Should the pressure be off or on in the use of oxygen in the treatment of carbon monoxide-poisoned patients?

Carbon monoxide intoxication: An updated review

“…For example in rat brains, it prevents lipid peroxidation and leukocyte adherence to brain microvascular endothelium while accelerating regeneration of inactivated cytochrome oxidase. Therefore, usually at 2.5 to 3 ATA for 90 to 120 min, it is considered the treatment of choice for those who present with syncope, coma, or seizure, and focal neurological deficit or COHb N 25% (15% in pregnancy) [59][60][61][62][63].…”

Carbon monoxide poisoning

“…Although they could not define absolutely a high-risk population for developing neurologic sequelae, patients in the extremes of age, patients with neurologic abnormalities, patients with loss of consciousness, and patients with a CO-Hgb level greater than 25% ''require special consideration'' [141]. Although the efficacy of one HBOT treatment protocol over another has not been determined [143,196,204,[224][225][226], one session of HBOT at 2.5 to 3.0 ATA is recommended initially, with further sessions considered if symptoms persist [141,202,221]. Patients not meeting criteria for HBOT should receive 6 to 12 hours of 100% oxygen delivered by tightfitting facemask [13,141,196,212,225,227].…”

Subacute normobaric oxygen and hyperbaric oxygen therapy in drowning, reversal of brain volume loss: a case report

“…Functional imaging has been used since 1990 in chronic neurological disorders,25262728293031323334353637383940414243 to document HBOT-induced neurological improvements. These improvements have evaded anatomical imaging due to the paucity of subacute pediatric cases, treatment of severe cases with large tissue loss, and the inability to capture metabolic252930 and microscopic changes,31354244 including microscopic neurogenesis 4245.…”