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Relationship between brain tissue oxygen (PbrO2) and cerebral perfusion pressure (CPP)
Critical Care volume 1, Article number: P008 (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.
Individual PbrO2 values depends from single patient and from PaO2. It is difficult to define precisely a PbrO2 value that can be used as a target for treatment. With PaO2 between 80 and 150 mmHg. PbrO2 values between 25 and 40 are expected, but whatever value decreasing in spite of a constant PaO2 can be regarded is an alarming sign of impinging on cerebral oxygenation
Dings J, Meixensberger J, Amschler J, Hamelbeck B, Roosen K: Brain tissue pO2 in relation to cerebral perfusion pressure, TCD findings and TCD-CO2-reactivity after severe head injury. Acta Neurochir (Wien). 1996, 138: 425-434. 10.1007/BF01420305.
van Santbrink H, Maas AIR, Avezaat CJJ: Continuous monitoring of partial pressure of brain tissue oxygen in patients with severe head injury. Neurosurgery. 1996, 381: 21-31. 10.1097/00006123-199601000-00007.
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Bruzzone, P., Bellinzona, G., Imberti, R. et al. Relationship between brain tissue oxygen (PbrO2) and cerebral perfusion pressure (CPP). Crit Care 1, P008 (1997). https://doi.org/10.1186/cc14
- Oxygen Diffusion
- Cerebral Perfusion Pressure
- Oxygen Availability