Targeting normoxemia in acute respiratory distress syndrome may cause worse short-term outcomes because of oxygen toxicity

Neil R. Aggarwal, Roy G Brower

Research output: Contribution to journalArticle

Abstract

It was suggested that targeting normoxemia (PaO2 85-110mmHg) in patients with acute respiratory distress syndrome (ARDS) might prevent neurocognitive dysfunction in survivors. However, targeting normoxemia may cause detrimental effects to the lungs from oxygen toxicity. Some have suggested that oxygen is not harmful to the lungs at FIO2 (fraction of inspired oxygen) levels less than 0.6-0.7, but contrasting evidence in normal humans suggests that there can be untoward effects of moderate FIO2 levels. Furthermore, in experimental models of the acute respiratory distress syndrome, coexisting lung inflammation increases susceptibility to oxygen toxicity. Coexisting lung inflammation may lower the threshold for oxygen toxicity in patients with ARDS or in other acute illnesses in the lung. Moreover, physicians frequently prescribe higher FIO2 levels than are necessary to achieve their arterial oxygenation goal, further increasing the risk of oxygen toxicity. Targeting normoxemia in patients with ARDS may prevent some long-term neurocognitive deficits in survivors, but it may increase lung inflammation and cause worse short-term clinical outcomes.Weadvocate for a clinical trial in patients with ARDS to determine more appropriate goals for arterial oxygenation.

Original languageEnglish (US)
Pages (from-to)1449-1453
Number of pages5
JournalAnnals of the American Thoracic Society
Volume11
Issue number9
DOIs
StatePublished - Nov 1 2014

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Adult Respiratory Distress Syndrome
Oxygen
Pneumonia
Lung
Survivors
Theoretical Models
Clinical Trials
Physicians

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Medicine(all)

Cite this

Targeting normoxemia in acute respiratory distress syndrome may cause worse short-term outcomes because of oxygen toxicity. / Aggarwal, Neil R.; Brower, Roy G.

In: Annals of the American Thoracic Society, Vol. 11, No. 9, 01.11.2014, p. 1449-1453.

Research output: Contribution to journalArticle

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