Ventricular tachycardia differential diagnosis

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

Overview

When wide QRS tachycardia is present on the [[electrocardiogram] ECG, it is necessary to rapidly differentiate whether it is caused by ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrant conduction. While the ECG 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 QRS 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.
• Wide complex tachycardia will be due to VT in 98% of cases if there's a history of structural heart disease.

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.

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. The 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. The 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

• If premature ventricular contractions (PVCs) are present on a prior tracing, and if the morphology of the wide complex tachycardia is the same, then it is likely to be ventricular tachycardia.
• Previous EKG may show a preexisting intraventricular conduction delay (IVCD) which would favor SVT with abberancy.
• If there are premature atrial contractions (PAC)s with aberrant conduction, then the origin of the wide complex tachycardia may be supraventricular.

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 similiar to that during the wide complex tachycardia:

The QRS Axis

• A "northwest axis" with a QRS axis in the RUQ between -90 and +180 degrees favors ventricular tachycardia.

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 suggests 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

Regular

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

Irregular

• The first 50 beats of VT can be irregular
• SVT with aberrancy: Atrial fibrillation, multifocal atrial tachycardia (MAT)
• Atrial fibrillation with bypass tract usch 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 be 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, the 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 and 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%

• The lead II R-wave-peak-time: sensitivity 60%, specificity 82.7%

• The aVR algorithm: sensitivity 87.1%, specificity 48%

• The Bayesian algorithm: sensitivity 89%, specificity 52%

• The Griffith algorithm: sensitivity 94.2%, specificity 39.8%

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. To aplly 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

Absence of an RS complex in all precordial leads?

Yes? VT (SN=0.21 SP=1.0)

No?

R to S interval>100 ms in one precordial lead?

Yes? VT (SN=0.66 SP=0.98)

No?

AV dissociation?

Yes? VT (SN=0.82 SP=0.98)

No?

Morphology criteria for VT present both in precordial leads V1, V2 and V6?

Yes? VT (SN=0.987 SP=0.965)

No?

SVT (SN=0.965 SP=0.987)

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

Vereckei Criteria

• 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 criteria.
• In this method, the voltage change during the initial 40 ms (V_i) and the terminal 40 ms (V_t) of the same QRS complex is used to estimate the (V_i) and terminal (V_t) ventricular activation velocity ratio (V_i/V_t).
• A V_i/V_t > 1 suggests SVT and a V_i/V_t ≤ 1 suggests VT.

AV dissociation present?

Yes? VT

No?

Initial R wave in aVR present?

Yes? VT

No?

QRS morphology unlike BBB or FB?

Yes? VT

No?

Vi/Vt≤1?

Yes? VT

No?

SVT

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

Calculation of V_i/V_t

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?

Regular

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 adenosine

Previous myocardial infarction or structural heart disease? If yes, VT is likely.

1 to 1 AV relationship?

Yes or unknown

No

V rate faster than A rate

A rate faster than V rate

QRS morphology in precordial leads

VT

Atrial tachycardia Atrial flutter

Typical RBBB or LBBB

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

SVT

VT

VT

VT

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

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. Verapamil should be avoided in patients with wide complex tachycardia as it can result in hemodynamic deterioration in patients with ventricular tachycardia.

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)	Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	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	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial Flutter	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	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Atrioventricular nodal reentry tachycardia (AVNRT)	Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R' in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. 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	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Multifocal Atrial Tachycardia	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	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal Supraventricular Tachycardia	Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature Atrial Contractrions (PAC)	Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 second May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node Ashman’s Phenomenon: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome	Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	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.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 - 300 per 100,000	Ebstein's anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular Fibrillation (VF)	Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular Tachycardia	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	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

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	Ischemic heart disease Illicit drug use such as cocaine and methamphetamine Structural heart diseases Electrolyte disturbances Congestive heart failure Myocarditis Obstructive sleep apnea Pulmonary artery catheter Long QT syndrome	Ventricular tachycardia originates from a ventricular focus. Lasts more than 30 seconds. Broad QRS complexes: rate of >90 BPM.
Ventricular fibrillation	Acute coronary ischemia Cardiomyopathies Congenital heart disease Myocardial infarction Heart surgery Electrolyte abnormalities	Poorly identifiable QRS complexes and absent P waves The heart rate is >300 BPM Rhythm is irregular
Ventricular flutter	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm
Asystole	Hypovolemia Hypoxia Acidosis Hypothermia Hyperkalemia or Hypokalemia Hypoglycemia Cardiac Tamponade Tension pneumothorax Thrombosis Myocardial infarction Thrombosis Pulmonary embolism Cardiogenic shock Degeneration of the sinoatrial or atrioventricular nodes Ischemic stroke	There is no electrical activity in the asystole
Pulseless electrical activity	Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hypothermia Electrolyte disturbances Hypoglycemia Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers Tamponade Tension pneumothorax Thrombosis (Myocardial infarction) Thrombosis (Pulmonary embolism) Trauma (Hypovolemia from blood loss)	Several pattern are possible including: Normal sinus rhythm Sinus tachycardia, with discernible P waves and QRS complexes Bradycardia, with or without P waves
Torsade de Pointes	*Electrolyte disturbances Medications such as: Amiodarone Azithromycin Clozapine Famotidine Flecainide Foscarnet Levofloxacin Lithium Mirtazipine Quetiapine Risperidone Tacrolimus Tamoxifen Ziprasidone	Paroxysms of VT with irregular RR intervals. A ventricular rate between 200 and 250 beats per minute. Two or more cycles of QRS complexes with alternating polarity. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion. Prolongation of the QT interval. Is often initiated by a PVC with a long coupling interval, R on T phenomenon. There are usually 5 to 20 complexes in each cycle.