-up assessment and with
left ventricular lead implantation procedures.
Optional Training in Device
Implantation (Applicable to Level 2 or 3)
Level 2 and 3 trainees may choose to obtain addi-
tional training in device implantation techniques.
The CEID implantation training may be obtained
545
concurrently or sequentially with Level 2 or 3
training, respectively. The CEID training must
include development of expertise in permanent
atrial, right and left ventricular lead and ICD lead
placement, threshold testing and programming of
devices, principles of surgical asepsis, surgical
techniques of implantation, and management of
implant-related complications. Trainees must
participate as the primary operator in at least 75
primary implants including at least 25 ICD, 25
dual-chamber, and 25 CRT (either pacing or
defibrillation) devices. Thorough ICD implant
evaluation including ventricular fibrillation
induction and defibrillation testing for a mini-
mum of 25 implants is necessary. Thirty CEID
revisions or replacements, including at least 10
ICD revisions as the primary operator, are also
necessary for this level. The trainee must partici-
pate in the follow-up of at least 200 CEID patient
visits and acquire proficiency in advanced pace-
maker ECG rhythm analysis, interrogation and
programming of complex pacemakers. Of the
follow-up visits, at least 100 should be in ICD
and 100 in pacemaker patients.
Level 2 training (6 months) with the option of
training in pacemaker implantation (6 months)
requires a total of 12 months of advanced training
beyond the cardiology core Level 1. This may be
obtained within a 3-year cardiology program if 1
of the 3 years is dedicated to acquiring pacemaker
implantation skills plus related management and
follow-up skills. The training does not meet the
ABIM requirements for admission to the CCEP
examination. As part of the training regarding
implantable pacemakers, exposure to the indica-
tions, implantation techniques, and follow-up of
implantable loop recorders is desirable.
The trainee pursuing a career in CCEP as
addressed under Level 3 also has the option of
obtaining expertise in the surgical aspects of pace-
maker or transvenous ICD implantation, or both.
The same amount of surgical experience with
bradycardia pacemaker implantation is required
and may be supplemented with surgical train-
ing for ICD implantation. If the Level 3 trainee
chooses this option, he/she must participate as the
primary operator in at least 25 ICD implantations
and possess the management and follow-up skills.
546
The Level 3 trainee wishing to become proficient
in biventricular pacing or defibrillating systems
requires the aforementioned training and involve-
ment in implantation and follow-up of 25 biven-
tricular systems. The trainee should be proficient
at interpreting data from echocardiography used
in the evaluation of resynchronization therapies.
Pacemaker lead extraction is a specialized pro-
cedure that requires special training but is not an
obligate part of training for CCEP examination eli-
gibility. Physicians being trained in lead extraction
should perform at least 20 lead extractions as the
primary operator under the direct supervision of a
qualified training physician.
Level 3 trainees for ICD implantation must have
an extensive knowledge of ICD indications, con-
traindications, and management of complications;
an ability to determine defibrillation thresholds and
manage high defibrillation thresholds; an under-
standing of drug- and pacemaker/ICD interactions;
and a thorough knowledge of ICD programming
and management of ICD malfunction and postop-
erative complications. Level 3 training with the
option of pacemaker or ICD implantation or both
requires a minimum of 1 year of dedicated CCEP
and device implantation training beyond the 3-year
cardiology program. Level 3 trainees must have an
extensive knowledge of left ventricular lead indica-
tions, contraindications, and management of biven-
tricular malfunctions and interactions, as well as
postoperative complications.
Level 3 trainees would be expected to have per-
formed a minimum of 300 procedures (including
150+ EP cases; 75 ablations; 75+ pacemakers/
ICDs).
Evaluation, Competence, and Privileges
The program director should maintain adequate
records of each individual’s training experi-
ences and performance of various procedures
for appropriate documentation for Levels 1, 2,
and 3. The trainees should also maintain records
of participation in the form of a logbook con-
taining clinical information, procedure per-
formed, and outcome of procedures, including
any complications.
22 Training in Pacing
The ACC, AHA, and the Heart Rhythm
Society (HRS) have formulated a clinical com-
petence statement on invasive EP studies, cath-
eter ablation, and cardioversion. Self-assessment
programs and competence exams in ECG are
available through the ACC. Training direc-
tors and trainees are encouraged to utilize these
resources.
The ACGME has published the essential com-
ponents of a specialized program for training in
CCEP. The ABIM provides a special examination
for additional certification in CCEP. Information
concerning the training requirements for admis-
sion to the examination can be obtained from the
ABIM; such requirements include one additional
year of training in an ACGME-accredited EP
program. Subsequent privileges to perform inva-
sive procedures should be granted primarily on
the basis of the technical expertise acquired in the
training program, the documented training, and
the recommendations of the directors of EP/pac-
ing programs.
Training in the UK
In the past, pacing skills have been gained by
“serving an apprenticeship” in a specialist ter-
tiary cardiac center, being taught by an experi-
enced pacemaker implanter who was often “self
taught” – having been one of the first cardiolo-
gists to have taken an interest in this treatment
in the 1960s and 1970s. Indeed, many of these
senior colleagues worked closely with industry
during the embryonic and infant stages of devel-
opment in pacemaker technology and were in no
small way responsible for the “pace” of prog-
ress. Although this apprenticeship was often the
best form of teaching one could hope for, it was
often not comprehensive and frequently lacked
structure.
In 2007, the Joint Royal Colleges of Physicians
Training Board (JRCPTB) in the UK published
the programme for training in cardiovascular
medicine which includes a curriculum, learning
objectives, and a detailed syllabus. The knowl-
edge, skills, and attitudes needed to fulfil the
learning objective are specified. Currently higher
Training in the UK
medical training (HMT) in cardiology last 6 years
and must be undertaken in Specialist Advisory
Committee (SAC)-approved posts. Some of the
training may be taken outside the UK if the train-
ing post involved has been approved by the SAC.
Two paths will either lead to a CCST in cardiol-
ogy or in cardiology/general medicine. Trainees
do not have to decide which path to take until the
beginning of the fifth year.
The Phase 1 (early training) lasts 3 years and
is designed to provide basic cardiology and GIM
in equal proportions in a district general hospital
(DGH) and a tertiary center. During phase 1, the
trainee will begin to acquire basic cardiac cathe-
terization, echocardiography, and pacing skills.
Specifically to training in pacing, the “basic”
objective of the syllabus is to ensure that the
trainee is able to assess patients for pacing and be
able to pace independently and safely. The knowl-
edge that should be achieved should include an
understanding of EP and cardiac anatomy rele-
vant to pacing, the importance of radiation pro-
tection, the indications for temporary and
permanent pacing, and the properties of different
pacing systems that are currently available. The
trainee should also become able to recognize and
treat complications of pacing systems and be able
to insert temporary pacing electrodes and perma-
nent single- and dual-chamber pacemaker sys-
tems and be able to monitor, interrogate, and
program pacemakers.
Phase 2 consists of 1 year of research relevant
to cardiovascular medicine. It may be extended to
>1 year but only 1 year will be counted toward
the HMT. This period of research would ideally
involve some aspects of pacing or EP if one had
this career path in mind.
Phase 3, which lasts 2 years, will be the time
at which trainees decide whether to concentrate
on dual accreditation in cardiology/GIM or take
their cardiology training to a higher level by
obtaining advanced subspeciality training – so-
called “advanced training.” This may be either in
percutaneous coronary intervention, electrophys-
iology/ablation techniques/ICD implantation,
adult congenital heart disease, nuclear cardiol-
ogy, or in pacemaker/CRT/ICD implantation. For
those opting to train in the latter subspecialty,
547
they will be expected to satisfactorily complete
all 4 “core modules” and “elective modules”
3 and 4. These are shown in Tables 22.1–22.6. It
is advised that a certain number of “procedures”
should be performed during training (Table 22.7)
and that after completion, methods such as DOPS
(Direct Observation of Procedural Skills) should
be used to assess practical competency.
Further competency examinations are encour-
aged but not mandatory (yet!). These may include
the exam set for pacing and electrophysiology by
Heart Rhythm UK. A step further would be the
European Heart Rhythm Association (EHRA)
examination which defines competencies for
device implantation.
More recently specific aspects of implan-
tation techniques are being taught in a more
structured manner to encourage better pocket
fabrication and wound closure. The courses may
be run by cardiologists with the help of industry
or under the auspices of the Royal Colleges of
Surgeons, UK.
Most established industry partners offer those
undergoing training in device implantation the
opportunity to attend their European Training
facilities to be taught implantation techniques
using models as well as skills in troubleshooting
after device implantation. These are invaluable
experiences for those with the intention of mak-
ing a career in device implantation.
In 2010, the JCRTB presented the 2010
Cardiology Curriculum intended to update the
previous curriculum in order to meet the GMC’s
new standards for curricula and assessment sys-
tems and to reflect recent medical advances and
the changes in service and training. The curricu-
lum includes five new assessment methods, Acute
Care Assessment Tool, Case-based Discussion,
Patient Survey, Teaching Observation, and Audit
Assessment, and became the training manual for
all trainees entering ST3 from 4th August 2010.
Within the Advanced Specialist Area Modules,
Advanced Rhythm Training consists of 12 mod-
ules (Table 22.8). For training in device therapy,
a minimum of modules 1, 2, and 3 must be
completed with optional additions of module 5
(CRT) and/or module 6 (lead extraction). Details
of the content of these modules are available on
Table 22.1 Royal College of Physicians’ Specialist Advisory Committee on training in pacing and electrophysiology
Core module 1: Training in pacemaker implantation and programming
Objectives
To understand the basic principles of
pacing including electrical parameters and
the engineering involved
To understand pacemaker lead
characteristics
To understand the published guidelines
for implantation of pacemakers and
clinical indications
To understand the implantation procedure
and the cardiac and thoracic anatomy
To master safe, sterile technique for all
procedures
To have detailed knowledge of the
programming of modern pacemakers
following implantation including
troubleshooting
Knowledge
Of the principles of pacing and the
engineering of pacemakers and leads
Of medico-legal issues concerning
consent and provision of information
Of the cardiac conduction system and its
disease processes
Of the cardiac and thoracic anatomy,
especially in venous access including the
cephalic vein approach
Of the indications and guidelines for
correct pacemaker prescription including
pacing mode
Of the safe implantation of pacemakers
including the operating environment and
antibiotic usage
Of management of complications of
pacemaker implantation including pneumo/ Competent programming of pacemakers
hemothorax, lead perforation/fracture
Of the management of lead problems –
when to extract and when not
Of programming issues related to leads
Of modern pacing systems and of
troubleshooting
Of rate-modulated pacing and sensor
technology
Of driving restrictions
Skills
Skills in correct patient selection
Safe implantation of single/dual chamber
pacemakers via cephalic/subclavian vian To foster a team approach to pacing
approaches
Intravascular catheter manipulation
Surgical skills in respect of opening,
manipulating and closing wounds
Managing complications, e.g., cardiac
tamponade
In the insertion and care of temporary
pacing wires
Detailed and safe approach to cephalic,
subclavian or internal jugular venous
access
and troubleshooting including the
programming of sensors and newer
anti-atrial tachycardia algorithms
548
Attitudes
Correct attitude to a surgical approach –
appreciating sterility and antibiotic usage
including a close relationship with
cardiac technicians
Committed to audit of long-term
outcomes including infections and lead
complications
To develop a critical attitude towards a
safe pacing programme in the hospital
and support patients in the community
with adequate pacing follow-up
To educate patients as to the treatment
options open to them and to explain
treatment strategies
To work closely with other HC
professionals, e.g., technicians,
cardiologists, geriatricians, neurologists,
infection control.
To appreciate the psychological impact
of the patient’s arrhythmia illness on the
patient and their family, and manage it
22
sensitively
Training in Pacing
Table 22.2 Royal College of Physicians’ Specialist Advisory Committee on training in pacing and electrophysiology

