• T G Di Salvo and P T O'Gara.
• Cardiac Unit, Massachusetts General Hospital, Boston 02114, USA.
• Clin Cardiol. 1995 May 1;18(5):285-90.

AbstractIntravenous haloperidol is the agent of choice for controlling severe agitated delirium in seriously ill cardiac patients in many institutions. Prior reports have proposed that high-dose intravenous haloperidol may be without untoward effects in these patients. Recently, however, a few reports of significant QTc prolongation and torsade de pointes as complications of high-dose intravenous haloperidol therapy have appeared. The present report describes three patients with definite haloperidol-induced QTc prolongation and torsade. In each case, QTc prolongation preceded the arrhythmia and disappeared following the discontinuation of haloperidol. Neither electrolyte imbalance, therapy with other cardiac drugs, bradycardia, ischemia, left ventricular dysfunction, nor other known cause of torsade was present in these patients. It is hypothesized that QTc prolongation and torsade likely are idiosyncratic, unpredictable reactions to high-dose haloperidol in select patients. Careful serial electrocardiographic monitoring and prompt discontinuation of the drug should suffice to prevent this relatively uncommon, life-threatening complication of high-dose intravenous haloperidol.

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