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 arrhythmias 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.* Submitted for publication June 10, 1964; accepted August 7, 1964. Supported in part by grants from the U. S. Public Health Service, National Institutes of Health (HE-05579), and from the Chicago and Illinois Heart Associations.Presented in part at the 55th annual meeting of the American Society for Clinical Investigation, Atlantic City, N. J., April 29, 1963. 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 over-all circulatory adjustments to the rhythm change would be anticipated. The technique of direct-current transthoracic shock, timed to occur during maximal ventricular depolarization, has been shown by Lown, Neuman, Amarasingham, 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 arrhythmias 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.
