title: Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia.
abstract: BACKGROUND
  Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia.
  
  
  METHODS
  Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation.
  
  
  RESULTS
  The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg.
  
  
  CONCLUSIONS
  Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.
authors.affiliation: Departments of Anesthesiology and Neurological Surgery, University of Washington School of Medicine, Seattle, Washington 98104, USA.
authors.forename: T J
authors.initials: TJ
authors.lastname: McCulloch
authors.forename: E
authors.initials: E
authors.lastname: Visco
authors.forename: A M
authors.initials: AM
authors.lastname: Lam
mesh_terms: D000328:Adult; D000768:Anesthesia, General / Q000009:adverse effects*; D018685:Anesthetics, Inhalation / Q000009:adverse effects*; D018686:Anesthetics, Intravenous / Q000009:adverse effects*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D018592:Cross-Over Studies; D005260:Female; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006935:Hypercapnia / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008738:Methyl Ethers / Q000009:adverse effects*; D008875:Middle Aged; D010313:Partial Pressure; D015742:Propofol / Q000009:adverse effects*; D000077149:Sevoflurane
chemical_list: D018685:Anesthetics, Inhalation; D018686:Anesthetics, Intravenous; D008738:Methyl Ethers; D002245:Carbon Dioxide; D000077149:Sevoflurane; D015742:Propofol