Premature infants who suffer from NRDS due to surfactant deficiency exhibit a high lining-fluid surface tension and hence a propensity for prominent atelectasis, decreased lung compliance, increased work of breathing and impaired gas exchange. The postnatal delivery of exogenous surfactant can significantly lower surface tension forces in the lung and has been established as a standard therapeutic intervention in the management of preterm infants with NRDS [ 24 ].
Therefore, the study of the rheological properties of airway surface liquid has both physiological and clinical significance. Unfortunately, due to a lack of suitable in vivo and in situ measurement techniques, thus far, all rheological measurements of human respiratory mucus came from in vitro studies that may not give a true picture of in vivo conditions.
Moreover, reported literature values of the viscoelasticity of human respiratory mucus show large orders of magnitude intersubject, intrasubject, and even within the same mucus -sample variations Table 1. It is imperative to heighten collaborations between clinicians, biomedical engineers, and applied scientists to explain these variations in perspective of both physiology and experimental techniques, to further develop tools to assess the quantitative properties of airway surface liquid, and finally to correlate the biophysical properties of airway surface liquid with healthy versus diseased states.
This article reviews the importance of airway surface liquid rheology and surface tension measurements in: 1 maintaining the stability of small airways and alveoli; 2 preventing ventilator-induced lung injury; 3 optimizing surfactant replacement therapy SRT ; and 4 characterizing lung barrier and clearance functions.
Subsequently, new methods and techniques for determining the viscosity and surface tension of airway surface liquid are described. The role of the surface tension and viscosity of airway surface liquid in maintaining airway stability is primarily two-fold: retarding small airway closure and preventing alveolar collapse.
As described in Section 1, the liquid lining usually forms a thin and relatively uniform layer on the inner surface of the airway, but sometimes it is possible for the airway to become occluded by the liquid, leading to airway closure. In the former case, liquid in a uniform film lining on the inner wall of an axisymmetric airway redistributes via a classical fluid-elastic instability known as the Plateau-Rayleigh instability [ 30 , 33 , 34 ].
Halpern and coworkers revealed that the growth rate for a viscoelastic layer was larger than for a Newtonian fluid with the same viscosity [ 36 ]. The overall timescale required for an occlusion to form is small compared with a single breathing cycle, provided that no surfactant is present.
Halpern and Grotberg further demonstrated that the closure time for a pulmonary surfactant-rich film can be approximately five times greater than that for a film free of pulmonary surfactant [ 37 ]. As lung volume falls during expiration, the radius of the airway is decreased, thus resulting in an increase of the curvature of the air-liquid interface. The initially uniform and axisymmetric liquid lining can become unstable, and pressure gradients are induced in the fluid that drive flows redistributing the fluid.
As a result, in the region where the liquid lining film is thickest, surface tension creates a large pressure jump over the highly curved air-liquid interface, causing negative pressure in the liquid. At the same time, parenchymal tethering forces on the external surface of the airway fall because of the gradual increase in lung volumes. This combination of reduced lining fluid pressure and parenchymal tethering subjects the airway wall to a significant compressive load and promotes the propensity of the airway to buckle inward, producing a compliant collapse.
In diseased conditions such as pulmonary oedema or neonatal RDS, this compliant collapse of the airways may occur due to an increase in the volume of fluid or in the surface tension. Surface forces also have a critical effect on airspace stability, as illustrated in Fig. Two connected bubbles alveoli with a common pressure and a constant surface tension are blown at the end of a Y-tube [ 1 , 38 ].
According to the Laplace equation, the pressure generated by surface tension in the small bubble is larger than that in one with a greater diameter, resulting in an inherently unstable system: the smaller alveolus will eventually collapse and the larger one will become over-distended. Of course, this is not the case in a healthy lung. The surface tension of the alveolar lining fluid is variable in situ as a function of expansion and compression of the alveolar surface area due to the presence of pulmonary surfactant.
The surface tension drops as the alveolar surface decreases, and it rises when the surface expands, allowing for equal pressure between two different sized alveoli; therefore, system stability is maintained.
Connected alveoli illustrating the driving force collapsing the smaller alveolus in the case of constant surface tension. A number of theoretical and experimental studies have demonstrated that the increase in viscosity and surface tension of airway surface liquid likely results in VILI. 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 , 40 , 41 ].
The prediction from an adjoining two-alveoli model by Chen et al. 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.
Consider a pair of juxtaposed alveoli: the maximum stress and strain within the septum shared by the two alveoli may occur at a low alveolar pressure; in contrast, as alveoli inflate to near total lung capacity TLC , the stress and strain of the alveolar walls may decrease instead. On the other hand, if the surface tensions in two adjacent alveoli are identical, then alveolar expansion is homogenous; that is, the stress and strain of all alveolar septa will appear to linearly increase as alveolar volume varies from functional residual capacity FRC to near TLC.
These calculations are in good agreement with the experimental phenomenon observed by Perlman and coworkers [ 43 ]. Using real-time optical section microscopy, these investigators quantified the micromechanics of an air-filled alveolus that shares a septum with a liquid-filled alveolus. Instilling liquid into the alveolus produced a meniscus that changed the septal curvature and consequently the pressure difference across the septum. As a consequence, the air-filled alveolus bulged into its liquid-filled neighbour even at FRC.
Given that liquid-filled and air-filled alveoli can be focal, diffuse or patchy in pulmonary oedema, these findings may provide a novel understanding of segmental heterogeneities and alveolar overdistension during mechanical ventilation. Using thin-walled polyethylene tubes to mimic bronchial walls held in apposition by airway lining fluid, Gaver III et al.
Gaver III et al. When Ca is larger than 0. In subsequent studies, Bilek and Kay et al. The narrow channel of the chamber was filled with either phosphate-buffered saline high surface tension or Infasurf ONY, Buffalo, NY , a biologically derived pulmonary surfactant with low surface tension.
Airway reopening was generated by the steady progression of a semi-infinite bubble of air along the length of the channel, which displaced the occlusion fluid. Two bubble progression velocities were investigated, and the results showed that for the saline-occluded channels, both slow and fast bubble velocities resulted in significant cellular injury compared with the control and that for the Infasurf-occluded channels, cellular injury was dramatically reduced at both bubble velocities, indicating that surfactant has a protective effect.
A comparison of the experimental and theoretical observations demonstrated that among four potentially injurious components of the stress cycle associated with airway reopening shear stress, pressure, shear stress gradient or pressure gradient , the pressure gradient was the most predominant mechanism underlying the observed cellular damage [ 45 ]. Recently, Chen et al. As discussed above, rheological measurements of airway surface liquid during the progression of the disease in many pulmonary disorders have an important role in the management of mechanical ventilation.
Measured values of surface tension and viscoelasticity provide clinical data for establishing and validating mathematical models of VILI. Knowing the values of viscosity and surface tension of airway surface liquid enables clinicians to quickly determine individualized inflation pressures and PEEPs and to roughly estimate lung stress and strain based on computational models, thereby adjusting the ventilation settings or therapeutic strategies in time to avoid VILI as much as possible.
Exogenous SRT has been established as a standard therapeutic intervention for preterm and term neonates with clinically confirmed respiratory distress syndrome since the early s [ 10 , 21 , 49 ]. During traditional SRT, natural or synthetic surfactant is administered via an endotracheal tube either as a bolus or by infusion via a thin catheter inserted into the endotracheal tube.
Thereafter, the infants are maintained on mechanical ventilation. The results showed that this strategy reduced the need for mechanical ventilation and improved survival rates [ 21 , 50 , 51 ]. A number of alternatives to the administration of surfactant include the use of aerosolized surfactant preparations, laryngeal mask airway-aided delivery of surfactant, instillation of pharyngeal surfactant, and administration of surfactant using laryngoscopy or bronchoscopy [ 21 , 51 ].
SRT has also been applied to adults whose surfactant systems are compromised by ARDS, but clear indications of a distinct surfactant-mediated decrease in mortality or improvement in ventilator care of ARDS patients are still lacking [ 49 , 52 ]. Additionally, recent randomized clinical trials have indicated that preventive surfactant administration to infants with suspected NRDS is no longer effective in groups of infants when CPAP is used routinely [ 21 ].
Most previous studies on SRT failures have focused on examining the biophysical mechanisms for surfactant inhibition due to plasma proteins or lipids [ 49 ].
However, the three-dimensional model of SRT recently proposed by Filoche and colleagues provides new insights into this issue, as it strongly suggests that inadequate delivery of surfactant may be a major cause of SRT failure [ 53 ]. Using similar surfactant mixtures and instilled dose volume, these investigators simulated the delivery of surfactant to neonates and adults in 3D structural models of the lung airway tree.
