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 electrophysiological effects of varying concentrations of extracellular K+ in 24 isolated, retrogradely perfused rabbit hearts. The left ventricular cavity was dilated with a fluid-filled balloon. Left ventricular effective refractory period decreased significantly (from 119 +/- 3 to 105 +/- 3 ms) with ventricular dilatation but was not influenced by K+ concentration. Conduction velocity was not changed by dilatation but was decreased 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 arrhythmias were induced in undilated hearts at a K+ concentration of 4.9 mM. Induced ventricular fibrillation was more frequent (38%; P < 0.01) in the dilated heart and increased markedly (92%; P < 0.01) with coexisting hypokalemia. The incidence of induced fibrillation was highly correlated with the wavelength of the ventricular impulse (wavelength = refractory period X conduction velocity). Thus dilatation and hypokalemia have very different electrophysiological effects that can interact synergistically to predispose the heart to reentrant arrhythmias in this model.