Relationship between brain tissue oxygen (PbrO₂) and cerebral perfusion pressure (CPP)

Introduction

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].

Methods

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.

Results

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.

Conclusions

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

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