No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in Po2 during decompression.

Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium-oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29-48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.

Effects of venous gas microemboli on pulmonary gas transfer function.

Dynamic lung volumes and flows, slope of phase III of the single breath oxygen test (delta-N2), closing volume (CV), and transfer factor for carbon monoxide (TICO) were measured before and 1 h after an air dive in a hyperbaric chamber to a pressure of 0.49 MPa for 40 min. Six divers had a bottom time of 20 min and a rate of decompression of 50 kPa x min-1, and six divers had a bottom time of 24 min and a rate of decompression of 100 kPa x min-1. Decompression stops were 5 min at 0.16 MPa and 10 min at 0.13 MPa for both groups. As control exposure they were breathing O2 at atmospheric pressure for 40 min. The dive and control exposure were done on different days within 1 wk, in random order. Doppler ultrasound monitoring for venous gas microemboli (VGM) was done during the first hour after the dive. VGM were detectable in all six divers with the fast decompression rate and in one subject with the slow rate (P < 0.01). In the subjects having VGM there was a significant reduction in TICO of -5.9 +/- 4.4% compared with -0.5 +/- 3.4% after the control exposure (P = 0.034). In the five subjects without detectable VGM, the changes in TICO were -2.8 +/- 3.7% and 0.2 +/- 3.8%, respectively. There were no significant changes in dynamic lung volumes and flows, CV, or delta-N2. A reduction in TICO may reflect effects of VGM after dives in which the effect of O2 exposure is negligible.

Bronchial response to breathing dry gas at 3.7 MPa ambient pressure.

In diving, pulmonary mechanical function is limited by the increased density of the gas breathed. Breathing cold and dry gas may cause an additional increase in airways resistance. We have measured forced vital capacity, forced expired volume in 1 s (FEV1) and forced midexpiratory flow rate (FEF25%-75%) before and after breathing dry or humid gas at 29-32 degrees C during a standardized exercise intensity on a cycle ergometer at an ambient pressure of 3.7 MPa. The atmosphere was a helium and oxygen mixture with a density of 6.8 kg.m-3. Six professional saturation divers aged 26-37 years participated in the study. There were no significant differences in convective respiratory heat loss between the exposures. The mean evaporative heat loss was 67 W (range 59-89) breathing dry gas and 37 W (range 32-43) breathing humid gas, corresponding to water losses of 1.7 g.min-1 (range 1.5-2.2) and 0.9 g.min-1 (range 0.8-1.1), respectively. There was a significant reduction in FEV1 of 4.6 (SD 3.6)% (P < 0.05), and in FEF25%-75% of 5.8 (SD 4.7)% (P < 0.05) after breathing dry gas. There were no changes after breathing humid gas. By warming and humidifying the gas breathed in deep saturation diving bronchoconstriction may be prevented.

Mechanisms of reduced pulmonary function after a saturation dive.

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.

Contribution of hyperoxia to reduced pulmonary function after deep saturation dives.

Pulmonary function was measured before and after a 28-day saturation dive to a pressure of 0.25 MPa in eight subjects. PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa for the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. A 28-day saturation dive with six subjects to a pressure of 0.15 MPa and a PO2 of 21 kPa was used as control. The measurements included static and dynamic lung volumes and flows, transfer factor for carbon monoxide (TLCO), and a cycle ergometer exercise test. There was a significant reduction in TLCO of 9.8 +/- 6.0% (P < 0.001) after the dive when values were corrected for hemoglobin concentration changes. Effective alveolar volume was unchanged. There was a reduction in forced midexpiratory flow rate of 9.8 +/- 7.0% (P < 0.01), but forced vital capacity and forced expired volume in 1 s were unchanged. Peak oxygen uptake was reduced by 10.1 +/- 5.3% (P < 0.001). There were no significant changes in any of the lung function variables after the control dive. Exposure to raised PO2 contributes significantly to the changes in pulmonary function that have been reported after deep saturation dives to pressures of 3.1-4.6 MPa with a similar profile of oxygen exposure. TLCO is apparently a more sensitive index than vital capacity for oxygen toxicity.

Pulmonary function one and four years after a deep saturation dive.

The pulmonary function of 24 Norwegian divers who had participated in a deep saturation dive to pressures of 3.1-4.6 MPa was reevaluated one and four years later. Twenty-eight divers performing ordinary saturation diving to pressures of 0.8-1.6 MPa and followed over a three-year period served as referents. A significant reduction in forced expiratory volume in 1 s (FEV1.0) of 210 (SD 84) ml (P < 0.001) occurred the first year after the dive. Thereafter the annual reduction in FEV1.0 was 28 (SD 62) ml.year-1; this value did not differ from the 35 (SD 80) ml.year-1 of the referents. The forced midexpiratory flow rate and forced expiratory flow rates at low lung volumes were also significantly reduced one year after the deep dive, and the closing volume was increased. No significant changes occurred in forced vital capacity. The results agree with those of cross-sectional studies on divers' lung function and indicate the development of airflow limitation in relation to diving exposure.

Respiratory effects of warm and dry air at increased ambient pressure.

We have measured in 7 divers forced vital capacity (FVC), forced expired volume in 1 s (FEV1), and forced midexpiratory flow rate (FEF25-75%) before and after exposure to dry or humid breathing gas of 35.3 degrees-36.8 degrees C (air) when diving to pressures of 117-600 kPa. The response was compared with the subjects' reactivity to pharmacologic bronchoprovocation with methacholine. Baseline FEV1 and FEF25-75% decreased in accordance with increasing gas density. Relative to baseline, there was a significant reduction after the dives in FEV1 of 4.0 +/- 6.1% (P less than 0.05) and in FEF25-75% of 8.6 +/- 9.7% (P less than 0.01) with exposure to dry breathing gas. By analysis of variance the reduction in the lung function variables below baseline were related to the breathing gas characteristic (dry/humid) (P less than 0.01), bronchial hyperreactivity (P less than 0.02), and ambient pressure (P less than 0.02) independently of each other. There was no significant change in FVC after the exposures. Humid breathing gas was considered more comfortable than dry breathing gas, and the upper comfort limit for breathing gas temperature was higher with humid breathing gas. Convective respiratory heat loss was negligible in these experiments, indicating that dry gas itself had a significant bronchoconstrictive effect. Bronchial hyperreactivity may cause increased risk of development of bronchial obstruction and air trapping during diving.

