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Pulmonary mechanical function and diffusion capacity after deep saturation dives.

E Thorsen1, K Segadal, E Myrseth

  • 1Norwegian Underwater Technology Centre A/S (NUTEC), Ytre Laksevåg, Norway.

British Journal of Industrial Medicine
|April 1, 1990
PubMed
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Deep saturation dives significantly increased lung volumes and closing volume, while reducing carbon monoxide transfer factor in divers. These pulmonary function changes may stem from lung tissue damage due to oxygen toxicity or gas emboli.

Area of Science:

  • Physiology
  • Occupational Health
  • Diving Medicine

Background:

  • Saturation diving involves prolonged exposure to high ambient pressures.
  • Understanding the physiological effects of deep saturation dives is crucial for diver safety.
  • Pulmonary function changes after saturation dives require detailed assessment.

Purpose of the Study:

  • To evaluate the impact of deep saturation dives on various pulmonary function parameters.
  • To assess changes in lung volumes, gas transfer, and closing volume post-dive.
  • To investigate potential mechanisms behind observed pulmonary function alterations.

Main Methods:

  • Pulmonary function tests including static/dynamic lung volumes, transfer factor for carbon monoxide (T1CO), and closing volume (CV) were performed.

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  • Measurements were taken before and after saturation dives to 3.1-4.6 MPa using helium-oxygen atmospheres.
  • Forty-three divers participated, with follow-up assessments conducted post-dive and several weeks later.

    • Main Results:

    • Total lung capacity (TLC) increased by 4.3% and residual volume (RV) by 14.8%.
    • Closing volume (CV) increased significantly by 16.7%.
    • Transfer factor for carbon monoxide (T1CO) decreased by approximately 9.2% (p < 0.01).

    Conclusions:

    • Deep saturation dives lead to significant alterations in pulmonary mechanics, including increased lung volumes and reduced gas exchange efficiency.
    • Observed changes, particularly the increase in TLC, RV, CV, and decrease in T1CO, suggest potential loss of pulmonary elastic tissue.
    • These effects may be linked to inflammatory responses from oxygen toxicity or venous gas emboli, necessitating further research and preventative strategies.