title: Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Irvine School of Medicine, University of California, Irvine, CA, USA.
authors.forename: B S
authors.initials: BS
authors.lastname: Alexander
authors.forename: A W
authors.initials: AW
authors.lastname: Gelb
authors.forename: W W
authors.initials: WW
authors.lastname: Mantulin
authors.forename: A E
authors.initials: AE
authors.lastname: Cerussi
authors.forename: B J
authors.initials: BJ
authors.lastname: Tromberg
authors.forename: Z
authors.initials: Z
authors.lastname: Yu
authors.forename: C
authors.initials: C
authors.lastname: Lee
authors.forename: L
authors.initials: L
authors.lastname: Meng
mesh_terms: D000328:Adult; D018685:Anesthetics, Inhalation / Q000097:blood / Q000494:pharmacology*; D018686:Anesthetics, Intravenous / Q000097:blood / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D002560:Cerebrovascular Circulation; D005260:Female; D006801:Humans; D006985:Hyperventilation / Q000097:blood* / Q000503:physiopathology*; D008297:Male; D008738:Methyl Ethers / Q000097:blood / Q000494:pharmacology; D010100:Oxygen / Q000097:blood*; D010880:Piperidines / Q000097:blood / Q000494:pharmacology; D015742:Propofol / Q000097:blood / Q000494:pharmacology; D000077208:Remifentanil; D000077149:Sevoflurane
chemical_list: D018685:Anesthetics, Inhalation; D018686:Anesthetics, Intravenous; D008738:Methyl Ethers; D010880:Piperidines; D002245:Carbon Dioxide; D000077149:Sevoflurane; D000077208:Remifentanil; D010100:Oxygen; D015742:Propofol