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(Circulation. 2000;102:817.)
© 2000 American Heart Association, Inc.

Images in Cardiovascular Medicine

Labile Repolarization From "Cell to Bedside"

Kalyanam Shivkumar, MD, PhD

From the Division of Cardiology, Department of Medicine, UCLA School of Medicine, Los Angeles, Calif.

Correspondence to Kalyanam Shivkumar, MD, PhD, Associate Director, Cardiac Electrophysiology, Division of Cardiology, Department of Internal Medicine, 4426 B, JCP, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City IA 52242. E-mail shivkumark{at}mail.medicine.uiowa.edu

A47-year-old man with end-stage renal disease on hemodialysis was taking quinidine for paroxysmal atrial fibrillation and clarithromycin for presumed bronchopneumonia. When he returned to the floor after hemodialysis, he complained of nausea and was given 10 mg of prochlorperazine intravenously. He then felt lightheaded and passed out. The rhythm monitor showed torsade de pointes, and a code was called. The rhythm required defibrillation; it recurred almost immediately and required repeated shocks. A serum electrolyte profile revealed a potassium concentration of 2.9 mEq/L. An ECG (FigureA) was obtained between shocks, and it shows the onset of torsade de pointes. A second ECG, which was obtained a few minutes later (Figure B), shows the dramatically prolonged QT interval, with prominent QU/bifid T waves. The QT interval was initially stabilized by infusion of isoproterenol and later by temporary transvenous pacing. The serum concentration of potassium was also corrected. A third ECG (Figure C) was obtained after 3 days, and it shows a resolution of the repolarization abnormalities. All offending drugs were discontinued, and the patient recovered without any further arrhythmias.

View larger version (83K): [in this window] [in a new window]   Figure 1. A, ECG obtained during code between shocks, demonstrating onset of torsade de pointes. B, ECG obtained a few minutes later shows a dramatically prolonged QT interval with prominent QU/bifid T waves. C, ECG obtained 2 days later shows normalization of QT interval.

In this patient, it is tempting to construct a scenario as follows: clarithromycin and quinidine blocked K channels, hypokalemia reduced repolarizing K currents (augmenting quinidine’s K channel–blocking effect), quinidine’s K channel–blocking effect was further augmented by the relative bradycardia when the patient was experiencing nausea (vagal effect), and prochlorperazine further compromised repolarization. This is an "ideal" setting for early after-depolarization–related tachyarrhythmias.

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