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


METHODS
Prospective interventional study.


METHODS
Neurosciences critical care unit of a university hospital.


METHODS
Eleven acutely head-injured patients requiring norepinephrine to maintain cerebral perfusion pressure.


METHODS
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.


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.
Johnston
Andrew J
AJ
University Department of Anaesthetics, Addenbrooke's Hospital, Cambridge, UK.
Steiner
Luzius A
LA
Coles
Jonathan P
JP
Chatfield
Doris A
DA
Fryer
Tim D
TD
Smielewski
Peter
P
Hutchinson
Peter J
PJ
O'Connell
Mark T
MT
Al-Rawi
Pippa G
PG
Aigbirihio
Franklin I
FI
Clark
John C
JC
Pickard
John D
JD
Gupta
Arun K
AK
Menon
David K
DK
D000293:Adolescent; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects*; D001921:Brain / Q000098:blood supply*; D001930:Brain Injuries / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D003422:Critical Care / Q000379:methods*; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D009638:Norepinephrine / Q000008:administration & dosage*; D010101:Oxygen Consumption / Q000187:drug effects*; D010104:Oxygen Radioisotopes; D049268:Positron-Emission Tomography; D012039:Regional Blood Flow / Q000187:drug effects; D016896:Treatment Outcome
D010104:Oxygen Radioisotopes; D009638:Norepinephrine