The brain is extremely sensitive to ischemia and hypoxia. Irreversible damage to brain cells occurs within 4–6 minutes after cardiac arrest. Hyperbaric oxygen therapy exerts its critical effects through three mechanisms:

Rapidly increase blood oxygen concentrationUnder hyperbaric conditions, the physically dissolved oxygen in plasma rises to 10–18 times that under normal atmospheric pressure. It supplies oxygen to brain tissue without relying on hemoglobin, directly penetrating the ischemic penumbra and rescuing dying neurons.

Relieve cerebral edema and reduce intracranial pressureHyperbaric oxygen constricts cerebral blood vessels and reduces tissue exudation. It quickly alleviates hypoxia-induced cerebral edema and prevents secondary compression of brain tissue caused by elevated intracranial pressure.

Promote nerve cell repairIt upregulates the secretion of neurotrophic factors and stimulates angiogenesis, creating conditions for the repair of damaged nerve cells and halting the progression of hypoxia-induced neurological injury.

2. Key Clinical Implications

Golden rescue time windowFor hypoxic-ischemic encephalopathy caused by asphyxia, drowning, cardiac arrest and other emergencies, every second counts. The 4–6 minute window is the critical threshold for irreversible brain cell damage. On-site CPR combined with early hyperbaric oxygen therapy is the core rescue protocol.

Timing of hyperbaric oxygen interventionFor patients with stable vital signs after resuscitation, hyperbaric oxygen therapy should be initiated as early as possible. Earlier intervention delivers better brain function protection and significantly reduces the risk of long-term neurological sequelae.