Objectives
- 1.
Describe static lung mechanics and the measurement of lung volumes.
- 2.
Define lung compliance and its measurement.
- 3.
Relate lung and chest wall compliance to lung volumes.
- 4.
Characterize lung and chest wall interactions in terms of pressure gradients and pressure volume relationships.
- 5.
Describe surfactant and its role in altering surface tension.
Static Lung Mechanics
Air movement in and out of the lung is controlled by the mechanical properties of the lung and chest wall. Static lung mechanics is the study of the mechanical properties of the lung and chest wall whose volume is not changing with time and is discussed in this chapter. Dynamic lung mechanics, which is the study of the lung and chest wall in motion (i.e., changing volume), is discussed in Chapter 3 .
The mechanics of the lung are composed of the combined mechanical properties of the airways, lung parenchyma, interstitial matrix (composed of fibrin, collagen, and a few cells), alveolar surface, and pulmonary circulation. The mechanical properties of the chest wall include the properties of all of the structures outside of the lungs that move during breathing, including the rib cage, diaphragm, abdominal cavity, and anterior abdominal muscles. The interaction between the lung and the chest wall determines lung volumes, and static lung volumes play a major role in gas exchange and in the work of breathing. They can be measured and are abnormal in many lung diseases.
Lung Volumes
The static volumes of the lungs are shown in Fig. 2.1 . All lung volumes are subdivisions of the total lung capacity (TLC) and are measured in liters. They are reported either as volumes (e.g., residual volume) or capacities (e.g., vital capacity). A capacity is composed of two or more volumes.
The total volume of air that is contained in the lung is called the TLC. It is composed of the volume of air that an individual can exhale from a maximum inspiration to a maximum exhalation, known as the vital capacity (VC), and the volume of air that is left in the lung after a maximal exhalation, known as the residual volume (RV). Two other important lung volumes are the tidal volume (TV, or V t ) and the functional residual capacity (FRC). The TV is the volume of air that is breathed into and out of the lung during quiet breathing. The FRC is the volume of air contained in the lung after a normal exhalation. The FRC is composed of the residual volume and the volume of air that can be exhaled from the end of a normal exhalation to residual volume. This latter volume is called the expiratory reserve volume (ERV). The FRC represents the resting volume of the respiratory system, in which the forces of the chest wall to increase in size and the forces of the lung to decrease in size are equal but opposite (see later in this chapter).
To get a sense of the importance of lung volumes in respiration, breathe quietly close to TLC (take a deep breath in, and breathe at this high lung volume for a few minutes). Now breathe out until you cannot force any more air out, and try breathing at this volume, which is close to your RV. Both of these maneuvers should be uncomfortable and associated with increased work; both increases and decreases in lung volume occur in lung disease as a result of a change in lung mechanics. The measurement of lung volumes is used to detect and follow the progression of lung disease and is discussed in Chapter 4 .
Using and Interpreting Results of Lung Volume Measurements
Two major types of pathophysiologic abnormalities involving the lung and chest wall can be described using lung volumes. One group of diseases is called obstructive pulmonary disease (OPD) . In OPD, during exhalation the airways close (premature airway closure, the hallmark of OPD) trapping air behind them (see Chapter 3 ). This results in an increase in TLC, RV, and FRC. In contrast, in restrictive pulmonary disease , the other major pathophysiologic abnormality involving the lung and chest wall, lung volumes are reduced.
One of the most useful tests for distinguishing obstructive and restrictive types of lung disease is the measurement of the RV/TLC ratio. In normal individuals, the RV/TLC ratio is less than 0.25, that is, approximately 25% of the air in the lungs is trapped and cannot be exhaled. An elevated RV/TLC ratio, characterized by an increase in RV out of proportion to any increase in TLC, is due to air trapping secondary to airway obstruction and is seen in individuals with OPD. An elevated RV/TLC ratio due to a decrease in TLC out of proportion to any change in RV is seen in individuals with restrictive types of pulmonary disease.
