Objectives: Prophylactic hyperventilation of patients with head injuries worsens outcome, presumably by exacerbating tissue hypoxia. Oxygen tension in brain tissue (P(br)O2) 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 P(br)O2 during hemorrhagic shock are not known. The aim of this study was to examine the effects of alteration in ventilation on P(br)O2 in hemorrhaged swine. Methods: Clark-type polarographic probes were inserted into the brain tissue of seven swine to measure P(br)O2 directly. To examine the effects of alterations in ventilation on hemorrhage-induced hypotension, swine were hemorrhaged to 50% estimated blood volume and P(br)O2 was monitored during hyperventilation (RR = 30) and hypoventilation (RR = 4). Results: After the 50% hemorrhage, P(br)O2 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 P(br)O2. Hypoventilation produced a 166% mean increase in P(br)O2. These changes were significant (p = 0.001) for absolute and percentage differences from baseline. Conclusion: During hemorrhage, alterations in ventilation significantly changed P(br)O2: 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.
|Number of pages||9|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Jun 2000|
- Cerebral oxygenation
- Cerebral resuscitation