Enriched Air Nitrox Breathing Reduces Venous Gas Bubbles after Simulated SCUBA Diving: A Double-Blind Cross-Over Randomized Trial

<div><p>Objective</p><p>To test the hypothesis whether enriched air nitrox (EAN) breathing during simulated diving reduces decompression stress when compared to compressed air breathing as assessed by intravascular bubble formation after decompression.</p><p>Methods</p><p>Human volunteers underwent a first simulated dive breathing compressed air to include subjects prone to post-decompression venous gas bubbling. Twelve subjects prone to bubbling underwent a double-blind, randomized, cross-over trial including one simulated dive breathing compressed air, and one dive breathing EAN (36% O₂) in a hyperbaric chamber, with identical diving profiles (28 msw for 55 minutes). Intravascular bubble formation was assessed after decompression using pulmonary artery pulsed Doppler.</p><p>Results</p><p>Twelve subjects showing high bubble production were included for the cross-over trial, and all completed the experimental protocol. In the randomized protocol, EAN significantly reduced the bubble score at all time points (cumulative bubble scores: 1 [0–3.5] vs. 8 [4.5–10]; P < 0.001). Three decompression incidents, all presenting as cutaneous itching, occurred in the air versus zero in the EAN group (P = 0.217). Weak correlations were observed between bubble scores and age or body mass index, respectively.</p><p>Conclusion</p><p>EAN breathing markedly reduces venous gas bubble emboli after decompression in volunteers selected for susceptibility for intravascular bubble formation. When using similar diving profiles and avoiding oxygen toxicity limits, EAN increases safety of diving as compared to compressed air breathing.</p><p>Trial Registration</p><p><a href="http://www.isrctn.com/ISRCTN31681480" target="_blank">ISRCTN 31681480</a></p></div

Intravascular bubble scores of two air dives.

<p>Intravascular bubble scores of two air dives.</p

Intravascular bubble score.

<p>Intravascular bubble score.</p

Inclusion and randomization flow diagram.

<p>EAN = Enriched air nitrox.</p

Simulated diving profile.

<p>Study compression profile as used for all simulated dives to a maximum depth of 28 msw, followed by two decompression steps at 6 msw and 3 msw. For further details see text.</p

Parameters of systemic hemodynamics, lung mechanics, pulmonary gas exchange, metabolism, and acid-base.

<p>^§ depicts p < 0.05 vs. the corresponding Non-CS group,</p><p>^$ depicts p < 0.05 vs. the corresponding air group (K-W ANOVA Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).</p><p>Parameters of systemic hemodynamics, lung mechanics, pulmonary gas exchange, metabolism, and acid-base status in mice without (Non-CS) and with (CS) cigarette smoke exposure over three to four weeks prior to blunt chest trauma and after four hours mechanical ventilation with air (FiO₂ 0.21) or 100% O₂ (FiO₂ 1.0) (n = 8 in each group). All data are median (quartiles).</p

Typical examples of the histopathological items scored.

<p><i>Upper panel</i>: Lung region with little histopathological abnormalities, i.e. no dystelectasis/ atelectasis, normal thickness of alveolar membranes, and little lymphocyte immigration. Dotted arrows show some degree of protein debris in the airspaces. <i>Lower panel</i>: Lung region with major histological injury (alveolar membrane thickening and lymphocyte immigration grade 1.5 each). Solid arrows show alveolar smokers’ macrophages within the airways.</p

Results of the immunohistochemistry for P2X₄.

<p>Typical examples (upper panel) and quantitative analysis (lower panel) of immunohistochemistry for lung tissue expression of the purinergic receptor P2X₄ from mice without (dotted boxplots) and with (hatched boxplots) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O₂ (grey boxplots) (n = 8 in each group). All data median (quartiles, range), § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).</p

Results of the immune blotting for HIF-1α.

<p>Original western blots and quantitative analysis of lung tissue expression of HIF-1α expression from mice without (open boxplots; n = 8 each) and with (hatched boxplots; n = 7 each) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O₂ (grey boxplots) together with two blots each (right part of blot panel) from control animals that did not undergo cigarette smoke exposure, anaesthesia, chest trauma, and surgery. All data are median (quartiles, range) as fold increase over values from control animals; § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).</p

Results of the immunohistochemistry for nitrotyrosine.

<p>Typical examples (upper panel) and quantitative analysis (lower panel) of immunohistochemistry for lung tissue nitrotyrosine formation from mice without (dotted boxplots) and with (hatched boxplots) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O₂ (grey boxplots) (n = 8 in each group). All data median (quartiles, range), § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).</p