Lung volume does not alter the distribution of pulmonary perfusion in dependent lung in supine humans.

There is a gravitational influence on pulmonary perfusion, including in the most dependent lung, where perfusion is reduced, termed Zone 4. Studies using xenon-133 show Zone 4 behaviour, present in the dependent 4 cm at total lung capacity (TLC), affects the dependent 11 cm at functional residual capacity (FRC) and almost all the lung at residual volume (RV). These differences were ascribed to increased resistance in extra-alveolar vessels at low lung volumes although other mechanisms have been proposed. To further evaluate the behaviour of perfusion in dependent lung using a technique that directly measures pulmonary perfusion and corrects for tissue distribution by measuring regional proton density, seven healthy subjects (age = 38 ± 6 years, FEV1 = 104 ± 7% predicted) underwent magnetic resonance imaging in supine posture. Data were acquired in the right lung during breath-holds at RV, FRC and TLC. Arterial spin labelling quantified regional pulmonary perfusion, which was normalized for regional proton density measured using a fast low-angle shot technique. The height of the onset of Zone 4 behaviour was not different between lung volumes (P = 0.23). There were no significant differences in perfusion (expressed as ml min⁻¹ g⁻¹) between lung volumes in the gravitationally intermediate (RV = 8.9 ± 3.1, FRC = 8.1 ± 2.9, TLC = 7.4 ± 3.6; P = 0.26) and dependent lung (RV = 6.6 ± 2.4, FRC = 6.1 ± 2.1, TLC = 6.4 ± 2.6; P = 0.51). However, at TLC perfusion was significantly lower in non-dependent lung than at FRC or RV (3.6 ± 3.3, 7.7 ± 1.5, 7.9 ± 2.0, respectively; P < 0.001). These data suggest that the mechanism of the reduction in perfusion in dependent lung is unlikely to be a result of lung volume related increases in resistance in extra-alveolar vessels. In supine posture, the gravitational influence on perfusion is remarkably similar over most of the lung, irrespective of lung volume.

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

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 < 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 < 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 < 0.05), remained elevated 24-h post SCUBA dive (5.06 +/- 0.2, p < 0.05), but was decreased 1-hr after the chamber dive (4.96 +/- 0.31 L to 4.87 +/- 0.32, p < 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.

Inhomogeneity of ventilation leads to unpredictable errors in measured D(L)CO.

We evaluated the effects of inhomogeneity of ventilation on single-breath (SB), rebreathing (RB) and open circuit (OC) D(L)CO using a mathematical model consisting of two alveolar compartments and a common dead space. Inhomogeneity in ventilation was studied by altering inspired volume, initial alveolar volume and compartment size independently. When distribution of inspired volume between alveolar compartments was inhomogeneous (9:1), D(L)CO was underestimated by 35% for SB, 25% for RB, and 16% for OC, and there was an underestimation in V(A) of 9%, 15% and 9%, respectively. With inhomogeneity in initial alveolar volume there was an overestimation in D(L)CO of 13%, 7% and 11% for SB, RB and OC techniques and an underestimation of V(A) of 7%, 12% and 9%. Finally inhomogeneity of compartment size led to an underestimation of D(L)CO of 18%, 35% and 36% with no change in measured V(A). These results suggest D(L)CO measurements are sensitive to inhomogeneity of ventilation, and importantly, all techniques were at times, significantly in error.

The heterogeneity of regional specific ventilation is unchanged following heavy exercise in athletes.

Heavy exercise increases ventilation-perfusion mismatch and decreases pulmonary gas exchange efficiency. Previous work using magnetic resonance imaging (MRI) arterial spin labeling in athletes has shown that, after 45 min of heavy exercise, the spatial heterogeneity of pulmonary blood flow was increased in recovery. We hypothesized that the heterogeneity of regional specific ventilation (SV, the local tidal volume over functional residual capacity ratio) would also be increased following sustained exercise, consistent with the previously documented changes in blood flow heterogeneity. Trained subjects (n = 6, maximal O2 consumption = 61 ± 7 ml·kg(-1)·min(-1)) cycled 45 min at their individually determined ventilatory threshold. Oxygen-enhanced MRI was used to quantify SV in a sagittal slice of the right lung in supine posture pre- (preexercise) and 15- and 60-min postexercise. Arterial spin labeling was used to measure pulmonary blood flow in the same slice bracketing the SV measures. Heterogeneity of SV and blood flow were quantified by relative dispersion (RD = SD/mean). The alveolar-arterial oxygen difference was increased during exercise, 23.3 ± 5.3 Torr, compared with rest, 6.3 ± 3.7 Torr, indicating a gas exchange impairment during exercise. No significant change in RD of SV was seen after exercise: preexercise 0.78 ± 0.15, 15 min postexercise 0.81 ± 0.13, 60 min postexercise 0.78 ± 0.08 (P = 0.5). The RD of blood flow increased significantly postexercise: preexercise 1.00 ± 0.12, 15 min postexercise 1.15 ± 0.10, 45 min postexercise 1.10 ± 0.10, 60 min postexercise 1.19 ± 0.11, 90 min postexercise 1.11 ± 0.12 (P < 0.005). The lack of a significant change in RD of SV postexercise, despite an increase in the RD of blood flow, suggests that airways may be less susceptible to the effects of exercise than blood vessels.