Enhancement of the vulnerability of the ventricle to fibrillation (VF) by regional hyperkalemia

A region of intermittent hyperkalaemia was produced in dogs by the intracoronary infusion of K+ in a concentration of 40 m-equiv/1. at a rate of 0·06-0·13 μ-equiv K+/kg/sec. The rate of K+ infusion was selected on the basis of its ability reproducibly to produce systolic and diastolic injury currents and Q-T shortening in electrocardiograms recorded from areas perfused by K + . Moreover, K+ infusion displaced the vulnerable period to the left, accompanied by a greater than 50% decrease in the stimulus strength necessary to induce MVR or VF, while the tendency for MVR to degenerate into VF was distinctly enhanced. These studies have documented that infusion of an amount of K+ into a local coronary bed which produces electrocardiographic evidence of injury resulted in changes in excitability and vulnerability similar to those occurring in acute experimental ischaemia. Further, they suggested that the electrophysiological effects on refractoriness and vulnerability to VF resulting from local enhancement of extracellular K+ may indeed contribute importantly to the 'excitatory factors' related to arrhythmias during acute myocardial ischaemia in man.