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Introduction
Diagnosis of VT
Medical history and clinical examination
the presentation of a patient with a widecomplex tachy
cardia (Qrs >120 ms) is a common diagnostic dilemma
in clinical practice. several arrhythmias can present
as widecomplex tachycardia, including vt, supra
ventricular tachycardia (svt) with aberrancy or bundle
branch block (BBB), and svt with antegrade conduction
over an accessory pathway (preexcited tachycardia). in
addition, Qrs widening can be seen with other condi
tions, such as repaired congenital heart disease, drug toxi
cities, and electrolyte imbalances. However, preexcited
tachycardias, and druginduced and electrolyteinduced
Cardiovascular
Research Center,
Department of
Cardiology, Royal
Adelaide Hospital,
North Terrace, Adelaide,
SA 5000, Australia
(K. c. robertsThomson,
d. H. lau, P. Sanders).
Correspondence to:
P. Sanders
prash.sanders@
adelaide.edu.au
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Key points
The diagnosis of ventricular arrhythmias can be accurately made using
electrocardiographic algorithms
The underlying heart disease determines the prognosis of patients with
ventricular arrhythmias
in patients without structural heart disease, the treatment of ventricular
arrhythmias is focused on the elimination of symptoms
in patients with structural heart disease, implantable cardioverter-defibrillators
can prevent sudden death
Antiarrhythmic therapy has limited efficacy in patients with ventricular
arrhythmias and can have substantial adverse effects
Catheter ablation is useful to prevent recurrences of ventricular arrhythmia
Ecg criteria
the 12lead eCG is the most reliable means of differenti
ating vt from svt. as mentioned above, patients with
vt usually present with a wide Qrs complex during
tachycardia. However, a widecomplex tachycardia with a
Qrs morphology consistent with either BBB or fascicular
block is indicative of svt with aberrancy, because this
arrhythmia conducts through part of the HisPurkinje
system. aberrations associated with sustained tachy
cardias are just as likely to have a right BBB (rBBB)
pattern as a left BBB (LBBB) pattern. vt is likely to be
present if the Qrs morphology is incompatible with these
patterns.7 therefore, the physician needs to be familiar
with these Qrs morphologies.8 in a few of the eCG leads,
vt can seem to have a fairly narrow Qrs complex and
the appearance of such a narrowcomplex tachycardia on
a single lead does not exclude the possibility of vt. thus,
obtaining a full 12lead eCG in patients with tachycardia
is essential.
a number of eCG criteria have been used to differenti
ate vt from svt with aberrancy (Box 1). Heart rate is not
usually a useful criterion, as both vt and svt can occur
over a wide range of heart rates. vt and svt usually
have a regular rate; a widecomplex tachycardia that is
irregular is most likely to represent atrial fibrillation with
BBB or antegrade conduction over an accessory pathway
(Figure 1). However, irregularity of heart rate does not
exclude vt. in particular, focal idiopathic vt can mani
fest with periods of acceleration and deceleration, and so
can be irregular (Figure 2).
the most useful eCG feature that differentiates vt
from svt is the presence of av dissociation. Complete
av dissociation is present in 1050% of vts and only
in exceedingly rare cases of svt (Figure 3). 4,911 in
addition, variable retrograde conduction, in a 2:1 or
wenckebach pattern, can be seen in patients with
vt. wenckebach retrograde conduction is characterized
by prolonged ventricularatrial intervals followed by a
beat with av block. the presence of av dissociation is
dependent upon the rate of the vt, and detection of this
sign is dependent upon the experience of the clinician in
interpreting the eCG. Fusion and capture beats during
a widecomplex tachycardia imply the presence of av
dissociation (Figure 4). a fusion beat is a Qrs complex
arising from two different sources within the ventricle,
one usually from a sinus beat propagating down the
normal conduction system and one beat from the vt. a
capture beat is a sinus beat that conducts down the His
Purkinje system producing a narrow Qrs complex during
tachycardia. Both beats usually require the presence of a
slow vt to affect ventricular activation.
the width of the Qrs complex has also been shown
to be useful in diagnosing vt. in 1978, wellens et al.
