Overview
What is ventricular tachycardia (VT)?
What are symptoms of ventricular tachycardia (VT)?
Which physical findings are characteristic of ventricular tachycardia (VT)?
How is ventricular tachycardia (VT) diagnosed?
Why are electrolyte levels measured in patients with suspected ventricular tachycardia (VT)?
Which lab studies are performed in the evaluation of ventricular tachycardia (VT)?
What is included in the diagnostic workup following ventricular tachycardia (VT) conversion?
What is the role of electrophysiologic study (EPS) in the diagnosis of ventricular tachycardia (VT)?
How should unstable patients with monomorphic ventricular tachycardia (VT) be treated?
Which medications are used in the management of ventricular tachycardia (VT)?
What is ventricular tachycardia (VT)?
In which conditions is ventricular tachycardia (VT) commonly seen?
What are the possible triggers of ventricular tachycardia (VT)?
What is the presentation of ventricular tachycardia (VT)?
What are the ECG criteria for diagnosing ventricular tachycardia (VT)?
What are the variants of ventricular tachycardia (VT)?
What is the pathophysiology of ventricular tachycardia (VT)?
What causes hemodynamic collapse in ventricular tachycardia (VT)?
What increases the mortality risk from monomorphic ventricular tachycardia (VT)?
What is the role of dilated cardiomyopathy in the etiology of ventricular tachycardia (VT)?
What is the role of hypertrophic cardiomyopathy in the etiology of ventricular tachycardia (VT)?
What are causes of ventricular tachycardia (VT)?
What is the role of QT prolongation in the etiology of ventricular tachycardia (VT)?
What are the most common cardiac causes of sudden death following ventricular tachycardia (VT)?
What is the role of long QT syndrome in the etiology of ventricular tachycardia (VT)?
What causes catecholaminergic polymorphic ventricular tachycardia (CPVT)?
What is the role of Brugada syndrome in the etiology of ventricular tachycardia (VT)?
What is familial ventricular tachycardia (VT)?
What is the incidence of ventricular tachycardia (VT) in the US?
How does the prevalence of ventricular tachycardia (VT) vary by age?
How does the prevalence of ventricular tachycardia (VT) vary by sex?
What is the prognosis of ventricular tachycardia (VT)?
What can alter the prognosis of ventricular tachycardia (VT)?
Presentation
What are symptoms of ventricular tachycardia (VT)?
What should be the focus of patient history in the evaluation of ventricular tachycardia (VT)?
Which physical findings are characteristic of ventricular tachycardia (VT)?
DDX
Which conditions should be included in the differential diagnoses of ventricular tachycardia (VT)?
Which rhythms must be distinguished from ventricular tachycardia (VT)?
What are the differential diagnoses for Ventricular Tachycardia?
Workup
How is ventricular tachycardia (VT) diagnosed?
How is ventricular tachycardia (VT) evaluated in unstable patients?
What is included in the evaluation of a ventricular tachycardia (VT)?
When is screening for ventricular tachycardia (VT) indicated?
How is family screening performed for ventricular tachycardia (VT)?
What is the role of chest radiography in the evaluation of ventricular tachycardia (VT)?
Which lab studies are performed in the diagnosis of ventricular tachycardia (VT)?
What is monomorphic ventricular tachycardia (VT)?
What causes monomorphic ventricular tachycardia (VT) in the absence of underlying heart disease?
In which sites do monomorphic ventricular tachycardia (VT) originate?
What is the morphology of a fusion beat in ventricular tachycardia (VT)?
What is the morphology of a capture beat in ventricular tachycardia (VT)?
What are the ECG discrimination criteria for ventricular tachycardia (VT)?
How is ventricular tachycardia (VT) differentiated from sinus tachycardia?
What is the role of echocardiography in the evaluation of ventricular tachycardia (VT)?
What is the role of cardiac imaging in the evaluation of ventricular tachycardia (VT)?
What is the role of genetic testing in the evaluation of ventricular tachycardia (VT)?
What is the role of myocardial biopsy in the evaluation of ventricular tachycardia (VT)?
What information can cardiac devices provide during the evaluation of ventricular tachycardia (VT)?
When is angiography performed with EPS for the evaluation of ventricular tachycardia (VT)?
When is EPS indicated in the workup of ventricular tachycardia (VT)?
Treatment
What are symptoms of hemodynamically unstable ventricular tachycardia (VT)?
What are the treatment options for hemodynamically unstable ventricular tachycardia (VT)?
Which factors affect treatment selection in hemodynamically stable ventricular tachycardia (VT)?
What are the treatment options for hemodynamically stable monomorphic ventricular tachycardia (VT)?
What are the treatment options for hemodynamically stable polymorphic ventricular tachycardia (VT)?
How is ventricular tachycardia (VT) managed following conversion?
What is included in prehospital emergent care for ventricular tachycardia (VT)?
What is the initial treatment of acute ventricular tachycardia (VT)?
What are the treatment options for pulseless ventricular tachycardia (VT)?
What is included in poststabilization management of ventricular tachycardia (VT)?
What are the long-term treatment options for ventricular tachycardia (VT)?
What is the role of radiofrequency ablation (RFA) in the treatment of ventricular tachycardia (VT)?
Which dietary modifications may be beneficial in the management of ventricular tachycardia (VT)?
Which activity modifications may be beneficial in the treatment of ventricular tachycardia (VT)?
Which specialist consultations are needed for the management of ventricular tachycardia (VT)?
Guidelines
What is AHA treatment algorithm for ventricular tachycardia (VT)?
What are the AHA guidelines for defibrillation in patients with ventricular tachycardia (VT)?
What are the AHA guidelines for airway control and ventilation in ventricular tachycardia (VT)?
Medications
What is the role of antiarrhythmic medications in the treatment of ventricular tachycardia (VT)?
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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 |
