Hemodynamic Effects of Nitroglycerin in Acute Myocardial Infarction

Decrease in Ventricular Preload at the Expense of Cardiac Output

WILLIAMS, DAVID O. M.D.
AMSTERDAM, EZRA A. M.D.
MASON, DEAN T. M.D.

From Section of Cardiovascular Medicine, Departments of Medicine and Physiology, University of California at Davis, School of Medicine, Davis; Sacramento Medical Center, Sacramento; and Martinez Veterans Administration Hospital, Martinez, California.

Supported in part by Research Program Project Grant HL 14780 and Postgraduate Training Grant HL 5901 from the National Heart and Lung Institute.

Address for reprints: David 0. Williams, M.D., Section of Cardiovascular Medicine, Department of Medicine, Martinez Veterans Administration Hospital, Martinez, California 94553.

Received August 21, 1974; revision accepted for publication October 24, 1974.

Circulation 51(3):p 421-427, March 1975.

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agent in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (≤ 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (> 12 mm Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 to 7 mm Hg; P < .01), mean systemic arterial pressure (MAP) (95 to 82 mm Hg; P < .01), cardiac index (CI) (1.79 to 1.46 L/min/m²; P < .02), stroke index (SI) (24 to 18 cc/m²; P < .01) and stroke work index (SWI) (27 to 20 gm•m/m²; P < .01). These alterations were significant in both subgroups, with the decline in PAW greater (P < .02) in group II (19 to 9 mm Hg) than in group I (7 to 4 mm Hg). The decrease in SWI related to the fall in PAW was significantly greater (P < .05) in group I (2.03 gm•m/m²) compared to group 11 (0.82), thereby indicating greater impairment of ventricular function in the group II patients. Heart rate (HR) increased slightly in the 16 patients (77 to 82 beats/min; P < .05) and in group I (71 to 80 beats/min, P < .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline of pump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accompanied by potentially deleterious fall in cardiac output and systemic blood pressure.