Dangers of hyperoxia

Critical Care

Mervyn Singer¹  John G. Laffey²  Christian S. Meyhoff³  Markus B. Skrifvars⁴  Fabio Silvio Taccone⁵  Pierre Asfar⁶  Peter Radermacher⁷  Paul J. Young⁸ 

[1] Bloomsbury Institute of Intensive Care Medicine, Division of Medicine, University College London, London, UK;Department of Anaesthesia and Intensive Care Medicine, Galway University Hospitals, and School of Medicine, National University of Ireland, Galway, Ireland;Department of Anaesthesia and Intensive Care, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark;Department of Emergency Care and Services, University of Helsinki and Helsinki University Hospital, Helsinki, Finland;Department of Intensive Care, Hôpital Erasme, Université Libre de Bruxelles, Bruxelles, Belgium;Département de Médecine Intensive - Réanimation Et Médecine Hyperbare, Centre Hospitalier Universitaire d’Angers, Angers, France;Institut für Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinikum, Helmholtzstrasse 8-1, 89081, Ulm, Germany;Medical Research Institute of New Zealand, and Intensive Care Unit, Wellington Hospital, Wellington, Wellington, New Zealand;Australian and New Zealand Intensive Care Research Centre, Department of Critical Care Medicine, University of Melbourne, Melbourne, VIC, Australia;

关键词: 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;   

DOI  :  10.1186/s13054-021-03815-y

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY