Central Inhibition of Sympathetic Overdrive by Clonidine in Acute Myocardial Infarction with Systolic Hypertension. Haemodynamic Study

Publisher Website
Google Scholar
Abstract
Intravenous clonidine was used to treat systolic hypertension (systolic blood pressure greater than 160 mm Hg) in 15 patients with acute myocardial infarction and documented sympathetic overactivity (high plasma norepinephrine). Its effects on haemodynamics and blood gases were studied. After one hour, clonidine significantly reduced the systolic (195±7 to 137±7 mm Hg, p < 0.01) and diastolic (81±4 to 60±3 mm Hg, p < 0.01) blood pressures as well as the systemic vascular resistance (26±2 to 20±1 IU, p < 0.01). The cardiac index was reduced from 2.8±0.2 to 2.4±0.2 l/min.m2, p<0.01. This change was related to a reduction of the heart rate (92±4 to 81±4 beats/ min, p < 0.01) as the stroke index was unchanged. Pulmonary wedge pressure (15±3 to 10±2 mm Hg, p < 0.01) and rate pressure product (18.034±1.159 to 11.274±917 mm Hg, beats/min, p < 0.01) were also significantly decreased. The arterial oxygen tension did not change significantly but there was a significant drop in the mixed venous oxygen saturation (63±2 to 61±2%, p<0.02) and oxygen transport (433±41 to 409±36, p < 0.01). Clonidine is thus able to normalize blood pressure in acute myocardial infarction ; this is accompanied by a reduction in myocardial oxygen requirements and pulmonary wedge pressure. Oxygen transport to the tissues, however, may be decreased.