Abstract:
The explanation for prone and supine differences in tissue density and pleural pressure gradients in the healthy lung has been inferred from several studies as compression of dependent tissue by the heart in the supine posture; however, this hypothesis has not been directly confirmed. Differences could also arise from change in shape of the chest wall and diaphragm, and because of shape with respect to gravity. The contribution of this third mechanism is explored here. Tissue density and static elastic recoil were estimated in the supine and prone left human lung at functional residual capacity using a finite-element analysis. Supine model geometries were derived from multidetector row computed tomography imaging of two subjects: one normal (subject 1), and one with small airway disease (subject 2). For each subject, the prone model was the supine lung shape with gravity reversed; therefore, the prone model was isolated from the influence of displacement of the diaphragm, chest wall, or heart. Model estimates were validated against multidetector row computed tomography measurement of regional density for each subject supine and an independent study of the prone and supine lung. The magnitude of the gradient in density supine (−4.33%/cm for subject 1, and −4.96%/cm for subject 2) was nearly twice as large as for the prone lung (−2.72%/cm for subject 1, and −2.51%/cm for subject 2), consistent with measurements in dogs. The corresponding pleural pressure gradients were 0.54 cmH2O/cm (subject 1) and 0.56 cmH2O/cm (subject 2) for supine, and 0.29 cmH2O/cm (subject 1) and 0.27 cmH2O/cm (subject 2) for prone. A smaller prone gradient was predicted without shape change of the “container” or support of the heart by the lung. The influence of the heart was to constrain the shape in which the lung deformed.
