title: CO2 reactivity and brain oxygen pressure monitoring in severe head injury.
abstract: OBJECTIVE
  To investigate the effect of hyperventilation on cerebral oxygenation after severe head injury.
  
  
  METHODS
  A prospective, observational study.
  
  
  METHODS
  Neurointensive care unit at a university hospital.
  
  
  METHODS
  A total of 90 patients with severe head injury (Glasgow Coma Scale score < or =8), in whom continuous monitoring of brain tissue oxygen pressure (PbrO2) was performed as a measure of cerebral oxygenation.
  
  
  METHODS
  Arterial PCO2 was decreased each day over a 5-day period for 15 mins by increasing minute volume on the ventilator setting to 20% above baseline. Arterial blood gas analysis was performed before and after changing ventilator settings. Multimodality monitoring, including PbrO2, was performed in all patients. Absolute and relative PbrO2/PaCO2 reactivity was calculated. Outcome at 6 months was evaluated according to the Glasgow Outcome Scale.
  
  
  RESULTS
  Effective hyperventilation, defined by a decrease of PaCO2 > or =2 torr (0.27 kPa), was obtained in 218 (84%) of 272 tests performed. Baseline PaCO2 averaged 32.3 +/- 4.5 torr (4.31 +/- 0.60 kPa). Average reduction in PaCO2 was 3.8 +/- 1.7 torr (0.51 +/- 0.23 kPa). PbrO2 decreased by 2.8 +/- 3.7 torr (0.37 +/- 0.49 kPa; p < .001) from a baseline value of 26.5 +/- 11.6 torr (3.53 +/- 1.55 kPa). PbrO2/PaCO2 reactivity was low on day 1 (0.8 +/- 2.3 torr [0.11 +/- 0.31 kPa]), increasing on subsequent days to 6.1 +/- 4.4 torr (0.81 +/- 0.59 kPa) on day 5. PbrO2/PaCO2 reactivity on days 1 and 2 was not related to outcome. In later phases in patients with unfavorable outcome, relative reactivity was increased more markedly, reaching statistical significance on day 5.
  
  
  CONCLUSIONS
  Increased hyperventilation causes a significant reduction in PbrO2, providing further evidence for possible increased risk of secondary ischemic damage during hyperventilation. The low PbrO2/PaCO2 reactivity on day 1 indicates the decreased responsiveness of cerebral microvascular vessels to PaCO2 changes, caused by generalized vascular narrowing. The increasing PbrO2/PaCO2 reactivity from days 2 to 5 suggests that the risk of compromising cerebral oxygenation by hyperventilation may increase over time.
authors.affiliation: Hospital Juárez de México SSA, Hospital de Traumatología Magdalena de la Salinas IMSS, México.
authors.forename: J A
authors.initials: JA
authors.lastname: Carmona Suazo
authors.forename: A I
authors.initials: AI
authors.lastname: Maas
authors.forename: W A
authors.initials: WA
authors.lastname: van den Brink
authors.forename: H
authors.initials: H
authors.lastname: van Santbrink
authors.forename: E W
authors.initials: EW
authors.lastname: Steyerberg
authors.forename: C J
authors.initials: CJ
authors.lastname: Avezaat
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood*; D002648:Child; D005260:Female; D016489:Head Injuries, Closed / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption / Q000502:physiology*; D010102:Oxygen Inhalation Therapy / Q000379:methods*; D016896:Treatment Outcome
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen