VT or not VT: How it can be differentiated?

Alisara Anannab M.D., CCDS, CEPS-AC

Central chest institute of Thailand

Ventricular tachycardia (VT) is one of the differential diagnosis of monomorphic wide QRS
complex tachycardia (WCT). It arises distal to the bifurcation of the His bundle in the specialized
conduction system, ventricular muscle or combination of both tissue types. Mechanisms of VT include
disorder of impulse formation (enhanced automaticity or triggered activity) and conduction (reentry).

The electrocardiographic diagnosis of VT is suggested by the occurrence of a series of three

or more consecutive PVCs whose duration exceeds 120 milliseconds, with the ST-T vector pointing
opposite the major QRS deflection. However several arrhythmia can manifest as WCTs (Table 1.).

Cause Description, Examples

VT Macroreentrant VT
Focal VT
SVT with aberrancy Functional BBB
Preexistent BBB
Preexcited SVT Antidromic AVRT
AT or AVNRT with bystander BT
Antiarrhythmic drug Class IA and IC agents, amiodarone
Electrolytes abnormalities Hyperkalemia
Ventricular pacing
Table 1. Causes of wide QRS complex tachycardia. Modified from Issa Z, Miller JM, Zipes DP. (2009). Clinical
arrhythmology and electrophysiology: a companion to Braunwalds Heart Disease. Philadelphia. PA: Suanders
Elsevier.

The most common of cause of WCTs is VT which accounts for 80% of all cases of WCT,
followed by supraventricular tachycardia (SVT) with aberrancy conduction or pre-existing block that
account for 15-20%. The minority (1-6%) of WCTs is SVT with bystander preexcitation and antidromic
atrioventricular reentrant tachycardia.

The importance to differentiating whether a WCT is VT or not is that misdiagnosis of VT as

SVT can lead to inappropriate and potentially dangerous therapy such as giving the calcium channel
blocking agent in case of indeed patient has VT and poor LVEF.

Accurate diagnosis of WCT requires information obtained from the history, physical
examination, response to certain maneuvers or medications and careful inspection of the ECG.
Comparison of the ECG during the tachycardia with that recorded during sinus rhythm can also provide
useful information.

When consider about the patients clinical characteristic, manifestation and history, WCT
in a patient older than 35 years is likely to be VT (positive predictive value of up to 85%) while SVT is
more likely in the younger patient (positive predictive value of 70%). The severity of symptom during
tachycardia is not useful in determining the tachycardia mechanism because of the symptoms during
WCT are primarily depend on how fast of the heart rate, the presence and extent of LV dysfunction.
One important clinical information which is strongly suggests VT as the cause of WCT is that the
presence of underlying structural heart disease, especially coronary artery disease and previous MI.

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 For the physical examination information, the important point for the physical examination
during an episode of WCT is to evaluate whether the patients have unstable hemodynamic status in
order to prompt giving them appropriate life safety therapy. For the stable hemodynamic WCT, sign
of AV dissociation, intermittent cannon A wave or if present on ECG, is strongly suggest VT, although
its absence is less helpful.

For electrocardiographic inspection, there are several ECG features help differentiate VT
from SVT including the QRS axis, the QRS duration and the QRS morphology (Table 2.).

AV Relationship
Dissociated P waves
Fusion beats
Capture beats
A/V ratio 1

QRS Duration
160 msec with LBBB pattern
140 msec with RBBB pattern
QRS during WCT is narrower than in NSR

QRS Axis
Axis shift of 40 degrees between NSR and WCT
Right superior (northwest) axis.
Left axis deviation with RBBB morphology
Right axis deviation with LBBB morphology

Precordial QRS Concordance

Positive concordance
Negative concordance

QRS Morphology in RBBB Pattern WCT

Monophasic R, biphasic qR complex, or broad R (40 msec) in lead V1
Rabbit ear sign: Double-peaked R wave in lead V1 with the left peak taller than the right peak rS complex in lead V6
Contralateral BBB in WCT and NSR

QRS Morphology in LBBB-Pattern WCT

Broad initial R wave of 40 msec in lead V1 or V2
R wave in lead V1 during WCT taller than the R wave during NSR
Slow descent to the nadir of the S, notching in the downstroke of the S wave in lead V1
RS interval 70 msec in lead V1 or V2
Q or QS wave in lead V6

Table 2. ECG criteria favoring ventricular tachycardia. Modified from Issa Z, Miller JM, Zipes DP. (2009). Clinical
arrhythmology and electrophysiology: a companion to Braunwalds Heart Disease. Philadelphia. PA: Suanders
Elsevier.

