Abstract
Chronic hypokalemia (2.9±0.2mEq/L) was induced in 10 dogs by a low potassium diet and furosemide administration. Five control dogs with normokalemia (5.0±0.3mEq/L) were fed an ordinary diet. Three of the 10 hypokalemic dogs had electrically induced, nonsustained ventricular tachycardia (NSVT) and ventricular fibrillation (VF); none of the 5 control dogs had these ventricular arrhythmias. After ligation of the left anterior descending coronary artery (LAD), 4 of the 10 hypokalemic dogs developed spontaneous VF and 6 had electrically induced NSVT and VF, whereas 2 of the 5 control dogs had only NSVT. The effective refractory period (ERP) of the ventricles of the hypokalemic dogs was slightly longer than that of the control dogs. After LAD ligation, only the ERP of the anterior wall of the left ventricle was prolonged significantly in either group (p<0.01). The ventricular fibrillation threshold (VFT) of hypokalemic dogs was significantly lower than the control dogs (p<0.05), and was reduced markedly (p<0.05) after LAD ligation. A positive correlation between VFT and serum potassium level was observed. Thus, chronic hypokalemia increases ventricular vulnerability. This effect depends upon the severity of hypokalemia and is markedly augmented by acute myocardial ischemia. These findings indicate that, in clinical settings, preexisting hypokalemia and its severity may play important roles in the occurrence of lethal ventricular arrhythmias during the acute phase of myocardial infarction.
