Pulmonary function was measured in 152 professional saturation divers and in a matched control group of 106 subjects. Static lung volumes, dynamic lung volumes and flows, transfer factor for carbon monoxide (Tl,), transfer volume per unit alveolar volume (K>), delta-N2, and closing volume (CV) were measured and compared with reference values from recent Scandinavian studies, British submariners, and the European Community for Coal and Steel (ECCS) recommended reference values. Diving exposure was assessed as years of diving experience, total number of days in saturation and depth, and as the product of days in saturation and mean depth. Divers had significantly lower values for forced expired volume in one second (FEVy), FEV,/forced vital capacity (FVC) ratio, FEF25-75% FEF7s45% FEF,(%q FEF7S%, Tly,,, and K,, compared with the controls and a significantly higher CV. There was a positive correlation between diving exposure and CV, whereas the other variables had negative correlations with diving exposure. Values for the control group were not different from the predictive values of Scandinavian reference studies or British submariners, although the ECCS standard predicted significantly lower values for the lung function variables both in divers and the control group. The pattern of the differences in lung function variables between the divers and controls is consistent with small airways dysfunction and with the transient changes in lung function found immediately after a single saturation dive. The association between reduced pulmonary function and previous diving exposure further indicates the presence of cumulative long term effects of diving on pulmonary function.Previous studies have shown that divers in general have larger than predicted vital capacities compared with a standard reference population.'-3 Possible development of bronchial obstruction in divers has been questioned in these studies because the forced expired volume in one second (FEV,)/forced vital capacity (FVC) ratio was lower than predicted, and in one study the forced expiratory flow rate (FEF) at 75% of FVC expired (FEF75%) was also shown to be lower than predicted.' This pattern of changes may result from the larger than predicted vital capacity, as there is a negative correlation between FVC and FEV1/FVC ratio,4 and thereby a result of respiratory muscle training because of breathing dense gases, or simply a result of the selection process of divers. There is a thorough screening of divers for cardiopulmonary disorders both at the start of their education and by annual medical examinations in both Norway and Britain. Effects of a single deep dive on pulmonary function, however, have been shown in several studies.'' A reduction in transfer factor for carbon monoxide (Tl,O) is the most consistent effect reported. A small increase in vital capacity is often, but not always seen, and in two studies an increase in residual volume and total lung capacity was found.67 Gas exchange abnormalities, changes in ventilatory requirements and physiologi...
M Me ec ch ha an ni is sm ms s o of f r re ed du uc ce ed d p pu ul lm mo on na ar ry y f fu un nc ct ti io on n a af ft te er r a a s sa at tu ur ra at ti io on n d di iv ve e E. Thorsen, K. Segadal, B.K. KambestadMechanisms of reduced pulmonary function after a saturation dive. E. Thorsen, K. Segadal, B.K. Kambestad. ERS Journals Ltd 1994. ABSTRACT: Deep saturation diving has been shown to have prolonged effects on pulmonary function. We wanted to assess the relative contribution of various factors that could contribute to these effects.Pulmonary function was, therefore, measured before and after 17 different saturation diving operations to depths of 5-450 m of sea water, corresponding to absolute pressures of 0.15-4.6 MPa. Four to fifteen divers participated in each operation. The measurements included static and dynamic lung volumes 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 microemboli encountered during decompression was measured in 41 divers 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 hyperoxic exposure and load of venous gas microembolism, independently of each other. Closing volume was increased and forced mid-expiratory flow rate reduced, in correlation with cumulative hyperoxic exposure. An increase in total lung capacity correlated with cumulative hyperbaric exposure.We conclude that hyperoxia, hyperbaria, and venous gas microembolism all contribute to the changes in pulmonary function after a single saturation dive, and all may explain some of the long-term effects of diving on pulmonary function.
To assess the effects of deep saturation dives on pulmonary function, static and dynamic lung volumes, transfer factor for carbon monoxide (T1CO), delta-N2, and closing volume (CV) were measured before and after eight saturation dives to pressures of 3.1-4.6 MPa. The atmospheres were helium-oxygen mixtures with partial pressures of oxygen of 40-60 kPa. The durations of the dives were 14-30 days. Mean rate of decompression was 10.5-13.5 kPa/hour. A total of 43 divers were examined, six of whom took part in two dives, the others in one only. Dynamic lung volumes did not change significantly but total lung capacity (TLC) increased significantly by 4.3% and residual volume (RV) by 14.8% (p less than 0.05). CV was increased by 16.7% (p less than 0.01). The T1CO was reduced from 13.0 +/- 1.6 to 11.8 +/- 1.7 mmol/min/kPa (p less than 0.01) when corrected to a haemoglobin concentration of 146 g/l. Effective alveolar volume was unchanged. The increase in TLC and decrease in T1CO were correlated (r = -0.574, p less than 0.02). A control examination of 38 of the divers four to six weeks after the dives showed a partial normalisation of the changes. The increase in TLC, RV, and CV, and the decrease in T1CO, could be explained by a loss of pulmonary elastic tissue caused by inflammatory reactions induced by oxygen toxicity or venous gas emboli.
Pulmonary function and exercise tolerance were measured before and after three saturation dives to a pressure of 3.7 MPa. The atmospheres were heliox with partial pressures of oxygen of 40 kPa during the bottom phase and 50 kPa during the compression and decompression phase. The bottom times were 3, 10, and 13 days. Decompression time was 13 days. Precordial Doppler monitoring was done daily during the decompression, and an estimate of the total bubble load on the pulmonary circulation was calculated as the accumulated sum of bubble scores recorded for each diver. Nine of the 18 divers had chest symptoms with retrosternal discomfort or nonproductive cough after the dive. There were no changes in dynamic lung volumes. Transfer factor for carbon monoxide was significantly reduced from 12.3 +/- 1.2 to 10.9 +/- 1.3 mmol.kPa-1.min-1 (P less than 0.01), and maximum oxygen uptake was reduced from 3.98 +/- 0.36 to 3.42 +/- 0.37 l/min STPD (P less than 0.01) after the dives. Resting heart rate was increased from 64 +/- 6 to 75 +/- 8 min-1 (P less than 0.01). The ventilatory requirements in relation to oxygen uptake and carbon dioxide elimination were significantly increased (P less than 0.01) after the dives. The physiological dead space fraction of tidal volume was significantly higher and showed an increase with larger tidal volumes (P less than 0.05). Anaerobic threshold estimated from gas exchange data decreased from an oxygen uptake of 2.30 +/- 0.25 to 1.95 +/- 0.28 l/min STPD (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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