Carbon monoxide (CO) is a colorless, odorless, tasteless, and nonirritating gas produced by the incomplete combustion of any carbon-containing material. Common sources of human exposure include smoke inhalation in fires, automobile exhaust fumes, faulty or poorly ventilated charcoal, kerosene, or gas stoves, and, to a lesser extent, cigarette smoke and methylene chloride. CO poisoning accounts for approximately 50,000 emergency department visits every year in the United States.

Toxicity is a consequence of cellular hypoxia and ischemia.

1. CO binds to hemoglobin with an affinity 250 times that of oxygen, resulting in reduced oxyhemoglobin saturation and decreased blood oxygen-carrying capacity. In addition, the oxyhemoglobin dissociation curve is displaced to the left, impairing oxygen delivery at the tissues.
2. CO may also directly inhibit cytochrome oxidase, further disrupting cellular function, and it binds to myoglobin, possibly contributing to impaired myocardial contractility.
3. In animal models of intoxication, damage is most severe in areas of the brain that are highly sensitive to ischemia and often correlates with the severity of systemic hypotension. Postanoxic injury appears to be complicated by lipid peroxidation, excessive release of reactive oxygen species and excitatory neurotransmitters, and inflammatory changes.
4. Fetal hemoglobin is more sensitive to binding by CO. Maternal exposure to CO results in a delayed rise in fetal carboxyhemoglobin (CO-Hgb) levels and slower elimination after maternal CO-Hgb levels fall.
5. Pharmacokinetics. The CO-Hgb complex gradually dissociates after removal from exposure. The approximate half-life of elimination of CO-Hgb during treatment with high-flow oxygen by tight-fitting mask or endotracheal tube is 74 minutes (range, 24-148 minutes). In room air the approximate half-life is as much as 200 minutes, and during hyperbaric oxygen therapy it is as short as 12-20 minutes.

The recommended workplace limit (ACGIH TLV-TWA) for carbon monoxide is 25 ppm as an 8-hour time-weighted average. The level considered immediately dangerous to life or health (IDLH) is 1,200 ppm (0.12%). However, the duration of exposure is very important. Exposure to 1,000 ppm (0.1%) eventually will result in 50% saturation of CO-Hgb, but it may take several hours to reach that level. Brief exposure to much higher levels may produce a more rapid rise in CO-Hgb.

Symptoms of intoxication are predominantly in organs with high oxygen consumption, such as the brain and heart.

1. The majority of patients describe headache, dizziness, and nausea. Patients with coronary disease may experience angina or myocardial infarction. With more severe exposures, impaired thinking, syncope, coma, convulsions, cardiac arrhythmias, hypotension, and death may occur. Although blood CO-Hgb levels may not correlate reliably with the severity of intoxication, levels greater than 25% are considered significant, and levels greater than 40-50% usually are associated with obvious intoxication.
2. Survivors of serious poisoning may experience numerous overt neurologic sequelae consistent with a hypoxic-ischemic insult, ranging from gross deficits such as parkinsonism and a persistent vegetative state to subtler personality and memory disorders. Some may have a delayed onset of several hours to days after exposure. Various studies suggest that the incidence of subtle neuropsychiatric sequelae, such as impaired memory and concentration and mood disorders, may be as high as 47%.
3. A significant proportion of patients with CO poisoning have myocardial injury which may be associated with increased long-term mortality.
4. Exposure during pregnancy may result in fetal demise.

Is straightforward when there is a history of exposure (eg, the patient was found in a car in an enclosed garage) but may be challenging in less obvious cases. There are no specific reliable clinical findings; cherry-red skin coloration or bright red venous blood is highly suggestive but rarely noted. The routine arterial blood gas instruments measure the partial pressure of oxygen dissolved in plasma (PO₂), but oxygen saturation is calculated from the PO₂ and is therefore unreliable in patients with CO poisoning. Conventional pulse oximetry also gives falsely normal readings because it cannot distinguish between oxyhemoglobin and CO-Hgb. Some newer pulse oximeters (eg, Masimo) can measure CO-Hgb and methemoglobin levels, however they are not in widespread clinical use and their role in diagnostic testing is uncertain.

1. Specific levels. Obtain a specific CO-Hgb concentration by co-oximetry with arterial or venous blood. Note:
   1. CO-Hgb levels may be as high as 2% in nonsmokers and 10% in smokers.
   2. The presence of the cyanide antidote hydroxocobalamin can falsely elevate CO-Hgb levels.
   3. Persistence of fetal hemoglobin may produce falsely elevated CO-Hgb levels in young infants.
2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, troponin, ECG, lactate, and pregnancy tests. Metabolic acidosis suggests more serious poisoning. With smoke inhalation, measure the blood methemoglobin level (use a co-oximeter) and cyanide level (not routinely available in clinical laboratories).

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary. If smoke inhalation has also occurred, consider early intubation for airway protection.
   2. Treat coma and seizures if they occur.
   3. Continuously monitor the ECG for several hours after exposure.
   4. Because smoke often contains other toxic gases, consider the possibility of cyanide poisoning, methemoglobinemia, and irritant gas injury (p 251).
2. Specific drugs and antidotes. Administer oxygen in the highest possible concentration (100%). Breathing 100% oxygen speeds the elimination of CO from hemoglobin to a half-life of approximately 1 hour, compared with about 6 hours breathing room air. Use a tight-fitting mask and high-flow oxygen with a reservoir (nonrebreather) or administer the oxygen by endotracheal tube. Treat until the CO-Hgb level is less than 5%. Consider hyperbaric oxygen in severe cases (see below).
3. Decontamination. Remove the patient immediately from exposure and give supplemental oxygen. Rescuers exposed to potentially high concentrations of CO should wear self-contained breathing apparatus.
4. Enhanced elimination. Hyperbaric oxygen provides 100% oxygen under 2-3 atm of pressure and can enhance elimination of CO (half-life reduced to 20-30 minutes). In animal models, it reduces lipid peroxidation and neutrophil activation, and in one randomized controlled trial in humans, it reduced the incidence of subtle cognitive sequelae compared with normobaric 100% oxygen, although other similar studies found no benefit. Hyperbaric oxygen may be useful in patients with severe intoxication, especially when there is ready access to a chamber. It remains unclear whether its benefits over normobaric oxygen apply to victims who present many hours after exposure or have milder degrees of intoxication. Consult a regional poison control center (1-800-222-1222) for advice and for the location of nearby hyperbaric chambers. See Table II-19 for a list of proposed indications for hyperbaric oxygen.