Abstract
The effects of diphenylhydantoin sodium (Dilantin) on ventricular automaticity, intraventricular conduction, atrioventricular (A-V) conduction, and sinus rate have been determined in the digitalis-intoxicated and normal heart. These effects have been compared with procaine amide. Diphenylhydantoin sodium depresses ventricular automaticity and enhances A-V conduction while having little or no effect on intraventricular conduction or sinus rate. Procaine amide differed from diphenylhydantoin sodium in that it caused depression of both A-V and the intraventricular conduction, as well as slowing of the sinus rate. The results indicate that the electrophysiological properties of diphenylhydantoin sodium make it superior to procaine amide in the treatment of digitalis toxicity. Both diphenylhydantoin sodium and procaine amide can suppress digitalis arrhythmias due to enhanced automaticity, but procaine amide may promote "re-entry" arrhythmias by potentiating the intraventricular conduction defect caused by the glycoside. In addition, diphenylhydantoin sodium appears to antagonize the action of digitalis on the A-V node, while procaine amide increases the digitalis-induced A-V block. It is concluded that the electrophysiological properties of diphenylhydantoin sodium make it an excellent agent in treating digitalis-induced arrhythmias.
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