Hyperoxic Acute Lung Injury

Prolonged breathing of very high F-IO2 (F-IO2 >= 0.9) uniformly causes severe hyperoxic acute lung injury (HALL) and, without a reduction of F-IO2, is usually fatal. The severity of HALL is directly proportional to P-O2 (particularly above 450 mm Hg, or an F-IO2 of 0.6) and exposure duration. Hyperoxia produces extraordinary amounts of reactive O-2 species that overwhelms natural antioxidant 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-IO2 exceeds 0.7, and may become problematic when F-IO2 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 HALL largely reflected such issues as the primitive control of F-IO2, 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-IO2, as well as lung-protective ventilation, and other adjunctive therapies for severe hypoxemia, has greatly reduced the risk of HALL 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.