Carbon Monoxide Poisoning: Incidence, Diagnosis & Treatment

Your ambulance is dispatched to a 42-year-old man following a syncopal episode. Over the weekend, he has had a headache, chills, nausea and dizziness -common flu-like symptoms. The patient is treated and transported to a local emergency department, where he is given intravenous hydration and is discharged neurologically intact with normal vital signs. Two days later, you are dispatched to the same address, where you find the patient unconscious on his living room floor. Following aggressive airway management, oxygenation and ventilation, the patient is transported to the ED, where he is diagnosed with carbon monoxide (CO) poisoning. He is treated with hyperbaric oxygen, and is discharged with chronic headaches and memory problems. After returning to his home two days earlier, he had again been exposed to CO from a faulty furnace, which caused permanent neurologic deficits.

Many substances can cause dramatic poisonings, and even death, but CO-an odorless, colorless, two-molecule gas produced by burning material containing carbon-accounts for greater mortality and morbidity than all other poisonings combined. Carbon monoxide causes thousands of needless deaths each year in the United States.1,2 It is the leading cause of accidental poisoning deaths in America. Patients who survive the initial poisoning still face the prospect of delayed neurologic dysfunction, which occurs in 14% to 40% of serious cases.

Initial symptoms of CO poisoning, such as headaches, nausea and fatigue, are often mistaken for the flu, because the deadly gas goes undetected in a home. Early confirmation of CO poisoning and continuous monitoring of carboxyhemoglobin levels can now be performed in the field with new, noninvasive pulse CO-oximetry.

Carbon monoxide, an insidious byproduct of incomplete hydrocarbon combustion, is generated in toxic amounts by internal-combustion engines, fossil-fuel heating systems and fires. Carbon monoxide emissions from modern automobiles, though reduced by regulatory standards, are still highly toxic in poorly ventilated spaces. A stable gas at physiologic temperatures, CO diffuses rapidly across the alveolar capillary membrane and binds tightly to iron centers in hemoglobin.

Dangers of CO Poisoning

Anything that creates a flame, even a candle, is a potential source of CO. During incomplete combustion, carbon, hydrogen and available oxygen combine to form carbon dioxide, water, heat and the deadly CO. Any disruption of the burning process or shortage of oxygen can increase CO production and accumulation to dangerous levels.

Carbon monoxide gas enters the blood system during normal breathing. Inhaled CO combines with hemoglobin to form carboxyhemoglobin (COHb). Once this conversion occurs, the hemoglobin is no longer available for transporting oxygen to other parts of the body. As the amount of CO increases in the bloodstream, the tissues become hypoxic. The rate at which carboxyhemoglobin accumulates in the body is a factor of the concentration of gas being inhaled (parts per million or percent) and duration of exposure. Smokers have a pre-existing build-up of carboxyhemoglobin dependent upon the frequency of smoking. Aggravating the effects of exposure is the long half-life of carboxyhemoglobin in the bloodstream.

Carboxyhemoglobin decreases blood oxygen content and hinders the release of oxygen from hemoglobin to tissues.3 Carbon monoxide quickly binds with hemoglobin with an affinity 200-250 times greater than that of oxygen to form COHb. The resulting

decrease in arterial oxygen content and shift of the oxyhemoglobin dissociation curve to the left explains the acute hypoxic symptoms (primarily neurologic and cardiac) seen in patients with CO poisoning; however, the toxic effects of CO cannot be explained by this process alone.4 COHb levels do not correlate well with symptoms or outcome, and this process cannot account for the phenomenon of delayed neurologic sequelae.5 In patients with severe poisoning, carboxyhemoglobin compromises delivery of oxygen to tissue and leads to tissue hypoxia and its immediate functional implications, especially for organs with high oxygen demands, such as the brain and heart.6,7