Abstract:Hypocapnia is a common pathophysiological abnormality in patients with acute brain injury (ABI) and is closely associated with impaired central respiratory regulation, stress responses, mechanical ventilator settings, and iatrogenic hyperventilation. Traditionally, hypocapnia has been used as a short-term intervention to reduce intracranial pressure. However, recent studies have shown that sustained or marked reductions in the arterial partial pressure of carbon dioxide (PaCO?) may aggravate secondary brain injury and affect patient outcomes by decreasing cerebral blood flow, impairing cerebral oxygen unloading, and increasing neuronal excitability. At present, there is no unified classification system for the severity of hypocapnia after ABI. Its clinical significance should not be determined solely by a single PaCO? threshold, but should be assessed comprehensively according to the degree and duration of hypocapnia, dynamic PaCO? trajectories, cumulative exposure burden, and pathophysiological differences among ABI subtypes. Regarding monitoring, arterial blood gas analysis remains the gold standard for diagnosing hypocapnia, whereas end-tidal carbon dioxide monitoring provides continuous trend information but requires regular calibration with arterial blood gas measurements. In patients at high risk of cerebral ischemia, multimodal monitoring, including intracranial pressure, brain tissue oxygen tension, and near-infrared spectroscopy, may be combined to guide individualized PaCO? regulation. This review summarizes recent research on hypocapnia after ABI, focusing on its occurrence, injury mechanisms, monitoring and management strategies, and current challenges, with the aim of improving understanding and further optimizing individualized management.