Mechanisms of Action of Hyperbaric Oxygen Therapy in Carbon Monoxide Poisoning

Current knowledge indicates that there are multiple mechanisms of action of hyperbaric oxygen therapy in CO poisoning. Based on the law of mass action, elevated partial pressures of O2 will accelerate the rate of CO dissociation from hemoglobin. Thus, COHb half-life can be decreased from approximately 5 .5 hours when breathing air and to approximately 20 minutes when breathing O2 at 3 ATA. Indeed, this was the reasoning behind the first clinical implementation of hyperbaric oxygen therapy for CO poisoning. As the COHb level is not associated with clinical risk, it is hard to accept that a more rapid dissociation of CO from hemoglobin could be the central factor for the benefit of hyperbaric oxygen . A fraction of the acute mortality from CO is due to hypoxia, however, and prompt removal of CO from hemoglobin will be of benefit . HBO2 also promotes normalization of tissue hypoxia. CO binds to cytochrome oxidase, particularly when the COHb level exceeds 40% to 50% . Brown and Piantadosi demonstrated that hyperbaric oxygen at 3 ATA markedly accelerates the dissociation of CO from cytochrome oxidase. Furthermore, it was shown that HBO2 completely reversed brain mitochondrial electron transport chain inhibition by CO. Hyperbaric oxygen also has effects related to the cascade of vascular injury triggered by CO poisoning. Hyperbaric oxygen was found to be effective for preventing brain oxidative injury through increased heme oxygenase and upregulation of antioxidants. The mechanism appears to be associated with denaturation of a membrane-associated guanylate cyclase that plays a role in coordinating the elevated affinity of beta 2 integrins expressed on the cell surface. Given that vascular changes are prominent in clinical CO poisoning, it is feasible that neurological sequelae in patients may involve a perivascular injury mediated by leukocyte sequestration and activation. Moreover, HBO2 reduces neuronal apoptosis and necrosis, and it also mobilizes stem cells via a nitric oxide–dependent mechanism. Hence, timely administration of hyperbaric oxygen may ameliorate the cascade leading to brain injury via multiple mechanisms.

Disposition

The critical determination in carbon monoxide–poisoned patients is the severity of the poisoning. The majority of patients seen in emergency departments have a mild exposure to CO and become asymptomatic after receiving 100% oxygen for 3 to 4 hours. These asymptomatic patients may be sent home as long as their place of residence is deemed safe and CO free. Adequate follow-up with a primary care doctor and referral for neuropsychiatric testing should be assured prior to discharge.

The ultimate decision to treat a patient with 100% oxygen at a local hospital or to transfer that patient to a hyperbaric facility will remain a difficult one to make. The community, length of transport, available staff, and severity of symptoms must be considered. However, even in severe poisonings, it can be both advantageous and safe to transport patients for hyperbaric treatment. Each area should establish its own specific criteria prior to a CO emergency, to determine which patients will be transferred. Information about the location of hyperbaric facilities in the continental United States and Canada is available from the Diver’s Alert Network (DAN) at Duke University in Durham, North Carolina. The poison center in each state will also have a list of the closest hyperbaric facilities.

Source Reference: Excerpted from Hyperbaric Medicine Practice 4th Edition with permission from the publisher. Reference Chapter 13, Carbon Monoxide by Jillian Theobald

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