Carbon Monoxide Poisoning
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Carbon Monoxide (CO) poisoning, also known as the “silent killer” can be a life-threatening situation. CO is an odourless, colourless gas (hence ‘silent’).

CO binds to haemoglobin (carboxyhemoglobin) with 240x greater affinity than oxygen.

Common clinical scenarios where CO poisoning alarm bells should start ringing include all patients involved in fire-related injuries, due to the risk of inhalation, as well as the typical story of the “family who are all feeling unwell, apart from Mum who has just gone to spend the weekend away with her parents”.

Carbon monoxide molecule
Carbon monoxide molecule


Intentional: CO poisoning may occur as a result of intentional suicidal poisoning, e.g. exposure to car exhaust fumes in a garage
Accidental: patients involved in fires (acute presentation), patients with unknown gas leaks at home (subacute presentation)

Signs and Symptoms

Symptoms: Headache, nausea and vomiting, malaise, lethargy, arrhythmia, deceased level of consciousness
Signs: very often, patients with CO poisoning will have no overt clinical signs but may be hypotensive. Oxygen saturations will be deceptively high – sats monitors cannot differentiate between oxyhemoglobin and carboxyhemoglobin. [The notion of “cherry red lips” common amongst medical students is an erroneous one – it is a rare and very late stage sign, so is of very little use clinically!]

Assessing neurological affects may be difficcult in the suicidal patient.


CO has a high affinity for haem proteins and so CO binds to haemoglobin with great ease – around 240x more effectively than oxygen – preventing oxygen from binding to the Hb, shifting the oxyhaemoglobin dissociation curve to the left and reducing the amount of oxygen accessible to cells and tissues.

CO can also bind to other tissues – such as myglobin.

CO causes its neurological effects likely to due hypoxia. It can also caused delayed neurological effects (sometimes referred to as Delayed Neurological Sequelae – DNS) through a poorly understood mechanism.

CO also has cardiac effects. About 30% of patients with moderate to severe CO poisoning will have ECG changes or raised cardiac markers (e.g. raised troponin). This causes increased mortality in both he short and long term. One study[i] of patients with moderate or severe CO poisoning found ECG changes or raised cardiac markers in 1/3 of cases. Mortality at 7.6 years for patients with evidence of myocardial injury was 24% – estimated to be 3x greater than background rate.

[i] Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. Satran D, Henry CR, Adkinson C, Nicholson CI, Bracha Y, Henry TD. J Am Coll Cardiol. 2005;45(9):1513.


ABG: COHb – >30% is considered serious; bear in mind that levels of up to 15% may be normal in heavy smokers (non smokers should have a level <3%. Patients may have a metabolic acidosis on ABG too.
ECG should be performed to exclude any arrhythmias/cardiac ischaemia


Clinical presentations can vary widely, are often non-specific and don’t always directly correlate with the CO concentration. Typical presenting features include headache, malaise, nausea, dizziness.

Assessing cognitive function and conscious level is the most important part of the examination.

Textbook signs – such as cherry red lips – are rare and not sensitive.

  • Use a systematic approach – e.g. ABCD
  • Patients should be started on 15L/min O2 (humidified) by tight fitting mask and reservoir for >24 hours – regardless of O2 saturations!
  • Hyperbaric O2 should be considered in patients with neurological impairment or very high HBCO (although the evidence of this is debatable). See below for more info.
  • Sats or not reliable as they can’t differentiate oxyhaemoglobin from carboxyhaemoglobin
  • All patients should have ECG, and consider cardiac markers to screen for myocardial involvement if there are ECG changes or a history of cardiac disease
  • Diagnosis is based on COHb level on a blood gas in combination with history. COHb levels do NOT correlate with the degree of poisoning and correlate poorly with DNS and myocardial injury. Blood gas is also useful to assess acidosis
  • Consider CT brain to screen for other causes of neurological impairment
  • Consider intubation in patients with low GCS – and use 100% to ventilate

Defining the severity of CO poisoning and the threshold for Hyperbaric O2 is not straightforward.  There are multiple sets of guidelines with differing criteria. For example, the suggest HBO2 at which hyperbaric oxygen should be given ranged from >25 to >40. There is also debate about the most appropriate pressure at which to give therapy (2.0-3.0 atmospheres).

Uptodate suggests HBO2 for:

  • COHb >25% (20% if pregnant)
  • Loss of consciousness
  • pH <7.1
  • Signs of end organ ischaemia (ECG changes, chest pain, reduced GCS)

To reduce the risk of DNS HBO2 should be given within 6 hours of exposure. Several large studies on the effectiveness of HBO2 therapy have conflicting and inconclusive evidence. Some have shown some benefit at reducing neurological sequlae in the long term, some showed worse outcomes, and some showed no difference.

There is also a newer technique – isocapnic hyperpnea. Using this technique, patients are hyperventilated with a mixture of O2 and CO2 on a ventilator. Because the relationship between CO binding is related to minute volume, it is possible to reduce the CO concentration as quickly as HBO2 using this method (half live can be decreased to about 30 minutes). However, there are as yet no studies demonstrating any benefit to outcomes using this technique.

The half-life of CO whilst breathing room air is about 300 minutes, on high flow oxygen, about 90 minutes, and whilst breathing hyperbaric oxygen is about 30 minutes

After recovery from the acute effects of CO poisoning, those with intentional CO poisoning need appropriate psychiatric follow-up before being discharged.


Cerebral oedema, pulmonary oedema, MI, arrhythmia, barotrauma secondary to hyperbaric O2 therapy [creation of a pressure gradient across tympanic membrane, followed by haemorrhage/serious effusion]

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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