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Cardiac Arrhythmias I:

Atrioventricular Conduction
Disturbances and
Bradyarrhythmias
Michael H. Lehmann, M.D.
Clinical Professor of Internal Medicine
Director, Electrocardiography Laboratory


Overview of Cardiac Arrhythmias


Why Are Arrhythmias Important?
Symptoms span palpitations, lightheadedness,
syncope (fainting) and cardiac arrest
May be the first manifestation of heart disease
May precipitate or exacerbate heart failure or
ischemia
Some arrhythmias can predispose to intracardiac
clot formation and embolic events (stroke,
myocardial infarction, peripheral emboli)
EKG Assessment of Arrhythmias
Is the rate slow (< 60 beats/min [> 5 big boxes])?
Is the rate fast (>100 beats/min [< 3 big boxes])?
What drives the P waves?
What drives the QRS complexes?
What is the relationship between Ps and QRSs?
Sites of Disturbances in Impulse Formation
or Conduction Leading to Bradyarrhythmias
SA Node
AV Node
His-Purkinje
System
Components of Atrioventricular (AV) Conduction
His-
Purkinje
System
AV
Node
Intraventricular Conduction
Disturbances
Left bundle branch
Left anterior fascicle
Septal fascicle
Left posterior
fascicle
Right bundle branch
Intraventricular (His-Purkinje) Conduction System
(AV node)
His bundle
Rule for QRS Width:
Any electrophysiologic process that engenders
a departure from synchronous activation
of the ventricles tends to widen the QRS
Normal synchronous
overlapping activation
of both ventricles:
On
time
Asynchronous
scenario I:
Late
Head start
On
time
(or late)
Asynchronous
scenario II:
QRS
Narrow
Wide
Wide
QRS Width: Synchronous vs. Asynchronous
Ventricular Activation
Generation of Narrow QRS Complex
(s .10 sec [2.5 little boxes])
Intact Purkinje system
assures synchronous,
overlapping activation
of right ventricle (RV)
and left ventricle (LV)
Horizontal
plane with
precordial
leads:
RV
LV
Bundle Branch Blocks
Right Bundle Branch Block (RBBB)
Late right ventricular
activation, with slow
muscle-to-muscle
conduction
RV is activated
via the left bundle
QRS Distortion Induced by RBBB
Note terminal rightward
delay with QRS widening
(> .12 sec [3 little boxes],
with complete RBBB)

rSR
pattern
Broad
S wave
Initial QRS
inscription is
normal due to
normal LV activation
Note T wave pointing in direction opposite to
late rightward component (2 repolarization effect)
Complete RBBB Pattern
V1 V6
rsR
complex
Broad
S wave
(Lead I
similar)
Left Bundle Branch Block (LBBB)
Delayed left ventricular
activation, with slow
muscle-to-muscle
conduction
LV is activated
via the right bundle
QRS Distortion Induced by LBBB
Broad
monophasic
R wave
Entire QRS dominated by
marked leftward delay
and is wide (> .12 sec
[3 little boxes], with
complete LBBB)

Broad
S wave
Note absence of septal-q in V6; andT wave pointing
in direction opposite to QRS (2 repolarization effect)
Broad
S wave
Broad
R wave
(Lead I
similar)
Complete LBBB Pattern
V1 V6
Fascicular Blocks
Mean QRS Axis Quadrants in the Frontal Plane
Lead I
L
e
a
d

A
V
F

(+) ()
(
+
)

(

)

Frontal Plane Mean QRS Axis Designations
I
AVF
r s S in Lead II
for Left Axis
Deviation
Left Anterior Fascicular (/Hemi-) Block (LAFB)
Lead I
Lead
AVF
1) Initial QRS forces
directed inferiorly
to the right
LV is activated via the
left posterior fascicle
2) Bulk of QRS forces
directed superiorly
to the left
Left Axis
Deviation
(to -45
or beyond)
3) Minimal or no
QRS widening
Left Anterior Fascicular (/Hemi-) Block (LAFB)
I
II
III
Initial QRS forces directed rightward (negative in Lead I)
and inferiorly (positive in Leads II and III
rS
rS
qR
Subsequent predominant forces directed leftward
(positive in I) and superiorly (negative in II and III)
Left Posterior Fascicular (/Hemi-) Block (LPFB)
Lead I
LV is activated via the
left anterior fascicle
1) Initial QRS forces
directed superiorly
to the left

2) Bulk of QRS forces
directed inferiorly
to the right
Lead
AVF
Right Axis
Deviation
(beyond
+90)
3) Minimal or no
QRS widening
Left Posterior Fascicular (/Hemi-) Block (LPFB)
rS qR qR
I
II
III
Initial QRS forces directed leftward (positive in Lead I)
and superiorly (negative in Leads II and III
Subsequent predominant forces directed rightward
(negative in I) and inferiorly (positive in II and III)
Bifascicular Block (RBBB + LAFB)
LV is activated via the
left posterior fascicle
RV is activated
from the left
Site of
RBBB
Site of
LAFB
Bifascicular Block (RBBB + LAFB)
Note RBBB
pattern plus
left axis
deviation of
unblocked
portion of QRS
(initial .06 sec
=1.5 little
boxes)

