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Cited by 438Respiratory Support and MechanismsNeonatal Respiratory Health ResearchInterstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

Hyperoxic Acute Lung Injury

Open access
Kallet, Richard H, Matthay, Michael A·2013·Respiratory Care
DOI 10.4187/respcare.01963PMC PMC3915523
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Abstract

Prolonged breathing of very high F(IO(2)) (F(IO(2)) ≥ 0.9) uniformly causes severe hyperoxic acute lung injury (HALI) and, without a reduction of F(IO(2)), is usually fatal. The severity of HALI is directly proportional to P(O(2)) (particularly above 450 mm Hg, or an F(IO(2)) of 0.6) and exposure duration. Hyperoxia produces extraordinary amounts of reactive O(2) species that overwhelms natural anti-oxidant defenses and destroys cellular structures through several pathways. Genetic predisposition has been shown to play an important role in HALI among animals, and some genetics-based epidemiologic research suggests that this may be true for humans as well. Clinically, the risk of HALI likely occurs when F(IO(2)) exceeds 0.7, and may become problematic when F(IO(2)) exceeds 0.8 for an extended period of time. Both high-stretch mechanical ventilation and hyperoxia potentiate lung injury and may promote pulmonary infection. During the 1960s, confusion regarding the incidence and relevance of HALI largely reflected such issues as the primitive control of F(IO(2)), the absence of PEEP, and the fact that at the time both ALI and ventilator-induced lung injury were unknown. The advent of PEEP and precise control over F(IO(2)), as well as lung-protective ventilation, and other adjunctive therapies for severe hypoxemia, has greatly reduced the risk of HALI for the vast majority of patients requiring mechanical ventilation in the 21st century. However, a subset of patients with very severe ARDS requiring hyperoxic therapy is at substantial risk for developing HALI, therefore justifying the use of such adjunctive therapies.

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  • Mice treated with 60% O2 indefinitely in a standard atmosphere with oxygen content between 20% and 100% showed no signs of toxicity.

    “For normobaric hyperoxic respiration, in a standard atmosphere with an oxygen content between 20% and 100%, mice were treated with 60% O2 indefinitely without signs of toxicity.”

    From Hypoxia signaling in cancer: Implications for therapeutic interventions (2023) · cites this paper as [199]

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  1. [46]Castleman B McNeely BU Case records of the Massachusetts General Hospital. Case 7-1967 N Engl J Med 1967 276 7 401 411 6024568

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Authors
Kallet, R. H., & Matthay, M. A.
Affiliations
  • San Francisco General Hospital (US)
  • University of California, San Francisco (US)
ORCID
Matthay, Michael A
Venue
Respiratory Care
Publisher
SAGE Publications
Published
2013-01-01
Volume
58
Issue
1
Pages
123-141
ISSN
0020-1324 (ISSN-L)
DOI
10.4187/respcare.01963
PMC
PMC3915523
OpenAlex
W2146682756
Cited by
438
References
129
Citations by year
2026: 21 · 2025: 21 · 2024: 44 · 2023: 28 · 2022: 50 · 2021: 51 · 2020: 42 · 2019: 30 · 2018: 31 · 2017: 30 · 2016: 27 · 2015: 28 · 2014: 21 · 2013: 14
FWCI
4.66
Type
journal article
Language
en
Open access
Licence
www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/ (tdm)
Locations
  • Respiratory Care (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
National Heart, Lung, and Blood Institute (R37HL051856)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Keywords
hyperoxia, oxygen fraction, reactive oxygen species, oxidative stress, antioxidant defense, genetic susceptibility, mechanical ventilation, positive end-expiratory pressure, lung-protective ventilation, acute respiratory distress syndrome, pulmonary infection, hypoxemia
MeSH terms
Animals, Humans, Oxygen, Oxygen Inhalation Therapy, Partial Pressure, Superoxide Dismutase, Time Factors, Cytokines, Reactive Oxygen Species, Hyperoxia, Acute Lung Injury

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