Characteristics of the response to exercise in professional saturation divers.

Exercise testing with measurements of expired minute ventilation (VE), oxygen uptake (VO2), and carbon dioxide elimination (VCO2) was done in 63 professional saturation divers, in the screening programs for selection of divers, to 10 different experimental and operational saturation dives. Their experience as divers averaged 9.8 yr (range 1-20), and they averaged 276 days (range 5-900) in saturation. The maximal pressure they had ever been exposed to averaged 2.01 MPa (range 0.8-5.1). The divers were compared with a control group of 47 offshore workers and policemen matched for age, height, and smoking habits and with reference values for the general healthy population. There were no significant differences in peak work load achieved, VO2peak and VCO2peak. VE at VO2peak and the corresponding ventilatory equivalents for oxygen uptake (VE(peak)/VO2peak) and carbon dioxide elimination (VE(peak)/VCO2peak) were significantly higher in divers (P less than 0.05), but VE, VE/VO2 and VE/VCO2 were not different at lower work loads. VE(peak)/VCO2peak correlated positively with years of diving experience when corrected for age (P less than 0.01). Divers had higher tidal volumes and lower breathing frequencies at ventilations lower than 40% of VE(peak), but maximal tidal volumes were not different. Tidal volume at a VE of 30 liter.min(-1) correlated negatively with FEV1 (P less than 0.05). The results are in agreement with the transient changes in pulmonary function and exercise tolerance demonstrated after a single saturation dive, and indicate that these changes may not be completely reversible.

Divers' lung function: small airways disease?

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 (T1CO), transfer volume per unit alveolar volume (KCO), 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 (FEV1), FEV1/forced vital capacity (FVC) ratio, FEF25-75%, FEF75-85%, FEF50%, FEF75%, T1CO, and KCO 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.

Exercise tolerance and pulmonary gas exchange after deep saturation dives.

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)

Pulmonary mechanical function and diffusion capacity after deep saturation dives.

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.

Respiratory changes with deep diving.

Deep diving refers to saturation diving to a depth of more than 180 m (1.9 MPa ambient pressure). In the 1990s diving to 400 m may be necessary on the Norwegian continental shelf. The safety margins are narrow and the respiratory system is subject to great strain at such depths. The respiratory resistance increases and the dynamic lung volumes are reduced as the pressure increases due to enhanced gas density. Helium is used together with oxygen as breathing gas and its lower density partly normalises the dynamic lung volumes. The respiratory system puts clear limitations on intensity and duration of physical work in deep diving. Systematic studies of lung mechanics, gas exchange and respiratory regulation in the different phases of deep dives are lacking. Detection of occupational respiratory disorder following diving are dependent on long-term follow-up.

[Respiratory changes in deep diving]. / Respirasjonsendringer ved dypdykking.

Deep diving refers to saturation diving to a depth of more than 180 m (1.9 MPa ambient pressure). In the 1990s diving to 400 m may be necessary on the Norwegian continental shelf. The safety margins are narrow and at such depths the respiratory system is subject to great strain. Respiratory resistance increases and the dynamic lung volumes are reduced as the pressure increases due to enhanced gas density. Helium is used together with oxygen as breathing gas and the lower density partly normalises the dynamic lung volumes. The respiratory system imposes clear limitations on the intensity and duration of physical work during deep diving. We lack systematic studies of lung mechanics, gas exchange and respiratory regulation in the different phases of deep dives. Demonstration of possible chronic occupational respiratory diseases connected to diving is dependent on follow-up over a long time.

Transcutaneous measurement of PCO2 at high ambient pressure (41 bar).

The accuracy of transcutaneous CO2 monitoring with the Kontron CO2 sensor was studied during compression to 41 bar and subsequent decompression. The PCO2 was stable and accurate during the test of the sensor in the pressure chamber, although an increase of 0.1-0.2 kPa during compression was found. The function of the transcutaneous sensor was tested in rats at 1 bar for the correlation between transcutaneous PCO2 (PtcCO2) and arterial PCO2 (PaCO2). The correlation coefficient between PtcCO2 and PaCO2 in the rat was found to be 0.93. The time difference between the 90% transcutaneous and 90% arterial response time was 4.6 +/- 0.6 min (mean +/- SEM). Finally, the use of the sensor in rats ventilated at constant minute volume during compression to 41 bar was examined. An increase in PtcCO2 of 0.2-0.4 kPa was found. The present results of transcutaneous PCO2 measurements indicate that this method may be useful in hyperbaric research and treatment.

Gas bubbles in the circulation of divers after ascending excursions from 300 to 250 msw.

The occurrence of intravascular bubbles in arteries and veins has been studied using pulsed Doppler ultrasound in six subjects who performed two ascending excursions each from 300 to 250 meters of seawater (msw) during a heliox saturation dive. Following decompression, high-intensity reflections could be observed not only in the venous system but also in the arteries, most notably in the carotid artery. Intravascular bubbles were more numerous during the first ascent than during the second. The arterial bubbles most probably come from the venous side of the circulation, indicating that the pulmonary filter is not as effective as previously thought during saturation diving.