TY - JOUR
T1 - Effects of adenosine-induced hypotension on myocardial hemodynamics and metabolism in fentanyl anesthetized patients with peripheral vascular disease
AU - Owall, A.
AU - Jarnberg, P. O.
AU - Brodin, L. A.
AU - Sollevi, A.
PY - 1988
Y1 - 1988
N2 - The effects of adenosine on central and myocardial hemodynamics and metabolism were evaluated during fentanyl anesthesia (100 μg·kg-1) in six patients with peripheral vascular disease. Adenosine was intravenously infused, at a rate of 90 ± 20 (SEM) μg·kg-1·min-1, to reduce mean arterial blood pressure by approximately 20% (23 ± 2% SEM, from 82 ± 3 to 63 ± 3 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 consumption. 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.
AB - The effects of adenosine on central and myocardial hemodynamics and metabolism were evaluated during fentanyl anesthesia (100 μg·kg-1) in six patients with peripheral vascular disease. Adenosine was intravenously infused, at a rate of 90 ± 20 (SEM) μg·kg-1·min-1, to reduce mean arterial blood pressure by approximately 20% (23 ± 2% SEM, from 82 ± 3 to 63 ± 3 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 consumption. 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.
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U2 - 10.1097/00000542-198803000-00016
DO - 10.1097/00000542-198803000-00016
M3 - Article
C2 - 3344997
AN - SCOPUS:0023928394
SN - 0003-3022
VL - 68
SP - 416
EP - 421
JO - Anesthesiology
JF - Anesthesiology
IS - 3
ER -