Lung Compliance and Lung Elastic Properties
Lung compliance (C l ) is a measure of the elastic properties of the lung and is a reflection of lung distensibility. These distensibility properties of the lung are seen in the pressure volume relaxation curve for the lung that is called the compliance curve of the lung . Compliance of the lungs is defined as the change in lung volume resulting from a change in the distending pressure of the lung equal to 1 cm H 2 O. The units of compliance are mL (or L)/cm H 2 O. A lung with high lung compliance refers to a lung that is easily distended. A lung with low compliance or a “stiff” lung is the one that is not easily distended. Thus the compliance of the lung (C l ) is:
CL=ΔV/ΔP
The compliance of the isolated lung is measured in animals by removing the lung and measuring the changes in lung volume that occur with each change in the pressure between the inside of the lung and the outside (also known as transpulmonary or translung pressure ). As transpulmonary pressure increases, lung volume increases ( Fig. 2.2A ). The line that is generated, however, is curvilinear, not linear. That is, at low lung volumes, the lung distends easily, but at high lung volumes, larger increases in transpulmonary pressure are needed to produce only small changes in lung volume. This is in part because at high lung volumes all of the elastic fibers in the alveolar units and airways have been maximally stretched. More important than elastic recoil in the determination of compliance is the surface tension at the air–water interface lining the alveoli due to surfactant (see later in this chapter).
Lungs that are highly compliant will have a steeper slope than lungs with a low compliance. Lung compliance or distensibility is the inverse of elasticity or lung elastic recoil (P el ). Compliance is the ease with which something is stretched, whereas elastic recoil is the tendency to resist or oppose stretching and return to its previous configuration when the distorting force is removed.
By convention, the compliance of the lung is measured as the slope of the line between any two points on the deflation limb of the pressure volume loop. The compliance of the lung is greater when measured from TLC to RV (deflation) than from RV to TLC (inflation) ( Fig. 2.3 ). This is due in large part to the changes in surface tension with changing lung volume and is discussed later in this chapter. This difference between the inflation and exhalation curve is called hysteresis . As we will see later in this chapter, the most important reason for hysteresis is changes in surfactant. Other reasons include redistribution of gas and recruitment of alveoli.
Compliance of the Chest Wall
When the lungs are removed, the chest wall has a springlike character with a relatively high resting volume. In much the same way as the lung, the compliance curve of the chest wall relates the volume of gas enclosed by the chest wall to the pressure across the chest wall. The curve (see Fig. 2.2B ) is relatively flat at low volumes; that is, the chest wall is stiff with the shortened respiratory muscles maximally contracted. The curve is also flat at high lung volumes where the respiratory muscles are maximally stretched. At both high and low lung volumes, large changes in pressure across the chest wall result in small changes in the volume enclosed by the chest wall.
Compliance of the Respiratory System
Both the lungs and the chest wall contribute to the compliance of the respiratory system ( Fig. 2.4 ). The lung and chest wall are held together by the thin layer of pleural fluid that functions like a liquid film holding two pieces of glass together. The glass pieces slide easily relative to each other, but it is difficult to pull them apart. The compliance of the respiratory system is also analogous to electrical capacitance, and in the respiratory system the compliances of the lung and chest wall are in parallel. Thus their individual compliances add as reciprocals; that is, 1/compliance of the respiratory system = 1/compliance of the lung + 1/compliance of the chest wall or
1/CRS=1/CL+1/CW
In contrast, the reciprocal of compliance is elastance, and the elastance of the lung and chest wall add directly. In addition, compliances in series add directly. For example, the compliance of the lungs in the two hemithoraces that are in series is the sum of the compliances of the lung in each hemithorax.
