4.6 Article Proceedings Paper

Effect of dexmedetomidine on cerebral blood flow velocity, cerebral metabolic rate and carbon dioxide response in normal humans

Journal

ANESTHESIOLOGY
Volume 108, Issue 2, Pages 225-232

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.anes.0000299576.00302.4c

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Background: Dexmedetomidine reduces cerebral blood flow (CBF) in humans and animals. In animal investigations, cerebral metabolic rate (CMR) was unchanged. Therefore, the authors hypothesized that dexmedetomidine would cause a decrease in the CBF/CMR ratio with even further reduction by superimposed hyperventilation. This reduction might be deleterious in patients with neurologic injuries. Methods: Middle cerebral artery velocity (CBFV) was recorded continuously in six volunteers. CBFV, jugular bulb venous saturation (Sjvo(2)), CMR equivalent (CMRe), and CBFV/CMRc ratio were determined at six intervals before, during, and after administration of dexmedetomidine: (1) presedation; (2) presedation with hyperventilation; at steady state plasma levels of (3) 0.6 ng/ml and (4) 1.2 ng/ml; (5) 1.2 ng/ml with hyperventilation; and (6) 30 min after discontinuing dexmedetomidine. The slope of the arterial carbon dioxide tension (Paco(2))-CBFV relation was determined presedation and at 1.2 ng/ml. Results: CBFV and CMRe decreased in a dose-related manner. The CBFV/CMRe ratio was unchanged. The CBFV response to carbon dioxide decreased from 1.20 +/- 0.2 cm center dot s(-1)center dot mm Hg-1 presedation to 0.40 +/- 0.15 cm center dot s(-1)center dot mm Hg-1 at 1.2 ng/ml. Sjvo(2) was statistically unchanged during hyperventilation at 1.2 ng/ml versus presedation (50 +/- 11 vs. 43 +/- 5%). Arousal for hyperventilation at 1.2 ng/ml resulted in increased CBFV (30 5 to 38 4) and Bispectral index (43 +/- 10 to 94 +/- 3). Conclusions: The predicted decrease in CBFV/CMRe ratio was not observed because of an unanticipated reduction of CMRe and a decrease in the slope of the Paco(2)-CBFV relation. CBFV and Bispectral index increases during arousal for hyperventilation at 1.2 ng/ml suggest that CMR-CBr coupling is preserved during dexmedetomidine administration. Further evaluation of dexmedetomidine in patients with neurologic injuries seems justified.

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