Site of
RBBB
LV is activated via the
left anterior fascicle
Site of
LPFB
RV is activated
from the left
Bifascicular Block (RBBB + LPFB)
Bifascicular Block (RBBB + LPFB)
Note RBBB
pattern plus
right axis
deviation of
unblocked
portion of QRS
(initial .06 sec
=1.5 little
boxes)

Non-Specific Intraventricular Conduction Block
Leads I & V1
inconsistent
with RBBB;
septal q in I
inconsistent
with LBBB
QRS > .12 sec
without a
typical BBB
pattern
Causes of Intraventricular Conduction
Disturbances
Ischemic heart disease or cardiomyopathic scarring
Degenerative changes in the conduction system
Antiarrhythmic drugs that depress the inward
sodium current
Hyperkalemia (|K
+
)
Myocardial infection, infiltration (e.g., tumor)
Trauma (e.g., cardiac surgery)
Congenital abnormality

AV Block
Components of AV Conduction
His-
Purkinje
System
AV
Node
AV Block - Definitions

First Degree: Prolonged conduction time
Second Degree: Intermittent non-conduction
Third Degree: Persistent non-conduction
First Degree AV Block
(PR > .20 sec [1 big box])
II

P P P
.36
Site of delay most commonly the AV node,
but may be localized to the His-Purkinje system
Second Degree AV Block - Type I
(Wenkebach or Mobitz I Block)
P P P P
Block
II

Example of 3:2 conduction ratio; general pattern, n:n-1
Note PR | prior to block and + post-block
Characteristic of AV nodal site of block
II
Block
P P P
P
P
4:3 conduction ratio
Note first RR longer than second RR
Second Degree AV Block - Type I
(Wenkebach or Mobitz I Block)
Ladder Diagram of AV Conduction
P
QRS
Schema of a Typical
4:3 AV Wenckebach Sequence
Second RR (VV) shortens due to diminution
in the increment of AV prolongation
Pause encompassing blocked beat < 2 x PP
Second Degree AV Block - Type I
V1
7:6 Conduction Ratio
Note atypical PR & RR features
Second Degree AV Block - Type I
(Repetitive Cycles)
Group beating
(Regularly irregular rhythm)
II
4:3
4:3
II
P
P P P P P
Second Degree AV Block - Type II
(Mobitz II)
Example of 3:2 conduction ratio; general pattern, n:n-1
Note fixed PR for all conducted beats
Characteristic of His-Purkinje system site of block
Block
Block
Second Degree AV Block - Type II
P P P P P
4:3 conduction ratio
Block
II
P P P P P P
2:1 Second Degree AV Block -
Type I or Type II?
Is site of block within the AV node or His-Purkinje System?
EKG/Clinical Clues
-
to site of
2:1 Second Degree AV block
QRS narrow
Improves with exercise
(catecholamine-facilitated
conduction)
Observed in setting of
increased vagal tone (e.g.,
sleep) or AV nodal
depressant drugs
QRS wide (BBB patterns)
Unchanged (possibly even
precipitated) during
exercise
May improve with heart
rate slowing during
increased vagal tone
Favoring AV Node Favoring His-Purkinje System
-
Rules-of-Thumb only

II
P P P P P P P P P
3:1 conduction ratio, with ventricular rate in the 30s
Advanced Second Degree AV Block
(Block of > 2 Consecutive P Waves)
Pacemaker Hierarchy
(Dominant vs Subsidiary/Escape Pacemakers)
SA
Node
(+Atria)
AV Junction
(=AVN/His Bundle)
Ventricles
(= Distal Purkinje System)
Intrinsic Rate of Firing
60-100 min
1

