Critical Care 2015, 19:284 doi:10.1186/s13054-015-0996-4
Helmerhorst H, et al
Oxygen administration is uniformly
used in emergency and intensive care medicine and has life-saving potential in
critical conditions. However, excessive oxygenation also has deleterious
properties in various pathophysiological processes and consequently both
clinical and translational studies investigating hyperoxia during critical
illness have gained increasing interest. Reactive oxygen species are notorious
by-products of hyperoxia and play a pivotal role in cell signaling pathways.
The effects are diverse, but when the homeostatic balance is disturbed,
reactive oxygen species typically conserve a vicious cycle of tissue injury,
characterized by cell damage, cell death, and inflammation. The most prominent
symptoms in the abundantly exposed lungs include tracheobronchitis, pulmonary
edema, and respiratory failure. In addition, absorptive atelectasis results as
a physiological phenomenon with increasing levels of inspiratory oxygen.
Hyperoxia-induced vasoconstriction can be beneficial during vasodilatory shock,
but hemodynamic changes may also impose risk when organ perfusion is impaired.
In this context, oxygen may be recognized as a multifaceted agent, a modifiable
risk factor, and a feasible target for intervention. Although most clinical
outcomes are still under extensive investigation, careful titration of oxygen
supply is warranted in order to secure adequate tissue oxygenation while
preventing hyperoxic harm.
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