Three groups of dogs were given ouabain (mean 60 μg/kg) until an accelerated ventricular escape (AVE) and repetitive ventricular response (RVR) followed cessation of pacing. In a group of six control dogs, the AVE and RVR were found to occur at stable escape intervals for periods of at least three hours. A second group of dogs received various antiarrhythmic agents in an attempt to suppress the AVE and RVR. Quinidine, diphenylhydantoin, lidocaine, procainamide, and propranolol, were successful in only 0 to 33% of trials. Potassium canrenoate, 12 mg/kg was unsuccessful in three dogs. Verapamil, by bolus, suppressed RVR in 41% and AVE in 21% of trials. KCl, infused until AVE and RVR were suppressed, was successful when the mean serum potassium rose from 3.8 mEq/L to 7.2 mEq/L. Aprindine, 2.86 mg/kg, suppressed AVE and RVR in 14 of 14 dogs. In the third group of dogs, verapamil was infused continuously and suppressed RVR and AVE at a mean cumulative dose of 2.93 mg/kg. Calcium chloride reversed aprindine and verapamil induced suppression of RVR and AVE. This study demonstrates that RVR and AVE resist suppression by available antiarrhythmic agents in clinically used doses. Only aprindine was 100% successful at doses used in man. The ionic pathogenesis of RVR and AVE is unknown, but some data suggest the slow current may play an important role.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)