Core module 2: Training in ICD implantation and programming

Objectives Knowledge Skills Attitudes
Understand the principles and guidelines Of cardiac/thoracic anatomy relevant to Select patients appropriately for ICD Appreciate importance of informed
Training in the UK

for ICDs
To carry out specialist investigation and
treatment of patients who may benefit
from ICD implantation
venous access
Of national/international guidelines for
ICD implantation and their evidence
base
implantation
Investigate patients appropriately prior to
implantation (inc. whether or not
revascularization is required)
consent and need to explain lifestyle
issues/driving restrictions to patient
Correct attitude to surgical approach
– appreciating sterility/antibiotic use

To understand the implantation procedure/ Of medico-legal issues concerning
cardiac and thoracic anatomy and master
safe sterile technique for all procedures
To be able to implant single and dual
chamber ICDs, recognize and treat
complications during and after
implantation
To be able to program ICDs, provide
zones for VT of various rates, algorithms
for discrimination between SVT and VT,
appropriate use of antitachycardia pacing
algorithms, and appropriate shock therapy
To be able to “troubleshoot” ICD
problems including the recognition of
drug-device interactions, appropriate/
inappropriate shocks, device and lead
complications, and problems that require
specialist intervention, e.g., ablation (for
SVT/VTs)
consent and provision of information
Up-to-date knowledge of recent clinical
trials in ICD therapy
The effects of antiarrhythmic drugs on
defib and pacing thresholds
Of proarrhythmic effects of anti-arrhyth-
mic drugs and their effect on LV
function
Of how to manage complications of ICD
implantation and problems during
long-term follow-up
Of the indications for VT ablation, AV
nodal ablation, and atrial tachycardia/
fibrillation ablation in patients with ICDs
Of current recommendations on fitness
to drive with an ICD
Explain procedure/possible complica-
tions/possible effects on patient lifestyle
to patient and relatives
Assess anesthetic/sedation needs of
patient pre/during the implant
Assess whether a single, dual or triple
chamber (BiV) device is best suited to
patient
Perform the implant procedure compe-
tently with an acceptably low complica-
tion rate
Perform tests of pacing, sensing and
defibrillation safely during the implant
Be able to program the device
appropriately
Perform post-implant (pre-discharge)
assessment and routine follow-up of ICD
patients
Appreciate importance of team-working
with nursing, technical, X-ray, anesthetic
and industry staff
Appropriate self-confidence and
recognition of limitations
Committed to audit of long-term
outcomes including infection/lead
complications
To educate patients as to treatment
options and explain treatment strategies
To work closely with cardiac techni-
cians, cardiologists, geriatricians,
infection control, neurologists
Appreciate the anxiety that patients with
ICDs suffer
Appreciate the psychological impact of
the arrhythmia illness on patient and
their family and manage it sensitively
549
Table 22.3 Royal College of Physicians’ Specialist Advisory Committee on training in pacing and electrophysiology
Core module 3: Training in the mechanisms of arrhythmias, complex electrocardiography and the principles of intracardiac electrophysiology
Objectives
To understand the principles underlying
the main causes of cardiac arrhythmias at
cellular and tissue level
Familiarity with the use of surface ECG
for arrhythmia management
To understand the classification of clinical
arrhythmias based on their site of origin
within the heart
A knowledge of the pathophysiology of
AF, atrial tachycardia/flutter, junctional
tachycardias (inc. AV nodal tachycardia
and WPW syndrome)
To be able to describe abnormal electrical
activity in terms of the 3D structure of the
heart in situ
Knowledge
Of re-entrant, automatic/triggered
arrhythmia mechanisms. An understand-
ing of the differences between anatomic
and functional reentry, including spiral
wave generation
Of the pathophysiology of AF/atrial
flutter/tachycardia, junctional tachycar-
dias (inc. AVnodal tachycardia, WPW
syndrome), ischemic/non-ischemic VT
Of distinguishing between the principles
of arrhythmias from the characteristics of
the 12-lead ECG, and response to
maneuvers inc. vagotonic actions and
administration of drugs
Of the causes of wide-complex tachy
cardias and morphological schemes for
diagnosis of VT
Of use of surface ECG to assess likely
location of critical tissue sustaining
arrhythmia, e.g., accessory AV connec-
tion in WPW syndrome
Of the ECG in Long QT and Brugada
syndromes, RV dysplasia (ARVD) and
cardiomyopathy (ARVC)
Of the understanding of invasive EPSs
and their clinical indications. To have
observed and understood invasive EPSs
and RF ablations
Skills
History taking/appropriate examination
in patients with or at risk of arrhythmias
Obtaining an adequate ECG record
during an arrhythmia
Demonstrate a systematic approach to
interpretation of surface ECGs during
arrhythmias
Demonstrate familiarity with ECG
schema for localizing accessory
pathways in WPW syndrome
An appreciation of relevance and
limitations of basic arrhythmia mecha-
nisms in terms of clinical arrhythmia
management
To be able to describe abnormal
electrical activity in terms of the 3D
structure of the heart in situ
550
Attitudes
Take a sensible, professional attitude to
management of patients with arrhyth-
mias, using non-invasive techniques/
conserving resources
To educate patients as to treatment
options available, to empower them to
make their own decisions as to treatment
they prefer
To appreciate the psychological impact
of the patient’s illness on patient and
family, and manage it sensitively
22
Training in Pacing
Table 22.4 Royal College of Physicians’ Specialist Advisory Committee on training in pacing and electrophysiology

Core module 4: Training in intracardiac electrophysiology techniques

Objectives Knowledge Skills Attitudes
To successfully evaluate a patient with Of the EP of SVTs and typical (counter- To communicate effectively with Take a sensible, professional attitude to
Training in the UK

sustained narrow-complex tachycardia
and identify all electrophysiological
mechanisms
To elicit key factors in the history to
distinguish between different SVTs
To understand and be able to direct
autonomic maneuvers in clinic
To be able to select appropriate investiga-
tions to diagnose the presenting
arrhythmia
To correctly select patients for EPSs and
catheter ablation
To safely/competently perform an invasive Of intracardiac electrographic patterns in
EPS and interpret findings
To perform curative catheter ablation
procedures
To safely/competently manage all drug
therapy for the patient
clockwise) atrial flutter
Of medico-legal issues concerning
consent and provision of information
Of range of varied presentations/clinical
findings associated with different
arrhythmias
Of range of ECG recording equipment
for detecting intermittent arrhythmias
Of 3-D cardiac anatomy
Of equipment needed for EPSs and
catheter ablation
SVT/atrial flutter and their interpretation
Of ablation techniques and ability to use
information from imaging/intracardiac
electrograms to guide/evaluate effective-
ness of ablation
Of complications of invasive EP
procedures and their management
patients/family/contacts to take effective
history
To communicate effectively in gaining
informed consent
Competence in performing autonomic
maneuvers
To prepare patient for EPS, safely/
competently insert sheaths and undertake
the procedure
To safely/accurately manipulate
electrodes in the circulation/heart
To accurately document records of all
aspects of care
Technique of transeptal puncture
arrhythmia management, learn under
supervision/request advice
Consent patients sensitively, give
objective risk assessment
Be aware of MDT work in cath lab in
safe performance of procedures
Communicate effectively with fellow
professionals involved in care
Remain calm/professional in event of
adverse complications
Be diligent in recording the management
of patient. Achieve effective communica-
tion with primary care colleagues
Appreciate the psychological impact of
patient’s illness on patient/family, and
manage it sensitively

