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Venous gas bubbles occur in recreational SCUBA divers in the absence of decompression sickness, forming venous gas emboli (VGE) which are trapped within pulmonary circulation and cleared by the lung without overt pathology. We hypothesized that asymptomatic VGE would transiently increase ventilation-perfusion mismatch due to their occlusive effects within the pulmonary circulation. Two sets of healthy volunteers (n = 11, n = 12) were recruited to test this hypothesis with a single recreational ocean dive or a baro-equivalent dry hyperbaric dive. Pulmonary studies (intrabreath V (A)/Q (iV/Q), alveolar dead space, and FVC) were conducted at baseline and repeat 1- and 24-h after the exposure. Contrary to our hypothesis V (A)/Q mismatch was decreased 1-h post-SCUBA dive (iV/Q slope 0.023 +/- 0.008 ml(-1) at baseline vs. 0.010 +/- 0.005 NS), and was significantly reduced 24-h post-SCUBA dive (0.000 +/- 0.005, p &lt; 0.05), with improved V (A)/Q homogeneity inversely correlated to dive severity. No changes in V (A)/Q mismatch were observed after the chamber dive. Alveolar dead space decreased 24-h post-SCUBA dive (78 +/- 10 ml at baseline vs. 56 +/- 5, p &lt; 0.05), but not 1-h post dive. FVC rose 1-h post-SCUBA dive (5.01 +/- 0.18 l vs. 5.21 +/- 0.26, p &lt; 0.05), remained elevated 24-h post SCUBA dive (5.06 +/- 0.2, p &lt; 0.05), but was decreased 1-hr after the chamber dive (4.96 +/- 0.31 L to 4.87 +/- 0.32, p &lt; 0.05). The degree of V (A)/Q mismatch in the lung was decreased following recreational ocean dives, and was unchanged following an equivalent air chamber dive, arguing against an impact of VGE on the pulmonary circulation.

Ventilation-perfusion inequality in the human lung is not increased following no-decompression-stop hyperbaric exposure