40-60 min
1
30-40 min
1
Site of AV Block vs. Escape Rhythm
AV Node: Junctional or ventricular
His-Purkinje System: Ventricular
Junctional and ventricular (= idioventricular)
escape beats or rhythms
Are suppressed (inhibited) as long as their intrinsic
rates are overdiven by a faster pacemaker tissue or
rhythm process capturing the heart
Become manifest (escape from suppression) in
the absence of faster competing rhythms
But, firing of these pacemakers at rates faster than
their upper-limit escape rates is abnormal (i.,e.,
accelerated rhythm or relative tachycardia )
EKG Appearance of Escape Beats
Sinus
Rhythm
Atrial Junctional Ventricular
(Retrograde P waves require
intact retrograde AVN cond.)
P P
Narrow
QRS
Wide
QRS
Normal synchronous
overlapping activation
of both ventricles:
On
time
Asynchronous
scenario I:
Late
Head start
On
time
(or late)
Asynchronous
scenario II:
QRS
Narrow
Wide
Wide
QRS Width: Synchronous vs. Asynchronous
Ventricular Activation
Third Degree AV Block
(Complete Heart Block)
P P P P P P
P waves at 60 beats/min
QRS complexes (junctional escape rhythm) at 45
beats/min
Atrial and ventricular activity are completely unrelated
Junctional escape rhythm suggests AV nodal site of block
II
Third Degree AV Block
(Complete Heart Block)
V1
P P
P P
P
P waves at 50-60 beats/min
QRS complexes (ventricular escape rhythm) at 35 beats/min
Atrial and ventricular activity are completely unrelated
Ventricular escape rhythm suggests His-Purkinje site of
block
Ladder Diagram of AV Dissociation
During Third Degree AV Block
Faster atrial rate
Slower ventricular (escape) rhythm
Note that impulses block anterogradely and retrogradely
within the AV conduction system
Unreliability of Ventricular Escape Rhythm
in Third Degree AV Block
P P (P) P P P
P P P P
P P
No QRS complexes!
P P P (P) P
15 s
Physiologic AV Block
First and second degree AV block may occur
physiologically at an AV Nodal level:
in response to premature atrial impulses or atrial
tachyarrhythmias
in settings of increased vagal tone (e.g., sleep,
Valsalva maneuver, well-trained athletes)
BUT persistent 3rd degree AV block is never
physiologic
Causes of NON-Physiologic AV Block
Ischemic heart disease, cardiomyopathy and
degenerative changes
Drugs that depress AV conduction
AV Node: digoxin, beta blockers, calcium channel
blockers, amiodarone
His-Purkinje System: Antiarrhythmic drugs that depress
the inward sodium current
Myocardial infection, infiltration (e.g., tumor)
Trauma (e.g., surgery; therapeutic ablation)
Congenital abnormalities

Sinus Bradyarrhythmias
Inspiration Expiration
SA nodal acceleration SA nodal deceleration
Sinus Arrhythmia
Pacemaker Hierarchy
(Dominant vs Subsidiary/Escape Pacemakers)
SA
Node
(+Atria)
AV Junction
(=AVN/His Bundle)
Ventricles
(= Distal Purkinje System)
Intrinsic Rate of Firing
60-100 min
1

40-60 min
1
30-40 min
1
Sinus Bradycardia
II
P wave upright in leads I and II, just as in normal sinus rhythm
Causes of Sinus Bradycardia
Increased vagal tone
Drugs: beta blockers, calcium channel blockers,
amiodarone, digoxin (indirect effect)
Myocardial ischemia/infarction
Hypothyroidism
Sick sinus syndrome - degenerative/fibrotic
atrial process

Sequence of P Wave Generation
Sinus
Node
SA
Junction
Atrium
(P wave)
Non-visible process on the EKG
Sinoatrial (SA) Exit Block - Definitions
First Degree: Prolonged SA conduction time
(non-detectable on EKG; no missing P waves)
Second Degree: Intermittent non-conduction
(intermittent absence of P waves)
Third Degree: Persistent non-conduction (complete
absence of P waves; escape rhythms only)
Second Degree SA Exit Block - Type I
(Wenkebach)
P P P P
4:3 pattern
Missing
P wave
PP intervals shorten prior to block
Note unaffected, fixed PR intervals
PP:
Schema of a Typical 4:3 Second Degree
SA Exit Block (Type I) Sequence
Second PP (AA) shortens due to diminution
in the increment of SA-A prolongation
Pause encompassing blocked beat < 2 x normal PP
Sinus
Node


SA
Junct.
A
Second Degree SA Exit Block - Type II
PP:
P P
P P P
One P wave abruptly drops out on time
Missing
P wave
X 2X
2X X
P P P P
P P P P
2:1 SA Exit Block
(Every Other P wave is Dropped)
Atrial rate is abruptly cut in half
Resolution of block
P
P P P P
Sinus bradycardia Sinus arrest Slow junctional escape rhythm
(with retrograde p waves)
Sinus Arrest
Tachycardia-Bradycardia
(Form of Sick Sinus) Syndrome
Atrial Flutter
Sinus arrest Junctional
escape (tardy)
Atrial Flutter
terminates
Sinus Arrest Asystole
Sinus rhythm
Sinus brady.
Sinus arrest
V. escape
rhythm
Failure of V.
escape rhythm
Asystole
P P P
P P P P
P
Causes of SA Exit Block and Sinus
Pauses/Arrest
Increased vagal tone (very intense for sinus arrest)
Drugs: beta blockers, calcium channel blockers,
amiodarone, digoxin (indirect effect)
Myocardial ischemia/infarction
Sick sinus syndrome
Sequela of open heart surgery