Of the pharmacology, side effects and

interactions of drugs used in manage-
ment of these conditions

Of arrhythmogenic RV dysplasia
(ARVD) or cardiomyopathy (ARVC)
551
Table 22.5 Royal College of Physicians’ Specialist Advisory Committee on training in pacing and electrophysiology
Elective module 1: Training in multi-site ventricular pacing for cardiac resynchronization (CRT)
Objectives
To appreciate role CRT plays in the
management of patients with CHF
To undertake implantation of CRT devices
with high success rates
To recognize/deal with complications of
implant or device behavior
To be able to optimize therapy delivery
Knowledge
Of techniques available to identify
patients likely to benefit from CRT and
be aware or their limitations
Of medico-legal issues concerning
consent and provision of information
To be able to determine which patients
for CRT also require back-up ICD
Of all equipment for implantation and
subsequent programming
Of relative benefits of different leads/
devices
Of implantation techniques/how to deal
with common problems
Of potential complications
Skills
To be able to select appropriate patients
for CRT
To consent a patient in a balanced/
informed way about success rate, risks/
benefits of CRT
To perform a CRT implant in a safe/
logical fashion
To recognize nature of implant
difficulties + take correct action
To appreciate when an alternative
technique/approach may be required
e.g., surgical device implantation
To program the devices appropriately,
advise on optimization using recognized
techniques such as echocardiography
552
Attitudes
Take a sensible/professional attitude to
CRT, learn under supervision and request
advice
Consent patients sensitively with
objective assessment of likely benefit
Be aware of MDT in heart failure
management and in maximizing benefit
of CRT
To deal appropriately with patients in
whom CRT has not been effective
To appreciate the psychological impact
of the patient’s illness on patient/family,
and manage it sensitively
22
Training in Pacing
Table 22.6 Royal College of Physicians’ Specialist Advisory Committee on training in pacing and electrophysiology

Elective module 2: Training in pacing/AICD implantation and lead extraction techniques

Objectives Knowledge Skills Attitudes
To understand basic principles of pacing Of the basic principles of pacing and the In correct patient selection Correct attitude to a surgical approach
Training in the UK

electrical properties of the heart – appreciate sterility/antibiotic use

To understand engineering of endocardial
lead
To understand implantation procedure,
and the cardiac/thoracic anatomy
Safe sterile techniques for procedures
To be able to select appropriate cases for
endocardial lead extraction
Of medico-legal issues concerning
consent and provision of information
Of the engineering of pacemakers/leads
Of published guidelines for lead
extraction
Of cardiac/thoracic anatomy
In implantation of single and dual
chamber pacemakers via cephalic/
subclavian approaches
In handling intravascular catheters
In wound repair/closure
In handling immediate complications of
implants, e.g., cardiac tamponade
To foster team approach to lead
extraction including close relationship
with cardiac surgeons
Use of self audit regarding complications
To educate patients as to treatment
options and to explain strategies
including surgical extraction

To be able to safely extract pacing leads
using available technology
Of management of pacemaker implant Ability to extract leads from both To work closely with other colleagues as
complications, e.g., pneumo/hemothorax, superior/femoral approaches necessary
lead perforation, fracture
In using cutting, laser and femoral To appreciate the psychological impact
Of safe implantation of pacemakers/the extraction techniques of patient’s illness on patient/family and
operating environment/antibiotic use manage sensitively

Of management of lead problems – when

to extract/when not to

Of programming issues, specifically

related to leads

Of the lead extraction systems, including

cutting, laser and diathermy sheaths, and
use of femoral approach to lead
extraction

