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

Author(s):  
Sulpicio Soriano
2008 ◽  
Vol 108 (2) ◽  
pp. 225-232 ◽  
Author(s):  
John C. Drummond ◽  
Andrew V. Dao ◽  
David M. Roth ◽  
Ching-Rong Cheng ◽  
Benjamin I. Atwater ◽  
...  

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 (Sjvo2), CMR equivalent (CMRe), and CBFV/CMRe 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 (Paco2)-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.s.mm Hg presedation to 0.40 +/- 0.15 cm.s.mm Hg at 1.2 ng/ml. Sjvo2 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 Paco2-CBFV relation. CBFV and Bispectral Index increases during arousal for hyperventilation at 1.2 ng/ml suggest that CMR-CBF coupling is preserved during dexmedetomidine administration. Further evaluation of dexmedetomidine in patients with neurologic injuries seems justified.


2014 ◽  
Vol 117 (10) ◽  
pp. 1090-1096 ◽  
Author(s):  
Nicole S. Coverdale ◽  
Joseph S. Gati ◽  
Oksana Opalevych ◽  
Amanda Perrotta ◽  
J. Kevin Shoemaker

To establish the accuracy of transcranial Doppler ultrasound (TCD) measures of middle cerebral artery (MCA) cerebral blood flow velocity (CBFV) as a surrogate of cerebral blood flow (CBF) during hypercapnia (HC) and hypocapnia (HO), we examined whether the cross-sectional area (CSA) of the MCA changed during HC or HO and whether TCD-based estimates of CBFV were equivalent to estimates from phase contrast (PC) magnetic resonance imaging. MCA CSA was measured from 3T magnetic resonance images during baseline, HO (hyperventilation at 30 breaths/min), and HC (6% carbon dioxide). PC and TCD measures of CBFV were measured during these protocols on separate days. CSA and TCD CBFV were used to calculate CBF. During HC, CSA increased from 5.6 ± 0.8 to 6.5 ± 1.0 mm2 ( P < 0.001, n = 13), while end-tidal carbon dioxide partial pressure (PetCO2) increased from 37 ± 3 to 46 ± 5 Torr ( P < 0.001). During HO, CSA decreased from 5.8 ± 0.9 to 5.3 ± 0.9 mm2 ( P < 0.001, n = 15), while PetCO2 decreased from 36 ± 4 to 23 ± 3 Torr ( P < 0.001). CBFVs during baseline, HO, and HC were compared between PC and TCD, and the intraclass correlation coefficient was 0.83 ( P < 0.001). The relative increase from baseline was 18 ± 8% greater ( P < 0.001) for CBF than TCD CBFV during HC, and the relative decrease of CBF during HO was 7 ± 4% greater than the change in TCD CBFV ( P < 0.001). These findings challenge the assumption that the CSA of the MCA does not change over modest changes in PetCO2.


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