Although cerebral blood flow is a more reliable indicator of cerebral perfusion, special techniques are required for its measurement and it does not correlate well with functional neurological recovery. Maintenance of cardiac output and blood pressure by optimizing preload and contractility may increase cerebral blood flow, and moderate hemodilution may optimize the rheological properties of blood supplying oxygen and substrate. Since functional neurological recovery may best correlate with the brain's ability to utilize oxygen (difference between arterial and mixed venous oxygen content), jugular venous bulb cannulation may aid in prognosis but not in therapy (Connors §L§i 1992).
Hyperglycemia has been shown to worsen neurological outcome in global cerebral ischemia and should be avoided. Hypothermia and the diving reflex have been hypothesized to be cerebroprotective at the time of immersion; however, therapeutic hypothermia confers no advantage.
The use of intravenous barbiturates in doses sufficient to produce an isoelectric EEG with the goal of decreasing cerebral metabolic rate and the critical level of oxygen extraction in the face of cerebral global ischemia, although an attractive hypothesis, has not been proven to be effective. Barbiturates may also decrease intracranial pressure. New strategies aimed at minimizing reperfusion injury following global cerebral ischemia include use of L and N calcium-channel blockers, deferoxamine (desferrioxamine), pyruvate dehydrogenase inducers such as dichloroacetate, and stimulators of aerobic metabolism distal to pyruvate dehydrogenase such as acetyl L-carnitine. However, although experimentally promising, they are clinically unproven.
In summary, strategies for the preservation of neurological function after global anoxia are aimed at the prevention of secondary neurological injury and are, in effect, empirical and supportive.
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