Carbon Monoxide Poisoning
And Hyperbaric Oxygen Therapy

Carbon Monoxide Poisoning is a leading cause of death by poisoning in the United States. ^{7, 8} Among causes of Carbon Monoxide Poisoning are automobile exhaust (accidental or purposeful), faulty heaters, and building fires.

Many factors affect the carbon monoxide poisoning symptoms and the outcome of treatment.

Most significant factors are: the inhaled CO concentration, duration of exposure, rate and depth of breathing, heart rate, co-morbid illnesses and most importantly, the time between discovery of the patient after exposure and arrival at a Hyperbaric Chamber.

Photo courtesy of "smokeshowing"

Carbon Monoxide Poisoning

Stephen R. Thom, M.D., Ph.D., FACEP and Lindell K. Weaver, M.D., FACP, FCCP, FCCM

The injuries caused by carbon monoxide (CO) traditionally have been viewed as due to a hypoxic stress mediated by an elevated carboxyhemoglobin (COHb) level. The two organ systems most susceptible to injury from CO are the cardiovascular and central nervous systems. Human and animal data indicate that major cardiac injury is due primarily to CO-induced hypoxic stress.

However, the COHb level does not correlate well with the development of neurological injuries. Recent investigations have established that systemic oxidative stress can arise from exposure to CO and that perivascular and neuronal injuries arise by mechanisms other than hypoxia. Neuropathology seems to be due to a complex cascade of biochemical events involving several pathophysiologic processes.

Administration of supplemental oxygen is the cornerstone of treatment of CO poisoning. Oxygen inhalation will hasten disassociation of CO from hemoglobin dissociation to occur at a rate greater than that achievable by breathing pure oxygen at sea-level pressure.

Additionally, HBO₂, but not ambient pressure oxygen treatment, has several actions which have been demonstrated in animal models to be beneficial in ameliorating pathophysiologic events associated with central nervous system (CNS) injuries mediated by CO.

These include an improvement in mitochondrial oxidative processes, inhibition of lipid peroxidation, and impairment of leukocyte adhesion to injured microvasculature. Animals poisoned with CO and treated with HBO₂ have been found to have more rapid improvement in cardiovascular status, lower mortality, and lower incidence of neurological sequelae.

Since 1960, the clinical use of HBO₂ for CO poisoning has occurred with increasing frequency. Over 2,500 CO-intoxicated patients were treated in North American hyperbaric chambers in 1992. However, this is only a small fraction of those poisoned with CO. Extrapolation of data from a 1994 survey across three western states projected that over 4,000 CO-poisoned patients are evaluated in emergency departments annually in the United States.

In reported series, clinical recovery among patients treated with HBO₂ appears to be improved beyond that expected with ambient pressure supplemental oxygen therapy. This has been observed both in terms of mortality and neurologic morbidity.

This research found that the optimal benefit from HBO₂ occurs in those treated with the delay after exposure and that repeat treatments may yield a better outcome than just a single treatment in selected patients.¹²¹

Photo courtesy of Kyle Kesselring