title: Cerebral oxygenation during hemorrhagic shock: perils of hyperventilation and the therapeutic potential of hypoventilation.
abstract: OBJECTIVE
  Prophylactic hyperventilation of patients with head injuries worsens outcome, presumably by exacerbating tissue hypoxia. Oxygen tension in brain tissue (PbrO2) provides a direct measurement of cerebral metabolic substrate delivery and varies with changing end-tidal carbon dioxide tension (ETCO2) and mean arterial pressure. However, the effects of hyperventilation and hypoventilation on PbrO2 during hemorrhagic shock are not known. The aim of this study was to examine the effects of alteration in ventilation on PbrO2 in hemorrhaged swine.
  
  
  METHODS
  Clark-type polarographic probes were inserted into the brain tissue of seven swine to measure PbrO2 directly. To examine the effects of alterations in ventilation on hemorrhage-induced hypotension, swine were hemorrhaged to 50% estimated blood volume and PbrO2 was monitored during hyperventilation (RR = 30) and hypoventilation (RR = 4).
  
  
  RESULTS
  After the 50% hemorrhage, PbrO2 declined rapidly from 39.8 +/- 4.6 mm Hg to 11.4 +/- 2.2 mm Hg. Hyperventilation resulted in a further 56% mean decrease in PbrO2. Hypoventilation produced a 166% mean increase in PbrO2. These changes were significant (p = 0.001) for absolute and percentage differences from baseline.
  
  
  CONCLUSIONS
  During hemorrhage, alterations in ventilation significantly changed PbrO2: hyperventilation increased brain-tissue hypoxia whereas hypoventilation alleviated it. This finding suggests that hyperventilation has deleterious effects on brain oxygenation in patients with hemorrhagic shock and those with head trauma. Conversely, hypoventilation with resultant hypercapnia may actually help resolve hemorrhagic shock-induced cerebral hypoxia.
authors.affiliation: San Francisco Injury Center, Department of Neurological Surgery, School of Medicine, University of California San Francisco, USA.
authors.forename: G T
authors.initials: GT
authors.lastname: Manley
authors.forename: J C
authors.initials: JC
authors.lastname: Hemphill
authors.forename: D
authors.initials: D
authors.lastname: Morabito
authors.forename: N
authors.initials: N
authors.lastname: Derugin
authors.forename: V
authors.initials: V
authors.lastname: Erickson
authors.forename: L H
authors.initials: LH
authors.lastname: Pitts
authors.forename: M M
authors.initials: MM
authors.lastname: Knudson
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D006439:Hemodynamics; D006985:Hyperventilation / Q000150:complications / Q000378:metabolism*; D007040:Hypoventilation / Q000378:metabolism*; D002534:Hypoxia, Brain / Q000209:etiology; D007427:Intracranial Pressure; D008297:Male; D010102:Oxygen Inhalation Therapy / Q000009:adverse effects*; D011048:Polarography; D012151:Resuscitation / Q000009:adverse effects / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D013552:Swine