However, there is difficult to apply a single criteria for diagnosis of WCT, because most
patients will have some, but not all, of the features described. Several algorithm have been proposed
to guide integrating each ECG features into a diagnosis strategy. One important point is that we have
to know the limitation of specific criteria proposed. Generally, conditions that effect to the QRS
morphology such as history of prior MI, preexcited tachycardia, antiarrhythmic medication usage,
precordial lead placement, heart transplantation status and the presence of congenital heart disease
should be taken into account while applying these elements.

Brugada algorithm is one of the most commonly used algorithm for diagnosis of VT
(Figure 1 and Table 3.). The reported sensitivity and specificity from different authors were range from
79-92% and 43-70%, respectively.

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 Absence of an RS complex
in all precordial leads?

yes No

sens = .21 R to S interval >100 ms in

VT one precordial lead?
spec = 1.0

Yes
No
sens = .66 VT
spec = .98
Atrioventricular
dissociation?

yes No

sens = .82 Morphology criteria for VT

VT
spec = .98 present both in precordial leads
V1-2 and V6 ?

Yes No

sens = .987 VT SVT

spec = .965

sens = .965
spec = .987

Figure 1. Brugada algorithm for distinguishing ventricular tachycardia (VT) from

supraventricular tachycardia (SVT). sens sensitivity; spec specificity. (From
Brugada P, Brugada J, Mont L, et al: A new approach to the differential diagnosis of
a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649). Modified
from Issa Z, Miller JM, Zipes DP. (2009). Clinical arrhythmology and electrophysiology: a
companion to Braunwalds Heart Disease. Philadelphia. PA: Suanders Elsevier.

RBBB configuration LBBB configuration

QRS width >140 msec, left axis QRS width > 160 msec , right axis
QR,R,RSr complex in V1 (A) Initial R in V1 > 30 msec
(B) Slurring or notching of the downstroke
of the S-wave in lead V1-V2
(C) Begin QRS-nadir S wave >70 ms in V1-
V2

RS < 1 in V6 , QS in V6 Any Q in V6

Table 3. Classical Wellens criteria favouring VT. Modified from Becker S.N. Alzand* and Harry J.G.M
Crijns*Europace (2011) 13, 465472

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 A newer algorithm has been proposed since 2008 by Vereckei A and colleagues. This new
algorithm was studied and based solely on QRS morphology in lead aVR with the principle of
differences in the direction and velocity of the initial and terminal ventricular activation during WCT
caused by VT and SVT (Figure 2.). The overall accuracy of the aVR algorithm was 91.5% which is
superior to the Brugada algorithm (84.8%). However, some limitations remaining for the new aVR
criteria including the inability to differentiate preexcited tachycardia from VTs and the possible
exception of the presence of initial R wave in lead aVR e.g. in case of inferior wall MI.

Initial R wave in aVR

present?

Yes No

VT Initial r or q wave >40 ms

present?

Accuracy
98.6%
Yes No

VT Notch on the downstroke of a

negative onset, predominantly
negative aVR?
Accuracy
87.8%

Yes No

VT
Vi /Vt 1

Accuracy
86.5%
Yes
No

Accuracy VT
89.3%

SVT

Figure 2. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. SVT supraventricular
tachycardia; VT ventricular tachycardia. (From Vereckei A, Duray G, Szonsi G, et al: New algorithm using only lead aVR for
differential diagnosis of wide QRS complex tachycardia). Modified from Issa Z, Miller JM, Zipes DP. (2009). Clinical arrhythmology and
electrophysiology: a companion to Braunwalds Heart Disease. Philadelphia. PA: Suanders Elsevier.

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