We have developed an experimental model to assess the ability of drugs to maintain slow supraventricular rhythm after electrical conversion of atrial fibrillation. Fibrillation was produced by application of a saturated solution of aconitine to the surface of the right atrium of open-chest dogs. Right and left atrial electrograms, the lead II electrocardiogram, and blood pressure were recorded. A capacitor discharge (30 watt-seconds) was applied through electrodes placed on the right atrium and the left ventricle. Atrial rhythm was improved for 1 to 20 s following defibrillation; then atrial fibrillation returned owing to the continued presence of aconitine. Quinidine in doses up to 4 mg/kg did not convert the arrhythmia but increased the duration of recovery after defibrillation up to 49 s. Pronethalol in doses up to 8 mg/kg and propranolol in doses up to 0.8 mg/kg occasionally converted atrial fibrillation to normal rhythm, but had no effect upon the duration of recovery after defibrillation. Diphenylhydantoin was tested in doses up to 20 mg/kg. Rapid injection of doses above 10 mg/kg slowed or converted the arrhythmia. Slow injections of diphenylhydantoin had no direct effect on the atrial fibrillation, but the period of recovery after defibrillation was prolonged up to 700 s. These experiments show that drugs can enhance the ability of the heart to maintain a slow rhythm following electrical conversion of atrial fibrillation. Those agents which most effectively convert atrial fibrillation are not the most effective agents for preventing the return of fibrillation after conversion.
AV junctional versus left atrial rhythm.