The Initiation of Ventricular Tachycardia and Fibrillation in Isolated Hearts by Potassium Chloride

An accelerating tachycardia ending in fibrillation can be initiated in isolated hearts by injections of KC1 after the administration of epinephrine, but not in untreated hearts. KC1 acts in two ways to do this. First, it causes an A-V block that enables epinephrine to cause a paroxysmal ventricular tachycardia. Secondly, it causes the latter to accelerate by delaying the recovery of excitability so that at least one premature systole can fall into the recoveiy phase of a preceding impulse. This event is necessary and sufficient for the initiation of a self-sustaining accelerating tachycardia that can end in fibrillation. PROCAINE is an effective antifibrilla-tory agent, as shown by suitable testsin experimental animals1 and, in addi-tion, has been successfully used clinically for this purpose.2 However, in certain circum-stances it can cause ventricular arrhythmias, both in experimental animals3 and in isolated hearts.4 The mechanisms involved in this action of procaine have been analyzed in the latter case.4 In order to determine whether these mechanisms are peculiar to antifibrillatory agents of the local anesthetic type, the ability of potassium salts to initiate ventricular ar-rhythmias in isolated hearts has been studied. They have long been known to have anti-fibrillatory actions6 and to cause ventricular fibrillation in intact animals.8 METHODS The electrical activity of isolated rabbit hearts perfused with Krebs-Henseleit solution in a Langen-dorff apparatus was recorded by a previously de-scribed method.7 Epinephrine solutions were made up in 1 per cent ascorbic acid to prevent oxidation. The vehicle alone had only a transient effect on the T wave which in control experiments was found to have no bearing on the phenomena to be described. KC1 in a 0.77M solution was used for producing rapid alterations in the K+ concentration of the tissue fluid