Non-uniform alveolar liquid phase thickness in alveolar edema: a conceptual analysis of the effect on oxygenation

This is the authors' abstract. We don't add key points for this paper.

Pulmonary edema reduces lung gas exchange, but multiple mechanisms limit the reduction. We propose an additional mechanism. In flooded alveoli of excised lungs, the distribution of alveolar edema liquid is often non-uniform. Oxygen flux through a given volume of edema liquid is greater for non-uniform than uniform liquid distribution. If alveolar oxygen transport were purely diffusive, one could quantify the difference analytically using Fick’s first law of diffusion. But capillary advection also influences alveolar oxygen transport. We assess alveolar oxygen transport computationally in an alveolar model generated by extruding five sides of a cube and dividing the thickness of each side into an aqueous domain (alveolar liquid and tissue, which constitute the barrier to diffusion) and a capillary blood domain. With a physiologic aqueous-domain thickness, t B , of 0.71 µm, outlet oxygen saturation is 98%. Increasing t B to 5 µm only reduces saturation to 97%, but increasing t B to 15 µm reduces saturation to 85%. For the same aqueous-domain volume and interfacial area, non-uniform liquid distribution can return saturation to 89%. How non-uniform liquid distribution may interact with other mechanisms affecting oxygenation is considered. For example, alveolar edema is often accompanied by non-uniform perfusion and we find that alveolar oxygen transport drops more sharply below physiologic flow rate than it increases above. Thus non-uniform perfusion acts counter to non-uniform alveolar liquid distribution and reduces oxygenation. Our model has a functional, if simplistic, geometry; uses fundamental gas-exchange relations; and raises questions about oxygenation capability in edematous lungs.