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Carbon monoxide poisoning

Author: Gus Mitchell, Science Writer, Wellington. DermNet New Zealand Editor in Chief: Hon A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy editor: Maria McGivern. March 2017.


What is carbon monoxide poisoning?

Carbon monoxide (chemical formula: CO) is an odourless, colourless gas produced from the incomplete combustion of hydrocarbons in propane and gasoline. Carbon monoxide poisoning (CO poisoning) is caused by the inhalation or absorption of carbon monoxide from the exhaust of gasoline- or propane-powered appliances or cigarette smoke.

Who gets carbon monoxide poisoning?

The level of carbon monoxide concentration in the body is measured by the concentration of carboxyhaemoglobin (COHb) in the bloodstream. A normal carboxyhaemoglobin concentration for non-smokers is 1–3%, but it can reach levels of up to 15% in chronic smokers. Symptoms of carbon monoxide poisoning occur at carboxyhaemoglobin levels of between 10% and 30% [1].

The main sources of carbon monoxide are [2]:

  • Tobacco smoke
  • Automotive fumes
  • Malfunctioning or poorly installed gas cookers
  • Propane- or gasoline-fuelled compressors
  • Smoke from house fires
  • Methyl chloride from paint strippers [3].

Poisoning occurs through the inhalation of carbon monoxide or absorption through the skin. Most cases of carbon monoxide poisoning occur in enclosed, poorly ventilated areas, which increase the likelihood of inhalation.

What causes carbon monoxide poisoning?

When carbon monoxide enters the bloodstream, it binds to the mitochondrial membrane of red cells. As mitochondria produce energy within the cell, carbon monoxide inhibits the cells’ ability to take up oxygen. It changes the structure of the haemoglobin in the red cell to make it bind more tightly to oxygen. This traps oxygen on the surface of the cells, preventing the distribution of oxygen to the tissues, and metabolising the carbon monoxide into carboxyhaemoglobin.

This process starves the body's tissues of oxygen, causing hypoxia and chemical asphyxiation, where the patient does not receive enough oxygen to their tissues and organs on a cellular level, but does not present any physical signs of asphyxiation [1].

What are the clinical features of carbon monoxide poisoning?

Mild effects of carbon monoxide poisoning include [2]:

  • Headache
  • Nausea
  • Fatigue
  • Vomiting
  • Chest pains.

Severe symptoms of carbon monoxide poisoning, occurring after long or extreme exposure to the gas, include:

  • Respiratory failure
  • Cardiac arrhythmia
  • Angina
  • Impaired memory
  • Loss of consciousness.

Victims of carbon monoxide poisoning may have continued neurological aftereffects and psychomotor impairments, even long after treatment [2]. Depending on the concentration and length of exposure, symptoms can include:

  • Hypotension
  • Impaired memory
  • Personality change
  • Delayed psychomotor response
  • Parkinson disease-like symptoms
  • Seizures
  • Coma or semi-coma.

Cutaneous features

Severe carbon monoxide poisoning can cause the skin to turn a cherry-red colour.

In some cases, carbon monoxide poisoning can cause erythema, blistering and necrotic skin lesions on the hands, legs, back and ankles. These lesions are often misdiagnosed as burns from the source of the gas, but can be caused by muscle necrosis resulting from hypoxia [5].

How is carbon monoxide poisoning diagnosed?

The severity of the symptoms of carbon monoxide poisoning is dependent on a number of factors, such as [3]:

  • Duration of exposure to the gas source
  • Concentration of carbon monoxide upon exposure
  • The metabolic rate of the patient
  • Time elapsed after exposure
  • Response to oxygen therapy treatment.

Beyond the varied physical symptoms, carbon monoxide poisoning can prove difficult to diagnose. As oxygen binds tightly to carboxyhaemoglobin, carboxyhaemoglobin may be misread as oxyhaemoglobin when examined under arterial blood gas analysis and pulse oximetry (a measurement of arterial oxygen saturation). This gives a false reading of oxygen content in the blood [3].

