CO2 reactivity and brain oxygen pressure monitoring in severe head injury

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Abstract
To investigate the effect of hyperventilation on cerebral oxygenation after severe head injury. A prospective, observational study. Neurointensive care unit at a university hospital. A total of 90 patients with severe head injury (Glasgow Coma Scale score ≤8), in whom continuous monitoring of brain tissue oxygen pressure (Pbro2) was performed as a measure of cerebral oxygenation. Arterial Pco2 was decreased each day over a 5-day period for 15 mins by increasing minute volume on the ventilator setting to 20% above baseline. Arterial blood gas analysis was performed before and after changing ventilator settings. Multimodality monitoring, including Pbro2, was performed in all patients. Absolute and relative Pbro2/Paco2 reactivity was calculated. Outcome at 6 months was evaluated according to the Glasgow Outcome Scale. Effective hyperventilation, defined by a decrease of Paco2 ≥2 torr (0.27 kPa), was obtained in 218 (84%) of 272 tests performed. Baseline Paco2 averaged 32.3 ± 4.5 torr (4.31 ± 0.60 kPa). Average reduction in Paco2 was 3.8 ± 1.7 torr (0.51 ± 0.23 kPa). Pbro2 decreased by 2.8 ± 3.7 torr (0.37 ± 0.49 kPa;p < .001) from a baseline value of 26.5 ± 11.6 torr (3.53 ± 1.55 kPa). Pbro2/Paco2 reactivity was low on day 1 (0.8 ± 2.3 torr [0.11 ± 0.31 kPa]), increasing on subsequent days to 6.1 ± 4.4 torr (0.81 ± 0.59 kPa) on day 5. Pbro2/Paco2 reactivity on days 1 and 2 was not related to outcome. In later phases in patients with unfavorable outcome, relative reactivity was increased more markedly, reaching statistical significance on day 5. Increased hyperventilation causes a significant reduction in Pbro2, providing further evidence for possible increased risk of secondary ischemic damage during hyperventilation. The low Pbro2/Paco2 reactivity on day 1 indicates the decreased responsiveness of cerebral microvascular vessels to Paco2 changes, caused by generalized vascular narrowing. The increasing Pbro2/Paco2 reactivity from days 2 to 5 suggests that the risk of compromising cerebral oxygenation by hyperventilation may increase over time.