Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Dec 19;25(1):440.
doi: 10.1186/s13054-021-03815-y.

Dangers of hyperoxia

Mervyn Singer  1 , Paul J Young  2   3 , John G Laffey  4 , Pierre Asfar  5 , Fabio Silvio Taccone  6 , Markus B Skrifvars  7 , Christian S Meyhoff  8 , Peter Radermacher  9
Affiliations
Review

Dangers of hyperoxia

Mervyn Singer et al. Crit Care. .

Abstract

Oxygen (O2) toxicity remains a concern, particularly to the lung. This is mainly related to excessive production of reactive oxygen species (ROS). Supplemental O2, i.e. inspiratory O2 concentrations (FIO2) > 0.21 may cause hyperoxaemia (i.e. arterial (a) PO2 > 100 mmHg) and, subsequently, hyperoxia (increased tissue O2 concentration), thereby enhancing ROS formation. Here, we review the pathophysiology of O2 toxicity and the potential harms of supplemental O2 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 O2 to maintain PaO2 within the normal range, avoiding both hypoxaemia and excess hyperoxaemia.

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

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no competing interests..

Figures

Fig. 1
Fig. 1
Potential harm of hyperoxia. AIS acute ischaemic stroke; MI myocardial infarction; ARDS acute respiratory distress syndrome; FIO2 fraction of inspired O2; HPV hypoxic pulmonary vasoconstriction; ICB intracranial bleeding; PaO2 arterial O2 partial pressure; NO nitric oxide; ONOO‒ peroxynitrite; O2•‒ superoxide anion; ROS reactive oxygen species; SAB subarachnoidal bleeding; TBI traumatic brain injury. * Note that while hyperoxia and hyperoxaemia are well defined as FIO2 > 0.21 and PaO2 > 100 mmHg, respectively, there is no general threshold for “tissue hyperoxia”, because the normal tissue PO2 depends on the macro- and microcirculatory perfusion and the respective metabolic activity. Nevertheless, it is noteworthy that PO2 levels as low as 0.3 – 0.7 mmHg suffice for correct functioning of the mitochondrial respiratory chain [17, 162]
See this image and copyright information in PMC

References

    1. West JB. Carl Wilhelm Scheele, the discoverer of oxygen, and a very productive chemist. Am J Physiol Lung Cell Mol Physiol. 2014;307(11):L811–L816. - PubMed
    1. West JB. Joseph Priestley, oxygen, and the enlightenment. Am J Physiol Lung Cell Mol Physiol. 2014;306(2):L111–L119. - PubMed
    1. West JB. The collaboration of Antoine and Marie-Anne Lavoisier and the first measurements of human oxygen consumption. Am J Physiol Lung Cell Mol Physiol. 2013;305(11):L775–L785. - PubMed
    1. Leverve XM. To cope with oxygen: a long and still tumultuous story for life. Crit Care Med. 2008;36(2):637–638. - PubMed
    1. Asfar P, Singer M, Radermacher P. Understanding the benefits and harms of oxygen therapy. Intensive Care Med. 2015;41(6):1118–1121. - PubMed