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Overview of Monitoring of Cerebral Blood Flow and Metabolism after Severe Head Injury

Published online by Cambridge University Press:  12 November 2018

J. Paul Muizelaar  and
Marc L. Schröder
J. Paul Muizelaar*
Affiliation:
Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia
Marc L. Schröder
Affiliation:
Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia
*
Reprint request to: J. Paul Muizelaar, M.D. Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Box 631, MCV Station, Richmond, VA U.S.A. 23298-0631.
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Abstract

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The relationships between cerebral blood flow (CBF), cerebral metabolism (cerebral metabolic rate of oxygen, CMRO2) and cerebral oxygen extraction (arteriovenous difference of oxygen, AVDO2) are discussed, using the formula CMRO2 = CBF × AVDO2. Metabolic autoregulation, pressure autoregulation and viscosity autoregulation can all be explained by the strong tendency of the brain to keep AVDO2 constant. Monitoring of CBF, CMRO2 or AVDO2 very early after injury is impractical, but the available data indicate that cerebral ischemia plays a considerable role at this stage. It can best be avoided by not "treating" arterial hypertension and not using too much hyperventilation, while generous use of mannitol is probably beneficial. Once in the ICU, treatment can most practically be guided by monitoring of jugular bulb venous oxygen saturation. If saturation drops below 50%, the reason for this must be found (high intracranial pressure, blood pressure not high enough, too vigorous hyperventilation, arterial hypoxia, anemia) and must be treated accordingly.

Résumé

Résumé

Nous discutons des relations entre le flot sanguin cérébral (FSC), le métabolisme cérébral (taux métabolique cérébral d'oxygène, TMCO2) et le taux d'extraction de l'oxygène (différence artérioveineuse en oxygène, DAVO2), et nous utilisons la formule TMCO2 = FSC × DAVO2. L'autorégulation métabolique peut être entièrement expliquée par la tendance marquée du cerveau à garder la DAVO2 constante. La surveillance du FSC, du TMCO2 ou de la DAVO2 très tôt après le traumatisme est impraticable. Cependant, les données disponibles indiquent que l'ischémie cérébrale joue un rôle considérable pendant cette période. La meilleure façon de l'éviter est de ne pas "traiter" l'hypertension artérielle et de ne pas trop utiliser l'hyperventilation, alors que l'utilisation généreuse du mannitol est probablement bénéfique. A l'unité de soins intensifs, le traitement peut être guidé de façon pratique par la surveillance de la saturation veineuse en oxygène au niveau du golfe de la jugulaire. Si la saturation s'abaisse au dessous de 50%, on doit en trouver la cause (pression intracranienne elevee, pression sanguine trop basse, hyperventilation trop vigoureuse, hypoxie artérielle, anémie) et on doit y remédier.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 21 , Issue S1: Neurocritical Care Symposium , February 1994 , pp. S6 - S11
Copyright
Copyright © The Canadian Journal of Neurological 1994

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