The results revealed well-mixed distributions in the neonatal lungs but very inhomogeneous distributions in the adult lungs.
When liquid surfactant mixtures are instilled into the trachea via an endotracheal tube, they form liquid plugs, which are then blown distally into the branching network of the airways by forced inspirations. Filoche and colleagues simplified the above complicated flow process into two separate steps: step A, deposition of the liquid onto the airway walls into a trailing film; and step B, liquid plug splitting at an airway bifurcation.
Step A determines the total amount of liquid reaching the acini, i. Theoretical work by Helpern et al. Step B governs the homogeneity of delivery. This feature can be explained by the driving pressure at the bifurcation. When the fluid viscosity or plug velocity is too small, the driving pressure is not large enough to overcome gravity; thus, no liquid enters the upper gravitationally opposed daughter airway after bifurcation. In summary, the viscosity and surface tension of surfactant mixtures have a profound effect on the distribution quality of the delivered surfactant.
Furthermore, in the distal regions of the lung, surface tension gradient-induced Marangoni flows drive the surfactant deeper into the lung. This requires that the surface tension of the endogenous surfactant be above that of the instilled exogenous surfactant [ 57 ].
The airway mucus gel layer acts as a solid physical barrier to foreign pathogens, toxins and environmental ultrafine particles while allowing rapid passage of selective small molecules, ions, capsid viruses and many proteins. These selective barrier properties of airway mucus are intimately related to its viscoelasticity, which shows order-of-magnitude variations in healthy versus diseased states. The rheological characterization of airway mucus has contributed greatly to both the understanding of mucocilliary clearance and the quantitation of the severity of airway diseases such as CF, COPD and chronic bronchitis [ 13 ].
For example, Hill et al. Below 3. In addition, Button and coworkers recently found that mucus concentration was also strongly correlated with the mucus-epithelial surface adhesive and mucus cohesive strengths. The increased mucus concentration and viscous energy dissipation in CF and COPD patients therefore make the cough mechanism fail to effectively clear accumulated mucus from the lungs [ 60 ].
The gel-on-brush model of the mucus clearance system by Button et al. Kesimer et al. The mean total mucin concentrations were higher in current or former smokers with severe COPD than in controls who had never smoked.
The relationships between total mucin concentration and prospective annualized respiratory exacerbation showed that mucin concentrations were higher in participants who had exacerbations than in those who had none. These results suggest that airway mucin concentrations may serve as a biomarker for the diagnosis of chronic bronchitis. Microrheology affords a detailed characterization of the barrier properties of airway mucus at a scale relevant to pathogens, toxins, and foreign particles.
When the scale approaches the mesh size of the mucus layer, the diffusion rates of particles are expected to be reduced due to steric or adhesive forces, thus leading to a higher apparent viscosity. A variety of conventional nanoparticle-based drug delivery systems for CF and other pulmonary diseases have been discouraged by the mucus barrier since nanoparticles are usually subjected to mucociliary clearance before they reach airway mucosal surfaces due to the extremely slow diffusion rates of these particles in the mucus.
As such, to engineer nanoparticles capable of penetrating this highly viscoelastic and adhesive mucus barrier, it is imperative to characterize the local viscoelasticity of mucus at scales relevant to nanoparticle delivery systems. Suk and coworkers investigated the effect of nanoparticle size and surface chemistry on transport rates in fresh, undiluted CF sputum.
In light of these findings, investigators have further designed various muco-inert nanoparticles that can rapidly penetrate the mucus layer, thus enhancing the efficacy of drug and gene delivery at mucosal surfaces [ 62 , 63 ]. When selecting an appropriate technique to investigate the viscosity of airway surface liquid, it is important to keep in mind that airway surface liquid has two particular features: 1 a relatively small available sample volume and 2 large variations in the range of viscosity depending on the patient, the sampling site in the lung, and healthy or diseased conditions [ 7 , 13 , 14 , 15 , 16 , 26 , 27 , 29 , 59 , 64 ].
Commonly used instruments for the measurement of viscosity include glass capillary viscometers, falling sphere viscometers, rotational viscometers, magnetic microrheometers and particle tracking microrheometers.
Among these instruments, the first four have been used to determine the macroscopic bulk viscosity, while the last one has been applied to the study of microrheology. Glass capillary viscometers are also known as tube-type viscometers, which consist of a U-shaped glass tube with a reservoir bulb on one arm of the U and a measuring bulb with a precise narrow bore the capillary on the other. There are two calibrated marks along the length of the capillary.
