Ventricular tachycardia as a cause of morbidity and mortality is grossly underdiagnosed, potentially leading to mismanagement.
This may be particularly true when the clinical presentation is
unexplained syncope because no concomitant electrocardiographic
(ECG) documentation is available. In the case of cardiac arrest
or SCD acute myocardial infarction rather than an arrhythmic problem
is often assumed to be responsible. Most persons who have suffered
sudden death have no evidence of acute myocardial necrosis, even
though the episode often occurs in patients with underlying coronary
artery disease. Managing the underlying coronary artery disease
with no regard to treating the concomitant VT is inadequate.
When hemodynamically stable VT is recorded on the surface ECG, it is often misdiagnosed as supraventricular tachycardia (SVT) with
aberrant conduction. Any subsequent management is therefore directed
toward SVT. Although the exact logic for this line of thinking is
unclear, the main reason may be that the hemodynamic stability is associated
with the broad QRS rhythm and thus the erroneous belief that the
problem cannot be VT.
The clinical presentation of VT depends on many factors, including rate, ventricular function, presence of concomitant coronary artery
disease, the presence or absence of cardioactive drugs, and even
the patient’s posture at the time of onset. Hemodynamic
tolerance of VT can, therefore, vary considerably in different situations;
at times, it can vary in the same patient, and it is prudent not
to exclude the diagnosis of VT on the basis of hemodynamic tolerance
alone. It must be understood that approximately 80% of
the patients with sustained wide QRS tachycardia have VT. To avoid
misdiagnosis, the clinician can either use the established ECG criteria (discussed
in the next section) that distinguish VT from SVT with aberrant
conduction or simply assume the presence of VT. The assumption of
VT is more often correct; it is also safer because misdiagnosing
VT as SVT is a riskier judgment error than vice versa.
Diagnostic Approach to the Patient with Wide QRS Complex Tachycardia
The diagnosis of wide QRS complex tachycardia by ECG analysis has always been a challenge for clinicians. The differential diagnosis includes VT, SVT with aberrant conduction, and preexcited tachycardia in patients with Wolff-Parkinson-White syndrome (WPW). Figure 23–1 depicts, schematically, the reasons for normal and broad QRS complexes. Preexcited tachycardia results from antegrade activation of the ventricle via an accessory pathway in patients with WPW syndrome, which can present with atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular nodal reentry tachycardia (AVNRT), or antidromic tachycardia. Preexcited tachycardia is a rare cause of wide QRS complex tachycardia (5–8% of cases); however, the QRS pattern of preexcited QRS complex can be difficult to distinguish from VT because in both instances the QRS starts with muscle-to-muscle conduction. Electrocardiographic artifact can also mimic wide QRS complex tachycardia and be misdiagnosed as VT, leading to expensive testing and even placement of implantable cardioverter-defibrillator (ICD). Clues to the diagnosis include absence of hemodynamic deterioration, an unstable baseline, association with body movement, and ability
to march the normal QRS complexes through the artifact (“notches
sign”) at sinus R-R interval. A number of surface ECG criteria,
including the atrioventricular (AV) relationship, the QRS complex
duration, specific QRS morphology, and the QRS complex axis, have
been established to distinguish VT from SVT with aberrant conduction. These
criteria are helpful in arriving at an accurate diagnosis if they
are used in a systemic fashion.
Mechanism of wide QRS. A: Narrow QRS from simultaneous activation of the right and left ventricles. In the three types of wide QRS shown in B–D, there is sequential rather than simultaneous activation of the left and right ventricle and a variable amount of muscle-to-muscle conduction. AP, accessory pathway; AVN, atrioventricular node; BBB, bundle branch block; HB, His bundle; LB, left bundle; RB, right bundle. (Reproduced, with permission, from Akhtar M et al. Electrophysiological spectrum of wide QRS complex tachycardia. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia: WB Saunders, 1990.)
In SVT, the arrhythmia arises in the atria or AV junction and reaches the ventricles through the AV node and His-Purkinje system.