Of the specific complications of lead

extraction and how to prevent/handle
them
553
554
Table 22.7 JRCPTB Suggested numbers of procedures
to be performed during training
Procedure Requirement
Pacemaker Minimum of 20 supervised single or
implantation dual chamber PM implantations
+ Minimum of 100 systems
implanted by trainee unsupervised
Pacemaker Pacemaker interrogation and/or
programming programming of 100 follow-up
patients
ICDs Minimum of 25 supervised ICD
implantations
Detailed knowledge of programming
to include 50 patients in follow-up
clinic
Biventricular Supervised training in implantation
pacemakers of a minimum of 30 devices
Programming/optimization of BiV
devices in at least 30 cases with heart
failure using modern techniques such
as tissue Doppler imaging
Lead extraction Knowledge and training in pacemaker
lead extraction and indications for
extraction
www.jrctb.org and of modules 1–3 in Table 22.9.
It is expected that trainees will complete a mini-
mum of 100 pacemaker implants, 100 follow-up
patients requiring pacemaker interrogation and/or
reprogramming, 25 ICD implants and supervision
of 50 patients in programming clinics, 30 BiV
devices and their programming plus optimization
of 30 patients with heart failure using modern
techniques such as tissue Doppler imaging.
Trainees are expected to have CCAD-verified
training logbooks for procedures and outcomes,
attendance of local and national training days (2
per year), certified attendance at Heart Rhythm
UK arrhythmia and device therapy training days/
year, and certified attendance at one international
EP meeting/year or EP/device course where
appropriate. Criteria for training centers and train-
ees are specifically outlined within the document.
Training in Australia
The Specialist Advisory Committee (SAC) in
Cardiology of the Royal College of Physicians of
Australia stipulate a 3-year “Core Training” in
22 Training in Pacing
Table 22.8 Advanced Rhythm Training Modules 2010
curriculum (JRCPTB)
Module 1: Pacemaker implantation and
programming
Module 2: Training in ICD implantation and
programming
Module 3: Training in the mechanism of arrhyth-
mias, complex electrocardiography and
the principles of intracardiac
electrophysiology
Module 4: Intracardiac electrophysiology
techniques
Module 5: Multi-site ventricular pacing for CRT
Module 6: Training in Pacing/ICD lead extraction
techniques
Module 7: Training in ablation of SVT, typical
atrial flutter and normal heart VT
Module 8: Training in catheter ablation for AF/AT
and non-isthmus dependent atrial flutter
Module 9: Training in catheter ablation for VT
Module 10: Training in transeptal puncture and
catheterization
Module 11: Training in advanced assessment of the
risk of life-threatening arrhythmias or
sudden cardiac death – both inherited
and acquired
Module 12: Training in management of cardiac
arrhythmias in patients with adult
congenital heart disease
clinical cardiovascular medicine (with at least
1 year in Australia/New Zealand) followed by
2 years of advanced training in the subspecialty
of permanent pacemaker implantation and man-
agement of patients with ICDs. Such later
advanced training may be combined with EP
including diagnostic and ablative techniques.
A training program must be approved and
approved sites suitable for training are available
from the SAC.
Trainees in the 3-year “core training” period
are required to become conversant with all diag-
nostic procedures available – with their strengths,
limitations, and appropriate application, with the
relevant literature and with research activities in
the cardiovascular field. Preferably time will be
spent in more than one institution. At least
6 months should be in an institution that performs
adult cardiac surgery and percutaneous coronary
intervention (PCI) in order to gain experience in
indications for these procedures, appropriate
Training in Australia
Table 22.9 Details of modules 1–3 of 2010 Advanced
Rhythm Training Curriculum
Module 1: Pacemaker implantation
and programming
To understand the basic principles of pacing including
electrical parameters and the engineering involved
To understand pacemaker lead characteristics
To understand the published guidelines for implanta-
tion of pacemakers and clinical indications
To understand the implantation procedure and the
cardiac and thoracic anatomy
To master safe sterile techniques for all procedures
To have detailed knowledge of the programming of
pacemakers following implantation including
troubleshooting
Knowledge
Demonstrate knowledge of:
The principles of pacing and the engineering of
pacemakers and of pacing leads
The cardiac conduction system and its disease
processes
The cardiac and thoracic anatomy, especially of
venous access including the cephalic vein approach
The indications and guidelines for correct pacemaker
prescription including pacing mode
The safe implantation of pacemakers including the
operating environment and antibiotic use
The management of complications of pacemaker
implantation including pneumo/hemothorax, lead
perforation, lead fracture
The management of lead problems – when to extract
and when not to
Programming issues specifically related to leads
Modern pacing systems and of troubleshooting
Rate-modulated pacing and sensor technology
Driving restrictions
Skills
Demonstrate:
Skills in correct patient selection for and safe
implantation of single and dual chamber pacemakers
via the cephalic, axillary and subclavian approaches
Intravascular catheter manipulation and surgical
skills in opening, manipulating and closing wounds
The ability to manage complications, e.g., cardiac
tamponade
Skills in insertion/care of temporary pacing wires
Detailed and safe approach to cephalic, subclavian or
internal jugular venous access
Competent programming of pacemakers and
troubleshooting including the programming of
sensors, newer sensors and newer anti-tachycardia
algorithms
555
Table 22.9 (continued)
Behavior
Demonstrate:
Correct attitude to a surgical approach – appreciating
sterility and appropriate antibiotic use
To foster a team approach to pacing including a close
relationship with cardiac physiologists
Being committed to audit of long-term outcomes
including infection and lead complications
The development of a critical attitude towards a safe
pacing programme in the hospital and to support
patients in the community with adequate pacing
follow-up
The ability to educate patients as to the treatment
options open to them and to explain treatment
strategies
The ability to work closely with other health care
professionals as necessary including cardiac physiolo-
gists, infection control, neurologists, care of the elderly
An appreciation of the psychological impact of the
patient’s illness on the individual and their family
and manage it sensitively
Module 2: Training in ICD implantation and
programming
Understand the principles and guidelines for ICDs
To carry out specialist investigation and treatment of
patients who may benefit from ICD implantation
To understand the implantation procedure, the cardiac and
thoracic anatomy and safe sterile technique for procedures
To be able to implant single and dual chamber ICDs
and recognize and treat complications which may occur
To be able to program ICDs, provide zones for VT of
various rates, algorithms for discrimination of VT and
SVT, appropriate use of anti-tachycardia pacing
algorithms, and appropriate shock therapy.
To be able to “troubleshoot” ICD problems, including
recognition of drug-device interactions, appropriate and
inappropriate shocks, device and lead complications
and problems that may require specialist intervention
such as ablation (for both supraventricular and
ventricular arrhythmias).
Knowledge
Demonstrate knowledge of:
The cardiac and thoracic anatomy, especially in
respect of venous access
National and international guidelines for ICD
implantation and their evidence base
Medico-legal issues concerning consent and
provision of information
Up-to-date knowledge of recent clinical trials in ICD
therapy
The effects of antiarrhythmic drugs on defibrillation
and pacing thresholds
(continued)
556
Table 22.9 (continued)
The proarrhythmic effects of antiarrhythmic drugs
and their effect on left ventricular function
How to manage complications of ICD implantation
and problems during long-term follow-up
The indications for VT ablation, AV nodal ablation
and atrial tachycardia/AF ablation in patients with
ICDs
Current recommendations regarding fitness to drive
with an ICD
Skills
Demonstrate the ability to:
Select and investigate patients appropriately for ICD
implantation (including whether revascularization is
required)
Explain the procedure, possible complications and
possible effects on the patient’s lifestyle to the
patient and relatives
Assess the anesthetic/sedation needs for the
implantation
Assess whether a single, dual or triple chamber
(BiV) device is best suited to the patient
Perform the implant procedure competently with an
acceptably low complication rate
Perform appropriate tests of pacing, sensing and
defibrillation safely and thoroughly during the
implant
Be able to program the device appropriately
Perform post-implant assessment of the patient
Perform routine follow-up of ICD patients
Behaviors
Demonstrate:
An appreciation of the importance of informed
consent, and the need to explain lifestyle issues and
driving restrictions to the patient
The correct attitude to a surgical approach – appreci-
ating sterility and antibiotic usage
An appreciation of the importance of team-working
with nursing, technical, radiographic, anesthetic and
(if appropriate) industry staff
Appropriate self-confidence and recognition of
limitations
A committed approach to audit of long term
outcomes
The ability to educate patients as to the treatment
options open to them and to explain treatment
strategies
The ability to work closely with other health care
professionals as necessary: cardiac physiologists,
infection control, care of the elderly, neurologists
An appreciation of the anxiety that patients may
suffer with an ICD
An appreciation of the psychological impact of the
patient’s arrhythmia illness on the patient and their
family, and manage it sensitively
22 Training in Pacing
Table 22.9 (continued)
Module 3: Training in the mechanisms
of arrhythmias, complex electrocardiography and
the principles of intracardiac electrophysiology
Knowledge
Demonstrate knowledge of:
Re-entrant, automatic and triggered arrhythmia
mechanisms. An understanding of the differences
between anatomic and functional
Re-entry, including spiral wave generation
The pathophysiology of atrial fibrillation, atrial
tachycardia and flutter, junctional tachycardias (including
AV nodal tachycardia and the Wolff-Parkinson-White
syndrome), ischemic and nonischemic VT
Distinguishing between the principle mechanisms of
arrhythmias from the characteristics of the 12-lead
surface ECG, and their response to certain
maneuvers such as vagotonic actions and drug
administration
The causes of wide-complex tachycardias and
morphological schemes for the diagnosis of VT
The use of the surface ECG to assess the likely location
of a critical tissue sustaining an arrhythmia, e.g. an
accessory AV connection in the WPW syndrome
The ECG in Long QT and Brugada syndromes and
right ventricular dysplasia (ARVD)/cardiomyopathy
(ARVC)
The understanding of invasive electrophysiological
studies (EPS) and their clinical indications. To have
observed and understood invasive EPSs and
radiofrequency ablations
Skills
Demonstrate:
The capability of history taking and appropriate
examination in patients with or at risk of cardiac
arrhythmias
The ability to obtain an adequate ECG record during
an arrhythmia using available technologies
A systematic approach to interpretation of surface
ECGs during arrhythmias
An appropriate use of vagal maneuvers and drugs for
arrhythmias
A familiarity with ECG schema for localizing
accessory pathways in WPW syndrome
An appreciation of the relevance and limitations of
basic arrhythmia mechanisms in terms of clinical
arrhythmia management
An ability to describe abnormal electrical activity in
terms of the 3-D structure of the human heart in situ
Behaviors
Demonstrate:
A sensible, professional attitude to the management
of patients with arrhythmias, using non-invasive
techniques and treatments appropriately, and
conserving resources
Training in Australia
Table 22.9 (continued)
An ability to educate patients as to the treatment
options open to them, to empower them to take their
own decisions as to their preferred treatment strategy
An appreciation of the psychological impact of the
patient’s illness on the patient and their family, and
manage it sensitively
Module 5: Multi-site ventricular pacing for cardiac
resynchronization (CRT)
To appreciate the role CRT plays in the management of
patients with CHF
To undertake implantation of CRT devices with a high
probability of success
To recognize and deal with complications of implant or
device behavior
To be able to optimize therapy delivery
Knowledge
Demonstrate knowledge of:
Cardiac anatomy including the venous system
Techniques available to identify patients likely to
benefit from CRT and to be aware of limitations of
these techniques
Medico-legal issues concerning consent and
provision of information
How to determine which patients for CRT also
require ICD back-up
All the equipment available, both for implantation
and also subsequent programming
Of relative benefits of different leads and devices
Of implantation techniques and how to deal with
common problems
Of potential complications
Skills
Demonstrate the ability to:
Be able to select appropriate patients for CRT
Be able to consent a patient in a balanced and
informed way about the success rate, risks and
benefits of CRT
Be able to proceed with a CRT implant in a safe and
logical fashion
Be able to recognize nature of implant difficulties
and to take appropriate action to overcome these
Appreciate when an alternative technique or
approach may be required e.g. surgical device
implantation
Be able to program the devices appropriately, and to
advise on optimization using recognized techniques
such as echocardiography
Behaviors
Demonstrate:
A sensible, professional attitude to CRT, learn under
supervision with appropriate requests for advice
An ability to consent patients sensitively whilst
presenting an objective assessment of likelihood of
benefit
557
Table 22.9 (continued)
Being aware of the importance of members of a
multi-disciplinary team in heart failure management
and in maximizing benefit of CRT
The ability to deal appropriately with patients in
whom CRT implantation has not been effective
An appreciation of the psychological impact of the
patient’s illness on the patient and their family, and
manage it sensitively
Module 6: Training in pacing/ICD lead extraction
techniques
To understand the basic principles of pacing
To understand the engineering of endocardial leads
To understand the implantation procedure, and the
cardiac and thoracic anatomy
To perform safe sterile techniques for all procedures
To be able to select appropriate cases for endocardial
lead extraction
To be able to safely extract pacing leads using all
available technology
Knowledge
Demonstrate knowledge of:
The basic principles of pacing and the electrical
properties of the heart
The medico-legal issues concerning consent and
provision of information
The engineering and construction of pacemakers,
ICDs and pacing leads
The published guidelines for lead extraction
The cardiac and thoracic anatomy
The safe implantation of pacemakers including the
operating environment and antibiotic usage
The management of complications of pacemaker
implantation including; pneumo/hemothorax, lead
perforation, lead fracture etc.
The management of lead problems – when to extract
and when not to
Programming issues specifically related to leads
The lead extraction systems including cutting, laser
and diathermy sheaths, and the use of the femoral
approach to lead extraction
The specific complications of lead extraction and of
how to prevent/handle them
Skills
Demonstrate an ability for:
Correct patient selection
Implantation of both single and dual chamber
pacemakers via the cephalic, axillary and subclavian
approaches
Handling intravascular catheters
Dealing with wound repair and closure
Handling immediate complications of implants, e.g.,
cardiac tamponade
(continued)
558
Table 22.9 (continued)
Extracting leads from both the superior and femoral
approaches
Using cutting, laser and femoral extraction
techniques
Behaviors
Demonstrate:
Correct attitude to a surgical approach – appreciating
sterility and antibiotic usage
The fostering of a team approach to lead extraction
including fostering a close relationship with cardiac
surgeons
The use of self audit regarding complications
The ability to educate patients as to the treatment
options open to them and to explain treatment
strategies including surgical extraction
The ability to work closely with other health care
professionals as necessary: cardiac technicians, other
cardiologists, infection control, cardiac surgeons
An appreciation of the psychological impact of the
patient’s illness on the patient and their family, and
manage it sensitively
Alongside the recommendations are stated possible
assessment methods for the trainer, e.g., case-based dis-
cussion, mini-CEX, MSF, DOPS. These are available on
the website: www.jrcptb.org under Cardiology 2010
Curriculum
patient selection, familiarity with these interven-
tions and post-intervention care including com-
plications, their diagnosis, and management.
Knowledge of EP, radiofrequency ablation tech-
niques, and their application must be obtained in
an institution that uses these diagnostic and ther-
apeutic procedures. Specifically, trainees should
become skilled in all aspects of the clinical diag-
nosis and management of acute and chronic adult
heart disease and gain experience in the emer-
gency department and CCU as well as in the ward
and ambulant care area and in cardiac rehabilita-
tion. A high standard of competence must be
achieved in performing and/or reporting ECGs,
chest radiographs, exercise stress tests, Holter
monitors, and transthoracic echocardiograms.
Significant experience must be obtained perform-
ing right and left heart catheters and coronary
angiography, temporary transvenous pacemak-
ers, pericardial aspiration, and jugular/subclavian
catheterization. Knowledge and experience must
be gained in nuclear cardiology including the
interpretation of myocardial perfusion studies
22 Training in Pacing
and the principles of radiation safety. There must
be development of a sound knowledge of physi-
ology, pathology, and some knowledge of genet-
ics and molecular biology. The indications for
cardiac surgery and the principles of postopera-
tive management of patients undergoing cardiac
surgery should be soundly understood.
A minimum number of procedures have to be
performed during the 3-year period of core
training. These include 100 supervised report-
ing of Holter monitor recordings; 100 super-
vised and reported exercise stress tests; 600
supervised reporting of echocardiograms (at
least 50 TOEs); 300 performed and reported
TTE; 10 DC cardioversions; 10 temporary trans-
venous pacemakers; 100 permanent pacemaker
function testings at pacemaker clinic (50%
should be dual chamber); 150 performed and
reported right heart catheterizations; 150 per-
formed and reported coronary angiograms; 6
pericardiocentesis procedures; 20 involvements
in decision making and some experience con-
cerning referral for EP studies and ablation
techniques, including report interpretation and
observation of procedures. Participating in
teaching, research, and clinical audit and in con-
tinuing medical education is essential. A log-
book must be used to document performance of
all clinical procedures including whether they
were supervised or not.
Education in Pacing, Device,
and Arrhythmia Therapy
Pacing/Arrhythmia Societies
International and national societies/associations
represent the leading opinions and views on sci-
ence, education, and advice for cardiac arrhyth-
mia professionals and patients and are the primary
information resource on heart rhythm disorders.
Their purpose is to improve care of patients by
providing research, education, and guidance to
those involved in the subspecialty.
The three best-known organizations are The
Heart Rhythm Society (HRS) (USA) www.hrson-
Education in Pacing, Device, and Arrhythmia Therapy
Table 22.10 HRUK certificate of accreditation syllabus
2007
Core syllabus
Anatomy and physiology
Arrhythmia mechanisms
Arrhythmias – clinical characteristics, diagnosis, ECG
interpretation
Clinical examination
Devices
Arrhythmias/electrophysiology/ablation
Pharmacology
Current DVLA regulations for patients with or at risk
of arrhythmias and those with implantable devices
National guidance and policy for arrhythmia
management
Clinical trials relating to arrhythmia management
Medico-legal issues
line.org/, The European Heart Rhythm Association
(EHRA) www.escardio.org/bodies/associations/
EHRA/, and Heart Rhythm UK (HRUK) www.
hruk.org.uk/
The websites provide details of research
data, educational opportunities and meetings,
certification of accreditation for pacing and EP.
Accreditation in Pacing
and Electrophysiology
It is now possible to gain a national or interna-
tional certificate of accreditation in pacing and
device implantation.
HRUK offer a UK Certificate of Accreditation
to those passing their set examination on a wide-
ranging syllabus. Their syllabus is available on
the website – www.hruk.org.uk. The core sylla-
bus and the specialist section on devices is shown
in Tables 22.10 and 22.11.
EHRA offer a European Certification
Examination for Competence in Cardiac Rhythm
Device Therapy for the Physician (with separate
certificates for the technician). Certificates can be
achieved in both invasive cardiac electrophysiol-
ogy and in cardiac pacing and ICDs. A syllabus
for the heart rhythm specialist and for the invasive
cardiac EP examination is published on the
EHRA website. The exam consists of two parts: a
559
Table 22.11 HRUK certificate of accreditation syllabus
2007
Specialist section – devices
Indications for pacing, ICDs and CRT; selection of
appropriate pacing mode
Hemodynamics of pacing and pacemaker syndrome;
basic technology for devices; battery technology;
shock wave forms; longevity calculations; circuit
technology – telemetry; sensors; connectors; lead
technology/materials; electrode design/shape; bipolar/
unipolar and when to use
Pacemaker, ICD and CRT implant technique and
complications; preparation of the patient; venous
approach; selection of appropriate lead; measurements
at implant; DFT testing and ideal values; intracardiac
electrograms; drugs affecting thresholds; agents used
for moderate sedation; reversal agents
Device troubleshooting – sensing issues, under/
oversensing; loss of capture/ threshold rise; lead
problems. Identification/ interpretation of electrograms
and counters; timing cycles; crosstalk; pacemaker
mediated tachycardia; electrical interference in
devices; ICD and CRT troubleshooting
Programming pacemakers/ICDs; optimizing CRT
programming; complications of pacemakers and ICDs;
pacemaker and ICD X-rays; identification of
appropriate/inappropriate shocks/ATP
Management of infected implanted devices; indica-
tions for lead extractions, techniques and
complications
Generator change; electromagnetic interference;
follow up; end-of-life/palliative care issues
MHRA reporting and traceability; pacemaker and ICD
follow-up and support; DVLA regulations for ICDs
and pacemakers
theoretical first part – a written exam of 130 mul-
tiple choice questions which has to be passed
before going on to part 2. The second practical
part is a “log book” section. Candidates must
submit a list of at least 100 implantations (includ-
ing 70 pacemakers, 20 ICDs, 10 CRT) and fol-
low-up of a total of 200 procedures (including
140 pacemakers, 40 ICDs, 20 CRT) performed
during a period of 3 years.
The International Board of Heart Rhythm
Examiners (IBHRE) (formerly NASPExam) offers
a North American examination for certification of
competence in pacing and EP.
560
Pacing Journals
There are three major peer-reviewed pacing
journals:
Europace – European Journal of Pacing,
Arrhythmias and Cardiac Electrophysiology
(Official Journal of the European Society of
Cardiology and the European Heart Rhythm
Association),
Heart Rhythm Journal – The Official Journal
of the Heart Rhythm Society
PACE – Pacing and Clinical Electro-
physiology.
Journal of Cardiac Electrophysiology
Circulation – Arrhythmia/Electrophysiology
Other Books on Pacing/Devices
Cardiac Pacing and ICDs by Kenneth A.
Ellenbogen MD and Mark A. Wood MD
(Blackwell Publishing).
Cardiac Pacing and Defibrillation: A Clinical
Approach by David L. Hayes and Paul A.
Friedman (Wiley-Blackwell).
The Nuts and Bolts of Cardiac Pacing by Tom
Kenny (Wiley-Blackwell).
Cardiac Pacing for the Clinician by Fred M.
Kusumoto and Nora F. Goldschlager (Springer).
A Practical Guide to Cardiac Pacing by H.
Weston Moses and James C. Mullin (Lippincott,
Williams & Wilkins)
Clinical Cardiac Pacing, Defibrillation and
Resynchronization Therapy by Kenneth A.
Ellenbogen MD, Bruce L. Wilkoff MD, G. Neal
Kay MD, and Chu Pak Lau (Saunders).
The Nuts and Bolts of Cardiac Resynchroniza-
tion Therapy by Tom Kenny (Wiley-Blackwell).
The Nuts and Bolts of ICD Therapy by Tom
Kenny (Blackwell-Futura).
Pacing Academic Meetings
Major academic meetings that focus on pacing
and electrophysiology include CARDIOSTIM
22 Training in Pacing
annual meeting, the European Heart Rhythm
Association Meeting, the Heart Rhythm Society
annual meeting, and the Heart Rhythm Congress
(HRUK). The American College of Cardiology
and American Heart Association Annual
Scientific Sessions contain significant amounts of
device-related topics, sessions, and even satellite
symposia.
Device Manufacturer Websites
The major manufacturers of pacemakers, CRT,
and ICD devices have their own websites
which provide lists of all their current and
recent devices, electrodes, and accessories.
Details of their programmability, unique and
most recently introduced features are provided.
Moreover, most have physician resources and
patient information sections, product manuals
and instructions for use, education sections
such as slide presentations, videos and ani-
mations, photos as well as details of clinical
studies outcomes and guidelines. Useful con-
tact numbers and e-mail addresses are also to
be found. The websites below are particularly
useful.
Medtronic: www.medtronic.com; https://
wwwp.medtronic.com/mdtConnectPortal/
Boston Scientific: www.bostonscientific.
com
St. Jude Medical, Inc.: www.sjm.com
Sorin Group: www.sorin.com
Biotronik: www.biotronik.com
Spectranetics: www.spectranetics.com
Other Useful Websites
HRUK audit Group: Heart Rhythm Devices: UK
National Clinical Audit Report: www.devicesur-
vey.com
Joint Royal College of Physicians Training
Board: www.jrcptb.org.uk
Bakken Museum and Artifact Collection:
www.thebakken.org
 Index

