Relationship between brain tissue oxygen (PbrO2) and cerebral perfusion pressure (CPP)
© Current Science Ltd 1997
Published: 1 March 1997
Ischemia is the leading cause of secondary brain damage after severe head injury (SHI). Adequacy of cerebral oxygenation can be assessed by monitoring: cerebral perfusion pressure (CPP), the driving pressure of cerebral perfusion; oxygen saturation of jugular bulb (SjO2), the ratio between global cerebral oxygen availability and consumption: partial pressure of brain tissue oxygen (PbrO2), the driving pressure of oxygen diffusion to mitochondria at tissue level [1,2].
Our preliminary evaluation of PbrO2 in 10 patients with SHI (GCS = 8), in which PbrO2 was recorded for more than 7 days along with CPP, is reported. Intracranial pressure (ICP) was measured with an intraparenchymal fiberoptic transducer (Camino Laboratories), PbrO2 was measured with a Cark-Type catheter (Catheter PO2 Micro-Probe, CMP, Licox GMS, Kiel, Germany); CPP was obtained as difference between mean ABP and mean ICP.
All patients, when ICP increased over 20 mmHg, were treated according to a standard protocol: better sedation; moderate hyperventilation; mannitol infusion; barbiturates. Two patients had severe and repeated increases in ICP and eventually underwent surgery for evacuation of hemorrhagic contusion.
Data were collected every minute and analysed recoding CPP values in classes of 5 mmHg between 40 and 90 mmHg and one class for values over 90 mmHg. Using two way analysis of variance with CPP classes and patients as factors, a significant dependency of mean PbrO2 from CPP can be demonstrated.
Although PbrO2, is directly influenced by PaO2, using appropriate statistical methods and a large number of data, significant low PbrO2 values can be associated to a low cerebral perfusion pressure.
Confidence for the
Confidence for the
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