Diagnostic Considerations
In addition to the conditions listed in the differential diagnosis (see below), other problems to consider in the differential diagnosis of ventricular tachycardia (VT) include the following:
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Ventricular fibrillation (VF)
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Supraventricular tachycardia (SVT) or atrial tachycardia (AT) with aberrant conduction
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Electrocardiographic (ECG) lead motion artifact (see the image below)
At first glance, this tracing suggests rapid polymorphic ventricular tachycardia. It is actually sinus rhythm with premature atrial complex and a superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backward from the final two QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
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Inappropriate rate-responsive pacing
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Dual-chamber pacemaker tracking of AT
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Pacemaker failure
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Pacemaker syndrome
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Premature ventricular contraction
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Multifocal AT
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Wolff-Parkinson-White syndrome
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Accelerated idioventricular rhythm
VF is a disorganized, rapid ventricular rhythm that varies in interval and waveform. It may be difficult to distinguish from rapid, polymorphic VT. Sudden death accounts for approximately half of all deaths from cardiovascular disease and is generally caused by VT and VF. [1, 2]
Accelerated idioventricular rhythm is defined as an enhanced ectopic ventricular rhythm with at least three consecutive ventricular beats that is faster than the normal intrinsic ventricular escape rhythm (≤40 beats/min) but slower than VT. However, there is a potential definitional overlap with accelerated idioventricular rhythm and an automatic VT of 100-120 beats/min.
Pacemaker-generated tachycardia
Permanent pacemakers occasionally generate rapid rhythms. The most common cause is tracking of atrial tachyarrhythmias, such as atrial flutter or atrial fibrillation (AF). The pacemaker typically paces around the programmed maximum tracking limit, which is often set at 120-140 beats/min in older patients (see the image below). If a pacemaker programmer is not available, a magnet placed over the pacer generator deactivates atrial sensing temporarily and allows for the diagnosis of the atrial arrhythmia.
Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If a smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have a left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to the rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis. Sometimes “pacing spike detection” must be programmed “ON” in the electrocardiographic system to make the spike apparent.
Supraventricular tachycardia
Wide-complex conduction during SVT can mimic VT. The two most common forms are atrioventricular (AV) reentrant tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT) with aberrant conduction.
AVRT can be either orthodromic or antidromic, depending on the direction of conduction through the AV node. All antidromic AVRTs cause wide-complex tachycardia as a result of ventricular activation outside of the His-Purkinje system, and some orthodromic AVRTs conduct with wide QRS complexes as a result of functional or preexisting bundle-branch block, bystander accessory pathway conduction, or intraventricular conduction delay (see the images below).
Aberrantly conducted SVT circuits can mimic VT, but careful analysis of the ECG can allow discrimination of VT from aberrant SVT in most cases.
Historically, the use of adenosine to distinguish VT from regular wide QRS complex SVT has been discouraged because, in theory, it could precipitate VF. Wide QRS complex tachycardia should be presumed to be VT if the diagnosis is unclear. [40]
However, a retrospective observational study in 197 consecutive patients with regular wide QRS complex tachycardia found that adenosine was useful and safe as a diagnostic agent for making this differentiation. [41] Adenosine produces transient AV nodal blockade and thus should terminate reentrant SVTs, which involve the AV node as a pathway, but not most VTs.
Adenosine should not be used for irregular wide QRS complex tachycardia, because that dysrhythmia may involve AF in the presence of an accessory pathway (see the image below). In such cases, adenosine may allow conduction of rapid atrial fibrillatory impulses exclusively through an amenable accessory tract and thereby cause very rapid, intolerable ventricular rates and eventuate in the induction of VF. [42, 43]
Preexcited atrial fibrillation. The patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over an accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia.
Differential Diagnoses
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Heart Failure
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Hypocalcemia
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Hypomagnesemia
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This electrocardiogram (ECG) shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. The tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic study. A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
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This electrocardiogram shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). The patient presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, which is most obvious in leads V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
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At first glance, this tracing suggests rapid polymorphic ventricular tachycardia. It is actually sinus rhythm with premature atrial complex and a superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backward from the final two QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
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Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
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Preexcited atrial fibrillation. The patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over an accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia.
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Curative ablation of ventricular tachycardia (VT). The patient had VT in the setting of ischemic cardiomyopathy. VT was induced in an electrophysiology laboratory, and an ablation catheter was placed at the critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy was applied to tissue through the catheter tip, and VT was terminated when the critical conducting tissue was destroyed.
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Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If a smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have a left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to the rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis. Sometimes “pacing spike detection” must be programmed “ON” in the electrocardiographic system to make the spike apparent.
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Supraventricular tachycardia with aberrancy. This tracing is from a patient with a structurally normal heart who has a normal resting electrocardiogram. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note the relatively narrow RS intervals in the precordial leads.
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Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator.
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Posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red, and late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
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This tracing depicts monomorphic ventricular tachycardia.
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This image demonstrates polymorphic ventricular tachycardia.
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This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.
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This electrocardiogram is from a 48-year-old man with wide-complex tachycardia during a treadmill stress test. Any wide-complex tachycardia tracing should raise the possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of a supraventricular rhythm. By Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from R-wave onset to the deepest part of the S wave is shorter than 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon lead aVR, which shows no R wave, an initial q wave width shorter than 40 ms, and no initial notching in the q wave. The last Vereckei criterion examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in lead aVR. In this case, the initial downward deflection in lead aVR is steeper than the terminal upward deflection, yielding Vi/Vt ratio above 1. All of these criteria are consistent with an aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with a sinus tachycardia mechanism.
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The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.
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A wide QRS complex tachycardia is evident on this electrocardiogram from a 64-year-old man with history of previous myocardial infarction (MI) and syncope. In patients with a prior MI, the most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
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This tracing depicts atrioventricular dissociation.
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Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.
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Note the retrograde P waves in this electrocardiogram.
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Retrograde P waves are also observed in this electrocardiogram.
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This electrocardiogram reveals torsade de pointes.
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Hematoxylin and eosin stain; intermediate power of a healed myocardial infarct. Note the areas of fibrosis (pale pink) dissecting between the myocytes (red).
Tables
| Recommendation | Class |
|---|---|
| Resting 12-lead electrocardiography (ECG) in all patients | Class I |
12-lead ambulatory ECG to evaluate QT-interval changes or ST changes |
Class I |
| Cardiac event recorders when symptoms are sporadic to rule out transient arrhythmias | Class I |
Implantable loop recorders when symptoms are sporadic and suspected to be related to arrhythmias and when a symptom–rhythm correlation cannot be established by conventional diagnostic techniques |
Class I |
Exercise stress testing in adult patients who have an intermediate or greater probability of having coronary artery disease (CAD) to provoke ischemic changes or ventricular arrhythmia (VA) |
Class I |
| Exercise stress testing in patients with known or suspected exercise-induced VA | Class I |
| Echocardiography in all patients | Class I |
Pharmacologic stress testing plus imaging modality study to detect silent ischemia in patients with VAs who have an intermediate probability of having CAD and are physically unable to perform a symptom-limited exercise test |
Class I |
Cardiac magnetic resonance imaging (cMRI) or computed tomography (CT) scanning in patients with VAs when echocardiography does not provide accurate assessment of left- and right-ventricular function and/or evaluation of structural changes |
Class IIa |
Electrophysiologic study in patients with CAD with remote myocardial infarction with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. |
Class I |
Coronary angiography to establish or exclude significant obstructive CAD in patients with life-threatening VAs or in survivors of sudden cardiac death, who have an intermediate or greater probability of having CAD by age and symptoms |
Class IIa |
