What are the possible triggers of ventricular tachycardia (VT)?

Updated: Dec 05, 2017
  • Author: Steven J Compton, MD, FACC, FACP, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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VT may also occur in the absence of structural heart disease. VT in this setting may result from enhanced automaticity, which most commonly originates in the right ventricular outflow tract or from the fascicles of the cardiac conduction system. Bundle-branch reentrant VT occurs in patients with conduction system disease distal to the bundle of His. Finally, functional reentrant VTs can occur in structurally normal hearts, in patients with inherited channelopathies. [11]  The VT morphology can provide a guide to the anatomic likely site of origin in the heart. [12, 13]

VT can also be triggered by the following (see Etiology):

  • Electrolyte deficiencies (eg, hypokalemia, hypocalcemiahypomagnesemia)
  • Systemic diseases that affect the myocardium (eg, sarcoidosis, amyloidosis, systemic lupus erythematosus, hemochromatosis, rheumatoid arthritis)
  • Sympathomimetic agents, including intravenous (IV) inotropes and illicit drugs such as methamphetamine or cocaine
  • Digitalis toxicity, which can lead to biventricular tachycardia
  • Drugs that prolong the QT interval (class IA and class III antiarrhythmics, azithromycin, levofloxacin, and many others); these may cause torsade de pointes
  • Drugs that slow conduction velocity, particularly when an underlying myocardial scar is present (eg, halothane and class IA and IC antiarrhythmics)

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