Because the atrial arrhythmia is the primary event, either a 1:1
AV response or a varying degree of AV block occurs, but in either
case the atrial rates equal or exceed ventricular rates. During
VT, a retrograde block often leads to either AV dissociation or
a varying degree of ventriculoatrial conduction ratios, but the
ventricular rates equal or exceed the atrial rate. When AV dissociation
can be recognized, it is the most reliable criterion for VT. This
criterion lacks sensitivity, however, because the P waves can be
identified on the surface ECG in only 25% of patients with
VT (Figures 23–2 and 23–3). In patients with slower VT and AV dissociation, intermittent ventricular capture can result in fusion with narrow QRS complexes during wide
QRS complex tachycardia. This useful but rarely observed finding
is also 100% specific for the diagnosis of VT.
A: Monomorphic ventricular tachycardia (VT), with a uniform QRS appearance for all complexes. Arrowheads indicate superimposed P waves. B: Polymorphic VT, with a beat-to-beat variation in the QRS morphology; QT-interval prolongation follows the termination of the VT episode. (Reproduced, with permission, from Akhtar M. Circulation. 1990;82:1561.)
A: Scar-related ventricular tachycardia (VT), with a left bundle branch block left axis morphology in a patient with ischemic cardiomyopathy and previous myocardial infarction. B: Right bundle branch block right axis morphology VT in the same patient at the same rate suggesting that both forms of VT have the same circuit (that revolves around the mitral annulus) with different exits causing the difference in morphology. Atrioventricular dissociation is noted in the rhythm strip on V1 (*) that is 100% specific for VT.
For the reasons listed earlier, the QRS complex duration is the widest in VT and narrowest in aberrant conduction. To distinguish
VT from SVT with aberrant conduction on the basis of QRS duration alone,
however, some specific aspects must be considered. In the absence
of cardioactive drugs and extensive myocardial fibrosis, aberrancy
rarely results in a QRS duration of more than 140 ms with a right
bundle branch block (RBBB) pattern (Figure 23–3)
or more than 160 ms with a left bundle branch block (LBBB) configuration.
In the presence of intramyocardial conduction delay from drugs (such
as class I antiarrhythmic agents) and myocardial fibrosis, the QRS
width may also exceed these values in SVT with aberrant conduction. Conversely,
on a rare occasion, VT can present as a narrow QRS tachycardia (less
than 120 ms that is narrower than the conducted QRS complex) when there
is near-simultaneous activation of the two ventricles, perhaps from
The prevalence of LBBB versus RBBB morphology among the causes of wide QRS is comparable in both VT and SVT with aberrant conduction; it is therefore of no diagnostic value. The typical RBBB is a triphasic
complex best seen in V1 as rsR′ or rSR' pattern and in lead I as qRs, qRS pattern. Similarly, a typical LBBB has
no initial q wave in lead I and a small r and a rapid S wave in
V1. Because of the myocardial origin of most forms of VT,
however, the QRS appearance is not exactly like a typical LBBB or
RBBB. Many ECG criteria, therefore, have exploited this difference to
separate VT from aberrant conduction. A study that analyzed the
morphology of premature ventricular complexes and aberrantly conducted
beats of RBBB morphology in V1 found that the triphasic
RsR′ pattern with R' > R was predominant in aberrant conduction (70%) compared with premature ventricular
complexes (6%). Monophasic pattern or R > R′ was
seen in the premature ventricular complex beats. The limitation of that study is that origin
of the anomalous beats (SVT vs VT) was also based on the ECG (presence
or absence of preceding P wave). A retrospective ECG analysis of 70
patients with SVT and 70 patients with VT in whom His bundle recordings were
used to determine the site of origin of the wide QRS complex tachycardia found
that VT was favored by monophasic or biphasic R waves in V1 and
R:S ratio less than 1 in V6 in patients with RBBB morphology
and any Q wave in V6 in patients with LBBB morphology. A study of 150 consecutive wide QRS complex tachycardia cases found that 12-lead QRS morphology during wide QRS complex tachycardia was different from that during preexisting bundle branch block in
sinus rhythm, favoring a diagnosis of VT. The investigators also noted that a positive QRS concordance (positive complexes V1–V6) is uncommon in aberrancy, but a negative QRS concordance can occur during aberrant conduction in a small percentage of cases. Another study that evaluated wide QRS complex tachycardia with LBBB morphology
in V1 found that an R wave of > 30 ms, notching in the down stroke of the S wave and an RS (beginning of QRS complex to nadir of S wave) interval > 60 ms in V1 or V2, and any Q wave in V6 favored a diagnosis of VT. In a prospective analysis of wide QRS complex tachycardia (with RBBB and LBBB morphology), the following two criteria for a diagnosis of VT were proposed: (1) absence of R-S in all precordial leads (2) R-S interval > 100
ms (measured from the beginning of the QRS complex to the nadir of the S wave) in any precordial lead. Finally, the presence of QR complex in any lead during wide QRS complex tachycardia also
favors a diagnosis of VT.
