Mechanisms of onset and termination of abnormal cardiac rhythm studied by constant monitoring

Digitalis accelerated the rate in atrial flutter resulting in atrial fibrillation, whereas the addition of quinidine slowed the atrial rate producing either asystole or interference dissociation. In some patients receiving both digitalis and quinidine, the atrial rate showed less of a tendency to slow or actually increased, resulting in atrial fibrillation followed by normal sinus rhythm. This suggests an overriding effect of digitalis. Since the spontaneous termination of atrial flutter occurred in unknown circumstances that usually slowed the atrial rate and asystole was observed, this suggests that asystole is not a toxic effect of quinidine. Atrial flutter, fibrillation, and atrial premature beats began more commonly in the P-T cycle than in the T-P cycle. Since atrial recovery is more likely incomplete during the P-T cycle, this favors reentry as the underlying mechanism in the patient studied. Atrial and nodal tachycardia begin with an irregular sequence of premature beats before a stable tachycardia is established. There is usually a significant slowing of the rate prior to termination of the abnormal rhythm. Sinus arrest with ventricular escape is the usual method of termination, regardless of the form of therapy used. Bursts of rapid ventricular rhythm resembling ventricular tachycardia were seen only after the use of pressor agents. Atrial tachycardia with block treated with digitalis shows an initial atrial slowing but, as the dose of digitalis was raised in one patient, abrupt increases in atrial rate occurred until the rhythm terminated. This is a mechanism similar to that seen in the digitalis-induced termination of atrial flutter.