Clinical Management of Ventricular
Cara N. Pellegrini, MD, and
Melvin M. Scheinman, MD, FACC
Abstract:Ventricular tachycardia (VT) may be mono-
morphic or polymorphic. Although commonly related
to organic heart disease, a significant percentage of
VTs are idiopathic (occurring in patients with other-
wise normal hearts). Correctly identifying the sub-
strate and mechanism of the tachycardia is essential for
proper management. Although therapy for monomor-
phic VT associated with structural heart disease fo-
cuses on tachycardia suppression and reduction of
sudden cardiac death (SCD) risk, idiopathic monomor-
phic VT generally does not entail an increased risk of
SCD and treatment is aimed primarily at symptom
reduction. Polymorphic VT associated with ischemia or
an acquired precipitant that prolongs the QT interval
the congenital arrhythmia syndromes, which demand
genetic testing to define the underlying problem. This
review describes the diagnosis, mechanisms, etiology, and
management of monomorphic and polymorphic VT, with
attention to recent advances in biological understanding
and the most current therapeutic recommendations.
(Curr Probl Cardiol 2010;35:453-504.)
entricular tachycardia (VT) is an arrhythmia defined by a rate
?100 bpm that originates in the ventricles and is usually associ-
ated with wide QRS complexes (?120 ms) in adults. In its
sustained form it can produce hemodynamic compromise or cardiac
arrest. Even if nonsustained, it can be associated with bothersome
The authors have no conflicts of interest to disclose.
Curr Probl Cardiol 2010;35:453-504.
0146-2806/$ – see front matter
Curr Probl Cardiol, September 2010453
symptoms, and if persistent, can lead to degeneration of cardiac function
because of a tachycardia-induced cardiomyopathy.
VT with a single, stable QRS morphology is identified as monomorphic,
whereas polymorphic VT has a changing QRS morphology. Specifically,
if a VT has no constant morphology for more than 5 complexes, has no
clear isoelectric baseline, or has QRS complexes that are asynchronous in
multiple simultaneously recorded leads, it is said to be polymorphic.1VT
is considered sustained if it lasts ?30 seconds, although some argue that
15 seconds is sufficient, as treatment may be required in this time frame.
The electrocardiographic (ECG) diagnosis of VT can prove difficult.
Although VT accounts for up to 80% of cases of wide complex
tachycardias in unselected populations, there is a broad differential
diagnosis.2About 15%-30% of the time, a wide complex tachycardia may
be the result of a supraventricular tachycardia (SVT) with abnormal
interventricular conduction.3This can be due to bundle branch block or
aberration or preexcitation over an anomalous atrioventricular connec-
tion, such as occurs in Wolff–Parkinson–White syndrome (Fig 1).
Additionally, a ventricular paced rhythm can produce a wide complex
History and Physical Examination
A focused history can be helpful. In an emergency department based
study of wide complex tachycardia, the presence of a history of prior
myocardial infarction (MI), heart failure, or recent angina each had a
positive predictive accuracy of 95% for VT, although no clinical factors
were strongly predictive of a SVT and many cases of VT occurred in
patients without any of the above characteristics.4Of note, patients with
organic cardiac disease, especially elderly patients, also commonly present
with atrial arrhythmias, such as atrial flutter, which if the patient happens
to have a baseline bundle branch block, may mimic VT. If the tachycardia
has recurred over a period of more than 3 years, SVT is more likely5;
conversely, if the first occurrence of the tachycardia was after an MI, VT
is extremely likely.6Of note, the hemodynamic stability of a patient does
not distinguish VT from SVT, but rather has more relation to the rate of
the tachycardia and overall substrate of the patient.7Inappropriate
treatment of a hemodynamically stable patient with VT and structural
heart disease, with verapamil for presumed SVT, for example, may create
a situation of hemodynamic instability.8
454 Curr Probl Cardiol, September 2010
Physical examination may also be revealing if atrioventricular (AV)
dissociation is evident. “Cannon” A waves in the jugular venous wave-
form (due to atrial contraction against a closed tricuspid valve), a
variable-intensity S1 (due to variation in tricuspid and mitral leaflet stage
of opening at the time of dissociated ventricular systole), and variation in
systolic blood pressure unrelated to respiration (due to the dissociated
atrial contraction producing variable left ventricular filling), are all
possible manifestations of AV dissociation. Valsalva, carotid sinus
FIG 1. Examples of leads V1and V6in both left bundle branch block and right bundle branch
block types of QRS complexes in different types of wide complex tachycardia. ECG,
electrocardiogram; SVT, supraventricular tachycardia; WPW, Wolff–Parkinson–White syn-
drome. (Reproduced with permission from Miller et al.3)
Curr Probl Cardiol, September 2010455
massage, or adenosine may facilitate diagnosis of AV dissociation; if the
tachycardia terminates, SVT is strongly suggested as the etiology,9although
VT due to a triggered mechanism may be terminated as well.10-12
ECG. The ECG remains the cornerstone of VT diagnostics (Table 1).
Unfortunately, despite the plethora of criteria to help distinguish VT from
the most common alternative, SVT with aberrancy, all have limitations;
many are complicated, and in certain rare instances, even perfect
application of the criteria results in the incorrect diagnosis. Particularly
difficult situations include VT in children, VT originating from the
ventricular septum, fascicular VT, and some idiopathic VTs. The mor-
phologic criteria described below may fail as these more narrow VTs
access the heart’s specialized conduction system. In addition, SVT in the
setting of a class 1C antiarrhythmic agent and antidromic atrioventricular
reentrant tachycardia can be virtually indistinguishable from VT. None-
theless, with proper criteria application, successful diagnosis can be
performed in most patients.
Fred Morady: In antidromic atrioventricular reentrant tachycardia, ventricular
activation occurs through ventricular muscle, as in most ventricular tachy-
cardias. The ventricular insertion of left-sided accessory pathways is at the
mitral annulus. Therefore, if ventricular tachycardia arises near the mitral
annulus, the QRS morphology often is identical to that of antidromic
atrioventricular reentrant tachycardia.
At the most simple level, if a wide complex tachycardia appears to be
consistent with a typical bundle branch block (BBB) pattern, SVT is
suggested, whereas if the tachycardia is not manifest by some combina-
TABLE 1. Characteristics of wide complex tachycardia favoring diagnosis of ventricular
● QRS complexes ?0.14 s for RBBB and ?0.16 s for LBBB tachycardias (in the absence
of antiarrhythmic drugs)
● A superior frontal plan axis in RBBB and in a right inferior axis in LBBB tachycardias
● Evidence of A-V dissociation (fusion complexes, capture beats)
Morphologic criteria, focusing on ECG leads V1-2and V6
RBBB: monophasic R, qR, Rr=, and RS in V1and RS ratio ?1 in V6
LBBB: initial r wave ?0.04 s or an interval of ?0.07 s from the QRS onset to the nadir
of the S wave in V1-2,notching of the downstroke of the S wave in V1-2or an initial q
wave in V6
(Reproduced with permission from Josephson ME.1)
Abbreviations: RBBB, right bundle branch block; LBBB, left bundle branch block, A-V,
456 Curr Probl Cardiol, September 2010
tion of typical BBB or fascicular block, then it is likely VT (Fig 2).13The
Kindwall criteria formalize morphologic differences to 4 specific criteria
for VT with left bundle branch block (LBBB): an R wave in V1or V2
?30-ms duration; any Q wave in V6; a duration of ?60 ms from the onset
of the QRS to the nadir of the S wave in V1or V2; and notching on the
downstroke of the S wave in V1or V2.14Although each had low
sensitivity alone, grouped criteria had a sensitivity of 100%, specificity of
89%, and a predictive accuracy of 96% for VT. In contrast to the wide
QRS and slow deflections described above, there is relatively rapid
penetration of the ventricular His-Purkinje system in LBBB, such that the
initial vector of depolarization produces a narrow R wave and a rapid,
smooth descent to the S wave. With typical right bundle branch block
(RBBB) the initial portion of the QRS does not change, but the later
portion of the QRS reflects the delayed right ventricular depolarization
and gives rise to rR= or rsr= patterns. A monophasic R, qR, Rr=, or RS in
V1, or an RS ratio ?1, or a monophasic R in V6suggest VT.
Brugada and coworkers published a stepwise algorithm, in which 4
criteria for VT are sequentially considered.15If any are satisfied, VT is
diagnosed, while if none are fulfilled, SVT is diagnosed. First the
precordial leads are assessed for the absence of an RS complex, which
would signify VT. If an RS complex is present, but the longest RS
interval in any precordial lead is ?100 ms, VT is diagnosed. Next the
presence of AV dissociation marks VT. Finally, the QRS morphology
criteria described above are applied. The sensitivity of the 4 consecutive
steps was reported to be 0.987, and the specificity was 0.965, although
significantly lower discriminatory power has been reported in real-world
study of the criteria’s application.16
FIG 2. Diagrammatic representation of common QRS morphologies encountered in VT and SVT
with aberration, in leads V1and V6for both LBBB and RBBB QRS patterns. LBBB, left bundle
branch block; RBBB, right bundle branch block. (Reproduced with permission from Miller et al.3)
Curr Probl Cardiol, September 2010457
Fred Morady: A limitation of the study by Brugada15is that antidromic
atrioventricular reentrant tachycardias were not included in the analysis. The
criteria for ventricular tachycardia would be met by many antidromic atrio-
ventricular reentrant tachycardias.
