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We study the effects of surface tension and yield stress on mucus plug rupture. A three-dimensional simplified configuration is employed to simulate mucus plug rupture in a collapsed lung airway of the tenth generation. The Herschel–Bulkley model is used to take into account the non-Newtonian viscoplastic fluid properties of mucus. Results show that the maximum wall shear stress greatly changes right prior to the rupture of the mucus plug. The surface tension influences mainly the late stage of the rupture process when the plug deforms greatly and the curvature of the mucus–air interface becomes significant. High surface tension increases the wall shear stress and the time needed to rupture since it produces a resistance to the rupture, as well as strong stress and velocity gradients across the mucus–air interface. The yield stress effects are pronounced mainly at the beginning. High yield stress makes the plug take a long time to yield and slows down the whole rupture process. When the effects induced by the surface tension and yield forces are comparable, dynamical quantities strongly depend on the ratio of the two forces. The pressure difference (the only driving in the study) contributes to wall shear stress much more than yield stress and surface tension per unit length. Wall shear stress is less sensitive to the variation in yield stress than that in surface tension. In general, wall shear stress can be effectively reduced by the smaller pressure difference and surface tension.

Human respiratory mucus has non-Newtonian rheological properties of viscoelasticity, shear-thinning and yield stress. They play significant roles in mucus clearance by ciliary motion as well as cough [5,7,9]. Mucus is hypersecreted in such lung diseases as cystic fibrosis and asthma. Mucus hypersecretion damages mucus clearance mechanism [6], and more likely causes plugs to block partial or total airways [4].Copyright © 2013 by ASME

Mucus in a human lung has non-Newtonian properties such as shear-thinning, yield stress, and viscoelasticity. Rheological changes of mucus may greatly affect its ability to function as a lubricant, selective barrier, and the body’s first line of defense against infection (Lai 2009). Patients with COPD, asthma, or cystic fibrosis often have mucus hyper-secretion. Mucus plugging can cause total airway obstruction (Kant 2007). If mucus is too thick, for example in severe bronchitis or cystic fibrosis where the sputum viscosity can be more than 105 times that of water, patients experience great difficulty in mucus clearance, resulting in bacterial overgrowth (Lai 2009). The understanding of the mechanisms involved in mucus clearance is far from complete. For instance, the relation is not known between the non-Newtonian properties of the mucus layer and ciliary function in thickened mucus (Button 2008).Copyright © 2011 by ASME

There are several mechanisms which may cause airway closure in the lung. In this paper, we focus on airway closure due to the capillary instability [1]. In Gauglitz and Radke’s study [2], they showed that once the ratio of film thickness to tube radius is larger than 0.12, airway closure could occur. The induced interfacial deformation creates a driving pressure which forces more liquid into a growing bulge. The interface will then deform rapidly towards the end of the closure process due to the presence of large curvatures, which create strong driving pressures and will eventually lead to the formation of a liquid plug. Due to the instability, stresses, including normal and shear stresses on the airway wall, will be induced. The epithelial cells on the inner wall of the airway may be injured by these induced stresses. The purpose of this study is to calculate the wall stresses for a two-layer system and determine if the magnitude of the stresses are sufficient to injure the epithelial cells.

The airway closure due to capillary instability [1] occurs in lung diseases such as asthma, cystic fibrosis, or emphysema. The reopening process involves displacement of plugs constituted from mucus, a non-Newtonian fluid with a yield stress, in the airways. In this work the transient propagation of mucus plugs in a 2D channel is studied numerically, assuming that the mucus is a Bingham fluid. The governing equations are discretized by a spectral element formulation and the free surface is resolved with an Arbitrary Lagrangian Eulerian (ALE) approach [2]. The constitutive equation for a Bingham fluid is implemented through a regularized constitutive equation. According to the numerical results, the yield stress behavior of the plug modifies the plug shape, the pattern of the streamlines and the distribution of stresses in the plug domain and along the walls in a significant way. The distribution along the walls is a major factor in studying cell injuries.Copyright © 2011 by ASME

There are several mechanisms which may cause airway closure in the lung. In this paper, we focus on airway closure due to the capillary instability [1]. In Gauglitz and Radke’s study [2], they showed that once the ratio of film thickness to tube radius is larger than 0.12, airway closure could occur. The induced interfacial deformation creates a driving pressure which forces more liquid into a growing bulge. The interface will then deform rapidly towards the end of the closure process due to the presence of large curvatures, which create strong driving pressures and will eventually lead to the formation of a liquid plug. Due to the velocity and pressure gradients in the liquid film caused by the instability, stresses, including normal and shear stresses on the airway wall, will be induced. The epithelial cells on the inner wall of the airway may be injured by these induced stresses. The purpose of this study is to measure the stresses on airway numerically and determine if the magnitude of the stresses are sufficient to injure the epithelial cells.Copyright © 2010 by ASME

