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Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study
Author(s) -
ALEXANDER B. S.,
GELB A. W.,
MANTULIN W. W.,
CERUSSI A. E.,
TROMBERG B. J.,
YU Z.,
LEE C.,
MENG L.
Publication year - 2013
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.12054
Subject(s) - hyperventilation , remifentanil , medicine , anesthesia , sevoflurane , propofol , hypocapnia , capnography , hemodynamics , ventilation (architecture) , hypercapnia , acidosis , mechanical engineering , engineering
Background While the decrease in blood carbon dioxide ( CO 2 ) secondary to hyperventilation is generally accepted to play a major role in the decrease of cerebral tissue oxygen saturation ( SctO 2 ), it remains unclear if the associated systemic hemodynamic changes are also accountable. Methods Twenty‐six patients ( A merican S ociety of A nesthesiologists 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 CO 2 ( ETCO 2 ) from 55 to 25 mm H g. Minute ventilation, SctO 2 , ETCO 2 , mean arterial pressure ( MAP ), and cardiac output ( CO ) were recorded. Results Hyperventilation led to a SctO 2 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 SctO 2 were not statistically different between these two groups ( P = 0.5). SctO 2 correlated significantly with ETCO 2 in both groups ( P < 0.001). SctO 2 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. Conclusion The main mechanism responsible for the hyperventilation‐induced decrease in SctO 2 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 SctO 2 but to a much smaller degree.