Pulseless ventricular tachycardia differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2] Homa Najafi, M.D.[3]Rim Halaby, M.D. [4] Syed Hassan A. Kazmi BSc, MD [5]


Pulseless ventricular tachycardia must be differentiated from other diseases that cause wide complex tachycardia, such as supraventricular tachycardia with aberrant conduction, SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia.[1] While an EKG provides the most reliable data to distinguish VT from SVT with aberrant conduction, the clinical history and the age of the patient may also provide additional discriminatory information regarding the cause of the wide complex tachycardia. While older patients with a prior history of myocardial infarction are more likely to have VT, young hemodynamically stable patients presenting with paroxysmal tachycardia are more likely to have SVT with aberrant conduction. Nevertheless, the primary tool to differentiate VT from SVT with aberrant conduction is the ECG. There are several findings that are more common in ventricular tachycardia, and there are also more sophisticated electrophysiologic algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish VT from SVT with aberrant conduction. The diagnosis of VT is more likely if: There is a history of myocardial infarction or structural heart disease, the electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis), the QRS is > 140 msec, there is AV dissociation, there are positive or negative QRS complexes in all the precordial leads, and the morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).

History of Ischemic Heart Disease

Risk factors for the ventricular tachycardia as a cause of wide complex tachycardia include a history of prior myocardial infarction, a history of congestive heart failure, and a history of recent angina pectoris. These three historical features have positive predictive values for VT of > 95% in a small study, but sensitivities of 66%, 24%, and 24%, respectively.[2] Wide complex tachycardia will be due to VT in 98% of cases if there's a history of structural heart disease. Only 7% of patients with SVT with aberrancy will have had a prior myocardial infarction (MI).[3]

Hemodynamic Stability

Hemodynamic stability does not reliably differentiate VT from SVT. Patients with ventricular tachycardia can often be hemodynamically stable, and stable vital signs do not rule out ventricular tachycardia. This is often a major mistake on the part of clinicians and can lead to inappropriate treatment of VT as SVT with poor outcomes. [4]

EKG Findings Suggestive of VT

The Presence of AV Dissociation

Although AV dissociation is highly suggestive of VT, it may also be seen in junctional tachycardias with retrograde block.

Example: Shown below is a wide complex tachycardia. AV dissociation is present as shown by the varying morphology highlighted by the red arrows. LBBB configuration. Absence of RS in the chest leads. The diagnosis is VT.

Example: Shown below is a wide complex tachycardia. AV dissociation is present as shown by the varying morphology highlighted by the red arrows. LBBB configuration. Absence of RS in the chest leads. The diagnosis is VT.

Duration of the QRS Complex

  • A wide complex tachycardia with a RBBB morphology and a QRS > 0.14, or a LBBB morphology with a QRS > 0.16 suggests VT.

Morphology of the QRS Complexes

  • The finding of a positive or negative QRS complex in all precordial leads is in favor of ventricular tachycardia.
  • A monophasic or biphasic RBBB QRS complex in V1. But none of their patients with SVT had a preexisting RBBB. Therefore, this finding is of limited importance (A Wellens criterion).
  • 80 to 85% of aberrant beats have a RBBB pattern, but ectopic beats that arise from the LV have a similar morphology.
  • LBBB with a rightward axis
  • LBBB with the following QRS morphology:
  • R wave in V1 or V2 > 0.03 second
  • Any Q wave in V6
  • Onset of the QRS to nadir of the S wave in V1 > 0.06 seconds
  • Notching of the S wave in V1 or V2
Morphological criteria
LBBB pattern
Initial R more than 40 ms? Yes ≥ VT
Slurred or notched downwards leg of S wave in leads V1 or V2? Yes ≥ VT
Beginning of Q to nadir QS > 60 ms in V1 or V2? Yes ≥ VT LR > 50:1
Q or QS in V6? Yes ≥ VT LR > 50:1
RBBB pattern
Monophasic R or qR in V1? Yes ≥ VT
R taller than R' (rabbit-ear sign)? Yes ≥ VT LR > 50:1
rS in V6? Yes ≥ VT LR > 50:1

Morphology of Premature Beats During Sinus Rhythm

Example: Shown below is a wide complex tachycardia. There is no AV dissociation. A RBBB morphology is present. The wide complex tachycardia resembles sinus rhythm from the same patient. The diagnosis in this patient is SVT with RBBB:
Shown below is the ECG from the same patient as above in sinus rhythm. The QRS complex is very similar to that during the wide complex tachycardia:

The QRS Axis

The image below illustrates the "Northwest axis" also known as "Extreme Right Axis" or "No Man's Land":

Capture Beats

  • Rare, but one of the strongest pieces of evidence in favor of VT.
  • SVT with aberrancy rarely follows a beat with a short cycle length.

