INTERACTION OF HYPOKALEMIA AND VENTRICULAR DILATATION IN ISOLATED RABBIT HEARTS

Potassium depletion has been implicated in the genesis of ventricular arrhythmias, especially in patients with congestive heart failure, but the nature of this interaction is unknown. We studied the electrophys iological effects of varying concentrations of extracellular K+ in 24 isolated, retrogradely perfused rabbit hearts. The left ventricular ca vity was dilated with a fluid-filled balloon. Left ventricular effecti ve refractory period decreased significantly (from 119 +/- 3 to 105 +/ - 3 ms) with ventricular dilatation but was not influenced by K+ conce ntration. Conduction velocity was not changed by dilatation but was de creased by hypokalemia (81 +/- 2 cm/s, K+ = 4.9 mM; 75 +/- 2 cm/s, K= 3.5 mM; 70 +/- 2 cm/s, K+ = 2.5 mM; P < 0.05). No ventricular arrhyt hmias were induced in undilated hearts at a K+ concentration of 4.9 mM . Induced ventricular fibrillation was more frequent (38%; P < 0.01) i n the dilated heart and increased markedly (92%; P < 0.01) with coexis ting hypokalemia. The incidence of induced fibrillation was highly cor related with the wavelength of the ventricular impulse (wavelength = r efractory period X conduction velocity). Thus dilatation and hypokalem ia have very different electrophysiological effects that can interact synergistically to predispose the heart to reentrant arrhythmias in th is model.