Some of the other published criteria that we have found to be
particularly helpful include the following:
● QRS complex duration greater than 160 ms with LBBB morphology or
greater than 140 ms with RBBB morphology strongly favors VT in
patients not taking drugs that slow intraventricular conduction.2,17
● A right superior axis (?90 to ?180 degrees) favors VT, and to a lesser
extent a shift in the QRS axis of ?40 degrees from baseline also
Fred Morady: If there is a bundle branch block during sinus rhythm,
ventricular tachycardia from the ventricle that is contralateral to the bundle
branch block may have a QRS morphology that is very similar to that of the
bundle branch block.
● Concordant precordial R-wave progression pattern, with leads V1-V6
all either predominantly positive, or more suggestively, all predomi-
nantly negative, is uncommon in SVT, with the exception of the
positive concordance sometimes seen in preexcited tachycardias (Fig
3). Although the specificity of concordance for VT is high (?90%), the
sensitivity is low (?20%).17,19
● The presence of AV dissociation is perhaps the most useful electro-
cardiographic feature in distinguishing VT from SVT with aberration.
Complete AV dissociation occurs in 20%-50% of all VTs, and another
15%-20% of VTs have second-degree ventriculoatrial block, both of
which seldom occur in those with SVT, and is thus very specific for
VT.2,17Unfortunately, AV dissociation can be difficult to recognize,
particularly with rapid VT rates. Increasing the amount of ECG
analyzed, reviewing simultaneously recorded ECG leads to avoid
mistaking the terminal portion of the QRS for a P wave, and attending
to variation in QRS complex amplitude, due to scalar summation of the
P wave on the QRS complex or changes related to variable ventricular
filling in AV dissociation, can improve diagnostic accuracy.20
458 Curr Probl Cardiol, September 2010
FIG 3. (A) Negative concordance during VT in a patient with a prior anterior MI; AV
dissociation is present as well. (B) Positive concordance during VT in a patient with a prior
inferior MI. QRS amplitude alternans is seen in leads 2, 3, and aVF. (C) Positive concordance
during preexcited atrial flutter with 2:1 conduction over an anomalous AV connection in a
patient with Wolff–Parkinson–White syndrome. Note the similarity of ECG patterns between B
and C. (Reproduced with permission from Miller et al.3)
Curr Probl Cardiol, September 2010459
● Fusion beats involve blended ventricular activation from 2 different
sources, whereas capture beats represent pure ventricular activation
over the His-Purkinje system. The presence of either during a wide
complex tachycardia imply AV dissociation and are similarly diagnos-
tic of VT, with the caveat that a ventricular premature beat ipsilateral
to the “blocked” ventricle can mimic a fusion beat; thus, the presence
of a P wave shortly before the beat in question adds considerable
● A narrower QRS complex during the wide complex tachycardia than at
baseline, a contralateral BBB in tachycardia compared with baseline,
or the presence of multiple wide complex tachycardia configurations
all suggest VT.3
Mechanisms and Etiology
Sustained monomorphic tachycardia may be related to associated
organic heart disease, occurring in the setting of ischemic or nonischemic
cardiomyopathy, or idiopathic, occurring in patients with normal hearts.
VT can originate anywhere within the left or right ventricle, including the
conduction system, the outflow tract, and the perivalvular areas; it commonly
involves areas of scar.
All VTs can be attributed to 1 of 3 mechanisms: abnormal automaticity,
triggered activity, and reentry. Abnormal automaticity refers to impulse
formation by a region of ventricular cells at an accelerated rate compared
with normal (?50 bpm), due to an altered threshold for inward ventricular
myocyte sodium influx.21Accelerated idioventricular rhythms, frequently
observed in the setting of acute myocardial infarction, reperfusion,
myocarditis, or cocaine intoxication, are thought to occur based on this
mechanism.22Triggered activity results from oscillations in the mem-
brane potential that is dependent on the preceding action potential. Early
afterdepolarizations occur during phase II or III of the action potential and
have been shown to be responsible for many forms of drug- and
electrolyte-induced Torsades de pointes, and some forms of polymorphic
VT due to congenital long QT syndrome. Delayed afterdepolarizations
occur during phase IV of the action potential and are responsible for many
forms of outflow tract tachycardia and VT associated with digitalis
toxicity.23,24Finally, reentrant VT occurs commonly, but not exclusively,
in structurally abnormal myocardium and requires unidirectional conduc-
tion, fixed or functional conduction block, and a region of “slow
conduction” in which the tachycardia cycle length is longer than the
460 Curr Probl Cardiol, September 2010
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