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  • Fast, wide QRS complex on ECG.

  • Associated with ischemic heart disease, particularly in older patients.

  • In the absence of reversible cause, implantable cardioverter defibrillator (ICD) is recommended if meaningful life expectancy is longer than 1 year.


Ventricular tachycardia is defined as three or more consecutive ventricular premature beats. It is classified as either nonsustained (lasting less than 30 seconds and terminating spontaneously) or sustained with a heart rate greater than 100 beats/min (see eFigure 10–57). In individuals without heart disease, nonsustained ventricular tachycardia is generally associated with a benign prognosis. In patients with structural heart disease, nonsustained ventricular tachycardia is associated with an increased risk of subsequent symptomatic ventricular tachycardia and sudden death, especially when seen more than 48 hours after MI.

Ventricular tachycardia is a frequent complication of acute MI and dilated cardiomyopathy but may occur in chronic coronary disease, hypertrophic cardiomyopathy, myocarditis, and in most other forms of myocardial disease. It can also be a consequence of atypical forms of cardiomyopathies, such as arrhythmogenic right ventricular cardiomyopathy. However, idiopathic ventricular tachycardia can also occur in patients with structurally normal hearts. Accelerated idioventricular rhythm is a regular wide complex rhythm with a rate of 60–120 beats/min, usually with a gradual onset (eFigure 10–88). It occurs commonly in acute infarction and following reperfusion with thrombolytic medications. Treatment is not indicated unless there is hemodynamic compromise or more serious arrhythmias.

eFigure 10–88.

Wide complex regular tachycardia. Differential diagnosis includes ventricular tachycardia versus supraventricular tachycardia with aberrancy. Diagnosis of ventricular tachycardia is made using the Brugada criteria and, in this case, noting that the R-S interval is greater than 100 milliseconds. Other Brugada criteria (concordance, A-V dissociation, and morphology criteria) are not met. (Used, with permission, from Jose Sanchez, MD.)

Torsades de pointes, a form of ventricular tachycardia in which QRS morphology twists around the baseline, may occur in the setting of severe hypokalemia, hypomagnesemia, or after administration of a medication that prolongs the QT interval (eFigure 10–89). In nonacute settings, most patients with ventricular tachycardia have known or easily detectable cardiac disease, and the finding of ventricular tachycardia is an unfavorable prognostic sign.

eFigure 10–89.

Polymorphic ventricular tachycardia (torsades de pointes) due to quinidine toxicity. The QRS configurations change from upright to inverted in this MCL1 monitor lead. The polymorphic tachycardia is initiated by an R-on-T premature ventricular depolarization. The tachycardia becomes monomorphic as it continues; this is a relatively uncommon sequence of events. (Reproduced, with permission, from Goldschlager N, Goldman MJ. Principles of Clinical Electrocardiography, 13th ed. Originally published by Appleton & Lange. Copyright © 1989 by The McGraw-Hill Companies, Inc.)


A. Symptoms and Signs


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