Fusion Beats

Fusion beats are rare but strongly suggest VT.

Vagal Manuevers

  • VT is generally not affected by vagal stimulation.
  • May terminate reentrant arrhythmias

Atrial Pacing

  • A pacing wire is placed in the RA and the atrium is stimulated at a rate faster than the tachycardia.
  • If ventricular capture occurs and the QRS is normal in duration, then one can exclude the possibility of aberrant conduction.

Onset of the Tachycardia

  • Diagnosis of SVT made if the episode is initiated by a premature P wave.
  • If the paroxysm begins with a QRS then the tachycardia may be either ventricular or junctional in origin.
  • If the first QRS of the tachycardia is preceded by a sinus p wave with a PR interval shorter than that of the conducted sinus beats, the tachycardia is ventricular.

His Bundle Recording

  • In SVT, each QRS is preceded by a His bundle potential.
  • In VT there is no preceding His deflection.
  • The retrograde His deflection is usually obscured by the much larger QRS complex.

Regularity of the Rhythm


  • VT (slight irregularity of RR)
  • SVT with aberrancy: Sinus, atrial tachycardia (AT), or flutter
  • Antidromic atrioventricular reentrant tachycardia (AVRT)


  • The first 50 beats of VT can be irregular
  • SVT with aberrancy: Atrial fibrillation, multifocal atrial tachycardia (MAT)
  • Atrial fibrillation with bypass tract such as WPW is a dangerous cause of a very rapid irregular rhythm as the atrial rate is conducted rapidly over the bypass tract. Shown below is the tracing of a patient with atrial fibrillation conducting down the bypass tract in WPW. Note that the rate is extremely rapid, and the rhythm is irregularly irregular. It is critical that this rhythm is recognized to avoid the administration of agents that would further accelerate conduction down the accessory pathway in this patient with WPW which could cause degeneration into ventricular fibrillation. The best treatment for this patient is Pronestyl 15 mg/kg load over 30 minutes then 2-6 mg/min gtt or DC cardioversion:
  • The mechanism of SVT with aberrancy is usually concealed retrograde conduction. The ventricular beat penetrates the right branch (RB) or left branch (LB). When the next supraventricular activation front occurs that bundle is refractory and if conduction can occur, it will proceed down the other bundle. Since the RB has a longer refractory period than the LB, a right bundle branch block (RBBB) morphology is more common.
  • Other mechanisms of “rate related aberrancy” are preexisting bundle branch block (BBB), physiologic (phase 3) aberration, and use-dependent aberration secondary to medication. In physiologic aberration, the stimulus comes to the His-Purkinje system before it has fully recovered from the previous stimulus. The ensuing activation is either blocked or conducts slowly. Again, RB is the one more at risk. Most commonly seen at the onset of paroxysmal supraventricular tachycardia (PSVT), but can become sustained.
  • In use-dependent aberration, a patient on an anti-arrhythmic (especially class Ic agents) will have a progressive decrement in ventricular conduction rate the more it is stimulated. During faster heart rates, less time is available for the drug to dissociate from the receptor and an increased number of receptors are blocked.

Sophisticated Electrophysiologic Criteria

Several ECG criteria and algorithms have been used to differentiate VT and SVT, the common one of which is Brugada algorithm. Below is a list of all algorithms:

  • Brugada algorithm: sensitivity 89%, specificity 59.2%[5]
  • The lead II R-wave-peak-time: sensitivity 60%, specificity 82.7%[6]
  • The aVR algorithm: sensitivity 87.1%, specificity 48%[7]
  • The Bayesian algorithm: sensitivity 89%, specificity 52%[8]
  • The Griffith algorithm: sensitivity 94.2%, specificity 39.8%[9]

The R Wave Peak Time

In 2010 Joseph Brugada et al. published a new criterion to differentiate VT from SVT in wide complex tachycardias: the R wave peak time (RWPT) in Lead II.[6] To apply the criteria, the duration of onset of the QRS to the first change in polarity (either nadir Q or peak R) is measured in lead II as shown below. If the RWPT is ≥ 50ms the likelihood of a VT very high (positive likelihood ratio 34.8). This criterion was successful in their own population of 163 selected patients and is awaiting prospective testing in a larger trial.

Example: As shown below, an R-wave to Peak Time (RWPT) of ≥ 50ms in lead II strongly suggests VT:

Brugada Criteria[10]

Absence of an RS complex
in all precordial leads?

VT (SN=0.21 SP=1.0)
R to S interval>100 ms in
one precordial lead?

VT (SN=0.66 SP=0.98)
AV dissociation?

