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Carboxyhemoglobin 

  • Author: Tany Thaniyavarn, MD; Chief Editor: Eric B Staros, MD  more...
 
Updated: Jan 21, 2014
 

Reference Range

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.

The reference range of COHb differs among smokers and nonsmokers, as follows:

  • Nonsmokers: Up to 3%
  • Smokers: Up to 10%-15%

Individuals with hemolytic anemia and neonates may have COHb levels of up to 5%.[1]

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Interpretation

Carboxyhemoglobin (COHb) is formed by the binding of carbon monoxide to hemoglobin. High COHb levels can be physiologic or pathologic.

Physiologic

COHb levels increase as a result of hemolysis. Carbon monoxide is a natural byproduct of the breakdown of protoporphyrin to bilirubin.[2]

Pathologic

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]

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Collection and Panels

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]

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Background

Description

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]

Indications/Applications

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.

Considerations

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.

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Contributor Information and Disclosures
Author

Tany Thaniyavarn, MD Resident Physician, Department of Internal Medicine, Albert Einstein Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Glenn Eiger, MD Director of Internal Medicine Residency Program, Associate Chairman, Department of Medicine, Albert Einstein Medical Center

Glenn Eiger, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Phi Beta Kappa, Association of Program Directors in Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Wright GR, Shephard RJ. Physiological effects of carbon monoxide. Int Rev Physiol. 1979. 20:311-68. [Medline].

  2. Wu L, Wang R. Carbon monoxide: endogenous production, physiological functions, and pharmacological applications. Pharmacol Rev. 2005 Dec. 57(4):585-630. [Medline].

  3. Austin CC, Ecobichon DJ, Dussault G, Tirado C. Carbon monoxide and water vapor contamination of compressed breathing air for firefighters and divers. J Toxicol Environ Health. 1997 Dec 12. 52(5):403-23. [Medline].

  4. Nager EC, O'Connor RE. Carbon monoxide poisoning from spray paint inhalation. Acad Emerg Med. 1998 Jan. 5(1):84-6. [Medline].

  5. Touger M, Gallagher EJ, Tyrell J. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med. 1995 Apr. 25(4):481-3. [Medline].

  6. Tomaszewski C. Carbon monoxide; Goldfrank’s Toxicologic Emergencies. 9th edition. ISBN 978-0-07-160593-9: Chapter 125.

  7. Zaouter C, Zavorsky GS. The measurement of carboxyhemoglobin and methemoglobin using a non-invasive pulse CO-oximeter. Respir Physiol Neurobiol. 2012 Jul 1. 182(2-3):88-92. [Medline].

  8. Weaver LK, Churchill SK, Deru K, Cooney D. False Positive Rate of Carbon Monoxide Saturation by Pulse Oximetry of Emergency Department Patients. Respir Care. 2012 Jul 10. [Medline].

  9. Coburn RF. Endogenous carbon monoxide production. N Engl J Med. 1970 Jan 22. 282(4):207-9. [Medline].

  10. Caughey WS. Carbon monoxide bonding in hemeproteins. Ann N Y Acad Sci. 1970 Oct 5. 174(1):148-53. [Medline].

  11. Stewart RD. The effect of carbon monoxide on humans. Annu Rev Pharmacol. 1975. 17:409-423.

  12. Hardy KR, Thom SR. Pathophysiology and treatment of carbon monoxide poisoning. J Toxicol Clin Toxicol. 1994. 32(6):613-29. [Medline].

  13. Cobern RF. The carbon monoxide body stores. Ann N Y Acad Sci. 1970. 174:11-22.

  14. Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med. 2009 Mar 19. 360(12):1217-25. [Medline].

  15. Olson KR. Carbon monoxide poisoning: mechanisms, presentation, and controversies in management. J Emerg Med. 1984. 1(3):233-43. [Medline].

  16. Livshits Z, Lugassy DM, Shawn LK, Hoffman RS. Falsely Low Carboxyhemoglobin Level after Hydroxocobalamin Therapy. N Engl J Med. September 2012. 367:1270-1271. [Medline]. [Full Text].

  17. Coburn RF. Enhancement by phenobarbital and diphenylhydantoin of carbon monoxide production in normal man. N Engl J Med. 1970 Sep 3. 283(10):512-5. [Medline].

  18. Delivoria-Papadopoulos M, Coburn RF, Forster RE. Cyclic variation of rate of carbon monoxide production in normal women. J Appl Physiol. 1974 Jan. 36(1):49-51. [Medline].

 
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