Intracranial pressure and cerebral blood flow

Cerebral ischaemia (and ultimately infarction) occurs when cerebral blood flow cannot meet the metabolic demands of brain tissue. Following trauma, hypotension, hypoxia and raised intracranial pressure result in diminished oxygenation to cerebral tissue, compounding the deleterious effects of the primary injury to the brain. These secondary insults to the brain result in a worse outcome at long-term follow-up. Understanding the relationships between intracranial pressure, mean arterial blood pressure and cerebral blood flow are fundamental to the effective management of cerebral trauma and other intracranial disease. Various monitoring techniques are used in the neurointensive care setting to monitor brain function. Transcranial Doppler, PET, jugular venous oxygen, brain tissue oxygenation and cerebral microdialysis help assess the adequacy of cerebral perfusion and/or brain metabolism. These techniques have improved the understanding of cerebral blood flow and brain metabolism, but significant limitations in the acquisition and interpretation of measurements have led to the limited use of several of these techniques. Monitoring of intracranial pressure is the mainstay parameter to assess brain physiology in cerebral trauma. Raised intracranial pressure causes a reduction in cerebral perfusion pressure and leads to the shift of intracranial structures within the cranial cavity. The therapeutic approaches to the management of elevated intracranial pressure and the effects upon cerebral blood flow are reviewed.