MECHANISMS OF REDUCED PULMONARY-FUNCTION AFTER A SATURATION DIVE

Deep saturation diving has been shown to have prolonged effects on pul monary function. We wanted to assess the relative contribution of vari ous factors that could contribute to these effects. Pulmonary function was, therefore, measured before and after 17 different saturation div ing operations to depths of 5-450 m of sea water, corresponding to abs olute pressures of 0.15-4.6 MPa Four to fifteen divers participated in each operation. The measurements included static and dynamic lung vol umes and flows, transfer factor of the lungs for carbon monoxide (TLCO ), and closing volume. The dives were characterized by the cumulative hyperoxic and hyperbaric exposures, and the load of venous gas microem boli encountered during decompression was hyperoxia measured in 41 div ers in three dives to 0.25, 1.2 and 3.7 MPa TLCO was reduced by 8.3+/- 7.0% mean+/-SD after the dives, this correlated with cumulative hypero xic exposure and load of venous gas microembolism, independently of ea ch other. Closing volume was increased and forced mid-expiratory now r ate reduced, in correlation with cumulative hyperoxic exposure, An inc rease in total lung capacity correlated with cumulative hyperbaric exp osure. We conclude that hyperoxia, hyperbaria, and venous gas microemb olism all contribute to the changes in pulmonary function after a sing le saturation dive, and all may explain some of the long-term effects of diving on pulmonary function.