VT (SN=0.82 SP=0.98)
Morphology criteria for VT present
both in precordial leads V1, V2 and V6?

VT (SN=0.987 SP=0.965)
SVT (SN=0.965 SP=0.987)

Based on the 2011 Nature Reviews Cardiology algorithm of broad complex tachycardia.[11]

Vereckei Criteria[12]

  • An algorithm has been proposed by Vereckei and colleagues, wherein in addition to do the traditional criteria, the voltage change on the EKG is used as a final discriminatory criterion.
  • In this method, the voltage change during the initial 40 ms (Vi) and the terminal 40 ms (Vt) of the same QRS complex is used to estimate the (Vi) and terminal (Vt) ventricular activation velocity ratio (Vi/Vt).
  • A Vi/Vt > 1 suggests SVT and a Vi/Vt ≤ 1 suggests VT.[7]

AV dissociation present?

Initial R wave in aVR present?

QRS morphology unlike BBB or FB?



Based on the 2011 Nature Reviews Cardiology algorithm of broad complex tachycardia.[13]

Calculation of Vi/Vt

Shown below is an image demonstrating the method used to calculate Vi/Vt. In this tracing, Vi/Vt is < 1 is suggestive of ventricular tachycardia according to Vereckei criteria.

Pacemaker Mediated Tachycardia

Pacer spikes are present. There is a ventricular-paced rhythm at or near the upper rate limit at approximately 120-130 beats per minute. Given the mechanical nature of the trigger, the EKG is absolutely regular.

Shown below is a rhythm strip demonstrating pacemaker mediated tachycardia:

Putting It All Together: The ACC Algorithm

Wide QRS complex tachycardia
(QRS duration greater than 120 ms)
Regular or irregular?
Is QRS identical to that during SR?
If yes, consider:
- SVT and BBB
- Antidromic AVRT
Atrial fibrillation
Atrial flutter / AT with variable
conduction and:
a) BBB or
b) Antegrade conduction via AP
Vagal maneuvers or
Previous myocardial infarction or structural heart disease? If yes, VT is likely.
1 to 1 AV relationship?
Yes or unknown
V rate faster than A rate
A rate faster than V rate
QRS morphology in precordial leads
Atrial tachycardia
Atrial flutter
Typical RBBB
Precordial leads:
- Concordant
- No R/S pattern
- Onset of R to nadir longer than 100ms
RBBB pattern:
- qR, Rs or Rr' in V1
- Frontal plane axis range
from +90 degrees to -90 degrees
LBBB pattern:
- R in V1 longer than 30 ms
- R to nadir of S in V1 greater than 60 ms
- qR or qS in V6

The above algorithm is adapted from the 2003 American College of Cardiology.[14]

Response to Pharmacotherapy As a Diagnostic Tool to Differentiate the VT from SVT

Although termination of a wide complex tachycardia by either adenosine, a calcium channel blocker, a beta blocker or digoxin is suggestive of supraventricular tachycardia with aberrant conduction, VT can also be terminated by these pharmacotherapies.[15][16] Verapamil should be avoided in patients with wide complex tachycardia as it can result in hemodynamic deterioration in patients with ventricular tachycardia.[17]

Differentiating Ventricular Tachycardia From Other Diseases

Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[18][19]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[20]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)[21][22][23][24]
  • Regular
  • 140-280 bpm
  • slow-fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R' in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Multifocal Atrial Tachycardia[25][26]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[27][28]
  • Regular except when disturbed by premature beat(s)
  • 80-120 bpm
  • Upright
  • > 0.12 second
  • Maybe shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
  • Ashman’s Phenomenon:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[29][30]
  • Regular
  • Atrial rate is nearly 300 bpm and the ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[31][32][33]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[34][35]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent

  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

The table below provides information on the differential diagnosis of ventricular tachycardia in terms of ECG appearance:

Disease Name Causes ECG Characteristics ECG view
Ventricular tachycardia [36][37][38][39][40]
Ventricular fibrillation [34][42][43][44]
Ventricular flutter [46][47][48]
Asystole [50][51]
  • There is no electrical activity in the asystole
Pulseless electrical activity [53][54]
Torsade de Pointes [56][57][58]
  1. Paroxysms of VT with irregular RR intervals.
  2. A ventricular rate between 200 and 250 beats per minute.
  3. Two or more cycles of QRS complexes with alternating polarity.
  4. Changing the amplitude of the QRS complexes in each cycle in a sinusoidal fashion.
  5. Prolongation of the QT interval.
  6. Is often initiated by a PVC with a long coupling interval, R on T phenomenon.
  7. There are usually 5 to 20 complexes in each cycle.


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