Ventilatory Effects of Prolonged Hyperoxia at Pressures of 1.5–3.0 ATA
Authors: Gelfand, Robert; Lambertsen, Christian J.; Clark, James M.
Source: Aviation, Space, and Environmental Medicine, Volume 77, Number 8, August 2006 , pp. 801-810(10)
Publisher: Aerospace Medical Association
Abstract:Gelfand R, Lambertsen CJ, Clark JM. Ventilatory effects of prolonged hyperoxia at pressures of 1.5–3.0 ATA. Aviat Space Environ Med 2006; 77:801–810.
Introduction: It was hypothesized that long-duration exposures to toxic levels of hyperoxia would have effects on respiratory control function or activity. Methods: Ventilatory parameters of human subjects breathing spontaneously at rest were measured before, during, and after hyperoxia in a study of organ systems’ tolerance to toxic O2 exposures at 1.5 ATA (17.7 h), 2.0 ATA (9.3 h), 2.5 ATA (5.7 h) and 3.0 ATA (3.5 h). Results: Average neurotoxic changes in ventilatory parameters during and after prolonged hyperoxia were mild. They included: 1) timing component of ventilation decreased progressively with exposure duration at all four O2 pressures, slopes increased with O2 pressure, changes were significant late in exposure at 1.5 ATA (−11%) and 3.0 ATA (−10%); 2) post-O2 exposure respiratory rates were significantly above controls by 15% to 59%; and 3) ventilation increased significantly by 20% late during the 1.5 ATA O2 exposures. There were severe neurotoxic changes prior to occurrence of an “O2 convulsion” at 3.0 ATA in one subject. Expiratory time increased by 184%; resultant reductions in respiratory rate and ventilation caused respiratory Pco2 increase, accelerating rate of brain O2 poisoning. Significant nontoxic physiological hyperventilation (21% to 45% above control) early in hyperoxia at all exposure pressures persisted throughout hyperoxia, and reversed post-O2 exposure. Hyperventilation increased and end-tidal Pco2 decreased as inspired Po2 increased. Changes reached maximum values at ∼2.0 ATA. Discussion: Hyperoxia has concurrent toxic and physiological effects on respiratory control; degrees depend on O2 dose (exposure pressure and duration).
Document Type: Research Article
Publication date: 2006-08-01
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