4.7 Review

Dangers of hyperoxia

Journal

CRITICAL CARE
Volume 25, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s13054-021-03815-y

Keywords

Hyperoxia; Hyperoxaemia; Reactive oxygen species; Reactive nitrogen species; ARDS; Sepsis; Trauma-and-haemorrhage; Traumatic brain injury; Subarachnoidal bleeding; Acute ischaemic stroke; Intracranial bleeding; Cardiopulmonary resuscitation; Myocardial infarction; Surgical site infection

Funding

  1. Projekt DEAL
  2. Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [251293561, CRC 1149]
  3. Health Research Council of New Zealand Clinical Practitioner Research Fellowship
  4. Health Research Council of New Zealand

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Oxygen toxicity is mainly related to the excessive production of reactive oxygen species, supplemental oxygen may cause hyperoxemia and hyperoxia which should be avoided, titrating oxygen to maintain PaO2 within the normal range is advisable to prevent deleterious side effects.
Oxygen (O-2) toxicity remains a concern, particularly to the lung. This is mainly related to excessive production of reactive oxygen species (ROS). Supplemental O-2, i.e. inspiratory O-2 concentrations (FIO2) > 0.21 may cause hyperoxaemia (i.e. arterial (a) PO2 > 100 mmHg) and, subsequently, hyperoxia (increased tissue O-2 concentration), thereby enhancing ROS formation. Here, we review the pathophysiology of O-2 toxicity and the potential harms of supplemental O-2 in various ICU conditions. The current evidence base suggests that PaO2 > 300 mmHg (40 kPa) should be avoided, but it remains uncertain whether there is an optimal level which may vary for given clinical conditions. Since even moderately supra-physiological PaO2 may be associated with deleterious side effects, it seems advisable at present to titrate O-2 to maintain PaO2 within the normal range, avoiding both hypoxaemia and excess hyperoxaemia.

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