The axis orientation on a 12-lead ECG ranging from normal (–30° –+90°), left (–31° – –90°) or right (+91° – +180°) has significant overlap across the causes of wide QRS complex tachycardia and is of little diagnostic value. The axis range of –91° to 180°, however, is usually not seen in aberrant conduction. The
axis location of this extreme during SVT is, therefore, unlikely
unless there was a nonarrhythmic reason for it, such as severe right
ventricular hypertrophy or lung disease. Similarly, a combination
of right axis with LBBB pattern is almost always seen in patients
with VT. A previous history of MI and an axis change of more than
40 degrees between sinus rhythm and wide QRS complex tachycardia
may independently favor VT over SVT.
Examination and 12-Lead ECG
A detailed history and physical examination can provide clues to the diagnosis of wide QRS complex tachycardia. A history of myocardial
infarction favors VT as the diagnosis of wide QRS complex tachycardia.
The presence of irregular cannon waves and variable intensity of
S1 suggest AV dissociation and are indicative of VT. Carotid
massage (performed carefully after ruling out a bruit) that leads
to termination of wide QRS complex tachycardia suggests SVT as the mechanism
of the arrhythmia (an exception is idiopathic VT arising from the
right ventricular outflow tract).
An old ECG in sinus rhythm showing Q waves indicates VT; SVT is the diagnosis if the old ECG shows bundle branch block pattern
that matches the 12-lead ECG during wide QRS complex tachycardia;
and preexcited tachycardia is inferred from the ECG showing WPW pattern
that is similar to wide QRS complex tachycardia ECG pattern. It is essential to obtain a 12-lead ECG during wide QRS complex tachycardia to compare it to the sinus rhythm ECG and look for subtle findings like AV dissociation and narrow beats (fusion and capture) that might not be evident in some leads. Table 23–1 outlines an approach to diagnosing wide QRS complex tachycardia by analyzing the ECG. The first step is to read the ECG with emphasis on rate, regularity (atrial fibrillation with preexcited tachycardia is irregular), axis (extreme northwest axis suggests VT), and morphology in V1. The next step is looking for AV dissociation (V > A) that is facilitated by marching the sinus P waves at the onset and termination of the wide QRS complex tachycardia if available. Narrow QRS complexes
in a wide QRS complex tachycardia (caused by capture and fusion of conducted beats through the AV node-His-Purkinje system) are also 100% specific for VT. The next step is to use the Brugada criteria by evaluating the R-S complexes in precordial leads. Absence of R-S complex in all
precordial leads or a R-S greater than 100 ms in one precordial lead favor a diagnosis of VT. The last step is using the morphology criteria for RBBB and LBBB in leads V1, V2, and V6 (as discussed earlier). The morphology criteria have certain limitations
as idiopathic VT (fascicular VT, outflow tract VT) and bundle branch reentrant VT can have a typical bundle branch block pattern on the ECG and can be misdiagnosed as SVT with aberrancy while some patients with SVT who take antiarrhythmic medications can have atypical bundle
branch block pattern on the ECG, leading to a misdiagnosis of VT.
Table 23–1. Approach to the ECG with Wide QRS Complex Tachycardia.
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Table 23–1. Approach to the ECG with Wide QRS Complex Tachycardia.
|1. Read the ECG: rate, rhythm, axis, morphology
in V1 (predominantly upright, RBBB; downward, LBBB)|
|2. AV dissociation|
|3. Narrow complex beat: fusion or capture|
|4. Brugada criteria: RS (measured from beginning
of QRS to the nadir of S wave) in precordial leads |
|a. Absence of RS in all precordial leads favors VT|
|b. RS > 100 ms in any precordial lead favors VT|
|5. Morphology criteria (V1, V2):
classic bundle branch block morphology favors SVT|
|a. RBBB (rsR'): R' > r favors SVT|
|b. LBBB: Kindwall criteria favors VT |
|R > 30 ms, notch in S wave, QRS onset to S > 60 ms Q wave in V6|
Miller JM et al. Value of the 12-lead ECG in wide QRS tachycardia. Cardiol Clin. 2006 Aug;24(3):439–51.