Ventilatory effects of prolonged hyperoxia at pressures of 1.5-3.0 ATA

It was hypothesized that long-duration exposures to toxic levels of hyperoxia would have effects on respiratory control function or activity.

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).

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 significantly 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 approximately 2.0 ATA.

Hyperoxia has concurrent toxic and physiological effects on respiratory control; degrees depend on O2 dose (exposure pressure and duration).