(Circulation. 2000;102:817.)
© 2000 American Heart Association, Inc.
Images in Cardiovascular Medicine |
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@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.
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In this patient, it is tempting to construct a scenario as
follows: clarithromycin and quinidine blocked K channels, hypokalemia
reduced repolarizing K currents (augmenting quinidines K
channelblocking effect), quinidines K channelblocking
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