Carbon monoxide poisoning: Too easily overlooked

Nursing, May 2004 by Balch, Coleen

Here's how to avoid being fooled by this master of disguises.

Carbon monoxide (CO) poisoning claims 6,000 lives and causes more than 10,000 sick days in the United States each year. But its vague symptoms are too easily attributed to a preexisting condition, or resemble another condition (such as cardiovascular disease), so sources of exposure can be tricky to pin down. As a result, CO poisoning is often misdiagnosed or missed altogether.

If you're alert to the possibility of CO poisoning, you may be able to identify it in the early stages. Read on to learn which clues to look for when assessing patients and how to intervene.

Beating oxygen to the punch

Inhaled CO binds with hemoglobin far more swiftly than inhaled oxygen does, forming carboxyhemoglobin (COHb) and causing hypoxia. Carbon monoxide also binds with myoglobin and mitochondrial cytochrome oxidase, depriving the brain and vasculature of oxygen, so COHb levels alone don't always reflect the seventy of toxicity. Tissue hypoxia leads to anaerobic metabolism and lactic acidosis, causing lipid peroxidation and free radical formation-which, in turn, provokes neurotoxicity.

The deeper and more rapidly a person breathes, the greater his exposure to CO. Once the exposure stops, bound CO molecules dissociate from hemoglobin and are excreted through the lungs, and normal oxygen transport resumes. By then, however, oxygen deprivation may have seriously damaged organs. The degree of organ damage depends on the severity and duration of exposure. Even low levels of exposure can be harmful, particularly in patients with underlying medical conditions.

Early in the exposure, the body tries to compensate for cellular hypoxia by increasing the heart and respiratory rates and boosting cerebral and coronary blood flow. Even if the heart is healthy, these compensatory mechanisms may be ineffective. If the heart is compromised by underlying cardiac disease, this increased myocardial workload can cause angina, myocardial infarction, arrhythmias, and pulmonary edema.

The brain is particularly susceptible to CO poisoning because of its continuous requirement for oxygen. Common neurologic complaints are a throbbing headache, weakness, fatigue, dizziness, memory loss, and concentration difficulties. Patients also may suffer syncope, seizures, cerebral edema, or coma.

Carboxyhemoglobin levels over 60% can cause death through cardiac toxicity, neurotoxicity; systemic acidosis, or respiratory arrest. Patients who survive CO poisoning may experience delayed consequences of brain or neurologic system damage, including serious and possibly permanent disabilities.

Low levels of chronic CO exposure, as from tobacco smoke, industrial CO production, or urban pollution, can affect long-term cardiovascular health by raising blood pressure, encouraging atherosclerosis or thrombotic tendencies, and triggering polycythemia and its increased clotting risk.

Long-term neuropsychiatric consequences of CO poisoning, which occur in some form in 20% of patients, include dementia, psychosis, and personality changes; visual, speech, and gait disturbances; tremor; and fecal and urinary incontinence. Parkinsonism is a rare complication. Many of these complications occur weeks to months after the actual poisoning. Factors that increase the risk of delayed neurologic syndrome include very young or old age, preexisting medical conditions, severe hypoxia, prolonged loss of consciousness, or persistent dizziness and fatigue after regaining consciousness.

Many guises of CO poisoning

Keep the possibility of CO poisoning in mind when you encounter mild, nonspecific symptoms such as malaise, dizziness, fatigue, and difficulty staying focused, especially in very young, elderly, or pregnant patients and in patients with coronary artery or pulmonary disease. Severe CO poisoning can trigger or resemble other serious conditions, such as acute coronary syndrome, syncope, stroke, chronic obstructive pulmonary disease, respiratory failure, or postictal state.

Headache, nausea, and vomiting are common symptoms of CO exposure. Be especially vigilant in cold weather because poorly vented heaters and woodstoves are a common source of CO poisoning. Other common causes are fires, explosions, automobile exhaust, and heavy machinery. Tobacco smoke, including secondhand smoke, also increases patients' CO blood levels.

If you suspect CO poisoning, ask the patient about her home and work environment. For example, are her family and pets feeling well? If everyone in the household is lethargic, the home atmosphere may contain unhealthy levels of CO-especially if fresh air relieves their symptoms and they have no lymphadenopathy fever, myalgia, or sore throat.

If you provide home health care, assess your patients for signs and symptoms and check the homes you visit for potential CO hazards and proximity to busy urban roads. Air pollution can contribute to chronic CO toxicity.

Seeking the clues

Some common diagnostic tools and observations aren't reliable in detecting CO poisoning. For example, the patient's nails and mucous membranes rarely are cherry red. What's more, conventional pulse oximeters don't distinguish between COHb and oxyhemoglobin, so the patient's SpO^sub 2^ will be falsely elevated.