EFFECTS OF DIPHENYLHYDANTOIN SODIUM (DILANTIN SODIUM) AND PHENOBARBITAL SODIUM UPON ECTOPIC VENTRICULAR TACHYCARDIA IN ACUTE MYOCARDIAL INFARCTION

Abstract

The concept that the mechanism of production of ectopic ventricular impulses in acute myocardial infarction may be due in part to factors that are similar to those which evoke focal cerebral impulses that produce epileptic seizures led to the trial of anti-epileptic drugs for suppressor effect upon ventricular ectopic activity. Diphenylhydantoin Na (dilantin) in sufficient dosage produced complete cessation of ectopic activity for a period of time followed by a longer period of marked reduction of ectopic frequency. The quantity of dilantin required was greater when the ectopic frequency was greater and less when the ectopic frequency was less. Dilantin reduced the frequency of discharge of the S-A node also, but the effect upon the frequency of ectopic discharges was much greater. Phenobarbital Na alone was effective in suppressing only relatively low-frequency ectopic rhythms. It markedly increased the effectiveness (reduced the required dose) of dilantin in the suppression of ectopic rhythms of all frequencies. Rapid intraven. admn. of dilantin produced a sharp drop in blood pressure and an increase in rate and depth of respiration. In 2 trials these phases were followed by cessation of respiration followed by cardiac standstill. Slow intraven. admn. produced little or no change in blood pressure or respiration. In a few trials the admn. of sufficient dilantin alone to suppress all ectopic activity produced toxic nervous symptoms; after phenobarbital, the relatively small amts. of dilantin required never produced such symptoms. In the discussion an incomplete listing of similarities of reactions of cardiac muscle, nerve and skeletal muscle is given. It is suggested that ventricular preparations with ectopic rhythms might be valuable for preliminary testing of drugs for anti-epileptic activity.