Carbon monoxide (CO) poisoning is a potentially life-threatening toxic exposure that can cause acute neurologic and cardiovascular injury as well as delayed neurocognitive complications. Because carbon monoxide is colorless and odorless and produces nonspecific symptoms, clinically significant poisoning may not be immediately recognized.
Hyperbaric Oxygen Therapy (HBOT) is an accepted treatment for carbon monoxide poisoning and is recognized by the Undersea & Hyperbaric Medical Society (UHMS) as an indication for hyperbaric treatment.
HBOT rapidly increases oxygen delivery, accelerates carbon monoxide elimination, and may help limit the cellular and inflammatory processes associated with neurologic injury following significant CO exposure.
Patients with suspected carbon monoxide poisoning should be removed from the exposure source and treated promptly with high-concentration oxygen.
For patients with significant neurologic symptoms, loss of consciousness, cardiovascular involvement, severe metabolic abnormalities, pregnancy, or other indicators of serious poisoning, early consultation with a hyperbaric medicine specialist should be considered.
The decision to use HBOT should be based on the overall clinical presentation rather than the carboxyhemoglobin level alone.
Carbon monoxide is a colorless, odorless gas produced by incomplete combustion of carbon-containing fuels.
Common sources of exposure include:
Residential fires
Furnaces and heating systems
Portable generators
Motor vehicles
Gas-powered equipment
Charcoal grills
Propane appliances
Boats and marine engines
Industrial combustion processes
Enclosed or poorly ventilated spaces containing combustion sources
Carbon monoxide binds strongly to hemoglobin, forming carboxyhemoglobin and reducing the blood's ability to transport oxygen.
Its toxicity, however, extends beyond impaired oxygen transport. Carbon monoxide also disrupts cellular respiration and initiates inflammatory, oxidative, vascular, and neurologic processes that can continue after the initial exposure has ended.
The brain and cardiovascular system are particularly susceptible to injury.
Carbon monoxide poisoning can produce a broad range of nonspecific symptoms. Because early symptoms often resemble viral illness, migraine, intoxication, or other common conditions, recognition of the exposure history is critical. Multiple people developing similar symptoms in the same environment should increase suspicion for a shared carbon monoxide exposure.
Carboxyhemoglobin Levels and Clinical Severity
Measurement of carboxyhemoglobin (COHb), generally by blood co-oximetry, is important in confirming carbon monoxide exposure. However, the COHb concentration should not be interpreted in isolation. COHb levels decrease once a patient is removed from the exposure and fall more rapidly after supplemental oxygen is administered. As a result, a level obtained after transport or oxygen treatment may substantially underestimate the patient’s earlier exposure. Additionally, the measured COHb concentration does not consistently correlate with neurologic injury, clinical severity, or the risk of subsequent cognitive complications. Clinical history, neurologic findings, cardiovascular involvement, duration and circumstances of exposure, pregnancy status, metabolic abnormalities, and response to treatment should therefore be considered alongside the COHb measurement.
HBOT may address several components of carbon monoxide toxicity.
Breathing oxygen decreases the half-life of carboxyhemoglobin. Hyperbaric oxygen accelerates this process further, allowing carbon monoxide to be displaced from hemoglobin more rapidly.
Under hyperbaric conditions, substantially more oxygen dissolves directly into plasma. This increases oxygen availability to tissues even while normal hemoglobin-mediated oxygen transport is impaired.
Carbon monoxide interferes with mitochondrial function and cellular respiration. Hyperbaric oxygen may improve cellular oxygen availability during recovery from this metabolic insult.
Carbon monoxide poisoning can initiate oxidative stress, lipid peroxidation, leukocyte-mediated vascular injury, inflammation, and other processes that may contribute to brain injury after the initial hypoxic event. HBOT appears to influence several of these pathways, providing a rationale for treatment beyond simply reducing the circulating COHb concentration. These mechanisms are particularly important in the central nervous system, where even temporary interruption of blood flow can produce significant neurologic injury.
The optimal selection of patients for HBOT remains an area of active clinical discussion, and treatment decisions should be individualized.
Hyperbaric consultation should be strongly considered when carbon monoxide poisoning is associated with findings such as:
The Centers for Disease Control and Prevention advises consideration of HBOT when COHb exceeds approximately 25–30%, or when cardiac involvement, severe acidosis, unconsciousness, neurologic impairment, or abnormal neuropsychiatric testing is present.
HBOT may also be appropriate at lower COHb concentrations when the clinical presentation or exposure history suggests significant poisoning.
A COHb threshold should not be used as the sole criterion for referral.
Pregnancy requires particular consideration because carbon monoxide exposure can threaten both the pregnant patient and the fetus. The fetus is especially vulnerable to carbon monoxide toxicity, and maternal symptoms or COHb concentrations may not fully reflect fetal exposure or risk. Current CDC clinical guidance supports a more aggressive approach to hyperbaric treatment in pregnancy and identifies HBOT as the treatment of choice for pregnant patients with carbon monoxide poisoning, including patients who may appear less severely poisoned than nonpregnant adults. Suspected significant CO poisoning during pregnancy warrants prompt consultation with specialists experienced in toxicology, maternal-fetal care, and hyperbaric medicine.
