CO2 reactivity and brain oxygen pressure monitoring in severe head injury

Citation
Jac. Suazo et al., CO2 reactivity and brain oxygen pressure monitoring in severe head injury, CRIT CARE M, 28(9), 2000, pp. 3268-3274
Citations number
37
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
28
Issue
9
Year of publication
2000
Pages
3268 - 3274
Database
ISI
SICI code
0090-3493(200009)28:9<3268:CRABOP>2.0.ZU;2-X
Abstract
Objective: To investigate the effect of hyperventilation on cerebral oxygen ation after severe head injury. Design:A prospective, observational study. Setting: Neurointensive care unit at a university hospital. Patients: A total of 90 patients with severe head injury (Glasgow Coma Scal e score less than or equal to 8), in whom continuous monitoring of brain ti ssue oxygen pressure (Pbro(2)) was performed as a measure of cerebral oxyge nation. Interventions: Arterial P-CO2 was decreased each day over a 5-day period fo r 15 mins by increasing minute volume on the ventilator setting to 20% abov e baseline. Arterial blood gas analysis was performed before and after chan ging ventilator settings. Multimodality monitoring, including Pbro(2), was performed in all patients. Absolute and relative Pbro(2)/Paco(2), reactivit y was calculated. Outcome at 6 months was evaluated according to the Glasgo w Outcome Scale. Measurements and Main Results: Effective hyperventilation, defined by a dec rease of Pace, greater than or equal to 2 torr (0.27 kPa), was obtained in 218 (84%) of 272 tests performed. Baseline Paco(2) averaged 32.3 +/- 4.5 to rr (4.31 +/- 0.60 kPa), Average reduction in Paco(2) was 3.8 +/- 1,7 torr ( 0.51 +/- 0.23 kPa) Pbro(2) 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) , Pbro(2)/Paco(2) 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, Pbro(2)/Paco(2) 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 o n day 5, Conclusions: Increased hyperventilation causes a significant reduction in P bro(2), providing further evidence for possible increased risk of secondary ischemic damage during hyperventilation, The low Pbro(2)/Paco(2) reactivit y on day 1 indicates the decreased responsiveness of cerebral microvascular vessels to Pace, changes, caused by generalized vascular narrowing, The in creasing Pbro(2)/Paco(2) reactivity from days 2 to 5 suggests that the risk of compromising cerebral oxygenation by hyperventilation may increase over time.