Carboxyhemoglobin
Updated: Nov 20, 2019
Author: Tany Thaniyavarn, MD; Chief Editor: Eric B Staros, MD
Carboxyhemoglobin (COHb) is a stable complex of carbon monoxide that forms in red blood cells when carbon monoxide is inhaled. COHb should be measured if carbon monoxide or methylene chloride poisoning is suspected. COHb is also useful in monitoring the treatment of carbon monoxide poisoning.
Normal findings for saturation of hemoglobin differ among smokers, nonsmokers, and newborns, as follows[1] :
Possible critical value is >20%.[1]
Carboxyhemoglobin (COHb) is formed by the binding of carbon monoxide to hemoglobin. High COHb levels can be physiologic or pathologic.
COHb levels increase as a result of hemolysis. Carbon monoxide is a natural byproduct of the breakdown of protoporphyrin to bilirubin.[2]
Increases in COHb can be caused by carbon monoxide inhalation or methylene chloride toxicity, either intentional or unintentional.
Carbon monoxide inhalation
Carbon monoxide results from incomplete combustion of hydrocarbons. Carbon monoxide toxicity tends to occur upon exposure to a source of carbon monoxide in a poorly ventilated environment (eg, warehouses, parking garages, ice rinks, other indoor facilities).
Potential sources of carbon monoxide may include motor-vehicle exhaust, ice-resurfacing machines, house fires, fireplaces, wood/charcoal camp stoves/lanterns, cooking ranges, natural gas (eg, methane, propane, kerosene) heaters, furnaces, hot water heaters, gasoline-powered equipment, and propane-powered forklifts. Compressed air for firefighters and divers has been implicated in carbon monoxide poisoning owing to faulty air compressors.[3]
Methylene chloride
Methylene chloride (dichloromethane) is a solvent that can be found in paint removers. The routes of absorption can be dermal, inhalation, or oral ingestion. Methylene chloride is metabolized in the liver to carbon monoxide, which subsequently forms COHb.[4]
The collection sample should be whole blood in an arterial blood gas syringe with lyophilized heparin or a purple- or green-top tube. The sample is then placed on ice.
The sample can be either arterial or venous blood,[5] although arterial blood is preferred for the diagnosis of carbon monoxide poisoning because of its precision in assessment of acidosis, especially lactic acidosis, which affects the assessment of the severity and management of carbon monoxide poisoning. Venous blood can be useful in screening large numbers of patients who may have been exposed to carbon monoxide or to monitor carboxyhemoglobin (COHb) during treatment.
Refrigerated heparinized samples can be used for retrospective evaluations, as COHb levels remain stable for months.[6]
Regular pulse oximetry cannot be used to detect COHb. Multiwavelength pulse oximetry may be a good screening tool for carbon monoxide poisoning in a large number of patients if the carbon monoxide hemoglobin saturation (SpCO) reading is less than 15%.[7] A low SpCO level in patients suspected of having carbon monoxide poisoning cannot be used to rule out carbon monoxide poisoning. In this situation, blood for COHb should always be measured for confirmation. SpCO measurements may not be used interchangeably with standard blood COHb measurements.[8]
Carboxyhemoglobin (COHb) is a stable complex of carbon monoxide that forms in red blood cells when carbon monoxide is inhaled. It is produced from hepatic metabolism of methylene chloride or as a byproduct in the process of hemoglobin degradation.[9]
In normal physiologic states, hemoglobin is metabolized by heme oxygenase into carbon monoxide, ferrous iron, and biliverdin. Heme oxygenase found in the liver and spleen is the major endogenous source of carbon monoxide, which is responsible for a small amount (< 3%) of COHb found in the blood.
Carbon monoxide binds to hemoglobin with 200-250 times greater affinity than oxygen,[10] leading to tissue hypoxia. Carbon monoxide also causes a leftward shift of the oxyhemoglobin dissociation curve, thereby decreasing oxygen release from hemoglobin to target tissues, further exacerbating tissue hypoxia.[11]
Approximately 85% of absorbed carbon monoxide binds with hemoglobin and remains in the intravascular compartment as COHb. The rest of the carbon monoxide is taken up by tissues and primarily bound to myoglobin. To a lesser extent, carbon monoxide can also bind to other molecules such as cytochromes and NADPH reductase. Binding of carbon monoxide to these molecules can disrupt normal physiologic processes, including mitochondrial dysfunction.[12, 13] The brain and the heart are the most commonly affected organs in carbon monoxide poisoning.
Elimination of carbon monoxide occurs predominantly via the pulmonary circulation through competitive binding of hemoglobin by oxygen. The rate of elimination is proportionate to the degree of oxygenation, atmospheric conditions, and minute ventilation.[2]
The half-life of COHb in an individual breathing room air is approximately 300 minutes. This can be decreased to 80 minutes with high-flow oxygen via a nonrebreather mask.[14] With hyperbaric oxygen at 3 times atmospheric pressure, COHb elimination half-life can be reduced even further, to about 20-30 minutes. Apart from decreasing COHb half-life, hyperbaric oxygen may improve tissue oxygenation by bypassing the normal transfer of oxygen through hemoglobin.[15]
The clearance of COHb in methylene chloride poisoning is prolonged. The half-life of COHb in this setting is approximately 13 hours because of ongoing carbon monoxide production from methylene chloride metabolism in the liver. The peak COHb level can be delayed in methylene chloride poisoning.[6]
COHb should be measured if carbon monoxide or methylene chloride poisoning is suspected. COHb is also useful in monitoring the treatment of carbon monoxide poisoning.
COHb levels can be falsely low if the patient receives oxygen prior to the test. For example, a patient who receives oxygen therapy in the ambulance prior to hospital arrival may have normal or lower-than-expected COHb levels despite carbon monoxide poisoning. Although high COHb levels confirm exposure to carbon monoxide, COHb levels are not always predictive of symptoms or outcome.[6]
An antidote for cyanide poisoning, hydroxocobalamin, is usually administered when co-intoxication with carbon monoxide is suspected. The presence of hydroxocobalamin may interfere with the co-oximetry used to detect COHb, causing falsely low COHb.[16]
Phenobarbital, phenytoin, and progesterone enhance carbon monoxide production, which may affect the level of COHb.[17, 18]
Co-intoxication with cyanide should also be considered in cases of carbon monoxide poisoning due to smoke inhalation and exposure to fires.