As noted previously, lung compliance varies with lung volume (see Fig. 2.2 ). It is greater at lower lung volumes than at higher lung volumes. For this reason, specific compliance, or compliance divided by the lung volume at which it is measured (usually FRC), is used ( Fig. 2.5 ). As an example, consider the individual with chronic bronchitis in whom FRC is increased. As a result, pulmonary compliance, which is now being measured at this higher lung volume, would also be increased. However, when corrected for the FRC (specific compliance), the compliance is normal. In individuals with normal FRC, the compliance of the lung is about 0.2 L/cm H 2 O, of the chest wall is 0.2 L/cm H 2 O, and of the respiratory system is 0.1 L/cm H 2 O. Note that the compliance of the respiratory system is lower than the compliance of either the lung or the chest wall. Lung compliance is not affected by age.
The compliance of the lung is not altered by airflow per se, but the compliance of the lung and chest wall is affected by a number of respiratory disorders. In emphysema, the lung is more compliant because of destruction of lung elastic tissue; that is, for every 1 cm of H 2 O pressure increase, there is a larger increase in volume than in the normal lung. In contrast, a proliferation of connective tissue in the lung called pulmonary fibrosis can be seen in lung diseases such as interstitial pneumonitis and sarcoidosis or in association with chemical or thermal lung injury. The lungs in these diseases are “stiff,” or noncompliant; that is, for every 1 cm H 2 O pressure change, there is a smaller change in volume. Similarly, in diseases associated with increased fluid in the interstitial spaces such as pulmonary edema or in diseases associated with fluid, blood, or infection in the intrapleural space ( pleural effusion, hemothorax, or empyema, respectively), lung compliance is reduced.
The compliance of the chest wall is decreased in individuals with obesity in whom adipose tissue results in an additional load on the chest wall muscles and the diaphragm.
Individuals with decreased mobility of the rib cage such as in kyphoscoliosis or other types of musculoskeletal diseases that affect chest wall movement also have decreased chest wall compliance.
Individuals with decreased compliance must generate greater transpulmonary pressures to produce changes in lung volume than individuals with normal compliance. This results in increased work associated with breathing (see Chapter 3 ).
Fibrosis/emphysema pressure–volume curve. TLC, total lung capacity.
The compliance of the lung is not altered by airflow per se, but the compliance of the lung and chest wall is affected by a number of respiratory disorders. In emphysema, the lung is more compliant because of destruction of lung elastic tissue; that is, for every 1 cm of H 2 O pressure increase, there is a larger increase in volume than in the normal lung. In contrast, a proliferation of connective tissue in the lung called pulmonary fibrosis can be seen in lung diseases such as interstitial pneumonitis and sarcoidosis or in association with chemical or thermal lung injury. The lungs in these diseases are “stiff,” or noncompliant; that is, for every 1 cm H 2 O pressure change, there is a smaller change in volume. Similarly, in diseases associated with increased fluid in the interstitial spaces such as pulmonary edema or in diseases associated with fluid, blood, or infection in the intrapleural space ( pleural effusion, hemothorax, or empyema, respectively), lung compliance is reduced.
The compliance of the chest wall is decreased in individuals with obesity in whom adipose tissue results in an additional load on the chest wall muscles and the diaphragm.
Individuals with decreased mobility of the rib cage such as in kyphoscoliosis or other types of musculoskeletal diseases that affect chest wall movement also have decreased chest wall compliance.
Individuals with decreased compliance must generate greater transpulmonary pressures to produce changes in lung volume than individuals with normal compliance. This results in increased work associated with breathing (see Chapter 3 ).
Fibrosis/emphysema pressure–volume curve. TLC, total lung capacity.
Factors Determining Lung Volume
Why can’t we inspire above TLC or exhale beyond RV? The answers lie in the properties of the lung parenchyma and in the interaction between the lungs and the chest wall. Both the lungs and the chest wall have elastic properties. Both have a resting volume (or size) that they would assume if there were no external forces or pressures exerted on them. Both expand when stresses are applied and recoil passively when stresses are released. If the lungs were removed from the chest and no external forces were applied, they would become almost airless. To expand, these lungs would require either the exertion of a positive pressure on the alveoli and airways or the application of a negative pressure from outside the lungs. Either would result in a positive transpulmonary pressure. These situations are analogous to the balloon and the vacuum canister. A balloon is airless until positive pressure is exerted at the opening to distend the balloon walls (positive-pressure “ventilation”). In the case of the vacuum, negative external pressure is applied and results in sucking materials (air) into the canister (negative-pressure “ventilation”).
