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Department of Anesthesiology, Medical College of Wisconsin and Veterans Affairs Medical Center, Milwaukee
Address correspondence to Thomas J. Ebert, MD, PhD, VA Medical Center/112A, 5000 West National Ave., Milwaukee, WI 53295. Address e-mail to tjebert{at}mcw.edu
We explored the possible mechanisms of hypotension during the administration of sedation-analgesia doses of remifentanil in young (ASA physical status I) volunteers (n = 24). Cardiorespiratory and sympathetic variables were collected at baseline and at plasma concentrations of remifentanil (2 and 4 ng/mL). Monitoring included electrocardiogram, heart rate (HR), direct blood pressure, muscle sympathetic nerve activity, and forearm blood flow (FBF). A cold pressor test (1-min hand immersion in ice water) quantified analgesia effectiveness (visual analog scale, 0–100). Visual analog scale to the cold pressor test (62 at baseline) decreased to 27 and 18 during remifentanil infusions. Respiratory rate decreased and end-tidal carbon dioxide (ETCO2) increased with increasing doses of remifentanil; HR, direct blood pressure, muscle sympathetic nerve activity, SpO2 remained unchanged, but FBF increased compared with placebo. In a second study (n = 7), timed respiration was used to maintain ETCO2 during remifentanil, but FBF still increased. In a third study (n = 11), direct effects of remifentanil on vascular tone were determined with progressive infusions from 1 to 100 µg/h into the brachial artery; FBF increased significantly from 3.5 to 4.3 mL/min per 100 mL of tissue (
13%–18% increase). Sedative doses of remifentanil resulted in analgesia but no changes in neurocirculatory end-points except FBF. Direct effects of remifentanil on regional vascular tone may play a role in promoting hypotension.
IMPLICATIONS: Remifentanil occasionally has been associated with hypotension, the mechanism of which is unclear. This study found that remifentanil directly causes the forearm arterial vasculature to dilate.
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