I. Pathophysiology

  1. Carbon monoxide (CO) is colorless and odorless produced by combusion of hydrocarbons, particularly petroleum-derived
  2. CO has higher affinity for hemoglobin than O2, so displaces O2 from hemoglobin molecules

II. Clinical Features

  1. With mild exposure:
    1. Headache
    2. Dizziness
    3. Nausea and vomiting
    4. Bright ("cherry") red discoloration of mucus membranes and skin (rare)
  2. With moderate-to-severe exposure
    1. Dyspnea
    2. Hypotension
    3. Cardiac dysrhythmias
    4. Seizures
    5. Altered mental status and coma
  3. Late effects
    1. Memory loss
    2. Chronic headaches
    3. Cerebellar dysfunction
    4. Parkinsonism

III. Diagnosis

  1. Carboxyhemoglobin levels (correlate poorly with symptoms)-Normal level in nonsmokers is 0.5-2.0% and 10-12% in smokers
  2. Note-arterial blood gas and pulse oximetry findings may be normal

IV. Management

  1. Remove from source of CO
  2. Supplemental 100% O2
  3. ECG and cardiac enzymes to assess for cardiac toxicity
  4. CXR to assess for pulmonary toxicity
  5. Consider brain imaging for infarction (esp. in globus pallidus) if neurologic abnormalities are present
  6. Hyperbaric O2 ASAP for high-risk patients, e.g.  with evidence of moderate-to-severe exposure

(Sources include Core Content Review of Family Medicine, 2012)