A diagnostics, 211
Abrams–Lucas inductive-coupled unit, 18 AV sequential pacing, 104
Accent MRI™ and Tendril MRI™, 115 AV synchrony, 27, 34
ACM. See Atrial capture management (ACM)
Activitrax™, 28, 29
Advanced pacemaker B
AF suppression, 210 Biotronik’s CardioMessenger I, 246
AIDA diagnostics, 211 Blanking period (BP), 204
arrhythmia, 211 Brachial plexus injury, 254–255
AT/AF diagnostic suite, 211 Bradycardias, permanent pacemaker implantation
auto-initialization, 211 bundle-branch block, 63–65
Auto Sense, 212 cardiogenic shock and A-V block, 68
hysteresis response, 210 carotid sinus hypersensitivity and MVS, 64, 65, 68
SBR and MV offset, 213 first-degree AV block, 59–61
VRR/VRS, 213 hypertrophic obstructive cardiomyopathy, 66, 68
VSP, 213 pediatrics and congenital heart disease, 68–69
Advisa MRI™ SureScan™, 114 post-cardiac transplantation, 68
AIDA. See Automatic interpretation for diagnosis second-degree AV block, 59, 62
assistance (AIDA) sick sinus syndrome, 63, 65–67
AID-B–first automatic implantable defibrillator from third-degree AV block, 59, 62–63
INTEC, 32, 33
Altrua™, 97, 100, 176, 508, 510
Altrua™ 50 DDDR pacemaker, 495, 496 C
Anthem™ RF CRT-P device, 375 Cardiac electrical implantable devices (CEID), 545
Antitachycardia pacing (ATP), 431–432 Cardiac Pacemakers Inc. (CPI), 17, 28, 31
Arrhythmia detection, ICDs Cardiac pacing devices
programming, 430–431 “artificial pacemaker”, 1, 2
sensing, 429–430 Bakken’s “old number one” pacemaker, 7, 8
ATP. See Antitachycardia pacing (ATP) demand pacing( see Demand pacing)
Atrial capture management (ACM), 36 flexibility, programmability and physiological
Atrial demand pacing, 100–101 pacing, 25–33
Atrial fibrillation (AF) suppression, 210 Grass physiological cardiac stimulator, 1, 4
Atrial synchronized, rate-adaptive pacing (VDDR), 106 transcutaneous cardiac stimulator, 4, 5
Atrial synchronized ventricular pacing (VDD), 105–106 wearable device, 8
Atrioventricular (AV) block Cardiac Resynchronization in Heart Failure (CARE-HF)
acute MI, 284–287 study, 401
children, 331–333 Cardiac resynchronization therapy (CRT)
congenital, 319 CARE-HF, 47
Attain StarFix®, 371 complications, 377–382, 386–389
Autolifestyle/Daily Learning™, 211 description, 357
Automatic interpretation for diagnosis assistance (AIDA) devices( see Devices, CRT)