observed that almost 70% of vts had a Qrs >140 ms,
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whereas all svts had Qrs duration of <140 ms, although
no patients in this study had preexisting BBB.11 in the late
1980s, akhtar and colleagues demonstrated that, because
the Qrs duration is slightly longer with LBBB, the diag
nostic accuracy of using a Qrs >140 ms with rBBB
morphology and a Qrs >160 ms with LBBB morphology
is excellent, with PPvs of 100% and 96%, respectively.10
However, a relatively narrow Qrs (<120 ms) does not
absolutely exclude the diagnosis of vt, as can be seen
when the tachycardia involves the Purkinje system. the
Qrs axis alone is fairly poor at differentiating vt from
svt, because block in the anterior and posterior fascicles
can produce vectors between 90o and +150o, which are
also commonly seen during vt. the one exception is the
combination of LBBB morphology and rightaxis devia
tion, which is almost always the result of vt.10 a right
superior (northwest) axis, which is a clear sign of vt, is
present in approximately one quarter of patients.10
single criteria are not particularly useful for differenti
ating between vt and svt; therefore, a number of algo
rithms have been proposed for diagnostic purposes.4,9,12
the most widely used and cited is the algorithm pro
posed by Brugada and collegues.12 this algorithm com
prises four steps, with the first two steps involving the
assessment of an rs complex in the precordial leads
(Figure 5a). the investigators reported that this sign
had a sensitivity and specificity for the diagnosis of vt
of 99% and 97%, respectively.12 Other researchers4,9 have
found this algorithm to be useful, but to be less accurate
than originally reported by Brugada and coworkers. in
2008, vereckei et al. provided a simpler algorithm for
the identification of vt (Figure 5b), which involves the
assessment of lead avr only.9 in a blinded comparison,
this new model was found to have greater sensitivity and
specificity (97% and 75%, respectively) than the widely
quoted Brugada algorithm.6
although eCG criteria are predominantly used for
diagnosing vt, for cases in which doubt exists about the
type of arrhythmia, an electrophysiological study can
provide the diagnosis. in patients with coronary artery
disease and vt, a high likelihood exists of inducing the
clinical arrhythmia with reasonable reproducibility. 13
in other disease states, however, this likelihood is much
lower. isoproterenol is useful in provoking idiopathic
PvCs and vt.14
Figure 1 | 12-lead electrocardiogram of atrial fibrillation with ventricular preexcitation over a left-sided accessory pathway. The morphology is right bundle
branch block and Northwest axis, suggestive of ventricular tachycardia. However,
the rhythm is irregular. The concordance suggests a basal location in the left
ventricle for the origin of the arrhythmia.
a
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
VI
II
V5
b
I
II
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aVR
V4
V1
II
aVL
V2
V5
III
aVF
V3
V6
25 mm/s; 1 cm/mV
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
Focal vT
the most common form of idiopathic vt is focal vt
arising from the right ventricular outflow tract, which
accounts for approximately 6070% of idiopathic vts.20
these focal vts can manifest as recurrent PvCs or paroxys
mal monomorphic vt, usually with LBBB morphology
and marked inferior axis. Patients, who are typically aged
3050 years, often present with palpitations and, occasion
ally, presyncope. Focal vt is also observed on the eCGs
of asymptomatic patients. exercise testing reproduces
the patients clinical vt in 2550% of cases.21,22 in some
patients, vt is suppressed by exercise and appears during
the recovery phase whereas, in other patients, vt initiates
during exercise. although the right ventricular outflow
tract is the origin of the majority of focal vts, many other
sites (particularly the structures around the outflow tract
regions) can also produce PvCs or paroxysmal vt (Box 2).
in addition, the papillary muscles, particularly in the left
ventricle, have been recognized as a fairly common site of
focal vt.2326 the main differential diagnosis that needs to
be excluded in patients with suspected focal vt is arvC,
which can also present as a vt with repetitive LBBB
morphology. twave abnormalities in leads v1v3 on
the baseline eCG, multiple vts with LBBB morphology,
a family history of arvC, and right ventricular structural
abnormalities support a diagnosis of arvC.18,27
Mechanisms
the majority of focal vts seem to be caused by cyclic
adeno sine monophosphate (aMP)related activity,
although the evidence for this mechanism, which was
presented by Lerman and colleagues, 14,28,29 is limited.
Catecholamine stimulation of the adrenergic receptor
results in a rise in intracellular cyclic aMP, producing an
increase in the levels of intracellular calcium and release
of calcium from the sarcoplasmic reticulum. this process
then gives rise to delayed afterdepolarizations and vt.
Focal vts can be induced with isoproterenol, atropine,
aminophylline, and rapid pacing, but not usually with
programmed ventricular stimulation.14 Other than the
work by Lerman and his group, very little research has
been carried out into the mechanisms of focal vt.
Management
the treatment of patients with focal vt depends on the
frequency and severity of symptoms, as this condition has
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2011 Macmillan Publishers Limited. All rights reserved
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a
Brugada algorithm
Absence of RS complex in all precordial leads
Yes
aVR algorithm
Presence of an initial R wave
No
Yes
VT diagnosed
No
VT Diagnosed
No
VT diagnosed
No
VT diagnosed
Presence of notch on descending limb of a
negative onset and predominantly negative QRS
AV dissociation
Yes
No
Yes
VT diagnosed
No
VT diagnosed
Vi/Vt 1
Yes
No
Yes
No
VT diagnosed
SVT diagnosed
VT diagnosed
SVT diagnosed
Figure 5 | Electrocardiographic algorithms of broad complex tachycardia to differentiate between VT and SVT. a | Brugada
algorithm. From Brugada, P. et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS
complex. Circulation 83, 16491659 (1991) with permission from Wolters Kluwer Health. b | aVR algorithm. Reprinted from
Heart Rhythm, 5, Vereckei, A. et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex
tachycardia. 8998, copyright (2008), with permission from Elsevier. vi /vt measures the vertical excursion (in mV) recorded
on the electrocardiogram during the initial (vi) and terminal (vt) 40 ms of the QRS complex. Abbreviations: AV, atrioventricular;
SVT, supraventicular tachycardia; vi /vt, ventricular activation velocity ratio; VT, ventricular tachycardia.
