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

2015 ◽  
Vol 119 (3) ◽  
pp. 190-201 ◽  
Author(s):  
Zheng-long Chen ◽  
Yuan-lin Song ◽  
Zhao-yan Hu ◽  
Su Zhang ◽  
Ya-zhu Chen
Keyword(s):  
Surface Tension ◽  
Respiratory Rate ◽  
Inflation Rate ◽  
Mechanical Stresses ◽  
Normal Lung ◽  
Shear Stresses ◽  
Fluid Viscosity ◽  
Small Airways ◽  
Protective Ventilation Strategy ◽  
Elevated Surface

Alveolar overdistension and mechanical stresses generated by repetitive opening and closing of small airways and alveoli have been widely recognized as two primary mechanistic factors that may contribute to the development of ventilator-induced lung injury. A long-duration exposure of alveolar epithelial cells to even small, shear stresses could lead to the changes in cytoskeleton and the production of inflammatory mediators. In this paper, we have made an attempt to estimate in situ the magnitudes of mechanical stresses exerted on the alveolar walls during repetitive alveolar reopening by using a tape-peeling model of McEwan and Taylor (35). To this end, we first speculate the possible ranges of capillary number ( Ca) ≡ μU/ γ (a dimensionless combination of surface tension γ, fluid viscosity μ, and alveolar opening velocity U) during in vivo alveolar opening. Subsequent calculations show that increasing respiratory rate or inflation rate serves to increase the values of mechanical stresses. For a normal lung, the predicted maximum shear stresses are <15 dyn/cm2 at all respiratory rates, whereas for a lung with elevated surface tension or viscosity, the maximum shear stress will notably increase, even at a slow respiratory rate. Similarly, the increased pressure gradients in the case of elevated surface or viscosity may lead to a pressure drop >300 dyn/cm2 across a cell, possibly inducing epithelial hydraulic cracks. In addition, we have conceived of a geometrical model of alveolar opening to make a prediction of the positive end-expiratory pressure (PEEP) required to splint open a collapsed alveolus, which as shown by our results, covers a wide range of pressures, from several centimeters to dozens of centimeters of water, strongly depending on the underlying pulmonary conditions. The establishment of adequate regional ventilation-to-perfusion ratios may prevent recruited alveoli from reabsorption atelectasis and accordingly, reduce the required levels of PEEP. The present study and several recent animal experiments likewise suggest that a lung-protective ventilation strategy should not only include small tidal volume and plateau pressure limitations but also consider such cofactors as ventilation frequency and inflation rate.

Three-dimensional airway reopening: the steady propagation of a semi-infinite bubble into a buckled elastic tube

2003 ◽  
Vol 478 ◽  
pp. 47-70 ◽  
Author(s):  
ANDREW L. HAZEL ◽  
MATTHIAS HEIL
Keyword(s):  
Surface Tension ◽  
Three Dimensional ◽  
Propagation Speed ◽  
Elastic Tube ◽  
Shear Stresses ◽  
Fluid Viscosity ◽  
Flow Topology ◽  
Airway Reopening ◽  
Bubble Pressure ◽  
Steady Propagation

