Patient-specific optimization of mechanical ventilation for patients with acute respiratory distress syndrome using quasi-static pulmonary P-V data.

Quasi-static, pulmonary pressure-volume (P-V) curves were combined with a respiratory system model to analyze tidal pressure cycles, simulating mechanical ventilation of patients with acute respiratory distress syndrome (ARDS). Two important quantities including 1) tidal recruited volume and 2) tidal hyperinflated volume were analytically computed by integrating the distribution of alveolar elements over the affected pop-open pressure range. We analytically predicted the tidal recruited volume of four canine subjects and compared our results with similar experimental measurements on canine models for the validation. We then applied our mathematical model to the P-V data of ARDS populations in four stages of Early ARDS, Deep Knee, Advanced ARDS and Baby Lung to quantify the tidal recruited volume and tidal hyperinflated volume as an indicator of ventilator-induced lung injury (VILI). These quantitative predictions based on patient-specific P-V data suggest that the optimum parameters of mechanical ventilation including PEEP and Tidal Pressure (Volume) are largely varying among ARDS population and are primarily influenced by the degree in the severity of ARDS.

Quasi-static pulmonary P-V curves of patients with ARDS, Part I: Characterization.

Quasi-static, pulmonary pressure-volume (P-V) curves are combined with a respiratory system model to analyze characteristics of patients with acute respiratory distress syndrome (ARDS). It is shown that there exist distinct differences between healthy- and injured-respiratory system in the order of magnitudes of parameters of their P-V model equation. Four stages of ARDS (Early ARDS, Deep knee, Advanced ARDS and Baby lung) are defined quantitatively in terms of these parameters.

Flow-induced endothelial surface reorganization and minimization of entropy generation rate.

Effects of hydrodynamic shear on the shape of the endothelial surface are examined based on evaluations of the rate of entropy generation at the cell surface. A linear solution of the flow over a sinusoidally varying endothelial surface is used to evaluate the entropy generation rate on the cell surface for which measured cell dimensions are available. Both the local rate of entropy generation (equivalent to the rate of energy dissipation by viscous shear) at the peak of a cell and the total entropy generation rate over the cell surface are minimized under conditions of a constant cell surface area and a constant cell peak height; which yields horizontal cell dimensions that are close to those obtained experimentally.