Carbon monoxide (CO) is an odorless, colorless gas that is produced when carbon containing materials ae burned such as gasoline, wood, oil, and natural gas.  The amount of oxygen present at the time of burning determines how much CO versus Carbon dioxide is produced.  Most individuals have low levels of CO in their blood and the levels are increased in smokers to about 15%.  Most deaths due to Co poisoning are secondary to automobile exhaust either accidentally or by suicide.  Lethal levels of CO may be reached in 10 minutes in an unventilated garage. 

Pathophysiology 
1. CO has an affinity for hemoglobin that is 250 times greater than oxygen.  It shifts the oxygen saturation curve to the left and oxygen is only released at low O2 tensions.  This results in a "functional" anemia. 
2. The CO dissolved in plasma has toxicity 
3. CO binds to other heme compounds such as myoglobin, catalases, cytochrome systems, and oxidases. 
4. Toxicity is secondary to hypoxia, reoxygenation toxicity, a d oxygen radical formation. 
5. Fetus' have an increased risk of toxicity because the oxygen saturation curve is already shifted to the left of the mother's curve. 

Clinical Symptoms 
1. The presentation may be similar to a viral illness and because the incidence is the highest in the winter, the diagnosis may be missed. 
2. Tachypnea, shortness of breath, fatigue, headache, dizziness, nausea, confusion, tinnatus, decreased hearing, visual changes, difficulty in thinking, and loss of consciousness. 
3.May have erythema of the skin 
4. Levels greater than 10% usually produce symptoms 
5. There may be delayed neurologic symptoms with personality and mental changes occurring weeks later 

Diagnosis 
1. History of exposure combined with physical findings 
2. Increased levels of carboxyhemoglobin (COHb) on a venous or arterial sample.  Levels in the blood do not always correlate with symptoms,  Levels may have fallen by the time that they are checked.  It is important to check the environmental levels at the site of exposure. 
3. Pulse oximetry will no be helpful in distinguishing COHb from normal saturation with oxygen 
4. CT scan will not be helpful but will rule out others neurologic causes for the symptoms. 

Treatment 
1. Remove the patient from the source of carbon monoxide 
2. Administer 100% oxygen to decrease the half-life of COHb 
   a. competes for hemoglobin sites 
   b. Improves the delivery of oxygen to the tissues 
3. Treat any related injuries such as burns or smoke inhalation 
4. Hyperbaric oxygen should be used if; 
   a. The patient is comatose of history of LOC 
   b. COHb levels greater than 40% 
   c. Pregnant woman and level greater than 15% 
   d. Cardiac arrhthymias or ischemia 

Prevention 
1. Public awareness and education concerning CO poisoning 
2. Proper maintenance of heating systems 
3. Make sure that exhaust system are free from obstruction.  Cars systems may be blocked by snow or leaves 
4. CO detectors in the home and at offices 

References 
1. Ernst, Armin and Zibrak, Joseph.  Carbon Monoxide Poisoning.  NEJM Vol. 339, No.22. Nov 26, 1998 
2. Conway, Edward Jr. Carbon Monoxide Poisoning.  Pediatrics in Review.  Vol 13. No. 1 Jan. 1992