The effects of arterial CO2 on the injured brain: Two faces of the same coin.

Abstract Serum levels of carbon dioxide (CO2) closely regulate cerebral blood flow (CBF) and actively participate in different aspects of brain physiology such as hemodynamics, oxygenation, and metabolism. Fluctuations in the partial pressure of arterial CO2 (PaCO2) modify the aforementioned variables, and at the same time influence physiologic parameters in organs such as the lungs, heart, kidneys, and the gastrointestinal tract. In general, during acute brain injury (ABI), maintaining normal PaCO2 is the target to be achieved. Both hypercapnia and hypocapnia may comprise secondary insults and should be avoided during ABI. The risks of hypocapnia mostly outweigh the potential benefits. Therefore, its therapeutic applicability is limited to transient and second-stage control of intracranial hypertension. On the other hand, inducing hypercapnia could be beneficial when certain specific situations require increasing CBF. The evidence supporting this claim is very weak. This review attempts providing an update on the physiology of CO2, its risks, benefits, and potential utility in the neurocritical care setting.