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The effect of sevoflurane-induced hypotension in combination with acute hypervolaemic haemodilution on middle cerebral artery flow velocity in surgical patients

Published online by Cambridge University Press:  01 August 2008

M. Fukusaki*
Affiliation:
Nagasaki Rosai Hospital, Department of Anesthesia, Sasebo, Nagasaki, Japan
M. Kanaide
Affiliation:
Nagasaki Rosai Hospital, Department of Anesthesia, Sasebo, Nagasaki, Japan
C. Inadomi
Affiliation:
Nagasaki Rosai Hospital, Department of Anesthesia, Sasebo, Nagasaki, Japan
M. Takada
Affiliation:
Nagasaki Rosai Hospital, Department of Anesthesia, Sasebo, Nagasaki, Japan
Y. Terao
Affiliation:
Nagasaki Rosai Hospital, Department of Anesthesia, Sasebo, Nagasaki, Japan
K. Sumikawa
Affiliation:
Nagasaki University School of Medicine, Department of Anesthesiology, Nagasaki, Japan
*
Correspondence to: Makoto Fukusaki, Department of Anesthesia, Nagasaki Rosai Hospital, 2-12-5 Setogoshi, Sasebo, Japan. E-mail: [email protected]; Tel: +81 956 49 2191; Fax: +81 956 49 2358
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Summary

Background and objective

This study was carried out to clarify the effect of the combination of acute hypervolaemic haemodilution and hypotensive anaesthesia induced with sevoflurane on human middle cerebral artery flow velocity using transcranial Doppler ultrasonography.

Methods

Thirty patients who were maintained with N2O–O2–sevoflurane anaesthesia undergoing hip surgery were randomly divided into two groups (no controlled hypotension group, Group A, and controlled hypotension group, Group B). Haemodilution was produced by acute preoperative infusion of 1000 mL of hydroxyethylstarch without removing blood in both groups. Mean arterial pressure was maintained at approximately 95 mmHg in Group A and at 55 mmHg for 80 min by increasing the inspired concentration of sevoflurane in Group B. Middle cerebral artery flow velocity was measured before haemodilution, after haemodilution, 80 min after starting hypotension, and 60 min after recovery from hypotension.

Results

Middle cerebral artery flow velocity significantly increased in both groups after haemodilution; by 28%, in Group A, P < 0.05 vs. before haemodilution and by 30% vs. before haemodilution in Group B, P < 0.05). During controlled hypotension, it decreased towards the pre-haemodilution value (P < 0.05 vs. after haemodilution).

Conclusions

Sevoflurane-induced hypotension to a mean arterial pressure of 55 mmHg would reduce middle cerebral artery flow that had been increased by acute hypervolaemic haemodilution, such as haematocrit value of 26%, whereas it could preserve the flow in pre-haemodilution condition during normocapnia.

Type
Original Article
Copyright
Copyright © European Society of Anaesthesiology 2008

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