Computational pulmonary edema: A microvascular model of alveolar capillary and interstitial flow.

Abstract

We present a microvascular model of fluid transport in the alveolar septa related to pulmonary edema. It consists of a two-dimensional capillary sheet coursing by several alveoli. The alveolar epithelial membrane runs parallel to the capillary endothelial membrane with an interstitial layer in between, making one long septal tract. A coupled system of equations is derived using lubrication theory for the capillary blood, Darcy flow for the porous media of the interstitium, a passive alveolus, and the Starling equation at both membranes. Case examples include normal physiology, cardiogenic pulmonary edema, noncardiogenic edema Acute Respiratory Distress Syndrome (ARDS) and hypoalbuminemia, and the effects of positive end expiratory pressure. COVID-19 has dramatically increased ARDS in the world population, raising the urgency for such a model to create an analytical framework. Under normal conditions, the fluid exits the alveolus, crosses the interstitium, and enters the capillary. For edema, this crossflow is reversed with the fluid leaving the capillary and entering the alveolus. Because both the interstitial and capillary pressures decrease downstream, the reversal can occur within a single septal tract, with edema upstream and clearance downstream. Overall, the interstitial pressures are found to be significantly more positive than values used in the traditional physiological literature that creates steep gradients near the upstream and downstream end outlets, driving significant flows toward the distant lymphatics. This new physiological flow may provide a possible explanation to the puzzle, noted since 1896, of how pulmonary lymphatics can function so far from the alveoli: the interstitium can be self-clearing.