Effects of cerebrovascular pressure reactivity-guided optimization of cerebral perfusion pressure on brain tissue oxygenation after traumatic brain injury.
OBJECTIVE
To evaluate the concept of a cerebrovascular pressure reactivity-guided optimal cerebral perfusion pressure after traumatic brain injury by analyzing the relationship between optimal cerebral perfusion pressure and brain tissue oxygen.


METHODS
Prospective observational cohort study.


METHODS
Neurosurgical intensive care unit of a university hospital.


METHODS
Thirty-eight patients after head injury.


METHODS
Continuous computerized monitoring of mean arterial pressure, intracranial pressure, and brain tissue oxygen for 5.3 +/- 2.6 days. The index of cerebrovascular pressure reactivity was calculated as a moving correlation coefficient between spontaneous low-frequency fluctuations of mean arterial pressure and intracranial pressure. Optimal cerebral perfusion pressure was defined as the cerebral perfusion pressure level with the lowest average index of cerebrovascular pressure reactivity.


RESULTS
Optimal cerebral perfusion pressure could be identified in 32 of 38 patients. Median optimal cerebral perfusion pressure was between 70 and 75 mm Hg (range, 60-100 mm Hg). Below the level of optimal cerebral perfusion pressure, brain tissue oxygen decreased in parallel to cerebral perfusion pressure, whereas brain tissue oxygen reached a plateau above optimal cerebral perfusion pressure. Optimal cerebral perfusion pressure correlated significantly with the cerebral perfusion pressure level, where brain tissue oxygen reached its plateau (r = .79; p < .01). Average brain tissue oxygen at optimal cerebral perfusion pressure was 24.5 +/- 6.0 mm Hg.


CONCLUSIONS
This study supports the concept of cerebrovascular pressure reactivity-based individual optimal cerebral perfusion pressure. Driving cerebral perfusion pressure in excess of optimal cerebral perfusion pressure does not yield improvements in brain tissue oxygen after head injury and should be avoided, whereas cerebral perfusion pressure below optimal cerebral perfusion pressure may result in secondary cerebral ischemia.
Jaeger
Matthias
M
Department of Neurosurgery, University of Leipzig, Leipzig, Germany. Matthias.Jaeger@sswahs.nsw.gov.au
Dengl
Markus
M
Meixensberger
Jürgen
J
Schuhmann
Martin U
MU
D000328:Adult; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply / Q000378:metabolism* / Q000503:physiopathology; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology* / Q000628:therapy; D002560:Cerebrovascular Circulation; D005260:Female; D006785:Hospitals, University; D006801:Humans; D007362:Intensive Care Units; D007427:Intracranial Pressure; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism; D011446:Prospective Studies
D010100:Oxygen