Abstract
Mechanical ventilation may cause and aggravate lung damage and contribute to the appearance of multiorgan failure. One of the mechanisms that has been described is alveolar hyperoxia. In experimental models, it has lead to the production of free oxygen radicals that exceed the cell defense capacity, giving rise to inflammation, cell damage and gene overexpression with necrosis and apoptosis phenomenon. However, these findings in humans are not as conclusive, although a functional alteration due to the exposure to high FiO 2, and greater lung de-recruitment in patients with lung injury has been clearly demonstrated. Moreover, both the FiO 2 used as well as the PaO 2 achieved in the first 24 h of admission are associated with mortality. Clinical trials are needed that assess the threshold of the safe oxygen level for FiO 2 and oxygen saturation.
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