Nature of abnormal ventricular complexes during quinidin treatment of auricular fibrillation.

Abstract

When quinidin is given to patients with auricular fibrillation there is almost invariably a considerable increase in the ventricular rate. This is accompanied in one-third to one-half of the cases by the appearance of groups of abnormal ventricular complexes. These abnormal complexes must be due either to abnormal impulse formation in the ventricular muscle or to defective intraventricular conduction. The former explanation has been advanced by Cohn, 1 Levy, 2 and Lewis 3 ; the latter by White, 4 and others.

We have studied two cases in which these abnormal ventricular complexes were unquestionably due to defective intraventricular conduction. In the first case, runs of abnormal ventricular complexes occurred after eighteen grains of quinidin. After twenty-four grains all of the ventricular complexes were of the abnormal type. The administration of one-eighth grain of pilocarpin, intravenously, slowed the ventricular rate, and the longer pauses were followed by relatively normal complexes. There was, however, no close relation between the length of the pause and the form of the complex which followed. About two hours later, the auricular fibrillation gave place to normal rhythm but the ventricular complexes were still of the abnormal type. The normal type of complex returned, however, as soon as the quinidin effect wore off. After the rhythm had been normal for 3 days, eighteen grains of quinidin failed to produce abnormal complexes. The patient was then given three grains of quinidin twice a day to prevent a return of fibrillation but without success. When fibrillation returned the ventricular rate was rapid and runs of abnormal complexes again occurred. These disappeared when quinidin was discontinued and could not be produced by the intravenous administration of one-fiftieth grain atropin, which greatly increased the ventricular rate.