We consider the steady propagation of an air finger into a buckled elastic tube initially filled with viscous fluid. This study is motivated by the physiological problem of pulmonary airway reopening. The system is modelled using geometrically nonlinear Kirchhoff–Love shell theory coupled to the free-surface Stokes equations. The resulting three-dimensional fluid–structure-interaction problem is solved numerically by a fully coupled finite element method.The system is governed by three dimensionless parameters: (i) the capillary number, Ca=μU/σ*, represents the ratio of viscous to surface-tension forces, where μ is the fluid viscosity, U is the finger's propagation speed and σ* is the surface tension at the air–liquid interface; (ii) σ=σ*/(RK) represents the ratio of surface tension to elastic forces, where R is the undeformed radius of the tube and K its bending modulus; and (iii) A∞=A*∞/(4R2), characterizes the initial degree of tube collapse, where A*∞ is the cross-sectional area of the tube far ahead of the bubble.The generic behaviour of the system is found to be very similar to that observed in previous two-dimensional models (Gaver et al. 1996; Heil 2000). In particular, we find a two-branch behaviour in the relationship between dimensionless propagation speed, Ca, and dimensionless bubble pressure, p*b/(σ*/R). At low Ca, a decrease in p*b is required to increase the propagation speed. We present a simple model that explains this behaviour and why it occurs in both two and three dimensions. At high Ca, p*b increases monotonically with propagation speed and p*b/(σ*/R) ∝ Ca for sufficiently large values of σ and Ca. In a frame of reference moving with the finger velocity, an open vortex develops ahead of the bubble tip at low Ca, but as Ca increases, the flow topology changes and the vortex disappears.An increase in dimensional surface tension, σ*, causes an increase in the bubble pressure required to drive the air finger at a given speed; p*b also increases with A*∞ and higher bubble pressures are required to open less strongly buckled tubes. This unexpected finding could have important physiological ramifications. If σ* is sufficiently small, steady airway reopening can occur when the bubble pressure is lower than the external (pleural) pressure, in which case the airway remains buckled (non-axisymmetric) after the passage of the air finger. Furthermore, we find that the maximum wall shear stresses exerted on the airways during reopening may be large enough to damage the lung tissue.

Effects of surface tension and viscosity on airway reopening

1990 ◽  
Vol 69 (1) ◽  
pp. 74-85 ◽  
Author(s):  
D. P. Gaver ◽  
R. W. Samsel ◽  
J. Solway
Keyword(s):  
Surface Tension ◽  
Fluid Viscosity ◽  
Opening Pressure ◽  
Viscous Forces ◽  
Considerable Portion ◽  
Airway Opening ◽  
Wall Compliance ◽  
Large Opening ◽  
Surface Tension Forces ◽  
The Relationship

We studied airway opening in a benchtop model intended to mimic bronchial walls held in apposition by airway lining fluid. We measured the relationship between the airway opening velocity (U) and the applied airway opening pressure in thin-walled polyethylene tubes of different radii (R) using lining fluids of different surface tensions (gamma) and viscosities (mu). Axial wall tension (T) was applied to modify the apparent wall compliance characteristics, and the lining film thickness (H) was varied. Increasing mu or gamma or decreasing R or T led to an increase in the airway opening pressures. The effect of H depended on T: when T was small, opening pressures increased slightly as H was decreased; when T was large, opening pressure was independent of H. Using dimensional analysis, we found that the relative importance of viscous and surface tension forces depends on the capillary number (Ca = microU/gamma). When Ca is small, the opening pressure is approximately 8 gamma/R and acts as an apparent “yield pressure” that must be exceeded before airway opening can begin. When Ca is large (Ca greater than 0.5), viscous forces add appreciably to the overall opening pressures. Based on these results, predictions of airway opening times suggest that airway closure can persist through a considerable portion of inspiration when lining fluid viscosity or surface tension are elevated.

Airway surface liquid thickness as a function of lung volume in small airways of the guinea pig

1994 ◽  
Vol 77 (5) ◽  
pp. 2333-2340 ◽  
Author(s):  
D. Yager ◽  
T. Cloutier ◽  
H. Feldman ◽  
J. Bastacky ◽  
J. M. Drazen ◽  
...  
Keyword(s):  
Surface Tension ◽  
Epithelial Cells ◽  
Guinea Pig ◽  
Cross Sections ◽  
Lung Volume ◽  
Longitudinal Direction ◽  
Small Airways ◽  
Airway Surface Liquid ◽  
Residual Capacity ◽  
Surface Liquid

The average thickness and distribution of airway surface liquid (ASL) on the luminal surface of peripheral airways were measured in normal guinea pig lungs frozen at functional residual capacity (FRC) and total lung capacity (TLC). Tissue blocks containing cross sections of airways of internal perimeter 0.188–3.342 mm were cut from frozen lungs and imaged by low-temperature scanning electron microscopy (LTSEM). Measurements made from LTSEM images were found to be independent of freezing rate by comparison of measurements at rapid and slow freezing rates. At both lung volumes, the ASL was not uniformly distributed in either the circumferential or longitudinal direction; there were regions of ASL where its thickness was < 0.1 micron, whereas in other regions ASL collected in pools. Discernible liquid on the surfaces of airways frozen at FRC followed the contours of epithelial cells and collected in pockets formed by neighboring cells, a geometry consistent with a low value of surface tension at the air-liquid interface. At TLC airway liquid collected to cover epithelial cells and to form a liquid meniscus, a geometry consistent with a higher value of surface tension. The average ASL thickness (h) was approximately proportional to the square root of airway internal perimeter, regardless of lung volume. For airways of internal perimeter 250 and 1,800 microns, h was 0.9 and 1.8 microns at FRC and 1.7 and 3.7 microns at TLC, respectively. For a given airway internal perimeter, h was 1.99 times thicker at TLC than at FRC; the difference was statistically significant (P < 0.01; 95% confidence interval 1.29–3.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of surface tension and intraluminal fluid on mechanics of small airways

1997 ◽  
Vol 82 (1) ◽  
pp. 233-239 ◽  
Author(s):  
Mark J. Hill ◽  
Theodore A. Wilson ◽  
Rodney K. Lambert
Keyword(s):  
Surface Tension ◽  
Bending Stiffness ◽  
Liquid Interface ◽  
Cross Sectional Area ◽  
Pressure Curve ◽  
Small Airways ◽  
Sectional Area ◽  
Cross Sectional ◽  
Inner Surface ◽  
Air Liquid Interface

Hill, Mark J., Theodore A. Wilson, and Rodney K. Lambert.Effects of surface tension and intraluminal fluid on the mechanics of small airways. J. Appl. Physiol.82(1): 233–239, 1997.—Airway constriction is accompanied by folding of the mucosa to form ridges that run axially along the inner surface of the airways. The muscosa has been modeled (R. K. Lambert. J. Appl. Physiol. 71: 666–673, 1991) as a thin elastic layer with a finite bending stiffness, and the contribution of its bending stiffness to airway elastance has been computed. In this study, we extend that work by including surface tension and intraluminal fluid in the model. With surface tension, the pressure on the inner surface of the elastic mucosa is modified by the pressure difference across the air-liquid interface. As folds form in the mucosa, intraluminal fluid collects in pools in the depressions formed by the folds, and the curvature of the air-liquid interface becomes nonuniform. If the amount of intraluminal fluid is small, <2% of luminal volume, the pools of intraluminal fluid are small, the air-liquid interface nearly coincides with the surface of the mucosa, and the area of the air-liquid interface remains constant as airway cross-sectional area decreases. In that case, surface energy is independent of airway area, and surface tension has no effect on airway mechanics. If the amount of intraluminal fluid is >2%, the area of the air-liquid interface decreases as airway cross-sectional area decreases, and surface tension contributes to airway compression. The model predicts that surface tension plus intraluminal fluid can cause an instability in the area-pressure curve of small airways. This instability provides a mechanism for abrupt airway closure and abrupt reopening at a higher opening pressure.

THE ALVEOLAR LINING LAYER

PEDIATRICS ◽  
1962 ◽  
Vol 30 (2) ◽  
pp. 324-330
Author(s):  
Mary Ellen Avery
Keyword(s):  
Surface Tension ◽  
Secretory Activity ◽  
Hyaline Membrane Disease ◽  
Normal Lung ◽  
Elastic Recoil ◽  
Alveolar Cells ◽  
Electron Microscopic ◽  
Hyaline Membrane ◽  
Surface Active ◽  
Air Liquid Interface

The alveoli of the normal lung are lined by a substance which exerts surface tension at the air-liquid interface. In the expanded lung the tension is high and operates to increase the elastic recoil of the lung. In the lung at low volumes the surface tension becomes extremely low. This confers stability on the airspaces and thus prevents atelectasis. This lining layer is a lipoprotein film, which is not found where alveoli are still lined by cuboidal epithelium. Its time of appearance coincides with the appearance of alveolar lining cells. Electron microscopic evidence of secretory activity in alveolar cells suggests that they may be the source of the surface-active film. The normal alveolar lining layer is not present in lungs of infants who die from profound atelectasis and hyaline membrane disease. Whether its absence is a failure of development or due to inactivation is not established.

