Cerebral Circulatory Response to Acute Brain Disease

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Abstract
Acute brain injury produces not only abolition of neuronal function but also tissue acidosis, edema, and a state of vasomotor paralysis. This altered vasomotion first affects autoregulation to blood pressure changes and later all cerebral vasomotor control, resulting in paradoxical flow changes with alteration of PCO2. In the initial state, these changes are reversible, and often there is absolute hyperemia. More profound, irreversible brain damage is characterized by very low perfusion. Nevertheless, provided no mechanical obstruction to blood flow exists, as from edema, blood flow in both situations is in excess of metabolic need. This stereotyped derangement is seen with brain tumors, acute cerebro-vascular accidents, hypoxia, and severe trauma to the head, and following neurosurgical intervention. The clinical management of all these conditions must, therefore, follow a similar pattern, which consists of the maintenance of normal levels of perfusion pressure, the avoidance of cerebrovasodilatation from hypercapnia and general anesthetics, and the induction of respiratory alkalosis to offset cerebral acidosis.

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