Ventricular tachycardia – management
Ventricular tachycardia – management: Ventricular tachycardia (VT) is a potentially life threatening cardiac arrhythmia. If the rate is very fast, hemodynamic deterioration can occur rapidly. On the electrocardiogram, ventricular tachycardia can be defined as three or more ventricular ectopic beats occurring in a sequence at a rate more than 100 per minute. Ventricular tachycardia which gets spontaneously terminated within 30 seconds is called non sustained ventricular tachycardia (NSVT). Sustained ventricular tachycardia is one which does not get spontaneously terminated within 30 seconds or needs cardioversion before that due to hemodynamic compromise.
Based on the morphology, ventricular tachycardia can be classified into monomorphic and polymorphic ventricular tachycardias. Monomorphic VT is usually due to reentrant circuits within the myocardial conduction tissue, while polymorphic VT is due to early afterdepolarizations. Classical example of polymorphic ventricular tachycardia is torsade de pointes associated with congenital or acquired QT interval prolongation. Another rare form of ventricular tachycardia is bidirectional ventricular tachycardia.
Monomorphic ventricular tachycardia is usually treated with an amiodarone bolus dose followed by infusion. Monomorphic ventricular tachycardia in the setting of acute myocardial ischemia can also be treated by intravenous lignocaine bolus followed by infusion. Predisposing causes for ventricular tachycardia like ischemia and electrolyte imbalance has to be treated simultaneously to prevent recurrence. Ventricular tachycardia not responding to pharmacotherapy and those having hemodynamic compromise at presentation need direct current cardioversion after appropriate sedation.
Cardioversion of ventricular tachycardia
Monitor screen shot showing ventricular tachycardia and restoration of sinus rhythm following cardioversion with a direct current shock
Chronic recurrent monomorphic VT like fascicular tachycardia and right ventricular outflow tract tachycardia are also amenable to electrophysiological mapping and ablation. Recurrent ventricular tachycardia in spite of radiofrequency catheter ablation needs an implantable cardioverter defibrillator. Those at risk of recurrent VT with previous myocardial infarction and left ventricular dysfunction also need an implantable defibrillator.
Polymorphic VT is managed by intravenous magnesium and measures to increase heart rate like pacing as it occurs most often in the setting of bradycardia and QT interval prolongation. Associated hypokalemia which is often present has to be corrected. Offending drug has to be withdrawn in case of drug induced polymorphic VT. Recurrent polymorphic VT in the setting of cardiac channelopathies or primary electrical disorders of the heart need implantation of a cardioverter defibrillator as response to pharmacotherapy is often poor. Beta blockers are needed in addition, for most persons with congenital long QT syndrome. Some of the polymorphic VTs in Brugada syndrome may be prevented by quinidine, though implantation of a defibrillator cannot be avoided by this method.