THE ROLE OF POTASSIUM IN EPINEPHRINE-INDUCED CARDIAC ARRHYTHMIAS

¹ Department of Pharmacology and Therapeutics, University of Manitoba, Faculty of Medicine, Winnipeg, Manitoba, Canada

Five series of experiments have been performed to investigate a possible causal relationship between the induced hyperkalemia and epinephrin-induced ventricular arrhythmias in pentobarbital anesthetized dogs. It is concluded that no causal relationship exists on the basis of the following observations.

The hyperkalemic response to epinephrine is not quantitatively correlated with the induction of arrhythmias, and the ability of subthreshold doses of epinephrine to induce arrhythmias is not potentiated by the injection of exogenous potassium unless the plasma levels attained are considerably above those occurring after an arrhythmia -inducing dose of epinephrine.

The ability of isoproterenol to induce cardiac arrhythmias is not enhanced by the infusion of potassium to produce blood levels comparable to those resulting from an arrhythmia-inducing dose of epinephrine.

Infusion of potassium chloride to produce blood levels comparable to those induced by a previously arrhythmia-inducing dose of epinephrine does not allow the production of arrhythmias after Dibenamine blockade.

Exclusion of the liver from the circulation and consequent abolition of the epinephrine-induced hyperkalennia does not prevent the production of arrhythmias by epinephrine.

It was observed that very high plasma potassium levels, above those resulting from an arrhythmia-inducing dose of epinephrine, can facilitate the production of arrhythmias. The administration of exogenous potassium is particularly effective when peak levels are reached early in the course of the epinephrine action before the beginning of the epinephrine hyperkalemia. After exclusion of the liver from the circulation, the animals become more sensitive to this action of potassium. In one case potassium infusion alone induced ventricular fibrillation.