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The Pathophysiology of Cerebral Anoxia
Author(s) -
Ingvar David H.
Publication year - 1968
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1968.tb00725.x
Subject(s) - medicine , hyperaemia , cerebral blood flow , cerebral perfusion pressure , cerebral autoregulation , vasomotor , ischemia , autoregulation , intracranial pressure , pathophysiology , cerebral circulation , anesthesia , cardiology , blood pressure , blood flow
SUMMARY Measurements of regional cerebral blood flow have demonstrated that cerebral anoxia destroys the normal “metabolic” regulation of the flow as well as the normal autoregulation of the cerebrovascular resistance. This leads to cerebral “vasomotor paralysis” or “luxury perfusion” (Lassen (1966) 22 ), during which the rate of flow is increased above the post‐anoxi‐cally lowered metabolic demands. Cerebral anoxia may also, apart from causing cerebral hyperaemia, lead to an increased fluid filtration in the capillaries and possibly also an increased cellular water uptake. Although these mechanisms are not fully understood, it seems likely that they contribute to the development of brain oedema in the postanoxic phase. In patients with focal occlusive (anoxic) lesions, several of the above events can be demonstrated directly by means of neuroradiological procedures and measurements of regional cerebral blood flow. Following general brain anoxia the cerebral vasomotor paralysis and ensuing oedema may set up a vicious circle which leads to an increase in the intracranial pressure, which may further augment the anoxia and—in severe cases—give rise to global brain ischaemia and extensive brain necrosis.