Transient changes in brain tissue oxygen in response to modifications of cerebral perfusion pressure: an observational study
- PMID: 19933525
- DOI: 10.1213/ANE.0b013e3181c0722f
Transient changes in brain tissue oxygen in response to modifications of cerebral perfusion pressure: an observational study
Abstract
Background: The relative merits of the mechanisms for the maintenance of brain tissue oxygenation (PbtO(2)) have been much debated. There is a wealth of studies regarding various factors that may determine the absolute value and changes in PbtO(2). However, only a few of them analyzed fast (few minutes) and transient behavior of PbtO(2) in response to variations (waves) of intracranial pressure (ICP) and cerebral perfusion pressure (CPP).
Methods: This was a retrospective analysis and observational study. PbtO(2), arterial blood pressure (ABP), and ICP waveforms were digitally monitored in 23 head-injured patients, admitted to the Neuroscience Critical Care Unit, who were sedated, paralyzed, and ventilated. Computer recordings were retrospectively reviewed. The dynamic changes in PbtO(2) in response to transient changes in ABP and ICP were investigated.
Results: Several patterns of response to short-lasting arterial hypotension and hypertension, intracranial hypertension, cerebral vasocycling, and cerebral hyperemia were observed and characterized. During the majority of the transient events, PbtO(2) generally followed the direction of changes in CPP. Only during episodes of hyperemia, CPP and PbtO(2) changed in the opposite direction. Changes in PbtO(2) were delayed after dynamic changes in ABP, CPP, and ICP. The CPP-PbtO(2) delay during changes provoked by variations in ABP was 35.0 s (range: maximum 827.0 s; minimum 0.0 s) compared with changes induced by variations in ICP of 0.0 s (range: maximum 265.0 s; minimum 0.0 s); the difference was significant at P < 0.0001.
Conclusions: PbtO(2) is more than a number; it is rather a waveform following rapid changes in ICP and ABP. We show that PbtO(2) generally tracks the direction of CPP irrespective of the state of cerebral autoregulation.
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