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Background
Carboxyhemoglobin (COHb) is a stable carbon monoxide compound. It develops in red blood cells after inhaling the carbon monoxide (CO). It is formed by the byproduct of the degradation of hemoglobin or the hepatic mechanism of methylene chloride.
Heme oxygenase metabolized hemoglobin into ferrous iron, carbon monoxide, and biliverdin in a normal physiological states. Heme oxygenase is found in the spleen and liver. It is a primary endogenous source of CO. It generates small amounts of COHb, about less than 3% which is found in the blood.
CO binds to Hb with 200 to 250 times high affinity than the oxygen. It leads to tissue hypoxia. CO can induce a leftward shift to oxyhemoglobin dissociation curve. It decreases the oxygen release from Hb to the target tissue and increases the tissue hypoxia.
About 85% of the absorbed CO binds to the hemoglobin and other stores in the intravascular compartment as COHb. The rest of the CO is absorbed by tissue and binds to myoglobin. CO can bind to the cytochromes and NADPH reductase to a lesser extent. CO to these compounds may affect the normal physiological processes, including the dysfunction of mitochondria. The heart and brain are the most affected organs by CO poisoning.
CO is mostly eliminated by pulmonary circulation because of the intense binding of hemoglobin to oxygen. The rate of elimination is proportional to the degree of oxygenation, minute ventilation, and atmospheric conditions.
The half life of COHb is around 300 minutes in individual breathing room air. It is reduced to 80 minutes with high flow of oxygen by a non-rebreather mask. COHb elimination half life may be reduced to 20 to 30 minutes by using the hyperbaric oxygen at three times of atmospheric pressure. Hyperbaric oxygen can also improve the oxygenation of tissue by bypassing the normal oxygen transfer by hemoglobin.
COHb clearance is prolonged in cases of methylene chloride poisoning. The COHb half life goes about 13 hours due to ongoing production of CO from metabolism of methylene chloride in the liver. Methylene chloride poisoning may cause the delay in reaching the peak level of COHb.
Indications/Applications
COHb level is measured if the CO or methylene chloride poisoning appeared. COHb is useful to monitor the treatment of CO poisoning.
Clinical Significance:
COHb levels may be falsely reduced if the patient receives the oxygen before the test. If the patient receives the oxygen treatment in the ambulance before the arrival to the hospital can have a lower than expected or normal level of COHb despite having the CO poisoning. High level of COHb indicate the exposure to the CO. COHb level is not always predict the symptoms or results.
Hydroxocobalamin is an antidote for cyanide poisoning. It is administered when the intoxication with CO appeared. Hydroxocobalamin can interfere with the co-oximetry which is used to detect the COHb. This can lead to falsely reduced levels of COHb.
Phenytoin, progesterone, and phenobarbital increase the production of CO which can affect the COHb level. Co-intoxication with cyanide must be considered in cases of CO poisoning because of the inhalation of smoke and fire exposure.
Reference Range
The normal level of hemoglobin saturation differs between nonsmokers, smokers, and newborns.
Nonsmokers: Less than 3%
Smokers: Less than or equal to 12%
Newborns: Greater than or equal to 12%
The critical level of COHb is greater than 20%
Interpretation
Increased levels of COHb may be pathological or physiological.
Pathological
Increased level of COHb may be occurred by inhalation of CO or toxicity of methylene chloride either unintentionally or intentionally.
Inhalation of CO
CO forms from incomplete hydrocarbon combustion. Toxicity of CO occurs when the source of CO is poorly exposed to the ventilated environment like parking garages, warehouses, other indoor facilities, and ice rinks.
CO sources may include the ice-resurfacing machines, motor-vehicle exhaust, fireplaces, house fires, wood or charcoal camp stoves or lanterns, natural gas like propane, kerosene, methane, cooking ranges, heaters, hot water heaters, furnaces, propane powered forklifts, and gasoline powered equipment. Compressed air for firemen and divers has been linked to poisoning of CO because of the defective air compressors.
Toxicity of methylene chloride
Methylene chloride or dichloromethane is a solvent. It found in the paint removers. It can be absorbed by inhalation, oral ingestion, or dermal. Methylene chloride is transformed to CO in the liver and generates COHb.
Physiological
COHb level elevates in hemolysis. CO is a natural byproduct of the metabolism of protoporphyrin to bilirubin.
Collection And Panels
Sample type: Whole blood
Sample collection container: Purple or green top tube or arterial blood gas syringe with lyophilized heparin
Sample collection method: Arterial or venous blood
Arterial blood is used to diagnose the CO poisoning because of the accuracy in acidosis assessment and, specifically, lactic acidosis. It influences the severity and treatment of CO poisoning. Venous blood is used in large screening number of patients who have been exposed to CO or to monito the treatment of COHb.
Sample storage: Samples can be stored in refrigerator.
Refrigerated heparinized sample can be used in the evaluation of retrospective because COHb level remains stable for month.
Methods used for test: Regular pulse oximetry is not used to detect COHb. Multiwavelength pulse oximetry can be used to detect CO poisoning in many patients if the carbon monoxide hemoglobin saturation (SpCO) results are below 15%. Low level of SpCO in patients with CO poisoning may not be used to exclude the poisoning of CO. In such a case, the COHb level must be confirmed with the blood. COHb measurement and SpCO measurement cannot be used interchangeably.
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