Carbon monoxide poisoning may occur in spaces with improper ventilation, even with doors and windows open The classically described cherry red skin color is not sensitive for diagnosis Pao2 and pulse oximetry arterial saturation (Sao2 ) are likely to be normal in carbon monoxide intoxication Current Evidence In the United States about 50,000 ED visits annually are attributed to carbon monoxide poisoning The rate of deaths has declined in recent years to approximately 1,300 deaths per year, with most cases related to house fires Patients exposed to house fire are at a higher risk of associated burns, severe metabolic acidosis, hemodynamic disorders, cyanide toxicity, and inhalation pneumonitis Exposure may occur in a variety of other settings unrelated to accidental fires, including incomplete combustion of any carbon-containing fuel Examples include propane-powered forklifts, gas stoves improperly used to heat residences, gas-powered generators used in a garage, faulty gas-powered hot water heaters or central heating units, improperly vented wood- or coal-burning stoves, and automobile exhaust in garages Poisoning may occur even with doors and windows open Passengers may be poisoned in vehicles or boats with open backs, or with faulty or blocked exhaust systems In the normal person, carboxyhemoglobin levels are less than 1% but may be 2% to 3% in urban dwellers In smokers, levels of 5% to 10% are common Inhaled carbon monoxide has two important effects that cause tissue hypoxia: (i) It binds to hemoglobin with an affinity 200 to 300 times greater than that of oxygen, and (ii) it shifts the oxyhemoglobin dissociation curve to the left and changes the shape from sigmoidal to hyperbolic ( Fig 90.4 ) The first effect decreases oxygen content of the blood, whereas the second only allows oxygen release at lower-than-normal tissue oxygen levels Other endogenous (e.g., anemia) and exogenous (e.g., displacement of ambient oxygen during fires) factors contribute further to hypoxia Although oxygen content of the blood is low, the PaO2 remains normal Because carotid body receptors respond to PaO2 , respiration may not be stimulated until late, when metabolic acidosis activates other centers Tissue hypoxia increases cerebral blood flow, cerebrospinal fluid pressure, and cerebral capillary permeability, which predispose the patient to cerebral edema