Carbon Dioxide Management in TBI: From Theory to Practice

Hyperventilation is a double-edged sword strategy for controlling intracranial volumes and therefore reducing intracranial pressure (ICP) after acute brain damage. The effect is linked to the induced local alkalosis producing a reduction in cerebral blood flow (CBF). Although this effect is short-lasting, hyperventilation carries a potential risk of cerebral ischemia. Although all patients with severe traumatic brain injury (TBI) are mechanically ventilated, the target for the partial pressure of carbon dioxide in arterial blood (PaCO2) remains poorly defined and there is insufficient evidence to support any recommendation. A target PaCO2 of ≈36–40 mmHg has been reported by clinicians and suggested by consensus statements. In presence of raised ICP, this is usually lowered to ≈30–35 mmHg. In this chapter, starting from physiological concepts, we will review the evidence around PaCO2 management in TBI and will present some data on current practice of the use of hyperventilation in TBI. We observed considerable variability in CO2 management between centers in Europe. Further research is needed to identify optimal ventilatory strategies in the management of severe TBI.