A micromechanical model for estimating alveolar wall strain in mechanically ventilated edematous lungs

Abstract

To elucidate the micromechanics of pulmonary edema has been a significant medical concern, which is beneficial to better guide ventilator settings in clinical practice. In this paper, we present an adjoining two-alveoli model to quantitatively estimate strain and stress of alveolar walls in mechanically ventilated edematous lungs. The model takes into account the geometry of the alveolus, the effect of surface tension, the length-tension properties of parenchyma tissue, and the change in thickness of the alveolar wall. On the one hand, our model supports experimental findings (Perlman CE, Lederer DJ, Bhattacharya J. Am J Respir Cell Mol Biol 44: 34-39, 2011) that the presence of a liquid-filled alveolus protrudes into the neighboring air-filled alveolus with the shared septal strain amounting to a maximum value of 1.374 (corresponding to the maximum stress of 5.12 kPa) even at functional residual capacity; on the other hand, it further shows that the pattern of alveolar expansion appears heterogeneous or homogeneous, strongly depending on differences in air-liquid interface tension on alveolar segments. The proposed model is a preliminary step toward picturing a global topographical distribution of stress and strain on the scale of the lung as a whole to prevent ventilator-induced lung injury.

Determination of rheology and surface tension of airway surface liquid: a review of clinical relevance and measurement techniques

“…Two main physical mechanisms for VILI are lung tissue overdistention caused by surface tension-induced alterations in interalveolar micromechanics and atelectrauma to the epithelial cells during repetitive airway reopening and closure [39–41]. The prediction from an adjoining two-alveoli model by Chen et al [42] shows that the pattern of alveolar expansion can appear heterogeneous or homogeneous, strongly depending on differences in air-liquid interface tension on alveolar segments. More specifically, if surface tension in the liquid-filled alveolus is much greater than that in the air-filled alveolus, then alveolar expansion is heterogeneous.…”

An estimation of mechanical stress on alveolar walls during repetitive alveolar reopening and closure

“…For a pair of juxtaposed alveoli a1-a3 or a2-a3, shown in Fig. 1, our prior study (8) showed that the wall-tension stress in rat lungs varied approximately in the range of 2.07 kPa Յ Յ 5.12 kPa during inflation, from 5 to near 15 cmH 2O. With an average human alveolar septum thickness of 8 m (37), we estimate the alveolar wall tension T approximately in the range of 16.56 dyn/cm Յ T Յ 40.96 dyn/cm.…”

A Physiologically Informed Strategy to Effectively Open, Stabilize, and Protect the Acutely Injured Lung

“…Stress-focus: edema-filled or collapsed alveoli adjacent to air-filled alveoli create a stress-focus causing the alveolar wall to bend toward the fluid-filled alveolus (green arrow), which can cause stress failure at the alveolar wall (Perlman et al, 2011). Stress-focus is another key mechanism of VILI (Perlman et al, 2011;Chen et al, 2014;Makiyama et al, 2014;Retamal et al, 2014). Thus, the pathologic tetrad sets up a vicious cycle of high microvascular permeability → edema → surfactant deactivation → high alveolar surface tension → more edema → alveolar R/D → further increase in microvascular permeability → severe ARDS (Nieman and Bredenberg, 1985).…”