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New Guidance for In-Hospital Torsades De Pointes

Steve Stiles


February 9, 2010 (Dallas, Texas and Washington, DC) — Many common, useful drugs have the side effect of electrocardiographic QT-interval prolongation, which substantially increases the risk of sudden death from torsades de pointes, a polymorphic ventricular tachycardia. A given QT-prolonging drug may more likely cause torsades in hospitalized patients than in the general population, as 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," observes a new scientific statement from the American Heart Association and American College of Cardiology [1]. Those features, including advanced age, have confirmed or suspected associations with development of the malignant arrhythmia, the document states.

The document, also endorsed by the American Association of Critical-Care Nurses, describes the state of the art of how to identify the arrhythmia and its precursors on the electrocardiogram (ECG), drugs and patient features that promote it, strategies for prevention and monitoring, and acute management of both QT prolongation and the manifest arrhythmia. Dr Barbara J Drew (University of California, San Francisco) chaired its writing group.

The benefits of using QT-prolonging agents must be weighed against the risk in patients with increased susceptibility to torsades, it states. The susceptibility can include certain genetic mutations that, when such drugs are given, can promote the arrhythmia.

In such cases, continuous monitoring of the corrected QT (QTc) interval is recommended; "prompt action" is needed if the QTc exceeds 500 ms compared with an ECG obtained before drug administration; the QTc must be measured by the same method and/or device each time.

Responses can include drug withdrawal, correction of electrolyte abnormalities, temporary pacing, and "the ready availability of an external defibrillator."

Other ECG features can signal impending torsades, including distortions of the T-U wave, visible T-wave alternans, new ventricular ectopic beats, and "couplets and nonsustained polymorphic ventricular tachycardia initiated in the beat after a pause."

Drugs that promote QTc prolongation and torsades, to different degrees, include the antiarrhythmics quinidine, disopyramide, procainamide, sotalol, dofetilide, and ibutilide as well as methadone, thioridazine, and haloperidol, according to the statement.

Still, it notes, "where benefit clearly outweighs risk, QT prolongation should not limit necessary therapy."

The report states that "the American Heart Association and the American College of Cardiology Foundation make every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel" and lists disclosures for individual members of the writing group.

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