ischemia in the damaged or edematous brain. Under normal circumstances CBF is tightly controlled by homeostatic mechanisms. Normal CBF is approximately 50 ml/100 g/min, coupled to a cerebral metabolic oxygen consumption rate of 3.2 ml/100 g/min. In patients with brain injury, CBF of 18-20 ml/100 g/min is generally considered to be the ischemic threshold, below which secondary injury may occur, although cellular integrity is usually preserved until CBF is <8-10 ml/100 g/min. Many factors control the cerebrovascular tone, including endothelial factors (nitric oxide, endothelin), cerebral metabolism, neurotransmitter release, systemic blood pressure, blood carbon dioxide content, blood viscosity and humoral substances. In physiological terms the important considerations include flow-metabolism coupling, CO2 reactivity, and pressure autoregulation. Under normal circumstances, blood flow to the brain is tightly coupled to its metabolism, globally as well as regionally. The cerebral vasculature is exquisitely sensitive to carbon dioxide, changing by 3-4% per mmHg change in PaCO2. In contrast, PaO2 has a negligible effect on CBF. Although the molecular mechanism of cerebral autoregulation remains unknown, CBF is generally maintained constant between CPP of 50-150 mmHg. Blood flow becomes pressure-dependent at blood pressures outside the normal range, and this flow-pressure curve is shifted to the right in the presence of chronic hypertension. The purported mechanisms of autoregulation control include metabolic feedback and myogenic feedback.

Intracranial pathology may impair one or more of these homeostatic mechanisms [1]. CO2 reactivity appears to be more robust than autoregulation, and is frequently preserved even with severe brain injury. With the exception of arteriovenous malformation and vasospasm (see below), the loss of CO2 reactivity is generally associated with a poor prognosis.

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