Cerebral blood flow with intracranial hypertension

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Abstract
The effect of diffuse intracranial hypertension on cerebral blood flow is dependent on the rapidity of its development and the height of the intracranial pressure. When an intracranial balloon is expanded rapidly, cerebral blood flow declines immediately and ceases when the intracranial pressure exceeds the mean blood pressure, but, with a gradual increase in intracranial tension to 35 to 50 mm. Hg, reduction in blood flow may be minimal. If the rise in intracranial pressure initiates a vasopressor response, the resultant increase in arterial pressure will improve cerebral blood flow despite a persistent increase in the intracranial pressure. Also, this may occur despite a minimal difference between the rising intracranial and mean blood pressures. Cerebral vasodilation increases cerebral blood flow and probably accounts for the maintenance of blood flow in the presence of chronic intracranial hypertension. Hypercapnia and anoxia are well-known cerebral vasodilators, and an acute increase in pressure or sudden evacuation of an intracranial mass also may produce marked vasodilation. However, vasodilation, augmenting blood flow, also increases cerebral blood volume and as intracranial pressure rises continued vasodilation begins to impede blood flow, and cerebral ischemia ensues. Evidence has been presented that this causes further vasodilation due to vasomotor paralysis, and ul -timately cerebral blood flow virtually ceases when the intracranial pressure equals the systemic arterial pressure.

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