Carbon Monoxide
GENERAL PRINCIPLES
Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that is produced during incomplete combustion of carbon-containing fuels.
Common sources of exposure include smoke inhalation in house fires, malfunctioning heaters and electric generators, automobile exhaust, smoking, forklifts, and chemicals such as methylene chloride.
Pathophysiology
CO binds with hemoglobin to form carboxyhemoglobin, which causes a functional anemia and shifts the oxyhemoglobin dissociation curve to the left.
CO inhibits cellular respiration by binding to mitochondrial cytochrome oxidase and disrupting the electron transport chain.
CO poisoning also increases nitric oxide levels, producing vasodilation.
DIAGNOSIS
Clinical Presentation
The diagnosis of CO poisoning is challenging because of its many vague signs and symptoms that can wax and wane depending on the patient's source of exposure.
Patients with mild poisoning may present with flu-like symptoms, which include headache, myalgias, fatigue, lethargy, nausea, vomiting, and dizziness. If these patients remove themselves from the exposure, such as when they leave their house to seek medical attention, the symptoms may improve before they are evaluated by a physician.
Patients with more severe poisoning present with symptoms of end-organ damage, which are predominantly cardiac or neurologic.
These may include chest pain, myocardial infarctions, cardiac dysrhythmias, syncope, stroke-like symptoms, seizures, coma, and other psychoneurological symptoms.
Patients may present late after significant exposure with delayed neurologic sequelae (DNS), which can occur anywhere between 2 and 40 days after the exposure.
Have a low threshold to consider CO poisoning during the winter months (when patients may be exposed to malfunctioning heating systems) and in groups of patients living or working in the same environment who present with similar symptoms.
Diagnostic Testing
LABORATORIES
Carboxyhemoglobin (CO-Hgb) levels are readily available.
They can be obtained on either arterial or VBG specimens.๎ CO-Hgb levels greater than 5% generally indicate an exogenous CO exposure.
๎ Levels do not always correlate well with a patient's symptoms or prognosis.
Standard pulse oximeters may be falsely reassuring because they cannot detect a difference between oxyhemoglobin and CO-Hgb.
๎ Specialized handheld pulse co-oximeters can be used to noninvasively measure CO-Hgb; they are accurate in ruling out significant CO poisoning, but elevated values should generally be confirmed with blood gas testing.
Metabolic acidosis and elevated lactate concentrations may suggest CO poisoning in the right clinical context but are not specific for this toxin.
ELECTROCARDIOGRAPHY
Obtain an ECG in any patient with known or suspected CO poisoning who has chest pain, tachycardia, palpitations, syncope, shock, coma, seizures, or neurologic deficits.
ECG may demonstrate evidence of myocardial ischemia.
TREATMENT
The mainstay of treatment is the administration of oxygen, which enhances the elimination of CO. Administration of 100% oxygen by nonrebreather face mask decreased the half-life of CO to about 60ญ90 minutes.
The use of hyperbaric oxygen (HBO) therapy in CO poisoning is controversial. 33 The theoretical indication for HBO is to prevent DNS, not to facilitate more rapid CO elimination. Consider for endญorgan dysfunction such as syncope, coma, CO-Hgb gt;25%, or in pregnancy.
Additional care includes airway and ventilatory support, vasopressors for hypotension, and treatment of any concurrent injury or poisoning, such as if the patient has a burn, trauma, or cyanide toxicity from a house fire.