Cerebral oxygenation during hemorrhagic shock: Perils of hyperventilation and the therapeutic potential of hypoventilation

Objectives: Prophylactic hyperventilation of patients with head injuries wo rsens outcome, presumably by exacerbating tissue hypoxia, Oxygen tension in brain tissue (PbrO2) provides a direct measurement of cerebral metabolic s ubstrate delivery and varies with changing end-tidal carbon dioxide tension (ETCO2) and mean arterial pressure. However, the effects of hyperventilati on 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 tissu e of seven swine to measure PbrO2 directly. To examine the effects of alter ations in ventilation on hemorrhage-induced hypotension, swine were hemorrh aged to 50% estimated blood volume and PbrO2 was monitored during hypervent ilation (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% me an decrease in PbrO2, Hypoventilation produced a 166% mean increase in PbrO 2. These changes were significant (p = 0.001) for absolute and percentage d ifferences from baseline. Conclusion: During hemorrhage, alterations in ventilation significantly cha nged PbrO2: hyperventilation increased brain-tissue hypoxia whereas hypoven tilation alleviated it. This finding suggests that hyperventilation has del eterious effects on brain oxygenation in patients with hemorrhagic shock an d those with head trauma. Conversely, hypoventilation with resultant hyperc apnia may actually help resolve hemorrhagic shock-induced cerebral hypoxia.