Direct oximetry using a spectrophotometer (a device that measures the amount of light absorbed by a substance — in this case, oxygen) is the best diagnostic test of oxygen saturation in plasma, and should be used as soon as possible in order to begin treatment [3,6]. Direct oximetry will often show the oxygen saturation to be much lower than it would appear through pulse oximetry, and this gap in saturation between the two tests is a typical indicator of carbon monoxide poisoning [3].

What is the differential diagnosis for carbon monoxide poisoning?

Skin lesions resulting from hypoxia can be mistaken for burns from the source of the gas, such as fires and malfunctioning heating systems [5].

Existing metabolic conditions, such as diabetes and uraemia (the accumulation in the blood of nitrogenous waste products [urea] in kidney disease or due to dehydration), may present with similar symptoms such as fatigue. These disease should not exclude a diagnosis of carbon monoxide poisoning [6].

What is the treatment for carbon monoxide poisoning?

A patient diagnosed with carbon monoxide poisoning should begin a treatment of 100% oxygen for at least 6 hours [1]. This is intended to lower the half-life of carboxyhaemoglobin, which is 4–6 hours, and provide oxygen to tissues that are underoxygenated [1,6].

In cases of severe poisoning where the patient has seizures, periods of unconsciousness or coma, treatment in a hyperbaric oxygen chamber is advised and should be started as soon as poisoning is suspected [1,6]. Hyperbaric oxygen therapy involves the inhalation of 100% oxygen in a total body chamber, where atmospheric pressure is increased and controlled. The recommended regime for carbon monoxide poisoning is 100% oxygen for 90–120 minutes at 2–3 atmospheres pressure, followed by 4 hours of 100% oxygen therapy [6].

To aid recovery and prevent further poisoning to the patient and others, the source of the carbon monoxide should be identified and repaired or removed.

What is the outcome for carbon monoxide poisoning?

If treated effectively and if the poisoning is not extreme, affected individuals will return to good health.

In cases of severe poisoning, the patient may experience delayed neurological and psychomotor symptoms, such as personality changes, disorientation and gait disturbances, loss of memory, and seizures. Neurological recovery should be monitored after treatment in addition to carboxyhaemoglobin blood saturation [2].

Prevention of carbon monoxide poisoning

Identify any potential source of carbon monoxide poisoning in your home or workplace, such as stoves, gas heaters or automotive exhaust, and ensure they are functioning and have had a recent maintenance check.  

If you work in a kitchen, ensure all gas appliances are working correctly and that the kitchen area is well ventilated. This is as simple as ensuring a window is open during work hours to allow air to circulate. A malfunctioning gas stove can produce five times more carbon monoxide than a functioning one. A malfunction is indicated by the production of a blue flame when operating instead of a consistent orange flame1. Consult the maintenance schedule on all gas appliances and ventilation hoods and update them if need be.

If you smoke or are frequently exposed to second-hand smoke and begin to experience any of the listed symptoms (nausea, headaches, shortness of breath), consult with your doctor. If you wish to quit smoking, in New Zealand call Quitline on 0800 778 778.

If you recently been in a house fire or exposed to open flame for extended periods and begin to experience any of the listed symptoms, see your doctor immediately.



  1. Jor HM, Dalton HR. Headache and drowsiness in a 22 year old student. BMJ 2008; 337: a1481. DOI: 10.1136/bmj.a1481. Journal
  2. Hardy KR, Thom SR. Pathophysiology and treatment of carbon monoxide poisoning. J Toxicol Clin Toxicol 1994; 32: 613–29. PubMed
  3. Doherty S. History, pathophysiology, clinical presentation and role of hyperbaric oxygen in acute carbon monoxide poisoning. Emerg Med Australas 2000; 12: 55–61. DOI: 10.1046/j.1442-2026.2000.00085.x. Journal
  4. Goldstein M. Carbon monoxide poisoning. J Emerg Nurs 2008; 34: 538–42. DOI: 10.1016/j.jen.2007.11.014. Journal abstract
  5. Myers RAM, Snyder SK, Majerus TC. Cutaneous blisters and carbon monoxide poisoning. Ann Emerg Med 1985; 14: 603–606. Article
  6. Balzan MV, Agius G, Debono AG. Carbon monoxide poisoning: easy to treat but difficult to recognise. Postgrad Med J 1996; 72: 470–3. Article

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