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J Appl Physiol 13: 15-29, 1958;
8750-7587/58 $5.00
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Mechanisms in Development of Interstitial Emphysema and Air Embolism on Decompression From Depth

Karl E. Schaefer 1, Wilbur P. McNulty JR. 1, Charles Carey 1, and Averill A. Liebow 1

1 From the U.S. Naval Medical Research Laboratory, U.S. Naval Submarine Base, New London, and the Department of Pathology, Yale University School of Medicine, New Haven, Connecticut

Unprotected dogs decompressed from 100- or 200-foot equivalent depth (water) with trachea closed developed pulmonary interstitial emphysema and air embolism, probably via the pulmonary veins, when the intratracheal pressure reached a critical level of approximately 80 mm Hg. The lungs became markedly distended by entrapped air expanding as the ambient pressure was reduced. The systemic aortic pressure fell in consequence of compression of postarterial vessels in the lungs, indicated by a higher gradient between pulmonary arterial and left atrial pressures. Interstitial emphysema and air embolism could be prevented by the application of thoraco-abdominal binders, despite a rise in intratracheal pressure to levels of 180 mm Hg or more. The effects of the binders were: a) to prevent overdistention of the lung as indicated by the small difference between the intratracheal and intrapleural pressures; b) to keep at a lower level the pressure gradient between the respiratory passages and the pulmonary veins-left atrium; c) to maintain the systemic aortic pressure, in part, at least, in consequence of a low transcapillary pressure gradient. These observations suggest the possible utility of compressive garments of the ‘G-suit’ type in escape procedures. The critical factor for the development of pulmonary interstitial emphysema and air embolism appears to be not an absolute level of the intratracheal pressure, but rather a transpulmonic pressure in excess of 60–70 mm Hg or a transatrial pressure in excess of 55–65 mm Hg.

Submitted on November 12, 1957




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