The occlusion of pulmonary airways can be caused by many respiratory diseases such as respiratory distress syndrome. It is believed that these occluded airways are reopened by the propagation of an air finger. The mechanics of airway reopening have been studied in-depth for an individual airway [1,2] without considering the frequent branching of pulmonary airways. The presence of a bifurcation leads to the question of whether the propagating air finger will clear both branches of the airway or will propagate through a single branch, leaving the other branch occluded. The propagation of a finite length liquid plug through a fixed bifurcation has been studied experimentally [3, 4]. We wish to develop a numerical model for the propagation of an air finger through bifurcating channel filled with a viscous fluid. In this model, the air finger is driven by a pressure difference between the parent channel and the two daughter branches. The presence of an additional pressure difference between the two branches can cause unsymmetrical splitting of the air finger and, above a critical pressure difference, prevent the clearance of both branches.Copyright © 2010 by ASME

The airway closure due to the capillary instability [1] occurs in lung diseases such as asthma, cystic fibrosis, or emphysema. The reopening process involves with displacement of plugs constituted from mucus, a non-Newtonian fluid with a yield stress, in the airways. In this work the steady propagation of mucus plugs in a 2D channel is studied numerically, assuming that the mucus is a Bingham fluid. The governing equations are solved by a mixed-discontinuous finite element formulation and the free surface is resolved with the method of spines. The constitutive equation for Bingham fluid is implemented through a regularized constitutive equation. According to the numerical results, the yield stress behavior of the plug modifies the plug shape, the pattern of the streamlines and the distribution of stresses in the plug domain and along the walls in a significant way. The distribution along the walls is a major factor in studying cell injuries.Copyright © 2010 by ASME

A thin liquid layer coating the airway can be unstable and forms a plug. Airway closure usually happens at the small airways near the end of expiration, often accompanied with hypersecretion or/and surfactant deficiency in the airway in a variety of lung diseases, such as chronic obstructive pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS). Modeling work by Halpern and Grotberg [1] has shown that several forces could contribute to airway closure, such as the surface tension instability and the wall compliance. Experiments in a capillary tube were conducted by Cassidy et al. [2] who found that adding surfactant increased the airway closure time and the critical film thickness. In vitro studies [3] [4] illustrated that exposure of primary human airway epithelial cells to plug propagation and rupture led to significant cell injury. Experimental studies [5] [6] on excised lungs or in vivo animal models have shown that severe tissue damage was found in surfactant-deficient lungs due to the repetitive airway reopening. However, mechanical forces induced by airway closure have not been experimentally evaluated.Copyright © 2009 by ASME

A thin annular film lining the inside of a rigid tube is modeled as a liquid-lined airway in this study. Due to the capillary instability, the liquid film can form a plug and obstruct the airway once the ratio of the film thickness to tube radius, e, is greater than a critical value ∼0.12. The dynamics of the closure process is simulated for a Newtonian viscous film with constant surface tension and a passive core gas phase. The numerical simulation employs the finite volume approach with a sharp interface method for the free surface. The computational results show that the wall shear stress and normal stress during closure can be strong enough to injure airway epithelial cells.Copyright © 2009 by ASME

The mucus layer which covers the respiratory tract is a non-Newtonian fluid with a yield stress. The amount of shear stress must exceed a certain value before significant deformation (i.e. flow) can occur. Therefore, for better understanding of some interesting phenomena in the airways, such as the propagation or rupture of a mucus plug, as may occur in asthma, cystic fibrosis, or emphysema, the yield stress behavior of the fluid needs to be considered as well.

A simplified model of alveolar liquid lining dynamics is developed using a stretchable two-dimensional slot and an insoluble surfactant. Using lubrication theory, a coupled set of evolution equations is derived that describes the film height and interfacial surfactant distribution during the oscillation cycle. This system is solved asymptotically in the limit of small stretching amplitudes. The unsteady flow field is characterized by vortices at the end positions of the oscillation cycle. The cycle-averaged flow field also contains vortical structures, whose number and size vary over parameter space. For large molecular species, like proteins and surfactants, the bulk Peclet numbers can be large, indicating the importance of this liquid layer in the transport process. This may have an impact on the effectiveness and optimization of several medical treatment modalities. Also, since the liquid lining covers many cells within an alveolus, the predicted flow/transport patterns can allow a communication pathway among cells of the same alveolus.