Ventricular conduction delay and arrhythmias during regional hyperkalemia in the dog. Electrical and myocardial ion alterations.

Coronary arterial potassium (K) infusion induces RS-T elevation and ventricular arrhythmias. To explore electrical and metabolic events in this model, which simulates ischemia-induced injury currents and rhythm disturbances, isotonic KC1 was infused at 0.5-2.0 ml/min into the left anterior descending or the left circumflex coronary artery of 37 intact anesthetized dogs. Conduction was monitored with His and left bundle branch recording catheters and with bipolar electrodes at endocardial and epicardial levels in the perfused zone. RS-T segments rose progressively in the perfused region despite normal coronary blood flow ('Kr); some dogs progressed rapidly to multifocal ventricular extrasystoles and ventricular fibrillation (group 1), but others continued for 20 minutes without developing fibrillation (group 2). His-Q and bundle branch conduction times were not altered by regional perfusion, but the QRS complex was locally prolonged. Ventricular extrasystoles were frequently coupled and left bundle branch depolarizations never preceded them, suggesting origin within the myocardium. Intramural electrodes showed increasing delay in the perfused region; epicardial depression was uniformly more profound and preceded significant arrhythmias, often with 2:1 or higher intramural block and slowing sufficient to allow reentry. Epicardial activation preceding endocardial activation was observed during extrasystoles in the perfused zone, further indicating origin within the myocardium. These phenomena were associated with tissue concentrations of K in the outer wall significantly higher than those in the inner wall; and sodium was also significantly elevated. Therefore, it was postulated that reentry from depressed epicardial layers into more normal surrounding tissue constitutes a possible basis for the arrythmias in this model.