Neurologic injury subsequent to decompression from diving may be due to paradoxical arterialization of venous gas emboli. Of 40 divers who performed 53 open water dives after being tested for a patent foramen ovale (PFO), arterial gas emboli were detected in 7 of 13 dives, which resulted in venous bubbles. In five of these seven dives, there was evidence of a PFO by contrast transcranial Doppler sonography, indicating an increased risk of arterializing venous bubbles in divers with a PFO.

This study evaluated the subacute respiratory effects of diving, to try to separate the effects of ambient temperature from those of depth. In the first experiment 10 healthy men made a compressed-air dive to 50 m that exposed them to cold. They were compared with 10 matched control subjects who underwent the same dive profile but were exposed to a comfortable temperature. In the second experiment 16 healthy subjects made randomized cold dives to both 50 m and 10 m. Pulmonary function tests were made before, after 1 h, and 24 h after the dives. In the first experiment there was an increase in residual volume (P < 0.05) and a decrease in forced expiratory volume at 1 s (FEV1), in forced vital capacity (FVC) and in mid-expiratory flow at 75% of FVC (MEF75) 1 h after the cold dives (P < 0.05). In the second experiment significant increases in specific airways resistance (sR(AW)) (P < 0.05) and decreases in FEV1 (P<0.01), in MEF75 (P<0.05), and in mid-expiratory flow at 25% of FVC (P<0.05), were obtained after the 50 m-dives, whereas SR(AW) increased after the 10 m-dives (P<0.05). The respiratory pattern observed 1 h after cold dives to 50 m indicated airway narrowing. The changes after cold dives to 10 m, however, were of minor magnitude. Both cold and depth seemed to contribute to the adverse effects of a single compressed-air dive on pulmonary function.

Increasing popularity of sports diving makes it likely that subjects with allergic respiratory diseases will be involved in diving with self contained underwater breathing apparatus (scuba). The present study evaluated the effects of a single scuba-dive on pulmonary function in subjects with respiratory atopy. Specific airways conductance (sGaw), residual volume (RV), forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), mid expiratory flow at 50% of FVC (MEF50), and transfer factor for carbon monoxide (TLCO) were measured in 9 sport divers with a history of hay fever and 9 matched healthy sport divers (control) before, 3 hours and 24 hours after a wet hyperbaric chamber dive to a depth of 50 m. Airway hyperresponsiveness (AHR) was assessed by methacholine challenge 4 weeks after the dive. Atopic subjects and controls did not differ with respect to anthropometric data, diving experience, and predive lung function. A 3% reduction in FVC was found 24h after the dive (p < 0.05) in both groups, whereas sGaw decreased by 15% 24 h after the dive (p < 0.05) in the subjects with respiratory atopy only. Postdive changes in RV, FEV1, MEF50, and TLCO did not reach level of statistical significance. AHR was obtained in 8/9 subjects with respiratory atopy. We conclude that subjects with atopic sensitization and asymptomatic AHR may be more susceptible to effects of diving on pulmonary function.

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Previous studies have inconsistently shown changes in expiratory flows and volumes as well as diffusion capacity of the lungs after single dives and several diving related occupational conditions were considered as possible underlying factors. In this study mechanical impedance of the airways was measured before and after simulated dives to non-invasively determine whether there is evidence for lung function impairment due to hyperbaric exposure. Thirty-three healthy male divers employing air self-contained underwater breathing apparatus were randomly assigned to dry and wet chamber dives in a cross-over design to 600 kPa ambient pressure (total duration 43 min, bottom time 15 min, water temperature 24 degrees C). Immediately before and after diving, oscillometric parameters-e. g. resistance and reactance of the respiratory tract-were measured at defined frequencies (5, 20 Hz). Spirometry was carried out as well (FVC, FEV(1), MEF 25-75). No significant changes between post-exposure values and baseline values were detected by respiratory impedance and spirometry. Diving in accordance to diving regulations and without excessive workload is not a source for acute obstructive lung function changes as the obtained oscillometric data suggested. Moreover this study could not confirm changes in spirometry after simulated diving exposure.