PMID- 23271823
OWN - NLM
STAT- MEDLINE
DCOM- 20130404
LR  - 20220408
IS  - 0020-1324 (Print)
IS  - 1943-3654 (Electronic)
IS  - 0020-1324 (Linking)
VI  - 58
IP  - 1
DP  - 2013 Jan
TI  - Hyperoxic acute lung injury.
PG  - 123-41
LID - 10.4187/respcare.01963 [doi]
AB  - 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.
FAU - Kallet, Richard H
AU  - Kallet RH
AD  - Respiratory Care Services, Department of Anesthesia, University of California, 
      San Francisco at San Francisco General Hospital, San Francisco, California 94110, 
      USA. rich.kallet@ucsf.edu
FAU - Matthay, Michael A
AU  - Matthay MA
LA  - eng
GR  - R37 HL051856/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Respir Care
JT  - Respiratory care
JID - 7510357
RN  - 0 (Cytokines)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Acute Lung Injury/*etiology/physiopathology
MH  - Animals
MH  - Cytokines/metabolism
MH  - Humans
MH  - Hyperoxia/*etiology/physiopathology
MH  - Oxygen/administration & dosage/adverse effects
MH  - Oxygen Inhalation Therapy/*adverse effects
MH  - Partial Pressure
MH  - Reactive Oxygen Species/adverse effects/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Time Factors
PMC - PMC3915523
MID - NIHMS444767
COIS- The authors have disclosed no conflicts of interest.
EDAT- 2012/12/29 06:00
MHDA- 2013/04/05 06:00
PMCR- 2014/02/06
CRDT- 2012/12/29 06:00
PHST- 2012/12/29 06:00 [entrez]
PHST- 2012/12/29 06:00 [pubmed]
PHST- 2013/04/05 06:00 [medline]
PHST- 2014/02/06 00:00 [pmc-release]
AID - 58/1/123 [pii]
AID - 10.4187/respcare.01963 [doi]
PST - ppublish
SO  - Respir Care. 2013 Jan;58(1):123-41. doi: 10.4187/respcare.01963.