Culture Medium With Blood Analog Mechanical Properties

2007 ◽  
Author(s):  
Chantal N. van den Broek ◽  
Marcel C. M. Rutten ◽  
Ole Frøbert ◽  
Frans N. van de Vosse
Keyword(s):  
Culture Medium ◽  
Arterial Wall ◽  
Ex Vivo ◽  
Shear Stresses ◽  
Fluid Viscosity ◽  
Endothelial Phenotype ◽  
Physiological Fluid ◽  
Wall Shear ◽  
Medium Viscosity

Culture of arteries has become increasingly important in studying atherosclerosis and the effect of clinical interventions [1]. Ideally, arterial culturing should imitate in vivo conditions within an ex vivo environment. Physiological wall shear stresses are important as they induce an atheroprotective endothelial phenotype [2], which is relevant for maintaining arterial wall integrity. The arteries in such ex vivo studies, however, are perfused with culture medium, which has a viscosity lower than blood. Previously, the culture medium has been supplemented with dextran to obtain physiological fluid viscosity and wall shear stresses. However, several researchers [3,4] reported side effects of dextran on the cells in the arterial wall independent of its effect on medium viscosity. Also, dextran increases medium osmolality to supraphysiological levels [5]. This suggests that dextran may not be the optimal substance to increase medium viscosity.

Gravity waves with effect of surface tension and fluid viscosity

2006 ◽  
Vol 18 (3) ◽  
pp. 171-176 ◽  
Author(s):  
Xiao-Bo CHEN ◽  
Wen-Yang DUAN ◽  
Dong-Qiang LU
Keyword(s):  
Surface Tension ◽  
Gravity Waves ◽  
Fluid Viscosity ◽  
Effect Of Surface

scholarly journals Experimental study of the wake behind a surface-piercing cylinder for a clean and contaminated free surface

2000 ◽  
Vol 402 ◽  
pp. 109-136 ◽  
Author(s):  
AMY WARNCKE LANG ◽  
MORTEZA GHARIB
Keyword(s):  
Surface Tension ◽  
Free Surface ◽  
Turbulent Flows ◽  
Cross Sections ◽  
Surface Deformation ◽  
Surface Condition ◽  
Free Surface Flows ◽  
Shear Stresses ◽  
Surface Contaminants ◽  
A New Technique

This experimental investigation into the nature of free-surface flows was to study the effects of surfactants on the wake of a surface-piercing cylinder. A better understanding of the process of vorticity generation and conversion at a free surface due to the absence or presence of surfactants has been gained. Surfactants, or surface contaminants, have the tendency to reduce the surface tension proportionally to the respective concentration at the free surface. Thus when surfactant concentration varies across a free surface, surface tension gradients occur and this results in shear stresses, thus altering the boundary condition at the free surface. A low Reynolds number wake behind a surface-piercing cylinder was chosen as the field of study, using digital particle image velocimetry (DPIV) to map the velocity and vorticity field for three orthogonal cross-sections of the flow. Reynolds numbers ranged from 350 to 460 and the Froude number was kept below 1.0. In addition, a new technique was used to simultaneously map the free surface deformation. Shadowgraph imaging of the free surface was also used to gain a better understanding of the flow. It was found that, depending on the surface condition, the connection of the shedding vortex filaments in the wake of the cylinder was greatly altered with the propensity for surface tension gradients to redirect the vorticity near the free surface to that of the surface-parallel component. This result has an impact on the understanding of turbulent flows in the vicinity of a free surface with varying surface conditions.

