Cerebral ischemia

The brain requires a constant supply of oxygen and glucose, as well as other metabolic substrates, for maintenance of structural integrity and electrophysiological function. This supply must be uninterrupted because the brain has little ability to store nutrients. Therefore an adequate cerebral blood flow must be maintained at all times.

Global cerebral ischemia, such as that occurring after cardiac arrest, results from hypoperfusion of the entire brain. Focal ischemia, resulting in local hypoperfusion, occurs secondary to localized lesions or vessel occlusion distal to the circle of Willis. As collateral flow may develop in focal ischemia, the area of damage is graded with the development of an ischemic core surrounded by a penumbral zone.

As blood flow to cerebral tissue is reduced there is sequential loss of cellular function. First neuronal electrical function ceases, followed by failure of energy-dependent ion pumps within the cell membrane. This is followed by total cessation of neuronal function, which results in uncontrollable movement of ions across the cell membrane and subsequent cell death. Neurons in the ischemic penumbra may continue to receive enough blood to maintain oxygenation above the level required to maintain ion pump function but below that required for electrical, and therefore clinical, function. Metabolic failure is likely to occur in the ischemic penumbra if its precarious oxygen supply is not reversed within 3 to 4 h. However, total cessation of blood flow to the brain leads to an isoelectric electroencephalogram within 30 s and total depletion of high-energy phosphate stores within 2 min. Ischemic brain tissue releases biochemical substances, such as excitatory amino acids and free radicals, which worsen cerebral damage.

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