• Oxygen is a treatment for hypoxaemia and has not been shown to have any effect on breathlessness in non-hypoxaemic patients.


  • Oxygen should be titrated to achieve oxygen saturations of between 94 – 98%, (or 88 – 92% for COPD patients). These are achieved through the use of different flow rates and oxygen masks.


  • All paediatric patients with significant illness or injury should receive oxygen. Newborn resuscitation should ideally be commenced with room air for the first couple of breaths.
  • Explosive or flammable environments
  • Normoxia
Precautions / Notes
  • If the target saturations cannot be maintained with the nasal cannula or medium concentration mask then change to a non-rebreather oxygen mask.
  • Oxygen increases the toxicity in paraquat poisoning, target saturations of 88–92%.
  • Remember that some conditions can affect SpO2 readings e.g. carbon monoxide poisoning and cold digits
  • Aim for target saturations of between 94 – 98% for critical conditions requiring supplemental oxygen, maintained via bag-valve-mask or reservoir bag.
  • In patients with COPD or other conditions requiring controlled or low-dose supplemental oxygen aim for target oxygen saturations range of 88 – 92% (or the patient’s prescribed range).
  • If the patient is hypoxaemic, oxygen saturations of between 94 – 98% should be maintained through the use of a mask or nasal cannulae as appropriate.

At the correct flow rate the following devices will deliver the following approximate FiO2:

MaskFraction of Inspired O2 (FiO2)Flow-rate
Nasal cannulae 24 - 35%1 - 4 litres per minute
Simple face mask 40 - 60%5 - 8 litres per minute
Non-rebreather mask 60 - 100%10 - 15 litres per minute
Bag-valve-mask 100%15 litres per minute


Special Considerations
  • Patients with acute episodes of COPD are at risk of developing carbon dioxide retention if they are given excessive supplemental oxygen. This can cause acidosis and subsequent organ dysfunction.
  • High oxygen concentrations can lead to increased production of reactive free radicals resulting in cellular damage. This may be responsible for the detrimental effects observed with the use of high flow oxygen in myocardial infarction and stroke.


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