Fascicular vT
Fascicular vt, which is less common than focal vt, arises
from the left ventricle and presents with a rBBB morph
ology and predominantly leftaxis deviation (Figure 4).
Fascicular vt usually manifests in patients aged between
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Box 2 | Common locations of focal VT
Right ventricular outflow tract
Left ventricular outflow tract
Aortic cusps
Pulmonary artery
Mitral annulus
Tricuspid annulus
Papillary muscles
Epicardium
Abbreviation: VT, ventricular tachycardia.
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and can be useful in vt associated with ischemia or
myocardial infarction.64 However, in patients with slow
and stable vt, the efficacy of lidocaine is limited.6567
intravenous procainamide is an appropriate therapy in
these patients, as it rapidly slows and terminates vt.65
although procainamide is successful for acute arrhyth
mia termination in around 75% of patients with sustained
monomorphic vt, its use can be limited by hypotension,
which occurs in approximately 20% of these indivi
duals.68,69 amiodarone is also useful, but its onset of action
is slower than lidocaine or procainamide, and the results
of acute termination studies have been variable. 67,7072
However, amiodarone is less likely to produce hypotension
than procainamide.68 in some areas of the world, intrave
nous sotalol (australia, europe) and ajmaline (europe)
are available and have been shown to be effective.66,73
transvenous catheter pace termination, by application
of ventricular pacing at a faster rate than the vt, can
also be performed to treat sustained vt. this approach
is often effective and can be used in combination with
antiarrhythmic agents.74,75
Secondary prevention
recurrence of vt is frequent, with approximately 50% of
patients having subsequent episodes in the 2year period
following the initial event.7679 Patients who have been
resuscitated from a cardiac arrest, or who have experienced
vt that has produced hemodynamic compromise, have
a death rate in the first year postevent of approximately
20%.80,81 in 1997, the aviD study 82 demonstrated that iCD
use reduced this risk by 31% over 3 years compared with
amiodarone. whether iCDs should be used in patients
who have sustained vt without hemodynamic compro
mise and LveF >35% is controversial, and currently little
data are available to answer this question. although iCDs
effectively treat ventricular arrhythmias, shocks from these
devices can have substantial psychological consequences
and may increase the risk of death.83,84
Medical therapy can also be beneficial in the secondary
prevention of vt. among patients with heart failure, who
are at high risk of vt, both angiotensinconvertingenzyme
inhibitors and blockers have been shown to reduce
mortality and the incidence of sudden death.8588 the
class i antiarrhythmic drugs flecainide and propafenone
actually increase mortality in patients at risk of ventricu
lar arrhythmias.89,90 in patients with an iCD, amiodarone
and sotalol can reduce the number of device therapies,
but do not reduce mortality.63,91 Connolly and colleagues
randomly assigned patients who had sustained ventricular
arrhythmia, an LveF of 40%, and an iCD, to receive a
blocker, sotalol, or amiodarone plus a blocker.78 Over
a 12month followup period, iCD shocks occurred in 39%
of patients in the blocker group, 24% of those receiving
sotalol, and 10% of those assigned to the combination of
amiodarone and a blocker. in addition, discontinuation
rates were high in the sotalol and amiodarone groups.78
Mexiletine can be used as a secondline therapeutic agent
for recurrent ventricular arrhythmias, particularly in com
bination with other antiarrhythmic medications, although
adverse effects can limit its use.9294
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iCD shocks (27% versus 47%) and a longer time to recur
rence of vt (median 19 months versus 6 months).77 to
date, no randomized trials comparing catheter ablation
with antiarrhythmic therapy in the prevention of vt have
been conducted.
Polymorphic vT
Polymorphic vt is defined by a changing Qrs morph
ology from beat to beat, which can be sustainedoften
requiring emergency cardioversionor selflimiting.
evaluation of the underlying substrate for polymorphic
vt is important. although the most common cause of
polymorphic vt is acute ischemia, patients with other
conditions such as long Qt syndrome, Brugada syndrome,
catecholaminergic polymorphic vt, and idiopathic vF
can also present with polymorphic vt.
Coronary angiography should be performed to
exclude ischemia in patients with recurrent poly
morphic vt. Correction of electrolyte abnormalities
and stabilization of heart failure are also important.
intravenous administration of a blocker is the treat
ment of choice for these patients3 and improves mortality
in those with myocardial infarction and recurrent poly
morphic vt.115 amiodarone is also effective in control
ling episodes of polymorphic vt.116,117 in patients with
myocardial infarction, PvCs arising from the Purkinje
system in the scar border zone can trigger episodes of
polymorphic vt. Catheter ablation can be used to target
these sites and suppress vt.118 Catheter ablation can
also be successful in other substrates causing PvCs and
polymorphic vt.119,120
Conclusions
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