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. 2021 Dec 19;25:440. doi: 10.1186/s13054-021-03815-y

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Potential harm of hyperoxia. AIS acute ischaemic stroke; MI myocardial infarction; ARDS acute respiratory distress syndrome; F_IO₂ 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 F_IO₂ > 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]