The purpose of this study was to examine the effects of
hyperventilation or
hyperoxia on cerebral hemodynamic parameters over time in patients with severe
traumatic brain injury (TBI). We prospectively studied 186 patients with severe TBI. CO₂ and O₂ reactivity tests were conducted twice a day on days 1-5 and once daily on days 6-10 after injury. During
hyperventilation there was a significant decrease in intracranial pressure (ICP), mean arterial pressure (MAP), jugular venous oxygen saturation (Sjvo₂), brain tissue Po₂ (Pbto₂), and flow velocity (FV). During
hyperoxia there was an increase in Sjvo₂ and Pbto₂, and a small but consistent decrease in ICP, end-tidal
carbon dioxide (etco₂), partial arterial
carbon dioxide pressure (Paco₂), and FV. Brain tissue
oxygen reactivity during the first 12 h after injury averaged 19.7 ± 3.0%, and slowly decreased over the next 7 days. The autoregulatory index (ARI; normal = 5.3 ± 1.3) averaged 2.2 ± 1.5 on day 1 post-injury, and gradually improved over the 10 days of monitoring. The ARI significantly improved during
hyperoxia, by an average of 0.4 ± 1.8 on the left, and by 0.5 ± 1.8 on the right. However, the change in ARI with
hyperoxia was much smaller than that observed with
hyperventilation.
Hyperventilation increased ARI by an average of 1.3 ± 1.9 on the left, and 1.5 ± 2.0 on the right. Pressure autoregulation, as assessed by dynamic testing, was impaired in these head-injured patients. Acute
hyperoxia significantly improved pressure autoregulation, although the effect was smaller than that induced by
hyperventilation. The very small change in Paco₂ induced by
hyperoxia does not appear to explain this finding. Rather, the vasoconstriction induced by acute
hyperoxia may allow the cerebral vessels to respond better to transient
hypotension. Further studies are needed to define the clinical significance of these observations.