Prolonged Cardiac Repolarization in the Critically Ill Patient
A 42-year-old woman who underwent single lung transplantation who received tacrolimus and a 58-year-old woman with pneumonia and multiple comorbidities who received haloperidol both experienced drug-induced prolongation of cardiac repolarization. The second woman also developed torsade de pointes. Critically ill patients are particularly susceptible to developing torsade de pointes due to various comorbidities, electrolyte disturbances, and receipt of numerous drugs. These two case reports illustrate the increased risk for drug-induced cardiotoxicity in the critically ill patient. They also indicate the need for current knowledge derived from basic research and retrospective case reports on drug-induced torsade de pointes to be integrated into the existing body of knowledge. Guidelines can then be developed to help prospectively reduce the frequency of adverse effects in intensive care patients. Research is necessary regarding identification of high-risk patients before drugs are administered, and clarification of the proper role of therapeutic QT monitoring in clinical practice.
Drug-induced prolongation of the QTc interval generally is accepted as a surrogate marker for cardiac action potential prolongation and represents an increased risk for development of torsade de pointes, a rare but life-threatening ventricular tachycardia. Recent years have witnessed a growing concern regarding the cardiac safety profile of noncardiac drugs. This attention arose, at least in part, from studies linking certain nonsedating antihistamines with QT prolongation and the subsequent development of torsade de pointes.
Subsequently, certain agents in numerous drug classes have been linked to QT prolongation and torsade de pointes. The critically ill patient is particularly susceptible to developing torsade de pointes due to various comorbidities, electrolyte disturbances, and receipt of numerous drugs in the intensive care unit (ICU). We describe two cases of drug-induced QT prolongation in critically ill patients after intravenous administration of tacrolimus and haloperidol.
A 42-year-old woman who underwent single lung transplantation who received tacrolimus and a 58-year-old woman with pneumonia and multiple comorbidities who received haloperidol both experienced drug-induced prolongation of cardiac repolarization. The second woman also developed torsade de pointes. Critically ill patients are particularly susceptible to developing torsade de pointes due to various comorbidities, electrolyte disturbances, and receipt of numerous drugs. These two case reports illustrate the increased risk for drug-induced cardiotoxicity in the critically ill patient. They also indicate the need for current knowledge derived from basic research and retrospective case reports on drug-induced torsade de pointes to be integrated into the existing body of knowledge. Guidelines can then be developed to help prospectively reduce the frequency of adverse effects in intensive care patients. Research is necessary regarding identification of high-risk patients before drugs are administered, and clarification of the proper role of therapeutic QT monitoring in clinical practice.
Drug-induced prolongation of the QTc interval generally is accepted as a surrogate marker for cardiac action potential prolongation and represents an increased risk for development of torsade de pointes, a rare but life-threatening ventricular tachycardia. Recent years have witnessed a growing concern regarding the cardiac safety profile of noncardiac drugs. This attention arose, at least in part, from studies linking certain nonsedating antihistamines with QT prolongation and the subsequent development of torsade de pointes.
Subsequently, certain agents in numerous drug classes have been linked to QT prolongation and torsade de pointes. The critically ill patient is particularly susceptible to developing torsade de pointes due to various comorbidities, electrolyte disturbances, and receipt of numerous drugs in the intensive care unit (ICU). We describe two cases of drug-induced QT prolongation in critically ill patients after intravenous administration of tacrolimus and haloperidol.
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