Authors: REINSFELT, B.; WESTERLIND, A.; RICKSTEN, S.-E.

Source: Acta Anaesthesiologica Scandinavica, Volume 55, Number 1, January 2011 , pp. 118-123(6)

Publisher: Wiley-Blackwell

Abstract:

Background:

Previous studies on non-cardiac surgical patients have shown that cerebral pressure-flow autoregulation and cerebral flow-metabolism coupling are maintained with sevoflurane. The effects of sevoflurane on cerebral blood flow (CBF) autoregulation and flow-metabolism coupling during cardiopulmonary bypass (CPB) have not been studied previously. Methods:

The effects of sevoflurane-induced burst suppression, monitored with electroencephalography (EEG), on cerebral blood flow velocity (CBFV), cerebral oxygen extraction (COE) and flow autoregulation, were studied in 16 patients undergoing cardiac surgery. The experimental procedure was performed during non-pulsatile CPB with mild hypothermia (34 °C) in fentanyl/droperidol-anesthetized patients. Middle cerebral artery transcranial Doppler flow velocity, right jugular vein bulb oxygen saturation and jugular venous pressure were measured continuously. Autoregulation was tested during changes in the mean arterial pressure (40-90 mmHg), induced by sodium nitroprusside and norepinephrine before (control), and during additional sevoflurane administration, in a dose that resulted in an EEG burst-suppression level of 4-6/min. Results:

Sevoflurane, at an inspired concentration of 3.36±0.03%, induced a 17% decrease in CBFV (P<0.05) and a 22% decrease in COE (P<0.05) compared with the control. The slope of the positive relationship between CBFV and cerebral perfusion pressure was steeper with sevoflurane (P<0.01) compared with control measurements, as was the slope of the negative relationship between CPP and COE (P<0.01). Conclusion:

Burst-suppression doses of sevoflurane exert an intrinsic cerebral vasodilatory effect, which impairs CBF autoregulation during mildly hypothermic CPB. Furthermore, during sevoflurane administration, CBF is in excess relative to oxygen demand, indicating a partial loss of the cerebral flow-metabolism coupling.

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1399-6576.2010.02324.x

Affiliations: 1: Department of Cardiothoracic Anaesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden

Publication date: 2011-01-01

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