Hypoxemia in Man Induced by Prolonged +Gz Acceleration
Report Number: AMRL TDR 62-137
Author(s): Bjurstedt, H.
Corporate Author(s): Laboratories of Aviation and Naval Medicine, Karolinska Institutet, Stockholm, Sweden
Laboratory: Biomedical Laboratory
Date of Publication: 1963-04
Pages: 15
Contract: AF 61(052)-153
DoD Project: 7220
DoD Task:
Identifier: AD0411465
Abstract:
Changes in the arterial oxygen saturation were re corded in healthy subjects on the human centrifuge by continuous cuvette oximetry before, during and after prolonged exposures to positive accelera tion. With the subjects breathing air and wear ing an automatically inflated anti-G suit, an im mediate fall in the arterial O2 saturation was observed upon exposure to 4.5-5.0 Gz. After one minute of the first exposure the O2 satura tion ranged between 95 and 81 per cent, the arterial pH remaining essentially unchanged. At the same time the respiratory minute volume had increased, indicating gross deterioration in the efficiency of pulmonary function. Re peated exposures caused the arterial O2 satura tion to fall at a faster rate and to a lower level with each consecutive run. The rate of resatura tion on returning to normal gravity was usually slow, and markedly so after several exposures. The last-mentioned observations are interpreted as being mainly the result of residual atelec tasis in dependent regions of the lungs. The potential dangers of acceleration-induced hypoxemia in high performance flight missions are discussed.
Provenance: RAF Centre of Aviation Medicine
Author(s): Bjurstedt, H.
Corporate Author(s): Laboratories of Aviation and Naval Medicine, Karolinska Institutet, Stockholm, Sweden
Laboratory: Biomedical Laboratory
Date of Publication: 1963-04
Pages: 15
Contract: AF 61(052)-153
DoD Project: 7220
DoD Task:
Identifier: AD0411465
Abstract:
Changes in the arterial oxygen saturation were re corded in healthy subjects on the human centrifuge by continuous cuvette oximetry before, during and after prolonged exposures to positive accelera tion. With the subjects breathing air and wear ing an automatically inflated anti-G suit, an im mediate fall in the arterial O2 saturation was observed upon exposure to 4.5-5.0 Gz. After one minute of the first exposure the O2 satura tion ranged between 95 and 81 per cent, the arterial pH remaining essentially unchanged. At the same time the respiratory minute volume had increased, indicating gross deterioration in the efficiency of pulmonary function. Re peated exposures caused the arterial O2 satura tion to fall at a faster rate and to a lower level with each consecutive run. The rate of resatura tion on returning to normal gravity was usually slow, and markedly so after several exposures. The last-mentioned observations are interpreted as being mainly the result of residual atelec tasis in dependent regions of the lungs. The potential dangers of acceleration-induced hypoxemia in high performance flight missions are discussed.
Provenance: RAF Centre of Aviation Medicine