Hypokalemia after cardioversion from ventricular tachycardia induced in the electrophysiology laboratory

Serum potassium is often low after resuscitation from out-of-hospital ventricular fibrillation. We hypothesized that hypokalemia develops after ventricular tachycardia induced by programmed electrical stimulation. We measured serum potassium in 10 patients before induction of ventricular tachycardia and 15 minutes, 45 minutes, and 3 hours following cardioversion from ventricular tachycardia. Ventricular tachycardia rate was 243 +/- 71 bpm and duration was 57 +/- 87 seconds. Mean serum potassium (mEq/L) decreased from 4.1 +/- 0.3 at baseline to 3.8 +/- 0.5 at 15 minutes (p less than 0.01 vs baseline) and 3.7 +/- 0.6 at 45 minutes (p less than 0.005 vs baseline), but returned to 4.1 +/- 0.5 at 3 hours. Although no patients were hypokalemic (potassium less than 3.5 mEq/L) at baseline, 33% were hypokalemic at 15 minutes and 40% were hypokalemic at 45 minutes (p = 0.06 vs baseline). A low serum potassium was found in several of these patients immediately after the clinical arrhythmia that led to electrophysiologic study, and rapid resolution of the hypokalemia was observed. Thus, serum potassium decreases rapidly in man after resuscitation from brief but hemodynamically significant ventricular tachycardia. This suggests that patients with hypokalemia after resuscitation from out-of-hospital ventricular fibrillation have hypokalemia secondary to the event. The electrophysiologic effects of post-cardioversion hypokalemia are unknown.