D.R. Ramsdale, A. Rao, Cardiac Pacing and Device Therapy, 561

DOI 10.1007/978-1-4471-2939-4, © Springer-Verlag London 2012
562 Index

Cardiac resynchronization therapy (CRT) (cont.) PMT( see Pacemaker-mediated tachycardia (PMT))
hemodynamic benefits, 399, 400 pneumothorax, 250–252
indications, 357–358 subclavian vein thrombosis/thrombophlebitis,
LV leads, 373, 377, 383–384 260–263, 272
optimization, 390–392 thoracic duct injury, 255
patient selection, LV dyssynchrony, 359 Twiddler’s syndrome, 274–276
programming, 392–393, 396 Conexus™ Wireless Telemetry, 244, 245
technique, 359–361, 372 CONTAK CD study, 400–401
trials, 400–401 Contak® Renewal™ TR CRT-P device, 374, 395, 396,
troubleshooting, 396–399 514, 515
Cardiac resynchronization therapy defibrillation CorDigital® MicroER® event recorder, 74, 77
(CRT-D), 418, 420, 421 Cordigital Micro LR™, 77
Cardiocall VS20 device, 74 Coronary sinus (CS)
CardioMessenger II and II®S, 246, 247 cannulation/left ventricular (LV) lead position,
Cardionetics C.Net5000 ECG recorder, 82 CRT, 362–370
Cardiovascular implantable electronic device (CIED), dissection, 382, 387
204 lead, 373
CARE-HF study, 401 CPI. See Cardiac pacemakers Inc. (CPI)
Carotid sinus hypersensitivity, 64, 65, 68 CRT. See Cardiac resynchronization therapy (CRT)
CCAD. See Central cardiac audit database (CCAD) CRT-D. See Cardiac resynchronization therapy
CCEP. See Clinical cardiac electrophysiology (CCEP) defibrillation (CRT-D)
CEID. See Cardiac electrical implantable devices (CEID) CS. See Coronary sinus (CS)
Central cardiac audit database (CCAD), 187 Current® DR dual-chamber, 421
Cephalic vein approach
description, 153
CHD. See Congenital heart disease (CHD) D
CIED. See Cardiovascular implantable electronic device Da Vinci Robotic SiHD system, 388, 391, 503
(CIED) Defibrillation threshold (DFT)
Clinical cardiac electrophysiology (CCEP), 543, 546 high, 426–427
Closed loop stimulation (CLS), 111 intra-cardiac electrogram (IEGM), 425
CLS. See Closed loop stimulation (CLS) “shock-on-T”, 425, 426
CMOS. See Complementary metal-oxide-semiconductor shock polarity, 427
(CMOS) testing, 424–426
CMOS-1 Intermedics Inc. programmable pacemaker, 25 “tilt value”, 427
Cognis® CRT-D device, 247, 250 Dermabond®, 178, 179
COMPANION and CARE-HF studies, 401 DFT. See Defibrillation threshold (DFT)
Comparison of Medical Therapy, Pacing and Digital signal processing (DSP), 117
Defibrillation in Heart Failure (COMPANION) DSP. See Digital signal processing (DSP)
trial, 401 Dual chamber pacing
Complementary metal-oxide-semiconductor (CMOS), 25 atrial synchronized ventricular, 102–104
Complications, pacemaker implantation AV sequential, 104
air embolism, 254 AV universal, 104–105
arrhythmias, 249 description, 101–102
brachial plexus injury, 254–255 Durata SJ4 lead version, 418, 420
connection failure, 256–258
exit block, 263–264
hemorrhage, 253–254 E
hemothorax, 254 EAS. See Electronic article surveillance systems (EAS)
inappropriate pacemaker inhibition, 264–266 Easytrak® LV leads, 366, 369
infection, 269–275 Ebstein’s asamaly, 317–319
insulation break, 267–269 ECT. See Electroconvulsive therapy (ECT)
lead displacement, 255–256, 261 EHRA. See European Heart Rhythm Association
lead fracture, 266–267 (EHRA)
muscle stimulation/twitching, 265 Elective generator change
myocardial perforation, 250–253 abdominally placed generator, epicardial system,
obstruction, SVC( see Superior vena cava (SVC), 449–453
obstruction) pacemaker generator replacements, 441, 442
pacemaker generator failure, 273, 279 prepectorally placed generator, endocardial system,
pacemaker lead/generator erosion, 273, 277–279 442–449
pacemaker syndrome, 273 replacement, ICDs, 454
Index
Electroconvulsive therapy (ECT), 220
Electrode positioning
atrial leads, 165–168
ventricular leads, 157–164
Electrogram (EGM)
atrial, 511, 513
dual-chamber systems, 234
intracardiac, 231, 234, 506, 525
Electromagnetic interference (EMI), 215
Electronic article surveillance systems (EAS), 220
Electronic medical record (EMR), 196
Electrosurgical dissection sheath (EDS) system, 463
Elema–Schonander devices, 12–14
EMI. See Electromagnetic interference (EMI)
EMR. See Electronic medical record (EMR)
End-of-life (EOL) parameters, battery depletion, 242
Endotak Reliance 4-site lead system, 418, 419
EnPulse™, 113, 115
EnRhythm™ and Adapta™ pacemakers, 113
Epicardial/epimyocardial pacing
indications, 487
lead fixation, 497–500
subxiphoid approach, 495, 497
temporary pacing, 504
thoracoscopic and robotic epicardial, 501–504
thoracotomy, 488–495
Epicardial pacing systems
description, 342–343
implantation, 342
Ethilon®, 162
European Heart Rhythm Association (EHRA), 547, 559
Event recorders
external “post-symptom”, 74–76, 77
external “pre/post-symptom”, 77–79
Explant procedures
anesthetic, 457
antistaphylococcal antibiotics, 456
closing, 477–478, 479
complications, lead extraction, 480–481
description, 455
excimer laser, 468–477
lead abandonment, 479, 480
lead extraction, 456
pre-erosion, 455
redundant/infected/eroded pacemaker system,
458–460
surgical removal, 480
temporary pacemaker, 457–459
“unscrewing and traction”, 456
External pulse generators, temporary pacing
antecubital vein puncture, 302–303
APC cardiovascular, 296, 298
AV sequential pacing, 310, 312
dual-chamber TPM, 296, 297
femoral vein puncture, 301–303
initiating pacing, 305, 308–311
internal jugular vein (IJV) puncture, 296–299
lead positioning, femoral vein, 305
PACE 300 three-chamber, 295–296, 298
pacing box, 295, 296
563
subclavian vein puncture, 298–301
venous anatomy, 296, 298
F
FasTac® Flex tool, 486–489
Femoral vein puncture, 301–303
Fixed “J-shaped” tined electrode, 124
Flextend®2, 118
Follow-up, pacemaker implantation
alerts/recall, medical device, 240–242
algorithms, technicians, 224–226
application, magnet, 224, 227
battery and lead data, 234, 237
battery depletion/EOL parameters, 242
CRT and ICD devices, 234–236
diagnostic counters, 239
diagnostic functions, 234
equipment and facilities, 224, 226
fluctuations, impedance, 231
frequency and timing, 239–240
Holter ECG monitoring, 239
home monitoring, 243–248
interrogation, Reply™, 231, 232
lead data, 228, 230
NIPS testing, 228, 231
Quick Look II Screen, Medtronic programmer, 231,
233
“therapy guide”, 234, 236
thresholds and impedance data, 231, 234
ventricular arrhythmia detection settings, 237, 240
“ventricular therapies” program, 234, 238
G
Guidant/Boston Scientific’s LATITUDE®, 247
H
Heart Rhythm UK (HRUK), 558–559
Holter monitoring
atrial and ventricular arrhythmias, 542
3-channel ECG, 73–75
Vision™ 5L ECG recorder, 73
Vista plus device (Novacor), 73, 76
HRUK. See Heart Rhythm UK (HRUK)
I
ICDs. See Implantable cardioverter defibrillators (ICDs)
Identification (ID) card, 185–188
Identity® ADx DR pacemaker, 36, 37
Implantable cardioverter defibrillators (ICDs)
arrhythmia detection, 429–431
ATP, 431–432
CRT, 400–401
device and lead issues, 346–350
device-based testing (DBT), 424
DF-4, lead connector system, 418–420
DFT( see Defibrillation threshold (DFT))
564 Index

