Cardiovascular effects of atropine in postoperative cardiac patients receiving digoxin for ventricular dysfunction.

Digoxin is clinically useful as a cardiac antiarrhythmic and inotropic agent. Its antiarrhythmic actions are mediated through the cholinergic nervous system. The cholinergic system, when activated, can depress ventricular function. We have sought to further increase the cardiovascular effects of digoxin by blocking its cholinergic effects with atropine. Atropine, 1 mg intravenously, was given to 10 postoperative cardiac patients. The cardiovascular time course was monitored by an ECG, radial arterial line, and pulmonary artery thermodilution catheter for 8 hours. A significant increase (p less than 0.05) in the cardiac output (CO), from 5.98 +/- 0.24 L/min to 6.60 +/- 0.34 L/min, was evident within 2 hours after atropine administration. The CO returned to control levels by 6 hours. There were no significant changes in heart rate, systemic vascular resistance, pulmonary artery wedge pressure, or systemic blood pressure. The results indicate that the cholinergic blockade of digoxin with atropine will acutely increase the cardiac output in postoperative cardiac patients.