Introduction As brain tissue pO2 (PbtO2) monitoring is becoming more wide-spread, it has been observed that PbtO2 values are influenced by changes in arterial pO2 (PaO2) to a greater extent that can be explained by changes in oxygen delivery, especially in the damaged brain. It has been proposed that this may reflect an impaired ability of the cerebral vessels to vasoconstrict in response to an increasing PaO2. The purpose of this study was to compare the changes in PbtO2 to changes in cerebral blood flow velocity during a step change in PaO2. Methods Twenty-eight patients in coma from severe head injury were studied serially during the first 10 days after injury. In addition to the usual physiological monitors, a Licox PbtO2 monitor was placed in the brain, usually in white matter underlying an evacuated hematoma, or in tissue surrounding a contusion. Flow velocity in the middle cerebral artery (mcaFV), PaO2, jugular venous pO2 (PjvO2), and PbtO2 were measured at the patient's baseline FiO2 (usually 0.4), then at an FiO2 of 1.0, then again after returning the FiO2 to the patient's baseline. Results PaO2 increased from 146±3 to 330 ±8 mmHg, PbtO2 increased from 32 ±3 to 57 ±4 mmHg, and PjvO2 increased from 45±1 to 67±6 mmHg as the FiO2 was increased to 1.0. In response to these changes in oxygenation, mcaFV fell from 75 ±2 to 73 ±2 cm/sec on the injured side and from 79 ±2 to 75 ±2 cm/sec on the uninjured side (both p<.001). ICP also significantly decreased from 19±1 to 17±1 mmHg (p<.001). There was no relationship between the change in mcaFV and the change in PbtO2. Conclusions Hyperoxia causes a small, but detectable reduction in mcaFV, even on the most severely injured side of the brain. This vascular response to hyperoxia does not seem to explain the variability in the response of PbtO2 to hyperoxia that occurs after injury, and perhaps other factors such as diffusion characteristics of the injured brain tissue are responsible.
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine