Ventilation and oxygenation

ICP is significantly influenced by the adequacy of ventilation and the level of carbon dioxide within the blood stream (PaCO₂). Cerebral blood vessel dilatation caused by a rise in PaCO₂ may result in an ICP increase and therefore contribute to cerebral oedema, likely resulting in a poor outcome^2,4. Conversely, when PaCO₂ drops cerebral blood vessels constrict, decreasing cerebral blood volume and ultimately resulting in a fall in ICP^2,4.

Although once widely used as a method of ICP control, hyperventilation has been shown to exacerbate cerebral hypoperfusion and may result in ischaemia^4,5. A PaCO₂ of 4.5-5.0kPa, or close control normocapnia is therefore now recommended by UK guidelines⁶.

Despite widespread agreement on the principles of early management there is less clarity on resuscitation endpoints regarding oxygenation. The Brain Trauma Foundation (BTF) suggests targeting an oxygen level within the blood stream (PaO₂) >8kPa⁷ to avoid hypoxia, but the European Brain injury Consortium advocates targeting PaO₂ >10kPa⁸ and the Association of Anaesthetists of Great Britain and Northern Ireland recommend >13kPa⁶. This is predominantly due to, other than the avoidance of hypoxia⁹, there being little high-quality evidence to support one precise limit over another.