Analysis of Decrements in Vital Capacity as an Index of Pulmonary Oxygen Toxicity

摘要

Exposure to hyperoxia produces progressive lung damage in animals and humans. Oxygen exposures from 6 to 74 h at pressures ranging from 0.83 to 2.0 ATA result in characteristic subjective symptoms and alterations in pulmonary function in normal humans. Substernal pain, sore throat, cough, headache, anorexia, and paresthesias develop after 6-14 h at 1 ATA, with shorter latencies at higher partial pressures of O2 (Po2) and increased severity as exposure is lengthened. Changes in pulmonary function include decreases in static and dynamic lung volumes and carbon monoxide diffusing capacity and increases in alveolar-arterial O2 differences. A noninvasive means for detecting early stages of pulmonary O2 toxicity to regulate human O2 exposures would be useful because O2 is widely used therapeutically and in diving operations. Clark and Lambertsen suggested in 1970 that decreases in vital capacity (VC) could be used to predict the onset, rate of development, and degree of severity of the toxic process in the lung caused by O2 exposure. They developed a predictive graphic model relating Po2, time of exposure, and toxicity, expressed as a decrement in VC. Subsequently, a mathematical description of this graphic process was developed and named the unit pulmonary toxicity dose (UPTD). In the present study, we updated the available data set and performed a quantitative statistical analysis to evaluate VC as an index of pulmonary O2 toxicity. Hyperbaric conditions; Reprints. (aw)