Carbon monoxide and cyanide toxicity may occur simultaneously in victims of smoke inhalation, particularly following structural fires. The combination can produce severe cellular hypoxia and cardiovascular toxicity. UHMS recognizes carbon monoxide poisoning complicated by cyanide poisoning within its accepted hyperbaric indications and recommends strong consideration of HBOT in these cases. HBOT does not replace appropriate cyanide antidotal therapy, airway management, burn care, or critical care. Treatment should be coordinated with emergency medicine, toxicology, critical care, and hyperbaric medicine specialists.
When HBOT is indicated, treatment should generally be initiated as early as practical after stabilization. The potential benefit of hyperbaric treatment is not limited to rapid elimination of carboxyhemoglobin. The inflammatory and neurologic consequences of carbon monoxide exposure may continue after COHb concentrations have fallen substantially. For this reason, normalization of the COHb level does not necessarily eliminate the potential rationale for HBOT in a symptomatic patient. Transfer decisions should balance the potential benefit of hyperbaric treatment against the patient’s clinical stability, transport time, distance to an appropriate hyperbaric facility, and the facility’s ability to manage critically ill patients.
Hyperbaric oxygen therapy does not replace initial emergency treatment. Management of suspected or confirmed carbon monoxide poisoning begins with immediate removal from the exposure and administration of high-concentration oxygen.
Additional management may include:
Patients should be medically stabilized to the extent possible before transport or hyperbaric treatment, particularly because management of an acutely deteriorating patient may be more complex within a hyperbaric chamber.
One of the major concerns following carbon monoxide poisoning is the development of delayed neurologic or neuropsychiatric complications. A patient may initially improve and subsequently develop new symptoms days or weeks after the exposure. Potential delayed manifestations include:
The possibility of delayed neurologic sequelae is one reason treatment decisions cannot be based solely on normalization of carboxyhemoglobin or resolution of immediate symptoms.
Patients discharged after carbon monoxide poisoning should receive appropriate follow-up instructions and should be advised to seek reevaluation if new neurologic, cognitive, or behavioral symptoms develop.
Carbon monoxide poisoning is an accepted indication for Hyperbaric Oxygen Therapy according to the Undersea & Hyperbaric Medical Society.
UHMS states that HBOT should be considered for acute symptomatic carbon monoxide poisoning based on randomized clinical trials, experimental evidence, physiologic mechanisms, and accumulated clinical experience.
The evidence regarding which patients derive the greatest long-term neurologic benefit remains less definitive.
A landmark randomized, double-blind clinical trial published in the New England Journal of Medicine found that a three-treatment hyperbaric oxygen regimen reduced cognitive sequelae at six weeks and at later follow-up in patients with symptomatic acute carbon monoxide poisoning.
Other randomized trials have not demonstrated the same benefit, however, and differences in patient selection, treatment protocols, timing, outcome assessment, and study design have contributed to continuing debate.
The American College of Emergency Physicians reviewed the evidence again in its 2025 clinical policy. ACEP concluded that, in symptomatic acute carbon monoxide poisoning, selected patients may benefit from HBOT based on the severity of symptoms and treatment availability, including distance and time to a capable hyperbaric facility.
Accordingly, early consultation with a hyperbaric medicine specialist is particularly valuable in patients with significant poisoning because the decision can incorporate clinical severity, individual risk factors, available evidence, transport considerations, and local treatment capabilities.
Acute carbon monoxide intoxication is specifically listed as a covered condition under the Centers for Medicare & Medicaid Services National Coverage Determination for Hyperbaric Oxygen Therapy (NCD 20.29).
Coverage recognition does not guarantee payment for an individual treatment. Applicable documentation, medical necessity, coding, facility, and payer-specific requirements should be reviewed.
Consider prompt hyperbaric medicine consultation for patients with acute carbon monoxide poisoning when there is:
Do not delay consultation solely because the carboxyhemoglobin concentration has fallen or normalized after oxygen treatment.
Clinical severity and the circumstances of exposure are more informative than a single COHb measurement when determining whether HBOT should be considered.
Explore Hyperbaric Medicine: Principles & Practice, 2nd Edition, a comprehensive 40-hour CME/CEU course designed for physicians, advanced practice providers, nurses, and allied health professionals seeking deeper clinical and operational knowledge in hyperbaric medicine.
Weaver LK. Carbon Monoxide Poisoning. Undersea & Hyperbaric Medicine. 2024;51(3):253–276. Reprinted from the Hyperbaric Oxygen Therapy Indications Manual.
American College of Emergency Physicians Clinical Policies Subcommittee. A Critical Issue in the Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Annals of Emergency Medicine. 2025;85–e59.
Centers for Disease Control and Prevention. Clinical Guidance for Carbon Monoxide Poisoning.
Centers for Medicare & Medicaid Services. National Coverage Determination 20.29: Hyperbaric Oxygen Therapy.
Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning. New England Journal of Medicine. 2002;347:1057–1067.