QTc Prolongation in the Intensive Care Unit

Abstract

Because of the routine use of medications that can have proarrhythmic effects, critically ill patients are at an increased risk of acquiring drug-induced cardiac conduction abnormalities, specifically drug-induced QT prolongation. Approximately 69% of critically ill patients are estimated to meet at least 1 criterion for QT monitoring as recommended by the American Heart Association. These criteria include the use of a QT-prolonging medication, the presence of cardiac dysrhythmias causing severe bradycardia or long pauses, and patients with hypomagnesemia or hypokalemia. 1 Drug-induced QT prolongation can lead to the development of torsade de pointes (TdP), a potentially fatal ventricular arrhythmia. The presentation of TdP can include syncope, palpitations, dizziness, seizures, and ventricular tachycardia. However, it is important to note that patients may exhibit no symptoms at all. 2 The QT interval, a measurement from the onset of the QRS complex to the end of the T wave, is a surrogate marker for the cardiac myocyte action potential. Prolongation of the QT interval is a result of delayed repolarization of the ventricular myocardium. Many cardiac medications have been implicated in causing this delay in ventricular myocardium repolarization, resulting in prolongation of the QT interval. However, an increasing number of noncardiac medications have also been associated with QT interval lengthening. Druginduced QT prolongation is the most common reason noncardiac medications have required Food and Drug Administration (FDA) relabeling or have been withdrawn from the market in the last decade. 3