• gaseous inorganic element


  • essential role in oxidative phosphorylation resulting in energy production in the form of ATP



  • compressed gas cylinders (137 bar @ 15 C)
  • black with white shoulders
  • available in six sizes
  • also available in liquid form (1 volume -> 840 volumes of O2)
  • colourless, odourless, tasteless gas
  • supports combustion

Physical characteristics

  • specific gravity of 1.1
  • critical temperature -118 C
  • critical pressure 51 atm
  • melting point -218 C
  • atomic weight 18


  • titrated to PaO2 and SpO2 via inhalational route; should specify both an upper and lower target
    • e.g. target SaO2 90-94% in a post-cardiac arrest patient


  1. Hypoxia (except histotoxic)
  2. Inadequate oxygen delivery (DO2) (e.g. shock states)
  3. Carbon monoxide poisoning (may promote dissociation of CO bound to haemoglobin)
  4. Pneumothorax and Pneumatosis coli (may reduce volume of trapped gas by denitrogenation)
  5. Decompression sickness (hyperbaric oxygen)
  6. Anaerobic infections (hyperbaric oxygen)
  7. Cluster headaches
  8. Pre-oxygenation for intubation
  9. Prevention of hypoxia during procedural sedation


Cellular injury due to increased ROS (reactive oxygen species)

  • Increased ROS eg superoxide anion, hydroxyl radical, hydrogen peroxide
  • ROS lead to inflammation and secondary tissue injury / apoptosis
  • deplete cellular antioxidant defences
  • react / impair function of intracellular macromolecules
  • cell death


  • pulmonary vasodilation resulting in V/Q mismatch and CO2 retention in COPD
  • Haldane effect leads to decreased affinity of of Hb for CO2 and contributes to CO2 retention in COPD
  • increased mortality in CO2 retainers from high flow O2 compared with titrated O2 in a prehospital RCT
  • increased respiratory rate
  • Denitrogenation of the lungs causing resorption atelectasis
  • Bronchopulmonary dysplasia: neonates
  • >60% O2 causes tracheal irritation, sore throat, substernal pain, pulmonary congestion, decreased VC
  • Dry nose and mouth, increased susceptibility to mucous plugging
  • Increased R to L shunt fraction
  • Accelerated lung injury from bleomycin toxicity and paraquat poisoning
  • Delay recognition of hypoventilation by SpO2 monitoring during sedation (irrelevant if using ETCO2 monitoring)


  • Increased risk of secondary lung infection due to:
    • impaired mucociliary clearance
    • decreased bactericidal capacity of immune cells


  • Increased mortality post-cardiac arrest with hyperoxia (PaO2>300 mmHg)
  • Systemic vasoconstriction leading to increased SVR, increased BP, decreased heart rate and decreased cardiac output
  • Normobaric hyperoxia reduces coronary blood flow by 8 to 29% in normal subjects and in patients with coronary artery disease or chronic heart failure
  • Increased myocardial infarct size (AVOID study, 2015)
  • No reduction in myocardial ischemia in the presence of coronary artery disease unless SpO2 <85-90%
  • Impairs endothelium-mediated vasodilation


  • Acute toxicity with hyperbaric 100% O2 causing altered mood, vertigo, LOC, convulsions
  • Retinopathy of prematurity
  • Hyperoxia decreases cerebral blood flow by 11 to 33% in healthy adults
  • Hyperoxia associated with increased mortality in stroke and TBI


  • Prolonged exposure to 100% O2 impairs erythropoiesis


  • Absorption – freely permeable through normal alveolar tissue
  • Distribution – transported as oxyHb primarily, and a smaller amount is dissolved in blood
  • Metabolism – O2 combined with H+ to form H2O and CO2 (derived from glucose) and produce ATP via the electron transport chain in mitochondria
  • Elimination – CO2 exhaled and water metabolized/ excreted


Oxygen is liberally administered to many critically ill patients, this risks exposing them to supranormal arterial oxygen levels

  • Normobaric hyperoxia only leads to a modest increase in oxygen content (CaO2) when hemoglobin is already saturated (0.03 ml/l per mmHg)
  • Hyperoxia can have adverse effects on the cardiovascular, pulmonary, CNS and immune systems
  • There is likely a U-shaped curve of mortality with PaO2, with increased mortality at the extremes of hypoxia and hyperoxia
  • Mechanisms are uncertain,though many of the harmful effects are hyperoxia may be mediated by reactive oxygen species (ROS) and due to hyperoxia-induced vasoconstriction (direct and indirect)
  • There is evidence from observational data (though it is conflicting in many cases) that hyperoxia is associated with increased mortality in:
    • post-cardiac arrest
    • ischaemic stroke
    • acute coronary syndrome, and
    • traumatic brain injury
  • Optimal PaO2 remains unknown in critical illness, but should be targetted to specific SaO2 range in most cases – targets and the evidence for particular targets is described in the Oxygen Saturation Targets in Critical Care CCC entry

