Analgesic and hemodynamic effects of buprenorphine in acute infarction of the heart.
The analgesic, hemodynamic and respiratory effects of buprenorphine (0.3 mg i.v.) were monitored in 15 coronary care unit-admitted patients presenting with myocardial infarction who were in functional class I according to the Killip classification. At the time of the study, 8 of them had unequivocal precordial pain (group 1); the remaining 7 were painfree (group 2). The agent showed a prompt and potent analgesic action. It also induced a slight decrease in mean aortic pressure associated with a reduction in systemic vascular resistance and an increase in cardiac index, a rise in the pulmonary arterial pressure and arteriolar resistance and right atrial pressure, a reduction in arterial pO2 and pH and an increase in pCO2. Tension-time-indices of the left and right ventricles varied in parallel with variations in aortic and pulmonary artery pressure, respectively. These responses were probably unrelated to analgesia since they were similar in groups 1 and 2. Changes in systemic circulation were such as to possibly decrease the contractile effort and the oxygen need of the left ventricle and the size of infarction. On the contrary, the rise in pulmonary arterial pressure imposes a hemodynamic burden on the right ventricle that, depending on the patient's condition, may assume clinical importance. It is felt that the use of buprenorphine in myocardial infarction should be restricted to uncomplicated and selected cases.
D002047:Buprenorphine / Q000627:therapeutic use*; D004341:Drug Evaluation; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D010146:Pain / Q000188:drug therapy / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000187:drug effects; D013997:Time Factors
D002047:Buprenorphine