Circulatory Consequences of Changes in Cardiac Rhythm Produced in Patients by Transthoracic Direct-Current Shock*

Abstract

Most arrhythmias have long been regarded as undesirable. The salutary clinical consequences of abolishing ventricular and atrial tachycardias are often immediately apparent, and, in general, the circulatory disadvantages of an inappropriately rapid ventricular rate in man would seem well accepted. The effect on the circulation of atrial arrhyth-mias without tachycardia, particularly atrial fibrillation, however, is not clear. Lower cardiac outputs have been reported in groups of patients with rheumatic heart disease and atrial fibrillation than in those with sinus rhythm (1, 2). Studies of the same patients first with atrial fibrillation and later in sinus rhythm after quinidine conversion have been reported by several investigators (3-7). Of the 35 patients in two of these studies in which only mean data are presented (4, 7), the majority of patients had increased outputs after conversion. Of the 27 patients in the other three studies (3, 5, 6), the output was increased at rest after conversion in eighteen and was unchanged or less in nine. In the two studies in which heart rates were available (4, 5), no rates of over 100 in atrial fibrillation were found. In published data, therefore, it is evident that restoration of sinus rhythm with quinidine does not regularly result in an increased cardiac output when measurements are made days to weeks after conversion. Since quinidine was used as the antiarrhythmic drug in all of these studies, the observations on circulatory function were necessarily made days to weeks after the instant of reversion, i.e., at a time when overall circulatory adjustments to the rhythm change would be anticipated. The technique of direct-current transthoracic shock, timed to occur during maximal ventricular depolariza-tion, has been shown by Lown, Neuman, Ama-rasingham, and Berkovits in animals and man (8, 9) to be safe and effective in terminating various arrhythmias; furthermore, it has made possible hemodynamic studies predictably timed to coincide with a change in cardiac rhythm in the absence of quinidine. We have made observations before, during, and after condenser-discharge shocks in 26 patients with various ar-rhythmias undergoing electrical conversion attempts. The majority of these patients had atrial fibrillation with varying rates of ventricular response ; 21 detailed hemodynamiiic studies were made in 20 of these patients in an effort to assess the relative importance of the ventricular rate and the absence of atrial systole on cardiac output. Methods The patients studied included four with ischemic, 16 with rheumatic, and two with hypertensive heart disease ; one patient had had an atrial septal defect closed, and three patients, one with borderline hyperthyroidism [BMR, +20%; PBI (protein-bound iodine), 9.2 ,ug per 100 ml] and one with labile blood pressure, had atrial fibrillation as the only sign we could detect of possible heart disease