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Carbon Monoxide Toxicity

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Other Names

  • Carbon Monoxide Poisoning
  • CO toxicity


  • This page refers to carbon monoxide (CO) toxicity, which can be seen in scuba diving



  • Epidemiology is not well described, limited to case reports
  • In a review of 451 diving fatalities occurring from 1993- 1997 in the Divers Alert Network database, only two that were felt to have been caused by carbon monoxide poisoning[1]


Potential effects of elevated CO at the surface[2]
  • General
    • Colorless, odorless gas which occurs due to incomplete combustion of hydrocarbons
    • Often called the "great mimmicker" because of the varied, nonspecific presentations
    • Uncommon in diving but thought to be under-reported as symptoms mimic decompression sickness and respond to oxygen therapy


Surface equivalent levels at depth[2]
  • Diving
    • Can occur as a result of a faulty air compressor
    • From air contamination by the exhaust of nearby petrol engines.
    • Seen in sport divers and inshore/ inland divers
    • Unlikely to occur in deep offshore divers where air is supplied by decanting mixtures of oxygen and inert gases
    • Symptoms get worse at depth as partial pressure of CO increases
      • Symptoms can be mild or asymptomatic at atmosphere/ surface
      • During descent, symptoms may be rapid and severe
  • Non-diving
    • Most toxic component of smoke inhalation
    • Can be seen in the following:
      • Automotive exhaust
      • Propane-fueled heaters
      • Wood or coal-burning heaters
      • Structure fires
      • Gasoline-powered motors
      • Natural gas-powered heaters
      • Waterpipe/Hookah[3]
      • Methylene chloride (a degreasing solvent found in most paint strippers) fume inhalation


  • Hypoxia
    • Binding affinity of hemoglobin for CO (carboxyhemoglobin) is 200x that of O2
    • Half-Life
    • Room air: ~5hrs
    • 100% O2: ~1hr
    • HBO 2.5atm: 24min
  • Lactic Acidosis
    • CO inhibits oxidative phosphorylation
  • Hypotension
    • CO induces NO2 and guanylate cyclase release → vasodilation release
    • CO binds to myoglobin and alters its function
  • CO Damage at cellular level
    • Due to reactive oxygen species, lipid peroxidation, and cellular apoptosis
    • Occurs in CNS and leads to neurological sequela

Risk Factors

Differential Diagnosis

Differential Diagnosis Dive Medicine

Clinical Features

Symptom[4] %
Headache 85
Dizzy 69
Fatigue 67
Nausea or Vomiting 52
Confusion 37
LOC 35
Dyspnea 7
  • History
    • Wide spectrum of clinical features from flu-like illness to coma
    • CNS: headache, visual disturbances, confusion, ataxia, seizure, syncope, focal deficit, coma
    • Ophtho: retinal hemorrhage
    • GI: Vomiting
    • Pulm: Dypsnea, tachypnea
    • Cardio: Chest pain, dysrhythmias
    • Derm: bullous skin lesions, cherry red oral mucosa
  • Physical Exam
    • Very important to perform a thorough neurological examination
  • Special Tests


  • Diagnosis
    • Requires high level of clinical suspicion
  • Carboxyhemoglobin level
    • Interpretation must take into account time since exposure and O2 treatment
    • Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
    • Symptoms and COhemoglobin levels do not always correlate well
  • Pulse oximetry is unreliable
    • COhemoglobin registers the same as O2hemoglobin so will have artificially high SpO2
    • O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG


  • VBG
    • Check co-oxemtry
    • ABG not necessary
  • Consider
    • Lactate
    • Metabolic panel
    • Troponin
    • Total CK
    • Pregnancy test


  • Co-oximetry
    • Special coixemeter can accurately determine CO level


  • Findings
    • Range from normal to STEMI
    • Most commonly ST-T wave changes and prolonged QTc


  • Head CT
    • Demonstrates findings within 12 hours of exposure
    • Bilateral hypodense lesions in the basal ganglia: globus pallidus, putamen, and caudate nuclei[5]


  • No explicit classification system


  • ABCs
    • In critically ill patient, ABCs must by prioritized
  • Oxygen therapy
    • Provide O2 until COhemoglobin value <10%
    • Positive pressure: Early PEEP prevents progressive atelectasis and improves O2 diffusion
    • In general, COhemoglobin levels fall rapidly to < 10% within 30 min of 100% O2
    • Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic Cometabolism is occuring due to cytochrome oxidase poisoning[6]
      • Anaerobic metabolism universally seen with COhemoglobin > 40%
      • Monitor for return of aerobic metabolism with normal serum bicarbonate levels
  • Disposition
    • Minimal or no symptoms
      • Discharge
    • Mildly symptomatic
      • Symptoms: headache, vomiting, elevated carboxyhemoglobin
      • Monitor for at least 4 hours in ED
    • Severe symptoms
      • Symptoms: ataxia, syncope, chest pain, focal deficit, dypsnea, ECG changes, pregnant
      • Admit, possibly ICU
      • Discuss with hyperbaric specialist

Hyperbaric Oxygen Therapy (HBOT)

  • General
    • Decision to initiate should be made in consultation with specialist
  • Generally accepted indications[7]
    • Syncope
    • Confusion/altered mental status
    • Seizure
    • Coma
    • Focal neuro deficit
    • Pregnancy with Cohemoglobin level >15%
      • Fetal Hb has a higher affinity for CO
    • Blood level >25%
    • Acute myocardial ischemia
    • Prolonged CO exposure with minor clinical findings
  • Controversy regarding benefit
    • Three HBO treatments within 24hrs shown to reduce risk of cognitive sequelae 6 weeks and 12 months after CO poisoning[8]
    • However, another study showed no benefit and suggested worse outcomes in HBO therapy[9]


  • See: Dive Medicine Prevention
  • Preventing carbon monoxide toxicity
    • Test the gas in scuba tanks for CO prior to each dive
    • Fill tank at a reputable dive shop that tests for CO

Rehab and Return to Play


  • No clear rehabilitation guidelines

Return to Play/ Work

  • Needs to be updated

Complications and Prognosis


  • Long term sequalae
    • Can occur days to weeks after apparent resolution in up to 46% of patients (need citation)
    • Cognitive sequalae lasting one month or more appear ot occur in 25-50% of patients with loss of consciousness or CO level > 25%


  • Cognitive
    • Cognitive effects
    • Motor disturbances
    • Ataxia
    • Neuropathies
    • Psychosis
    • Dementia

See Also


  2. 2.0 2.1 Image courtesy of dan.org, "Carbon Monoxide Safety"
  3. Eichhorn, L., Michaelis, D., Kemmerer, M., Jüttner, B., & Tetzlaff, K. (2018). Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study. Clinical Toxicology , 56(4), 264–272
  4. Lavonas EJ. Carbon monoxide poisoning. In: Shannon M, Borron S, Burns M, eds. Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose. Philadelphia, Pa: Elsevier; 2007:1297-1307.
  5. Lee, DC: Hydrocarbons, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 156:p 2035-2038
  6. MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
  7. Practice Recommendations in the Diagnosis, Management and Prevention of Carbon Monoxide Poisoning. Hampson NB et al. Am J Respir Crit Care Med 2012 Oct 18
  8. Weaver, L. et al. Hyperbaric Oxygen For Acute Carbon Monoxide Poisoning. NEJM. 2002:347(14):1057 http://emed.wustl.edu/Portals/2/Answer%20Key%20PDF/2012/January2012/SecondYear.pdf
  9. Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised
Created by:
John Kiel on 11 July 2022 14:02:42
Last edited:
11 July 2022 15:05:13