Abstract

Cardiac arrest due to torsade de pointes (TdP) in the acquired form of drug-induced long-QT syndrome (LQTS) is a rare but potentially catastrophic event in hospital settings. Administration of a QT-prolonging drug to a hospitalized population may be more likely to cause TdP than administration of the same drug to an outpatient population, because hospitalized patients often have other risk factors for a proarrhythmic response. For example, hospitalized patients are often elderly people with underlying heart disease who may also have renal or hepatic dysfunction, electrolyte abnormalities, or bradycardia and to whom drugs may be administered rapidly via the intravenous route. In hospital units where patients’ electrocardiograms (ECGs) are monitored continuously, the possibility of TdP may be anticipated by the detection of an increasing QT interval and other premonitory ECG signs of impending arrhythmia. If these ECG harbingers of TdP are recognized, it then becomes possible to discontinue the culprit drug and manage concomitant provocative conditions (eg, hypokalemia, bradyarrhythmias) to reduce the occurrence of cardiac arrest. The purpose of this scientific statement is to raise awareness among those who care for patients in hospital units about the risk, ECG monitoring, and management of drug-induced LQTS. Topics reviewed include the ECG characteristics of TdP and signs of impending arrhythmia, cellular mechanisms of acquired LQTS and current thinking about genetic susceptibility, drugs and drug combinations most likely to cause TdP, risk factors and exacerbating conditions, methods to monitor QT intervals in hospital settings, and immediate management of marked QT prolongation and TdP. The term torsade de pointes was coined by Dessertenne in 1966 as a polymorphic ventricular tachycardia characterized by a pattern of twisting points.1 Several ECG features are characteristic of TdP and are illustrated in Figure 1. First, a change in the amplitude and morphology (twisting) of the QRS …

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