Impairment of autonomically mediated heart rate control in patients with cardiac dysfunction

Patients with cardiac disorders have defective parasympathetic control of heart rate. To evaluate the possibility of similar changes in sympathetic control of heart rate, reflex chronotropic responses to 80° upright tilt and nitroglycerin induced hypotension were compared in 31 cardiac patients and 7 normal individuals before and after partial parasympathetic blockade with atropine. Tilting revealed an attenuation of the normal heart rate increase in patients; the magnitude of this defect was greatest in patients with more severe symptoms (class III) and evidence of left ventricular dysfunction (the heart rate increase averaged 25 ± 3 beats/min in normal subjects, 12 ± 2 beats/min in class I-II patients, and 7 ± 1 beats/min in class III patients). Class III symptoms due to mechanical causes (mitral stenosis), however, were not associated with the defect. A marked reduction in heart rate with hypotension was seen only in those class III patients without mitral stenosis (0.4 ± 0.1 beats/min/mm Hg vs. 3.0 ± 0.5 beats/min/mm Hg in normal subjects). This abnormality also persisted after atropine administration thus confirming a defect in the sympathetic as well as the parasympathetic component of baroreceptor mediated reflex heart rate control in patients with cardiac dysfunction. Infusions of isoproterenol produced equivalent rises in heart rate in patients and normal individuals, excluding a reduction in beta receptor responsiveness as a cause of impaired sympathetic influence. Norepinephrine depletion, however, is a well recognized concomitant of cardiac failure. It is possible that the reduction in sympathetically mediated heart rate responses results in part from depletion of the sympathetic neurotransmitter.