Effects of Adenosine-induced Hypotension on Myocardial Hemodynamics and Metabolism in Fentanyl Anesthetized Patients with Peripheral Vascular Disease

Open Access
Publisher Website
Google Scholar
Abstract
The effects of adenosine on central and myocardial hemodynamics and metabolism were evaluated during fentanyl anesthesia (100 .mu.g .cntdot. kg-1) in six patients with peripheral vascular disease. Adenosine was intravenously infused, at a rate of 90 .+-. 20 (SEM) .mu.g .cntdot. kg-1 .cntdot. min-1, to reduce mean arterial blood pressure by approximately 20% (23 .+-. 2% SEM, from 82 .+-. 3 to 63 .+-. SEM mmHg) during a 20-min period. Systemic and pulmonary vascular resistance indices decreased by 36 .+-. 3 and 32 .+-. 6% (SEM), and cardiac index increased by 18 .+-. 5%. Heart rate, ventricular filling pressures, and whole body oxygen consumption were not affected by adenosine. Despite the reduced mean arterial blood pressure, coronary sinus flow increased by 128 .+-. 26% (SEM) in parallel with a 96 .+-. 11% (SEM) increase in coronary sinus oxygen content. Left and right ventricular stroke work indices, as well as myocardial oxygen consumption, were maintained. ECG (12-lead) demonstrated signs of ischemia in one subject, while myocardial lactate uptake was unchanged in all subjects. In conclusion, adenosine-induced hypotension in patients with peripheral vascular disease increased cardiac index without affecting myocardial work, whole body, and myocardial oxygen consumptions. The marked increase in coronary sinus blood flow, indicating coronary vasodilation, was not related to increased myocardial work. Further information regarding myocardial effect of adenosine in patients with ischemic heart disease is warranted.