One of the less frequent underlying mechanisms of ventricular tachycardia (VT) is triggered activity. Triggered activity refers to an extrasystole due to a premature depolarization that occurs when the amplitude of an early or delayed afterdepolarization brings the cardiac membrane to its threshold potential. Hydrochlorothiazide and hydroxyzine can prolong repolarization and QT interval and are associated with early afterdepolarizations. Cyclic AMP-mediated, delayed afterdepolarizations can occur as a result of catecholaminergic surge. Delayed afterdepolarization is classically associated with outflow tract (OT) tachycardia, a type of VT that is uniquely defined by its termination with adenosine. We present a case of triggered OT tachycardia for which intravenous amiodarone through its antiadrenergic effect may have been effective. Infusions of magnesium and a cardioselective, β-receptor antagonist that does not prolong repolarization may have been more appropriate given the concurrent, acquired prolonged QT syndrome. After initial stabilization, considering the underlying VT mechanism may prompt the clinician to select the most appropriate, further treatment.
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