Effect of cerebral perfusion pressure augmentation on regional oxygenation and metabolism after head injury.

Détails

ID Serval
serval:BIB_43021D850CF5
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Effect of cerebral perfusion pressure augmentation on regional oxygenation and metabolism after head injury.
Périodique
Critical Care Medicine
Auteur(s)
Johnston A.J., Steiner L.A., Coles J.P., Chatfield D.A., Fryer T.D., Smielewski P., Hutchinson P.J., O'Connell M.T., Al-Rawi P.G., Aigbirihio F.I., Clark J.C., Pickard J.D., Gupta A.K., Menon D.K.
ISSN
0090-3493
Statut éditorial
Publié
Date de publication
2005
Peer-reviewed
Oui
Volume
33
Numéro
1
Pages
189-195; discussion 255-257
Langue
anglais
Résumé
OBJECTIVE: In this study we have used O positron emission tomography, brain tissue oxygen monitoring, and cerebral microdialysis to assess the effects of cerebral perfusion pressure augmentation on regional physiology and metabolism in the setting of traumatic brain injury. DESIGN: Prospective interventional study. SETTING: Neurosciences critical care unit of a university hospital. PATIENTS: Eleven acutely head-injured patients requiring norepinephrine to maintain cerebral perfusion pressure. INTERVENTIONS: Using positron emission tomography, we have quantified the response to an increase in cerebral perfusion pressure in a region of interest around a brain tissue oxygen sensor (Neurotrend) and microdialysis catheter. Oxygen extraction fraction and cerebral blood flow were measured with positron emission tomography at a cerebral perfusion pressure of approximately 70 mm Hg and approximately 90 mm Hg using norepinephrine to control cerebral perfusion pressure. All other aspects of physiology were kept stable. MEASUREMENTS AND MAIN RESULTS: Cerebral perfusion pressure augmentation resulted in a significant increase in brain tissue oxygen (17 +/- 8 vs. 22 +/- 8 mm Hg; 2.2 +/- 1.0 vs. 2.9 +/- 1.0 kPa, p < .001) and cerebral blood flow (27.5 +/- 5.1 vs. 29.7 +/- 6.0 mL/100 mL/min, p < .05) and a significant decrease in oxygen extraction fraction (33.4 +/- 5.9 vs. 30.3 +/- 4.6 %, p < .05). There were no significant changes in any of the microdialysis variables (glucose, lactate, pyruvate, lactate/pyruvate ratio, glycerol). There was a significant linear relationship between brain tissue oxygen and oxygen extraction fraction (r = .21, p < .05); the brain tissue oxygen value associated with an oxygen extraction fraction of 40% (the mean value for oxygen extraction fraction in normal controls) was 14 mm Hg (1.8 kPa). The cerebral perfusion pressure intervention resulted in a greater percentage increase in brain tissue oxygen than the percentage decrease in oxygen extraction fraction; this suggests that the oxygen gradients between the vascular and tissue compartments were reduced by the cerebral perfusion pressure intervention. CONCLUSIONS: Cerebral perfusion pressure augmentation significantly increased levels of brain tissue oxygen and significantly reduced regional oxygen extraction fraction. However, these changes did not translate into predictable changes in regional chemistry. Our results suggest that the ischemic level of brain tissue oxygen may lie at a level below 14 mm Hg (1.8 kPa); however, the data do not allow us to be more specific.
Mots-clé
Adolescent, Adult, Blood Pressure/drug effects, Brain/blood supply, Brain Injuries/drug therapy, Brain Injuries/physiopathology, Critical Care/methods, Energy Metabolism/drug effects, Female, Humans, Infusions, Intravenous, Male, Microdialysis, Middle Aged, Norepinephrine/administration & dosage, Oxygen Consumption/drug effects, Oxygen Radioisotopes/diagnostic use, Positron-Emission Tomography, Regional Blood Flow/drug effects, Treatment Outcome
Pubmed
Web of science
Création de la notice
16/12/2009 15:59
Dernière modification de la notice
03/03/2018 16:39
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