Hyperoxaemia-induced vasoconstriction has been described in most vascular beds

  • examples of affected vascular beds include: brain, cardiac, renal and skeletal muscle (whereas hypoxia causes pulmonary vasoconstriction)
  • Paradoxically, oxygen delivery may be decreased due to hyperoxia-induced vasoconstriction
    • e.g. hyperoxia decreases cerebral blood flow by 11 to 33% and coronary blood flow by 8 to 29%
  • hyperoxia causes systemic vasoconstriction (heart rate slows reflexively and stroke volume is maintained, but cardiac output falls) and may decrease systemic oxygen delivery
    • may decrease levels of vasodilator prostaglandin PGI2
    • hyperoxia may reduce the bioavailability of nitric oxide (inactivated by superoxide)
    • RBCs may sense PO2, modulating ATP release which binds to endothelial P2Y receptors that increase NO production
    • hyperoxia may alter RBC deformability impairing flow through microvascular beds
    • Oxygen is a respiratory stimulant resulting in hyperventilation and hypocapnia that may lead to paradoxical vasoconstriction in C02-sensitive vascular beds (such as the brain)
      • may be mediated by CO2 release from increased haemoglobin oxygenation (‘Haldane effect’)
      • may be mediated by the effects of reactive oxygen species on the brainstem

Hyperoxia causes respiratory failure in CO2-retaining COPD by worsening V/Q mismatch and through the Haldane effect

Take Home Point: Carefully titrate oxygen to the lowest tolerable level to meet the patient’s needs



  • plants and algae contain chlorophyll which uses photoenergy from the sun to convert CO2 to O2

Fractional distillation of air

  • O2 can be obtained from the atmosphere by liquefication and fractional distillation of air
  • liquid air is a mixture of liquid nitrogen (BP -196 C) and liquid O2 (BP – 183 C)
  • nitrogen is more volatile and boils off first during evaporation
  • some of the O2 evaporates with nitrogen, so separation of the two gases is bought about by fractionation: the evolved gas mixture is bubbled through liquid air rich in O2 in a tall rectifying column
  • the O2 in the gas mixture condenses as almost pure nitrogen gas leaves the top of the column leaving almost pure liquid O2, which is then evaporated to give O2 gas
  • O2 gas is distributed as compressed gas in high pressure cylinders

O2 concentrators

  • device for extracting O2 from atmospheric air
  • air passed under pressure through a column of zeolite (molecular sieve), which traps nitrogen and H2O vapour whilst leaving O2 and trace gases
  • nitrogen removed by depressurising the column
  • produces a continuous supply of over 90% O2
  • can range from small (individual) or large (supplying hospitals)

References and Links


Journal articles

  • Bitterman H. Bench-to-bedside review: oxygen as a drug. Critical care (London, England). 13(1):205. 2009. [pubmed]
  • Budinger GR, Mutlu GM. Balancing the risks and benefits of oxygen therapy in critically III adults. Chest. 143(4):1151-62. 2013. [pubmed]
  • Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev. 2013 Aug 21;8:CD007160. doi: 10.1002/14651858.CD007160.pub3. Review. PubMed PMID: 23963794.
  • Cornet AD, Kooter AJ, Peters MJ, Smulders YM. The potential harm of oxygen therapy in medical emergencies. Crit Care. 2013 Apr 18;17(2):313. [Epub ahead of print] PubMed PMID: 23635028; PubMed Central PMCID: PMC3672526.
  • Damiani E, Adrario E, Girardis M. Arterial hyperoxia and mortality in critically ill patients: a systematic review and meta-analysis. Critical care (London, England). 18(6):711. 2014. [pubmed]
  • Helmerhorst HJ, Schultz MJ, van der Voort PH, de Jonge E, van Westerloo DJ. Bench-to-bedside review: the effects of hyperoxia during critical illness. Critical care (London, England). 19(1):284. 2015. [pubmed] [free full text]
  • Helmerhorst HJ, Roos-Blom MJ, van Westerloo DJ, de Jonge E. Association Between Arterial Hyperoxia and Outcome in Subsets of Critical Illness: A Systematic Review, Meta-Analysis, and Meta-Regression of Cohort Studies. Critical care medicine. 43(7):1508-19. 2015. [pubmed]
  • Iscoe S, Beasley R, Fisher JA. Supplementary oxygen for nonhypoxemic patients: O2 much of a good thing? Critical care (London, England). 15(3):305. 2011. [pubmed] [free full text]
  • Iscoe S, Fisher JA. Hyperoxia-induced hypocapnia: an underappreciated risk. Chest. 128(1):430-3. 2005. [pubmed] [free full text]
  • MacIntyre NR. Tissue hypoxia: implications for the respiratory clinician. Respiratory care. 59(10):1590-6. 2014. [pubmed]
  • Sjöberg F, Singer M. The medical use of oxygen: a time for critical reappraisal. J Intern Med. 2013 Dec;274(6):505-28. doi: 10.1111/joim.12139. Review. PubMed PMID: 24206183. [Free Full Text]
  • Stub D, Smith K, Bernard S, et al. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation. 131(24):2143-50. 2015. [pubmed]
  • Wang CH, Chang WT, Huang CH. The effect of hyperoxia on survival following adult cardiac arrest: a systematic review and meta-analysis of observational studies. Resuscitation. 85(9):1142-8. 2014. [pubmed]

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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