Clinical manifestations of pulmonary oxygen toxicity.
Despite the seriousness of pulmonary O2 toxicity, patients can generally withstand 1 atm. of PO2 for at least 24 hours. Also, there is no evidence that clinically relevant pulmonary O2 toxicity occurs in humans at inspired partial pressures below 0.4 to 0.5 ATA, even with prolonged exposures. Neither is there clinical or experimental evidence to indicate that patients with preexisting pulmonary disease are more sensitive to O2 toxicity than are normal volunteers. Although the florid manifestations of pulmonary O2 toxicity may have dire consequences, a lower dosage of O2, though still potentially toxic, may well be acceptable. The lung itself can generate some level of self-protection with prolonged O2 exposure, ultimately healing itself to a significant degree. Therefore, no patient should be exposed to dangerous levels of hypoxia out of fear of causing pulmonary O2 toxicity. Pulmonary hyperoxia and systemic hypoxia can usually be avoided with skillful, titrated management of respiratory insufficiency.
D000818:Animals; D001761:Bleomycin / Q000009:adverse effects; D002374:Catalase / Q000378:metabolism; D004198:Disease Susceptibility; D004702:Endocrine Glands / Q000503:physiopathology; D005122:Exudates and Transudates; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D008171:Lung Diseases / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D008657:Metabolic Clearance Rate; D009420:Nervous System / Q000503:physiopathology; D010100:Oxygen / Q000009:adverse effects* / Q000097:blood; D012138:Respiratory Therapy / Q000009:adverse effects; D013482:Superoxide Dismutase / Q000378:metabolism
D001761:Bleomycin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D010100:Oxygen