Abstract
This study examined the relationship between hypokalemia and ventricular tachyarrhythmia in nonischemic heart, and tried to determine whether hypokalemia enhances the proarrhythmic effect of ventricular repolarization-prolonging drugs. In 12 mongrel dogs (group 1), hypokalemia was produced by infusion of 5.0 g/kg of polystyrene sulfonic acid calcium into the colon while 8 other dogs (group 2) were maintained normokalemic. Programmed ventricular stimulation (PVS) was performed in the two groups before and after injection of disopyramide (i.v., 2.0 mg/kg). In group 1, serum potassium decreased from 4.1 ± 0.3 to 2.7 ± 0.4 mEq/L. QRS duration increased from 49 ± 2 to 60 ± 3 msec (p < 0.01). Effective refractory period (ERP) increased (p < 0.01). Monophasic action potential at 90% (MAP90) lengthened by 10% (not significant). Disopyramide significantly increased the above parameters, as well as the slope of the linear relation between percentage changes of MAP90 and potassium. Before production of hypokalemia, none out of 12 dogs (group 1) developed ventricular tachyarrhythmia in response to PVS. Five (42%) our of 12 hypokalemic dogs showed positive responses to PVS (four ventricular fibrillation, one nonsustained ventricular tachycardia). After administration of disopyramide, 7 (57%) out of 12 hypokalemic dogs showed positive responses to PVS (three ventricular fibrillation, four nonsustained ventricular tachycardia). In normokalemic dogs (group 2), no ventricular tachyarrhythmia could be induced before administration of disopyramide. After disopyramide administration, two (25%) out of eight normokalemic dogs developed ventricular fibrillation in response to PVS. Thus, hypokalemia is predictive of ventricular tachyarrhythmia even in nonischemic heart. Moreover, disopyramide-related prolongation of ventricular repolarization time can be a condition for proarrhythmic effect in a non-ischemic heart in the presence of hypokalemia.
