Carbon monoxide (CO) is a colorless, odorless gas produced as a byproduct of combustion. Poisoning occurs by inhalation, either accidentally or intentionally (suicide attempt). CO poisoning is responsible for an estimated 40,000 emergency department visits and 1,000 accidental deaths in the United States annually. Approximately 5-6% of patients evaluated in emergency departments for CO poisoning are treated with hyperbaric oxygen (HBO2).

CO binds to hemoglobin in red blood cells at the sites usually utilized to carry oxygen to tissues. Oxygen, and especially hyperbaric oxygen, accelerates the clearance of CO from the body, thereby restoring oxygen delivery to sensitive tissues such as brain and heart. This has traditionally considered to be the mechanism of benefit of HBO2. However, research published in the past few years has demonstrated a number of other mechanisms of toxicity from CO. Blood vessel (vascular) injury from CO has been demonstrated to result from CO-induced production of nitric oxide-derived oxidants and cellular injury from activated white blood cells (neutrophils). CO also causes direct central nervous system cellular injury through mechanisms that include disturbance of energy metabolism and intracellular production of oxygen free radicals. In animal experiments, hyperbaric oxygen, but not normobaric oxygen (NBO2), has been demonstrated to block each of these mechanisms of toxicity.

Until ten years ago, the benefit of hyperbaric oxygen treatment of CO poisoning was demonstrated by comparing the clinical experience at institutions where HBO2 was used with that at facilities where it was not available. Since 1989, six randomized prospective trials have been reported comparing HBO2 with NBO2 treatment of acute CO poisoning. Of these, three demonstrate improved patient outcomes with hyperbaric oxygen, two report no difference between the two therapies, and one remains blinded with regard to the treatment administered. A full listing of the investigations, as well as a discussion of the study designs and findings, can be found in the UHMS Hyperbaric Oxygen Therapy Committee Report (available for purchase through this web site).

The UHMS currently recommends HBO2 treatment of individuals with serious CO poisoning, as manifest by transient or prolonged unconsciousness, abnormal neurologic signs, cardiovascular dysfunction, or severe acidosis.

Also see a very nice discussion put forward by Dr. Neil Hampson on the benefits of HBO in CO poisoning in 2001.


  1. Thom SR, Fisher D, Xu YA, Garner S, Ischiropoulos H. Role of nitric oxide-derived oxidants in vascular injury from carbon monoxide in the rat. Am J Physiol 1999;276:H984-992.
  2. Brown SD, Piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J Clin Invest 1991;89:666-672.
  3. Hyperbaric Oxygen Therapy Committee. Hyperbaric Oxygen Therapy: 1999 Committee Report. Hampson NB, ed. Kensington, MD: Undersea and Hyperbaric Medical Society; 1999.
  4. Hampson N, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995;13:227-231.


Other references on Carbon Monoxide Poisoning:



  • Bartlett, R: Carbon monoxide poisoning. Clinical management of poisoning and drug overdose. WB Saunders, Lester M Haddad, James F Winchester editors; 3rd edition; 1997
    General review article, emphasizing both the modern appreciation of the complex pathophysiology involved, and the multifactorial benefits of HBO therapy.
  • Thom, SR: Carbon monoxide-mediated brain lipid peroxidation in the rat. J. Appl. Physiol. 1990;68(3): 997-1003
    A publication that advanced the pathophysiology of CO poisoning from the simple concept of inhibition of hemoglobin function. This data indicates that critical cellular toxicity occurs.
  • Thom, SR: Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol. Appl. Pharmacol. 1990; 105: 340-344
    In reference to the above elucidation of a cellular poisoning, this companion study demonstrates the ability of HBO therapy to inhibit the toxic process.
  • Thom, SR: Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol. Appl. Pharmacol. 1993; 123: 243-247
    Recent evidence of complex tissue injury, here involving a leukocyte –mediated brain injury as a result of acute CO poisoning.
  • Thom, SR: Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon- monoxide-mediated brain injury in rats. Toxicol. Appl. Pharmacol. 1993; 123: 248-256
    A companion article to that pathophysiology noted in the previous article. This research demonstrates the functional inhibition of leukocytes by HBO therapy, thereby antagonizing CO medicated oxidative brain injury. Clearly, CO poisoning involves multiple and complex pathologies. Hyperbaric oxygen has been consistently demonstrated as antagonistic to these processes: something no other intervention, including oxygen delivered without a hyperbaric chamber, has been demonstrated.
  • Myers RAM, Snyder SK, Emhoff TA: Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med. December 1985; 14: 1163-1167
    A large case series that reports the ability of HBO therapy to minimize/eliminate post exposure relapse, which occurred in 12% of CO poisoned patients not treated hyperbarically. The reader is asked to consider the morbidity and cost (work-related absence, etc.) associated with such sequelae.
  • Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: A review of 115 cases. Ann Emerg Med. December 1985; 14: 1168-1171
    Further evidence of the significant (43%) relapse/ late complications that characterize CO poisoned patients who do not receive hyperbaric oxygenation.
  • Van Hoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. JAMA 1989; 261: 1039-1043
    A report of the heightened risk/morbidity/mortality to the fetus in maternal CO poisoning. The authors provide a recommended management protocol that centers around HBO therapy.
  • McNulty JA, Maher BA, Chu M, ET AL.: Relationship of short-term verbal memory to the need for hyperbaric oxygen treatment after carbon monoxide poisoning. Neuropsychiatry, Neuropsychology and Behavioral Neurology 1997;10: 174-179
    A case controlled study demonstrating the benefit of HBO therapy in improving short-term memory following CO exposure.
  • Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB: Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Annuals of Emergency Medicine. April 1995; 25:4: 474-480
    Prospective randomized clinical trial that confirms the findings of above noted and non-controlled reports: namely: HBO therapy "decreased the incidence of delayed neurological sequelae after CO poisoning."
  • Ducasse JL, Celsis P, Marc-Vergnes JP: Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperbaric Med 1995; 22(1): 9-15
    Prospective and randomized blinded clinical trial. The authors conclude that HBO therapy "reduces the time of initial recovery and the number of delayed functional abnormalities…"
  • Jiang J, Tyssebotn I: Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats. Undersea Hyperbaric Med 1997; 24(2): 107-116
    A comparative trial of various groups; involving no treatment, pressurized air treatment and pressurized oxygen treatment, in a severe CO and cerebral ischemic model. "Compared to normoxic treatments, the HBO… significantly reduced the mortality and neurologic morbidity." HBO was also significantly better than ‘normal oxygen’ in increasing survival rate…"