TENSIONAL CHANGES OF ALVEOLAR GAS IN REACTIONS TO RAPID COMPRESSION AND DECOMPRESSION AND QUESTION OF NITROGEN NARCOSIS

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Abstract
Rapid compression of the ambient atmosphere induces a temporary asphyxial state of hypercapneia-hyperoxia. In such compression to 8 atmospheres, alveolar CO2 is elevated to levels little below those of a comparable period of mechanical asphyxia. This is caused by the compressional inflow which "blocks" expulsion of CO2, compresses dead space and alveolar air into the periphery of the lungs and drives CO2 and O2 into the blood before mixing of the inflow air is complete. This compressional elevation of CO2 is an important contributor to, if not the chief cause of, those reactions attributed by some authors solely to a hypothetical nitrogen narcosis. Rap-id decompression results in an asphyxial state of hypocapneic anoxia because the decompressional outflow "sucks" CO2 and O2 out of the lungs and the blood and "blocks" inspiratory entrance of O2. The immediacy and efficacy of this removal of O2 and CO2 from the blood may well explain those cardiac effects of rapid decompression and various responses attributed to aeroembolism. The importance of this in rapid ascent to high altitude, explosive decompression from one atmosphere,and in submarine escape procedures is emphasized.

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