Matthias Jaeger1, Erhard W Lang. 1. Department of Neurosurgery, Liverpool Hospital, University of New South Wales and University of Western Sydney, Locked Bag 7103, Liverpool BC, NSW, 1871, Australia. matthias.jaeger@sswahs.nsw.gov.au
Abstract
BACKGROUND: To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury. METHODS: Continuous monitoring of the partial pressure of brain tissue oxygen (PbrO2), mean arterial blood pressure (MAP), and intracranial pressure (ICP) in 11 patients. The cerebrovascular pressure reactivity index (PRx) was calculated as the moving correlation coefficient between MAP and ICP. For assessment of the cerebral oxygen regulation system a brain tissue oxygen response (TOR) was calculated, where the response of PbrO2 to an increase of the arterial oxygen through ventilation with 100 % oxygen for 15 min is tested. Arterial blood gas analysis was performed before and after changing ventilator settings. RESULTS: Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. PbrO2 increased from 28 ± 7 mmHg to 78 ± 29 mmHg, resulting in a mean TOR of 0.48 ± 0.24. Mean PRx was 0.05 ± 0.22. The correlation between PRx and TOR was r = 0.69, P = 0.019. The correlation of PRx and TOR with the Glasgow outcome scale at 6 months was r = 0.47, P = 0.142; and r = -0.33, P = 0.32, respectively. CONCLUSIONS: The results suggest a strong link between cerebrovascular pressure reactivity and the brain's ability to control for its extracellular oxygen content. Their simultaneous impairment indicates that their common actuating element for cerebral blood flow control, the cerebral resistance vessels, are equally impaired in their ability to regulate for MAP fluctuations and changes in brain oxygen.
BACKGROUND: To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury. METHODS: Continuous monitoring of the partial pressure of brain tissue oxygen (PbrO2), mean arterial blood pressure (MAP), and intracranial pressure (ICP) in 11 patients. The cerebrovascular pressure reactivity index (PRx) was calculated as the moving correlation coefficient between MAP and ICP. For assessment of the cerebral oxygen regulation system a brain tissue oxygen response (TOR) was calculated, where the response of PbrO2 to an increase of the arterial oxygen through ventilation with 100 % oxygen for 15 min is tested. Arterial blood gas analysis was performed before and after changing ventilator settings. RESULTS: Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. PbrO2 increased from 28 ± 7 mmHg to 78 ± 29 mmHg, resulting in a mean TOR of 0.48 ± 0.24. Mean PRx was 0.05 ± 0.22. The correlation between PRx and TOR was r = 0.69, P = 0.019. The correlation of PRx and TOR with the Glasgow outcome scale at 6 months was r = 0.47, P = 0.142; and r = -0.33, P = 0.32, respectively. CONCLUSIONS: The results suggest a strong link between cerebrovascular pressure reactivity and the brain's ability to control for its extracellular oxygen content. Their simultaneous impairment indicates that their common actuating element for cerebral blood flow control, the cerebral resistance vessels, are equally impaired in their ability to regulate for MAP fluctuations and changes in brain oxygen.
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