A Numerical Study of Friction in Isothermal EHD Rolling-Sliding Sphere-Plane Contacts With Spinning

2010 ◽  
Vol 132 (2) ◽  
Author(s):  
H. Dormois ◽  
N. Fillot ◽  
W. Habchi ◽  
G. Dalmaz ◽  
P. Vergne ◽  
...  
Keyword(s):  
Film Thickness ◽  
Numerical Study ◽  
Friction Reduction ◽  
Shear Stresses ◽  
Fluid Viscosity ◽  
Stress Distributions ◽  
Eyring Model ◽  
Element Approach ◽  
Transverse Shear Stresses ◽  
Shear Heating

This paper presents a study of the spinning influence on film thickness and friction in EHL circular contacts under isothermal and fully flooded conditions. Pressure and film thickness profiles are computed with an original full-system finite element approach. Friction was thereafter investigated with the help of a classical Ree–Eyring model to calculate the longitudinal and transverse shear stresses. An analysis of both the velocity and shear stress distributions at every point of the contact surfaces has allowed explaining the fall of the longitudinal friction coefficient due to the occurrence of opposite shear stresses over the contact area. Moreover in the transverse direction spinning favors large shear stresses of opposite signs, decreasing the fluid viscosity by non-Newtonian effects. These effects have direct and coupled consequences on the friction reduction that is observed in the presence of spinning. They are expected to further decrease friction in real situations due to shear heating.

On the interaction of Taylor length scale size droplets and isotropic turbulence

2016 ◽  
Vol 806 ◽  
pp. 356-412 ◽  
Author(s):  
Michael S. Dodd ◽  
Antonino Ferrante
Keyword(s):  
Surface Tension ◽  
Surface Area ◽  
Dissipation Rate ◽  
Isotropic Turbulence ◽  
Droplet Surface ◽  
Rate Of Change ◽  
Length Scale ◽  
Fluid Viscosity ◽  
Carrier Fluid ◽  
Two Fluid

Droplets in turbulent flows behave differently from solid particles, e.g. droplets deform, break up, coalesce and have internal fluid circulation. Our objective is to gain a fundamental understanding of the physical mechanisms of droplet–turbulence interaction. We performed direct numerical simulations (DNS) of 3130 finite-size, non-evaporating droplets of diameter approximately equal to the Taylor length scale and with 5 % droplet volume fraction in decaying isotropic turbulence at initial Taylor-scale Reynolds number $\mathit{Re}_{\unicode[STIX]{x1D706}}=83$. In the droplet-laden cases, we varied one of the following three parameters: the droplet Weber number based on the r.m.s. velocity of turbulence ($0.1\leqslant \mathit{We}_{rms}\leqslant 5$), the droplet- to carrier-fluid density ratio ($1\leqslant \unicode[STIX]{x1D70C}_{d}/\unicode[STIX]{x1D70C}_{c}\leqslant 100$) or the droplet- to carrier-fluid viscosity ratio ($1\leqslant \unicode[STIX]{x1D707}_{d}/\unicode[STIX]{x1D707}_{c}\leqslant 100$). In this work, we derive the turbulence kinetic energy (TKE) equations for the two-fluid, carrier-fluid and droplet-fluid flow. These equations allow us to explain the pathways for TKE exchange between the carrier turbulent flow and the flow inside the droplet. We also explain the role of the interfacial surface energy in the two-fluid TKE equation through the power of the surface tension. Furthermore, we derive the relationship between the power of surface tension and the rate of change of total droplet surface area. This link allows us to explain how droplet deformation, breakup and coalescence play roles in the temporal evolution of TKE. Our DNS results show that increasing $\mathit{We}_{rms}$, $\unicode[STIX]{x1D70C}_{d}/\unicode[STIX]{x1D70C}_{c}$ and $\unicode[STIX]{x1D707}_{d}/\unicode[STIX]{x1D707}_{c}$ increases the decay rate of the two-fluid TKE. The droplets enhance the dissipation rate of TKE by enhancing the local velocity gradients near the droplet interface. The power of the surface tension is a source or sink of the two-fluid TKE depending on the sign of the rate of change of the total droplet surface area. Thus, we show that, through the power of the surface tension, droplet coalescence is a source of TKE and breakup is a sink of TKE. For short times, the power of the surface tension is less than $\pm 5\,\%$ of the dissipation rate. For later times, the power of the surface tension is always a source of TKE, and its magnitude can be up to 50 % of the dissipation rate.

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