Cardiac Output as a Function of Ventricular Rate in a Patient with Complete Heart Block.

THE physician occasionally encounters a situation in clinical practice that offers unique opportunities to study physiologic principles relating to cardiac function that cannot be evaluated under ordinary circumstances. We recently studied a patient who had developed complete heart block without evidence of other cardiac or systemic disease. With heart rate controlled by an external pacemaker, the effects of rate, position, and exercise on cardiac output, systemic pressure, and stroke volume were assessed. Benchimol et al.1 reported hemodynamic findings in a 45-year-old man with complete heart block associated with coronary artery disease. No significant changes in stroke index were found with exercise. Our results suggest that this may have been due to the existence of coronary artery disease and myocardial damage. The work of Miller et al.2 in dogs with induced chronic heart block lends support to the concept that stroke volume may alter appreciably in response to exercise with its increased demand on the heart. Case Report D.P., a 33-year-old married Caucasian woman, was entirely well until April 1960, when she suddenly developed complete heart block with a ventricular rate of 30 beats per minute and con-gestive heart failure. Cardiac catheterization revealed only mild pulmonary hypertension, high end-diastolic ventricular pressure, and mild tri-cuspid insufficiency. Subsequent extensive laboratory studies have revealed no evidence of general or intracardiac disease other than the heart block. Medical management did not completely relieve the patient's congestive heart failure, and 592 isoproterenol increased the ventricular rate to only 48 beats per minute. A thoracotomy was performed, therefore, and bipolar electrodes were sutured into the ventricular myocardium and connected to an external pacemaker. Biopsy of the right atrial appendage showed moderate myo-cardial hypertrophy; pericardial biopsy revealed old, healed, nonspecific pericarditis. With heart rate fixed at 60 beats per minute, the patient was markedly improved. Two years later, it was necessary to replace the myocardial electrodes because of localized fibrosis. With an internal pacemaker set at 68 beats per minute, the patient was able to perform all household tasks for her family of six and to participate in athletics without difficulty. She remained well until May 1963, when she suddenly developed a ventricular rate of 200 beats per minute. The electrocardiogram at this time revealed a pacemaker rate of 400 (fig. 1). An external pacemaker was connected to the implanted electrode leads to re-establish the normal rate. One week later, a series of cardiac function tests were performed, …