Clinical
Carbon Monoxide Poisoning

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Causes of Carbon Monoxide Poisoning

Carbon monoxide comes from both natural and manufactured sources. The largest risk of exposure comes from the household environment.8 Such exposures come from the inhalation of combustible fumes such as those produced by small gasoline engines, stoves, generators, lanterns, and gas ranges or by burning charcoal and wood. Carbon monoxide is usually inhaled from an enclosed or confined space such as a garage, kitchen, basement, or workroom. The fire-related injuries and deaths result from a

Mechanisms of Carbon Monoxide Poisoning

The best established and most important toxic action of carbon monoxide is incapacitation of the cell’s mechanism for using oxygen resulting in chemical asphyxiation and hypoxia (e.g., effective oxygen deprivation). Hypoxia is a deficiency of oxygen at the tissue level.16 Hypoxemia-induced hypoxia occurs when the oxygen tension of arterial blood is reduced—generally, a partial pressure of oxygen (Po2) of less than 80 mm Hg.17 Carbon monoxide prevents cells from using oxygen by inhibiting the

Manifestations of Carbon Monoxide Poisoning

The body relies on oxygen to reach the cells to function; therefore all body systems are affected by carbon monoxide poisoning. The heart, brain, and lungs require large continuous amounts of oxygen for normal function and are most susceptible to the effects of carbon monoxide poisoning. Early signs and symptoms reflect reflexive attempts of the respiratory, cardiovascular, and neurologic systems to overcome tissue hypoxia. Carbon monoxide poisoning often mimics a viral illness with flu-like

Recognition of Carbon Monoxide Poisoning

Carbon monoxide remains a challenge to detect because of the chemical properties of being a colorless, odorless, tasteless, nonirritating gas. Acute carbon monoxide poisoning should be suspected in anyone who inhales smoke in a closed-space fire. The clinical manifestation and diagnostic findings in carbon monoxide poisoning reflect hypoxia caused by carbon monoxide deactivation of cellular oxygen-utilization mechanisms. The development of toxicity is generally rapid, at a rate dependent on the

Treatment of Carbon Monoxide Poisoning

Acute carbon monoxide poisoning is treated by terminating exposure and administering supportive care.29 Termination of carbon monoxide exposure can entail removal of the patient from the exposed environment. Immediate initial emergency care involves the basic life support airway, breathing, and circulation process.30 Administration of 15 L/min of oxygen via a non-rebreather mask (NRB) is an integral part of the initial management of acute carbon monoxide poisoning. High-flow oxygen by an NRB

Special Consideration (Pregnancy)

Pregnancy and carbon monoxide exposure does not increase the maternal risk of carbon monoxide toxicity.37 However, the fetus is susceptible to the toxic effects of maternal hypoxia.38 Fetal hemoglobin has an even greater affinity than adult hemoglobin for carbon monoxide binding.39 COHb levels above 15% represent severe poisoning. Therefore recommendations for treatment with HBO therapy for pregnant patients should be considered early on.

Injury Prevention Education

Injury prevention and education are the key to awareness of carbon monoxide exposure and poisonings.40 Fire departments, EMS providers, public health departments, and hospitals have provided sundry opportunities for public awareness and education. Despite substantial educational efforts, carbon monoxide exposures and poisonings still are an important topic of discussion. Injury prevention activities, such as lowering the cost of carbon monoxide and smoke detectors for purchase at a commercial

Conclusion

Acute carbon monoxide poisoning can be challenging to diagnose even for the seasoned emergency nurse. It can also be a debilitating and sometimes lethal illness if not recognized immediately. Therefore emergency nurses should have a comprehensive understanding with regard to recognition and treatment of carbon monoxide poisoning. Carbon monoxide affects all body systems, and progression and severity of toxicity vary according to concentration and duration of exposure. Morbidity and death are

Mark Goldstein, Michigan ENA, is EMS Coordinator, Department of Emergency Medicine, William Beaumont Hospital, Royal Oak, Mich.

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    Mark Goldstein, Michigan ENA, is EMS Coordinator, Department of Emergency Medicine, William Beaumont Hospital, Royal Oak, Mich.

    Earn Up to 8.5 CE Hours. See page 592.

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