Oxygen Toxicity Although supplemental oxygen is valuable in many clinical situations, excessive or inappropriate supplemental oxygen can be deleterious. Hyperoxia is poorly defined, but probably exists whenever oxygen tension exceeds 21 percent of atmospheric pressure. It appears to produce cellular injury through increased production of reactive oxygen species, such as the superoxide anion, the hydroxyl radical, and hydrogen peroxide. When the production of these reactive species increases and/or the cells antioxidant defenses are depleted, oxygen radicals can react with and impair the function of essential intracellular macromolecules, resulting in cell death. Oxygen free radicals may also promote a deleterious inflammatory response, leading to secondary tissue damage and/or apoptosis. Lung tissue is exposed to the highest concentrations of oxygen in the body, placing cells that line the tracheobronchial tree and alveoli at the greatest risk for hyperoxic cytotoxicity. Hyperoxia may also increase susceptibility to mucous plugging, atelectasis, and secondary infection by impairing both mucociliary clearance and the bactericidal capacity of immune cells. High fractions of inspired oxygen (FiO2) have been associated with several pulmonary consequences: increased intrapulmonary right-to-left shunt fraction and diminished lung volumes due to absorptive atelectasis; accentuation of hypercapnia; and damage to airways and pulmonary parenchyma. The term oxygen toxicity is usually reserved for the last of these consequences, ie, tracheobronchial and pulmonary parenchymal damage. References: To be posted
Posted on: Wed, 05 Nov 2014 15:40:54 +0000