Implantable cardioverter defibrillators (ICDs) (cont.) Kearns-Sayre syndrome, 63

dual-chamber and triple-chamber, 35 King of Hearts Express™, 77
ID card, 187, 188
implantation, 422–424
indications, children, 334–336 L
lead testing, 424, 425 Latitude® home monitoring system, 373, 381, 382
“magnet deactivation”, 217 LBBB. See Left bundle branch block (LBBB)
pacing, 424, 425, 426 Lead locking device (LLD), 462–463, 468–470,
postoperative care, 427–429 473, 474, 477
preparation, implant, 421–422 Lead measurements, implantation
SCD( see Sudden cardiac death (SCD)) anchoring, atrial, 174
subcutaneous( see Subcutaneous implantable anchoring, ventricular, 173
defibrillator (S-ICD)) black and red “crocodile clips”, 170
therapy, 405–406 electrogram, atrial, 170, 172
waveforms, 427 insertion, 175
Implantable loop recorders pacing/stimulation threshold, 170–172
activator applied, Reveal® device, 79, 80 sensing threshold, 170–172
chest X-ray, 80 suturing, ventricular, 173, 174
Reveal®, 79 threshold, atrial, 170, 173
Implantation technique Legend™, 29, 31
antiseptic solution, 144, 145 Left bundle branch block (LBBB), 357
axillary vein approach, 156–157 Lithotripsy, 220
cephalic vein approach( see Cephalic vein approach) LLD. See Lead locking device (LLD)
electrode positioning( see Electrode positioning) LLD EZ™ lead locking device, 468–470, 471,
epicardial devices, 137 474, 478
equipment and personnel, 138–141
instrument pack, 140–144
Ioban™, 146, 147 M
lead measurements( see Lead measurements, MADIT-CRT study, 401
implantation) Malignant vasovagal syndrome (MVS), 64–66
left pectoral region, 144, 145 Managed Ventricular Pacing® (MVP®), 212
operating theatre/pacing room, 137–138 Maximum tracking rate (MTR), 206
pacemaker pocket, 176–180 Medical implant communications service
pacemaker programming, 180–181 (MICS), 196, 243, 245
“scrub-up” room, 144 Medicines and Healthcare products Regulatory Agency
subclavian approach, 147–153 (MHRA), 241–243
unusual anatomy, 157 Medtronic/Alcatel nuclear-powered pacemaker, 22
InSync® III CRT-P device, 374 Medtronic CareLink® service, 244, 245
InSync Marquis™, 373, 375 Medtronic MINIX™ SSI pacemaker, 25
InSync Maximo™, 373, 375 Medtronic programmer, 392, 393
International standard (IS) Medtronic SelectSecure®, 344, 345
IS-1, 205 Medtronic’s Activitrax™, activity-sensing rate-responsive
IS-4, 205 pacemaker, 28, 29
Interventricular mechanical delay (IVMD), 399 Medtronic’s CareLink® service, 244, 245
Ioban™ (3M Health Care), 146, 147 Medtronic’s InSync® CRT device, 36
IRSplus (Intrinsic Rhythm Support), 212 Merlin.net™ PCN, web-based management
IVMD. See Interventricular mechanical system, 248
delay (IVMD) Merlin™ patient care system, 82
MHRA. See Medicines and Healthcare products
Regulatory Agency (MHRA)
J MICS. See Medical implant communications service
Joint Royal Colleges of Physicians Training Board (MICS)
(JRCPTB), 543, 546, 554 Microthin P1® 0522 unipolar
JRCPTB. See Joint Royal Colleges of Physicians device, 31, 32
Training Board (JRCPTB) Minute ventilation (MV) offset, 213
MIRACLE-ICD study, 401
MTR. See Maximum tracking rate (MTR)
K MultiBIOrate®, 35
Kappa® DDDR device, 500 Multicenter In Sync Randomized Clinical Evaluation
Kappa 700 series DDDR pacemaker, 110 (MIRACLE) study, 399–400
Index 565

Multisite Stimulation in Cardiomyopathy (MUSTIC) cross-talk, 204

trial, 399 demand pacing (inhibited), 204
MVS. See Malignant vasovagal syndrome (MVS) DF-1, 204
MyoDex™, 486, 487 DF-4/SJ4, 204
entrance block, 205
escape interval, 205
O exit block, 205
Omnicell® cabinets, 96, 100 filar, 205
Orchestra™ programmer, 231, 232 fixed-rate pacing, 205
Oscor® Inc., 129, 130 housekeeping current, 205
Over the wire (OTW) technique, 366, 370 hysteresis, 205
interval, 207
intracardiac electrogram, 205
P IS-1, 205
Pacemaker and ICD implantation, children IS-4, 205
active vs. passive endocardial leads, 344, 345 lead impedance, 205–206
anesthesia, 339 magnet rate, 206
AV block, 331–332 minute ventilation, 206
bradycardia pacing indications, 331, 332 missing, 206
CHD( see Congenital heart disease (CHD))CRT, 336 mode, 206
device and lead issues, ICD, 347–350 MTR, 206
device choice, 352–356 multisite pacing, 206
endocardial leads placement, 350–351 myocardial lead, 207
epicardial pacing systems, 342–343 myopotential inhibition, 207
indications, ICD, 334–336 non-committed, 207
lead, 345–346 optimal AV delay, 207
normal heart rates, 331, 333 output pulse, 207
right ventricular lead placement, 344–345 oversensing, 207
side and site, 339–340, 342 pacemaker Wenckebach, 207
tachyarrhythmias, permanent pacing, 332, 334 PMT, 207–208
venous access, 341, 343 programmed standby rate,208
Pacemaker-mediated tachycardia (PMT) PVARP, 208
24 h ECG Holter monitoring, 520 rate drop response, 208
PVARP, 276, 281 rate-responsive pacing, 208
retrograde conduction, atrial activity, 207 reed switch, 209
telemetered ECG tracing, 518, 519 refractory period, 209
troubleshooting, 279 relative threshold, 208
Pacemaker programming, 180–181 RRAVD, 208–209
Pacesetter® Systems Inc. desk-top/semi-portable safety margin, 209
programmer, 26, 28 sensitivity, 209
Pacesetter® Systems Inc. Vivalith™ 10 unipolar and sequential pacing, 209
bipolar devices, 31, 32 slew rate, 209
Pacing systems analyzer (PSA) strength-duration curve, 209
atrial and ventricular electrogram, 170 switching, mode, 206
cathode and anode, 172 synchronous pacing, 209
description, 207 TARP, 209
uni/bipolar electrodes, 169 threshold, 208, 209
Pacing terminology triggered pacing, 209–210
accelerometer, 196 undersensing, 210
acute-chronic threshold change, 196 unipolar pacing, 210
asynchronous pacing, 200 upper rate behavior, 210
automatic (basic) interval, 202 ventriculoatrial (VA) interval, 210
auto rest rate, 202 voltage threshold, 210
A-V interval/delay, 200, 202 VRP, 210
AV synchrony, 202 VS-1, 210
base rate, 202 Paradym CRT 8750 biventricular device, 194, 197
bipolar pacemakers, 204 Paradym™ 8750 CRT-D device, 394, 396, 397,
capture, 204 434, 435
coaxial lead, 204 Paradym DR 8550 ICD, 194, 198
committed, 204 Pathology, pacing, 51–57
566 Index