During use, liquid is suctioned into the measuring bulb and then allowed to flow downward through the capillary into the reservoir. The principle of the glass capillary viscometer is based on the Poiseuille law [ 66 ]:. Theoretically, the more viscous the liquid, the longer it takes to flow. Basch et al. Despite a variety of modified versions later, using a wide-bore or horizontal tube, for instance, the measurements with sputum were still widely scattered and not reproducible, as the sputum frequently either slipped through the tube as a solid plug or remained stuck somewhere in the tube.
In addition, lung fluids such as mucus and sputum behave as a non-Newtonian viscosity that is dependent on shear rate. Thus, capillary viscometers are further limited since they can only measure viscosity for one shear rate at a time. A small sphere is allowed to move through the test fluid.
As the falling velocity of the sphere increases, the frictional force also increases, and eventually, a terminal velocity Vs is reached when the gravitational force is balanced with the buoyant force and this frictional force. Falling sphere viscometers have undergone important modifications over the years; some commercially available instruments, for example, use cylindrical needles or pistons with hemispheric ends instead of spheres [ 65 ]. Unlike the traditional falling sphere viscometer that only applies for viscosity measurements of Newtonian fluids, the falling needle also possesses the ability to measure non-Newtonian rheological parameters [ 70 ].
In terms of sputum viscosity, there are several drawbacks associated with the falling sphere viscometers, including the requirement of a significant sample volume, operation at low shear rates and poor measurement stability and reproducibility.
For instance, Elmes and White measured sputum viscosity employing a rolling ball viscometer and found that the ball moved along the line of least resistance and rolled around the aggregation of viscous material suspended in the sputum [ 71 ]. Rotational viscometers use the concept that viscosity is defined as the ratio of shear stress to shear rate.
They measure the torque required to rotate an immersed element the spindle in a fluid at a known speed. The spindle is driven by a motor through a calibrated spring. By utilizing a multiple speed transmission and interchangeable spindles, a wide range of viscosities can be measured, thus enhancing the versatility of the instruments. There are two basic types of rotational viscometers, one with two coaxial cylinders and the other with a cone and plate [ 65 , 66 ].
In the cylinder viscometer, the liquid to be tested is placed in a narrow space between the rotating cylinder and the fixed cylinder. The more viscous the fluid is, the greater the torque required to spin the rotating cylinder. The primary disadvantage of the cylinder viscometer is the relatively large sample volumes required.
Baldry and Josse found that the rotating cylinder did not move at all or rotated with a very low speed when sputum viscosity was relatively high [ 66 ]. For these reasons, they are not extensively used in clinical laboratories.
In the cone and plate viscometer, a nearly flat cone with cone angle between 0. This cone and plate spindle geometry requires a sample volume of only 0. The viscosity can easily be determined from shear stress the torque and shear rate the angular velocity by the following equation:. Furthermore, both the elastic and viscous characteristics of the material can be studied by using a strain-controlled cone and plate rheometer [ 72 , 73 ].
The cone and plate viscometer has been widely employed in the measurement of the rheological properties of airway surface liquid [ 26 , 64 , 66 , 74 ]. As a result of measurements taken with a cone and plate viscometer, Baldry and Josse showed that comparable readings could be obtained with duplicate sputum samples at different shear rates [ 66 ]. Lieberman found that sputum viscosity could reach a relatively steady state after a limited amount shearing in a cone and plate viscometer [ 74 ].
Similarly, King et al. The magnetic micrcorheometer involves a pair of permanent magnets or electromagnets for generating a rotating magnetic field [ 13 , 76 , 77 , 78 ]. The test fluid sample is placed in a small test tube with a concave and clear bottom. A metal microsphere is inserted in the sample.
The tube, sealed to prevent evaporation of the sample, is centred between the two magnets. The rotating magnetic field generates a magnetic driving force that rotates the metal sphere. In the case of low frequencies and small sphere diameters, the sphere inertia can be neglected. Therefore, the angular speed of the sphere is determined by the rotational speed and strength of the magnetic field as well as the viscosity of the sample around the sphere.
The motion of the sphere is monitored by a high-resolution video microscope set below the sample cell. Images of the bead are captured by a charge-coupled device CCD camera to measure bead displacement. The two remarkable features of the magnetic microrheometer are the need for only microlitre quantities of sample volume and freedom from contamination.
