Cerebral hemodynamic effects of acute hyperoxia and hyperventilation after severe traumatic brain injury

Abstract

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.

FIG. 1.

Protocol for the experiment. Dynamic pressure autoregulation was tested by the cuff deflation method in triplicate (tests are indicated by the arrows), after equilibrating for 10–15 min in four test conditions: baseline, hyperventilation, baseline, and hyperoxia (MV, minute ventilation, Fio₂, fraction of inspired oxygen).

FIG. 2.

Graphs of changes in arterial Po₂ (Pao₂; the circles in the upper graph), brain tissue Po₂ (Pbto₂; the triangles in the upper graph), and brain tissue oxygen reactivity (Btor; lower graph), over the first 7 days post-injury (mean ± standard error). The values represent 900 sets of o₂r tests in 186 patients over the 7 days, and the number of data points for each time period are shown at the bottom of the graph. For the Po₂ values, the closed symbols are the baseline pre-hyperoxia values, and the open symbols are the values during hyperoxia (the p values are given in Table 3). The changes in Pao₂ and in Pbto₂ during the first exam were significantly smaller than all of the other exams. The average values for Btor during the first six exams (admission through day 3) were significantly greater than the average Btor during the last six exams (days 3.5–7; p = 0.043).

FIG. 3.

Graphs of baseline (pre-hyperventilation) autoregulatory index (ARI) and co₂ reactivity (co₂r) over time after injury (mean ± standard error). The p values for these changes in ARI and co₂r over time are given in Table 2.

FIG. 4.

Graphs of the baseline (closed circles) and hyperventilation (HV, open circles) autoregulatory index (ARI) over time after injury (mean ± standard error). The p values for these changes in ARI with hyperventilation over time are given in Table 2.

FIG. 5.

Graphs of the baseline (closed circles) and hyperoxia (HO, open circles) autoregulatory index (ARI) over time after injury (mean ± standard error). The p values for these changes in ARI with hyperoxia over time are given in Table 3.