Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study
Version of Record online: 2 JAN 2013
© 2013 The Acta Anaesthesiologica Scandinavica Foundation
Acta Anaesthesiologica Scandinavica
Volume 57, Issue 5, pages 604–612, May 2013
How to Cite
ALEXANDER, B. S., GELB, A. W., MANTULIN, W. W., CERUSSI, A. E., TROMBERG, B. J., YU, Z., LEE, C. and MENG, L. (2013), Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study. Acta Anaesthesiologica Scandinavica, 57: 604–612. doi: 10.1111/aas.12054
- Issue online: 10 APR 2013
- Version of Record online: 2 JAN 2013
- Manuscript Accepted: 3 DEC 2012
- National Center for Research Resources (NCRR)
- Institute for Clinical and Translational Science (ICTS). Grant Number: UL1 RR031985
- Laser Microbeam and Medical Program. Grant Number: P41-RR01192
- US Army SBIR Program. Grant Number: W81XWH-09-C-0006
- Laboratory for Fluorescence Dynamics (LFD). Grant Number: P41 RR03155
- Department of Anesthesiology and Perioperative Care
While the decrease in blood carbon dioxide (CO2) secondary to hyperventilation is generally accepted to play a major role in the decrease of cerebral tissue oxygen saturation (SctO2), it remains unclear if the associated systemic hemodynamic changes are also accountable.
Twenty-six patients (American Society of Anesthesiologists I–II) undergoing nonneurosurgical procedures were anesthetized with either propofol-remifentanil (n = 13) or sevoflurane (n = 13). During a stable intraoperative period, ventilation was adjusted stepwise from hypoventilation to hyperventilation to achieve a progressive change in end-tidal CO2 (ETCO2) from 55 to 25 mmHg. Minute ventilation, SctO2, ETCO2, mean arterial pressure (MAP), and cardiac output (CO) were recorded.
Hyperventilation led to a SctO2 decrease from 78 ± 4% to 69 ± 5% (Δ = −9 ± 4%, P < 0.001) in the propofol-remifentanil group and from 81 ± 5% to 71 ± 7% (Δ = −10 ± 3%, P < 0.001) in the sevoflurane group. The decreases in SctO2 were not statistically different between these two groups (P = 0.5). SctO2 correlated significantly with ETCO2 in both groups (P < 0.001). SctO2 also correlated significantly with MAP (P < 0.001) and CO (P < 0.001) during propofol-remifentanil, but not sevoflurane (P = 0.4 and 0.5), anesthesia.
The main mechanism responsible for the hyperventilation-induced decrease in SctO2 is hypocapnia during both propofol-remifentanil and sevoflurane anesthesia. Hyperventilation-associated increase in MAP and decrease in CO during propofol-remifentanil, but not sevoflurane, anesthesia may also contribute to the decrease in SctO2 but to a much smaller degree.