Patient symptoms, troubleshooting “printout”, time of discharge, 187, 189

arrhythmia, 516, 518 wound inspection, 183–184
dizziness/presyncope and syncope, 508–509, 511 Premature ventriclar complexes (PVCs), 541
fatigue and shortness, breath, 511–514 Post-ventricular atrial blanking period (PVAB), 393
loss of capture, 521–523 Programmers, 194, 196
loss of output, 523, 524 Promote Accel™ II, 416
pacemaker syndrome, 520 Promote Quadra™ CRT-D, 419, 421
phrenic nerve stimulation, 514 Promote™ RF, 418
PMT, 518, 519 PSA. See Pacing systems analyzer (PSA)
Pediatrics and congenital heart disease, 68–69 Pseudomalfunction, troubleshooting
Peel-away plastic introducer kits, 27, 28 algorithms, ventricular pacing, 534–537
Permanent pacemakers and leads auto capture algorithms, 534
accessories, 129–131 back-up pacing mode, 534
active fixation, 124–126 battery depletion, 536
advanced programmability, 112 magnet operation, 536, 538, 539
analyzers/programmers, 132, 135–136 noise reversion, 540
digital pacemaker technology, 117–118 rate drop response, 531, 533
dual chamber pacing( see Dual chamber pacing) rate response, 531, 534
electrode insulation and tip structures, 118, 122–124 sleep function and hysteresis, 539–540
endocardial, 119–121 upper rate behavior, 530–532
IS-1 bipolar connector pin, 122, 129 VSP, 541
lithium-iodine power source, 89 PVAB. See Post-ventricular atrial blanking period
multisensor pacing, 111–112 (PVAB)
NASPE/BPEG generic (NBG) code, 87–89 PVARP. See Post-ventricular atrial refractory period
passive fixation, 124 (PVARP)
physiological pacing( see Physiological pacing) PVCs. See Premature ventriclar complexes (PVCs)
polarity, 126–127
prescription, 131–132
single chamber pacing, 89, 97 Q
size reduction, 89, 95 Q-T sensors, 282
special functionality, 112–116 Quartet™ quadripolar, 385
storage, 95–97 Quick Look II Screen, Medtronic programmer, 231, 233
terminal pin sizes, 127 Quik-Combo™ (Medtronic) external pacing, 288, 289
“tined” and “screw-in”, 118, 121 Quintech® TX 911 rate-adaptive, multiprogrammable
Physiological pacing, 105 device, 28, 29
PMT. See Pacemaker-mediated tachycardia (PMT)
Pneumothorax
chest drain insertion, 250, 251 R
Post-ventricular atrial refractory period (PVARP) Rate-adaptive pacemakers, 280, 282
automatic, adjustment, 212 Rate-adaptive/rate-responsive pacing (VVIR, DDDR),
description, 208 106–109
Precautions, permanent pacemaker implantation Rate-responsive AV delay (RRAVD), 208–209
ablation, RF, 219 Reply™ DR pacemaker, 106, 111, 193, 194
cardiacmonitoring systems, 221 Reveal® DX, 80, 81
cardioversion/defibrillation, 220 Reveal® XT, 80, 81
cellular phones, 220 RF. See Radio frequency (RF)
diathermy, 219 RRAVD. See Rate-responsive AV delay (RRAVD)
EAS/metal detectors, 220
ECT, 220
EMI, 215 S
lithotripsy, 220 SAC. See Specialist Advisory Committee (SAC)
magnets, 215, 217 SafeR™, 213
SCUBA diving, 220 SafeSheath®, 361, 365
TENS, 220 SBR. See Sudden bradycardia response (SBR)
vigorous sports, 220 SCD. See Sudden cardiac death (SCD)
Predischarge pacemaker SCV. See Subclavian vein (SCV)
advice, patients, 187–188, 190, 191 Sensia™ DR device, 106, 110
device interrogated/programmed, patient, 183 S-ICD. See Subcutaneous implantable defibrillator
identification (ID) card, 185 Sick sinus syndrome
pneumothorax and lead displacement, 183 paroxysmal atrial flutter and fibrillation, 63, 66
Index 567

sino-atrial block, 63, 65 coils, 410, 418, 419, 426

“tachy–brady” syndrome, 63, 67 obstruction, 271–272, 275, 277, 328–329
Siemens-Elema 659 pacemaker, 26 persistent left-sided, 316–318
Sigma™ series, 96, 101 SVC. See Superior vena cava (SVC)
Single chamber pacing Symphony D 2450, 508, 510
atrial demand, 100–101 Symphony® DR, 115
fixed rate VOO, 89, 97, 101
ventricular demand, 97–100
SJM Confirm™, 81–82 T
SLS II. See Spectranetics Laser Sheath (SLS II) “Tachy–brady” syndrome, 63, 67
Specialist Advisory Committee (SAC) TARP. See Total atrial refractory period (TARP)
medical training, cardiology, 546–547 Telectronics Autima® dual-chamber pacemaker, 26, 31,
training program, 544 32
Spectranetics CVX-300® Excimer Laser generator, 468, Telectronics 120 VVI pacemaker, 20
469 Teligen™ ICD device, 275, 280, 410, 418
Spectranetics laser sheath (SLS II), 463, 469–471, 474, Temporary pacemaker (TPM)
477, 479 clinical indications, 284–286
Spectranetics® laser extraction, 37 complication rates, 287–288
Stille ImagiQ™ imaging table, 140, 141 description, 283
St. Jude Medical’s Merlin@home™ transmitter, 248 insertion and venous anatomy, 296, 298
Stratos® LA, 116 placing electrode pad, 284, 290
Structural cardiac abnormalities Temporary pacing
atrial septal defect/persistent foramen ovale, 319 aortic valve replacement, 283
congenitally corrected L-transposition, great vessels, AV block, acute MI( see Atrioventricular (AV) block)
319–320 box, 283–284
dextrocardia, 315, 316 cardiac surgery, during/after, 287
D-transposition, great vessels, 322–327 clinical indications, 284
Ebstein’s abnormality, 317–319 complications, 310, 312–314
epicardial pacing, structural defects, 324–327 description, 283–284
persistent left-sided SVC, 316–317 ECG indications, 284, 285
preoperative investigations, 315 external and transthoracic, 288–290
prosthetic valves, 329 external pulse generators( see External pulse
SVC obstruction/occlusion, 328–329 generators, temporary pacing)
tetralogy of Fallot, 320–321 leads, 292–296
tricuspid atresia/univentricular heart, 321–322 methods, 292–293
ventricular septal defects, 320 techniques, 287–288
Subclavian vein (SCV) TPM( see Temporary pacemaker (TPM))
head-down tilt, 148, 149 transvenous, requirements, 289, 290–292
punctures, 153, 298–301 Tendril™ ST electrode, 99
Subcutaneous implantable defibrillator (S-ICD) TENS. See Transcutaneous electrical nerve stimulation
device positions, 432 (TENS)
ICD follow up, 432, 434 Tetralogy of Fallot
interrogation, 434–437 active fixation leads, 321
possible sensing vectors, 433 description, 320–321
precautions, 437–439 pulmonary regurgitation, 321
Q-Trak™ subcutaneous electrode, 432 structure, 321, 322
remote monitoring, 437 The Concerto™, 373, 376
SQ-RX™ pulse generator, 432 The Frontier™ II RF CRT-P device, 375
tunneling, leads, 432, 434 The Livian®, 373, 376
VF detection, 432, 434 The Lumax 340 HF-T, 373, 377
Sudden bradycardia response (SBR), 213 The Promote™, 373, 377
Sudden cardiac death (SCD) Thoracic duct injury, 255
Brugada syndrome, 403, 404 Thoracoscopic and robotic epicardial lead placement,
definition, 403 501–503
long-QT syndrome, 403 Tilt table testing
LV aneurysm and myocardial scar, 403, 405 defined, 82
prevention, 403, 405 Task Force® monitor, 83, 84
ventricular tachyarrhythmias (VT), R-on-T ectopic, “Tined” passive-fixation lead, 124
403, 404 Total atrial refractory period (TARP), 34, 209
Superior vena cava (SVC) TPM. See Temporary pacemaker (TPM)
568
Training, pacing
academic meetings, 560
arrhythmia societies, 558–559
Australia, 554, 558
books and journals, 560
device manufacturer websites, 560
and electrophysiology, accreditation, 559
UK, 546–554
USA, 543–546
Transcutaneous electrical nerve stimulation (TENS), 220
Transtelephonic monitoring, 542
Troubleshooting, device implantation
defibrillation and anti-tachycardia pacing, 501
description, 501, 508
diagnostics, pacemaker, 505–510
patient and device familiarization, 501–504
patient symptoms( see Patient symptoms,
troubleshooting)tests, 541–542
Twiddler’s syndrome
description, 274–275
V W
Vario® (noninvasive) measurement of threshold, 26
VCM. See Ventricular capture management (VCM)
Ventak®, 32
Ventricular capture management (VCM), 36
Ventricular high rate (VHR) episode, 516, 517
Ventricular-inhibited (VVI) pacemaker, 97–100
Index
Ventricular rate regulation (VRR), 213
Ventricular rate stabilization (VRS), 213
Ventricular refractory period (VRP), 210
Ventricular safety pacing (VSP), 213, 541
Ventricular-triggered (VVT) pacing mode, 97–98, 100
Virtuoso™ ICD, 410
Vision™ 5L Holter ECG recorder, 74
Vista plus device (Novacor), 73, 76
Vitatron C-series, 117
Vitatron fixed-rate (VOO) device, 16, 17
Vitatron handheld programmer, 27
Vitatron T20 SR pacemaker, 110
Vitatron’s Quintech® TX rate-responsive
pacemaker, 28
Vitatron’s Vitalith™ VVI pacemaker, 20, 21
V-Pace™, 295
VRP. See Ventricular refractory period (VRP)
VRR. See Ventricular rate regulation (VRR)
VRS. See Ventricular rate stabilization (VRS)
VSP. See Ventricular safety pacing (VSP)
Wavelet technology, 78
Wolff–Parkinson–White (WPW) syndrome, 56, 57
Z
Zucker® and Myler® catheter, 293, 295