The lungs are enclosed by the chest wall, which expands during inspiration. The lungs and chest wall always move together in healthy individuals. Lung volumes are determined by the balance between the lung’s elastic recoil properties and the properties of the muscles of the chest wall. TLC occurs when the forces of inspiration decrease because of chest wall muscle lengthening and are insufficient to overcome the increasing force required to distend the lung and chest wall (see Fig. 2.4 ). Thus TLC is limited by the distensibility of both the lungs and the chest wall and the amount of force that the inspiratory muscles can generate. Disease that affects any of these three components will affect TLC.
At RV, a significant amount of gas remains within the lung. As RV is approached, the chest wall becomes so stiff that additional effort by the expiratory chest wall muscles to contract is unable to further reduce the volume. Thus RV occurs when the expiratory muscle force is insufficient to cause a further reduction in chest wall volume (see Fig. 2.4 ). As the chest wall is squeezed by the expiratory muscles, the recoil pressure of the chest wall (the chest wall wanting to increase in size) increases. The expiratory muscles shorten, and their capacity to generate force decreases; the point at which the force generated by the expiratory muscles is insufficient to overcome the outward recoil of the chest wall determines the RV. This simple model of RV applies to (young) individuals with normal lungs. In older individuals and in individuals with lung disease, premature airway closure, a property of the lung (see Chapter 3 ), becomes the major determinant of RV rather than outward chest wall recoil.
The FRC is the volume of the lung at the end of a normal exhalation and is determined by the balance between the elastic recoil pressure generated by the lung parenchyma to become smaller and the pressure generated by the chest wall to become larger (see Fig. 2.4 ). FRC occurs when these two forces are equal and opposite. In the presence of chest wall weakness, the FRC decreases (lung elastic recoil is greater than chest wall muscle force). In the presence of airway obstruction, the FRC increases because of premature airway closure that traps air in the lung. Always, however, the FRC occurs at the lung volume at which the outward recoil of the chest wall is equal to the inward recoil of the lung.
Lung–Chest Wall Interactions
The lung and chest wall move together in healthy people. The pleural space that separates the lung and the chest wall is best thought of as a “potential” space because of its small volume. Because the lung and chest wall move together, changes in their respective volumes are the same. The pressure changes across the lung and across the chest wall are defined as the transmural pressures . Transmural pressure refers to any pressure difference across a wall and by convention represents the inside of the wall pressure minus the outside of the wall pressure. For the lung, this transmural pressure is called the transpulmonary pressure (P l ; also called the translung pressure) and is defined as the pressure difference between the airspaces (alveolar pressure [P a ]) and the pressure surrounding the lung (pleural pressure [P pl ]); that is,
PL=PA−PPL
The lung requires a positive P l to increase its volume and lung volume increases with increasing P l . The lung assumes its smallest size when the transpulmonary pressure is zero. The lung, however, is not airless when the P l is zero because of the surface tension–lowering properties of surfactant (discussed later). The transmural pressure across the chest wall (P w ) is the difference between the pleural pressure and the pressure surrounding the chest wall (inside pressure minus outside pressure), which is the barometric pressure (P b ) or body surface pressure. That is,
PW=PPL−PB
During the inspiratory phase of quiet breathing, the chest wall expands to a larger volume. Because the pleural pressure is negative relative to atmospheric pressure during quiet breathing, the transmural pressure across the chest wall is negative. The pressure then across the respiratory system (P rs ) is the sum of the pressure across the lung and the pressure across the chest wall; that is,
PRS=PL+PW=(PA−PPL)+(PPL−PB)=PA−PB