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Carbon Monoxide

Carbon monoxide poisoning is a rare cause of problems when diving, it does occur when there is contaminated air in recreational diving tanks. CO poisoning is the leading cause of poisoning deaths in the U.S.(about 8600 deaths per year) and is easily missed unless health care providers are especially vigilant.

The most commonly observed result related to CO poisoning is neurological dysfunction; abnormalities in the cardiac, pulmonary and renal organ systems do occur. About 14% of patients sustain permanent brain damage, and delayed neurological sequelae do occur 3-21 days later in about 12% of people.


CO risk factors include:

  • Pre-existing cardiovascular disease
  • Age greater than 60 years
  • An interval of unconsciousness (longer the higher the risk)
  • Little association with COHgb (carboxy hemoglobin)
Carbon Monoxide signs:
  • Tachycardia (rapid pulse)
  • Tachypnea (rapid breathing)
  • Retinal venous engorgement (as seen through an ophthalmoscope)
  • Ekg conduction defects
  • COHgb greater than 20%

Carbon monoxide in diving is the product of incomplete combustion of hydrocarbons and is usually from compressors and cigarette smoking. In addition to the effect on the hemoglobin molecule, it has a toxic effect on the cytochrome A3 system. Prevention requires periodic air sampling. The maximal allowable level is 10 ppm (0.001%).


Treatment of Carbon Monoxide Poisoning With Hyperbaric Oxygenation

Here is an interesting article from the New England Journal of Medicine:

Hyperbaric Oxygen Treatments Reduced the Risk for Cognitive Sequelae after Acute Carbon Monoxide Poisoning

Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347:1057-67. [PMID: 12362006][Abstract/Free Full Text]

This study examined oxygen therapy given in a hyperbaric chamber to patients referred with carbon monoxide poisoning. The results were so significant that the trial was stopped early so that all patients could benefit from the hyperbaric therapy. Traditionally, patients with carbon monoxide poisoning are treated with 100% oxygen delivered by a tightly fitting or nonrebreather face mask. This is done to displace carbon monoxide from hemoglobin by providing a high partial pressure of oxygen. Weaver and colleagues rationalized that patients with carbon monoxide poisoning may have lingering neuropsychological effects that may or may not be related to the carboxyhemoglobin level with which they present to the hospital and that hyperbaric oxygenation may have benefits above and beyond displacing carbon monoxide from hemoglobin molecules.

In this randomized, double-blind trial, the investigators assigned patients with symptomatic acute carbon monoxide poisoning to 3 hyperbaric oxygen treatments within a 24-hour period or 1 normobaric oxygen treatment plus 2 sessions of exposure to normobaric room air within a 24-hour period. The carbon monoxide poisoning was the result of various factors, including an indoor heating fire and a suicide attempt, and the patients had carboxyhemoglobin levels of at least 10% when enrolled in the study. The patients received the oxygen treatments from an endotracheal tube or from a high-flow reservoir through a face mask to prevent rebreathing. The investigators administered neuropsychological tests immediately after chamber sessions 1 and 3 and at 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae at 6 weeks after carbon monoxide poisoning.

When the investigators stopped the trial, they had enrolled 76 patients in each group. At 6 weeks, cognitive sequelae (poor functioning) affected 25% of the hyperbaric oxygen group (19 of 76 patients) and 46.1% of the normobaric oxygen group (35 of 76 patients), even after adjustment for variables. At 6 months and 12 months, corresponding rates were 21% versus 38% and 18% versus 33%, respectively.

Three hyperbaric oxygen treatments within a 24-hour period appeared to reduce the risk for cognitive sequelae after acute carbon monoxide poisoning. This strongly positive study suggests that, if possible, hyperbaric oxygenation should be provided for symptomatic patients with acute carbon monoxide poisoning. The ideal number of chamber sessions, however, is unknown. It is also not known how hyperbaric oxygenation works to eradicate carbon monoxide. In animal models, such oxygenation affects lipid peroxidation in the brain; it also alters brain glutamate levels the same way that hypothermia does. Therefore, benefits of hyperbaric oxygenation may be related to improving oxygenation of cells above and beyond the displacement of carbon monoxide from hemoglobin.



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