Consequently, it is well suited to the investigation of the rheological properties of lung fluids partially because only small lung fluid samples can be obtained in normal or disease conditions. King and coworkers pioneered the use of a magnetic rheometer to determine the viscoelastic properties of normal tracheal mucus from canines and discussed the significance of these rheological behaviours in terms of the clearance of secretions from the lung [ 77 ].
Particle tracking microrheology can be used to characterize the linear viscoelasticity of complex fluids with the accuracy of bulk rheology measurements but with smaller sample volumes on the order of picolitres to microlitres required [ 13 , 81 , 82 ].
A modern experimental set up to perform particle tracking microrheology experiments primarily consists of a light source, a colloidal probe, optical microscopy, a fast COMS camera, and specialized particle tracking software.
Colloidal spheres are embedded into a soft viscoelastic fluid, and movies are made of the Brownian motion of the colloidal probes in the sample using the fast COMS camera. The positions of the centroids of the colloidal probes are subsequently matched frame by frame using a specialized routine to identify each particle and generate its trajectory.
Mathematical analysis of MSD can provide a measure of the linear viscoelasticity of the test fluid as a function of time or frequency. The simplest method, for example, is to calculate the creep compliance J t in the form [ 81 , 82 , 83 , 84 ]:. The frequency-domain representation of the GSE equation takes the following form:.
Combining Eq. Dawson et al. They found that CF sputum microviscosity was an order of magnitude lower than its macroviscosity, suggesting that the enhanced viscoelasticity of CF sputum correlates with the increased microheterogeneity in particle transport [ 28 ].
A primary problem with a particle tracking micorheology-based characterization of airway mucus is a possible overestimation of the true mucus viscoelasticity due to adhesive interactions between colloidal probes and mucus.
In addition, the maximally achievable viscosity and shear rate ranges are limited due to restrictions on particle sizes and the temporal resolution of tracking, respectively. Over the past few decades, a variety of measuring techniques have been developed for determining the surface activity of surfactant materials derived from the lung.
Among these are film balances, bubble methods and drop shape analysis methods. In addition, the surface tension of pulmonary surfactant can be inferred from pressure-volume data. In the following section, we will discuss classical methods and recent techniques in terms of their basic principles, advantages and limitations to help research workers select the method s best suited to their needs.
Clements first introduced the Langmuir-Wilhelmy surface balance to determine the surface tension-area relationship in his pioneering studies of lung extracts [ 86 , 87 ]. In this method, lung extracts are dropped onto the surface of a subphase substance usually normal saline contained in the trough of the surface balance, while the exposed surface area is varied over a wide range by means of a movable barrier. A roughened and clean platinum plate is attached to a balance with a thin metal wire.
When the plate is perpendicularly dipped into the liquid, the downward force F on it due to wetting is measured by a balance connected to a transducer.
Although the Langmuir-Wilhelmy balance is one of the most commonly used tools for measuring surface tension, there are still some drawbacks to this apparatus in terms of investigating the tension-area behaviour of lung extracts. One of the most intractable problems has been the film leakage that occurs on the surfaces of the restraining walls and barrier, causing experimental artefacts [ 89 ].
Furthermore, large sample volumes are required on the Langmiur-Wilhelmy surface balance because of its large size. Finally, the apparatus does not seem readily adaptable to rapid oscillations of surface area at rates corresponding to a normal cycle of breathing [ 57 ]. In this method, a lung surfactant suspension is placed into a glass flow-through chamber, and a bubble of atmospheric air is introduced and allowed to float against the slightly concave hydrophilic agarose ceiling of the chamber Fig.
As the air inside the lungs is moist, there is considerable surface tension within the tissue of the lungs. Because the alveoli of the lungs are highly elastic, they do not resist surface tension on their own, which allows the force of that surface tension to deflate the alveoli as air is forced out during exhalation by the contraction of the pleural cavity.
The force of surface tension in the lungs is so great that without something to reduce the surface tension, the airways would collapse after exhalation, making re-inflation during inhalation much more difficult and less effective.
Collapse of the lungs is called alectasis. Fortunately, the type II epithelial cells of the alveoli continually secrete a molecule called surfactant that solves this problem. Surfactant is a lipoprotein molecule that reduces the force of surface tension from water molecules on the lung tissue. The main reason that surfactant has this function is due to a lipid called dipalmitoylphosphatidylcholine DPPC which contains hydophilic and hydrophobic ends. The hydrophilic ends are water soluable and attach to the water molecules on the surface of the lungs.
