CO2 reactivity and brain oxygen pressure monitoring in severe head injury


    loading  Checking for direct PDF access through Ovid

Abstract

ObjectiveTo investigate the effect of hyperventilation on cerebral oxygenation after severe head injury.DesignA prospective, observational study.SettingNeurointensive care unit at a university hospital.PatientsA 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.InterventionsArterial 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.Measurements and Main Results: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.ConclusionsIncreased 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.

    loading  Loading Related Articles