The hydrophilic ends are water insoluable and face towards the air and pull away from the water. The net result is that the surface tension of the lungs from water is reduced so that the lungs can still inflate and deflate properly without the possibility of collapse from surface tension alone.
The force of these covalent bonds effectively creates an inward force on surfaces, such as lung tissue, with the effect of lowering the surface area of that surface as the tissue is pulled together.
As the air inside the lungs is moist, there is considerable surface tension within the tissue of the lungs. Because the alveoli of the lungs are highly elastic, they do not resist surface tension on their own, which allows the force of that surface tension to deflate the alveoli as air is forced out during exhalation by the contraction of the pleural cavity.
The force of surface tension in the lungs is so great that without something to reduce the surface tension, the airways would collapse after exhalation, making re-inflation during inhalation much more difficult and less effective. Collapse of the lungs is called alectasis.
Fortunately, the type II epithelial cells of the alveoli continually secrete a molecule called surfactant that solves this problem. Surfactant is a lipoprotein molecule that reduces the force of surface tension from water molecules on the lung tissue.
The main reason that surfactant has this function is due to a lipid called dipalmitoylphosphatidylcholine DPPC which contains hydophilic and hydrophobic ends. The hydrophilic ends are water soluable and attach to the water molecules on the surface of the lungs.
The hydrophilic ends are water insoluable and face towards the air and pull away from the water. The net result is that the surface tension of the lungs from water is reduced so that the lungs can still inflate and deflate properly without the possibility of collapse from surface tension alone. Therefore prematurely born infants are at a high risk of respiratory distress syndrome from airway collapse, which can cause death if untreated.
Other diseases may cause atelectasis, such as COPD, or any sort of lung trauma and inflammation that involves extensive damage to the pleural cavity or the lung parenchyma. Diagram of an Alveoli : An alveoli with both cross-section and external views. Lung compliance refers to the magnitude of change in lung volume as a result of the change in pulmonary pressure.
Low lung compliance can be the result of interstitial lung diseases resulting from the inhalation of particulate substances such as asbestos asbestosis and silicon silicosis.
Compliance is the ability of lungs and pleural cavity to expand and contract based on changes in pressure. Lung compliance is defined as the volume change per unit of pressure change across the lung, and is an important indicator of lung health and function. Measurements of lung volumes differ at the same pressure between inhalation and exhalation, meaning that lung compliance differs between inhalation and exhalation.
Lung compliance can either be measured as static or dynamic based on whether only volume and pressure static is measured or if their changes over time are measured as well dynamic. Compliance depends on the elasticity and surface tension of the lungs. Compliance is inversely related to the elastic recoil of the lungs, so thickening of lung tissue will decrease lung compliance. The lungs must also be able to overcome the force of surface tension from water on lung tissue during inflation in order to be compliant, and greater surface tension causes lower lung compliance.
Therefore, surfactant secreted by type II epithelial cells increases lung compliance by reducing the force of surface tension. A stiff lung would need a greater-than-average change in pleural pressure to change the volume of the lungs, and breathing becomes more difficult as a result. Low lung compliance is commonly seen in people with restrictive lung diseases, such as pulmonary fibrosis, in which scar tissue deposits in the lung making it much more difficult for the lungs to expand and deflate, and gas exchange is impaired.
Pulmonary fibrosis is caused by many different types of inhalation exposures, such as silica dust. Pulmonary Fibrosis : Pulmonary fibrosis stiffens the lungs through deposits of scar tissue, decreasing low compliance and making it more difficult for the lungs to inflate and deflate. A high lung compliance means that the lungs are too pliable and have a lower than normal level of elastic recoil.
This indicates that little pressure difference in pleural pressure is needed to change the volume of the lungs. Exhalation of air also becomes much more difficult because the loss of elastic recoil reduces the passive ability of the lungs to deflate during exhalation.
High lung compliance is commonly seen in those with obstructive diseases, such of emphysema, in which destruction of the elastic tissue of the lungs from cigarette smoke exposure causes a loss of elastic recoil of the lung. Those with emphysema have considerable difficulty with exhaling breaths and tend to take fast shallow breaths and tend to sit in a hunched-over position in order to make exhalation easier.
Airway resistance can change over time, especially during an asthma attack when the airways constricts causing an increase in airway resistance. Airway resistance is the resistance to flow of air caused by friction with the airways, which includes the conducting zone for air, such as the trachea, bronchi and bronchioles.
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