Interpretation of Pulmonary Function Tests A Practical Guide, 3. ed

7. Other Tests of Lung Mechanics: Resistance and Compliance

The tests described here are usually performed in fully equipped laboratories. In the outpatient setting, they add relatively little to the basic evaluations discussed in prEV1ous chapters (spirometry, lung volumes, diffusing capacity, and arterial blood gases). However, these tests might be encountered in either graduate training or in laboratory reports and therefore are considered briefly. Also, understanding these concepts is important in the management of patients requiring mechanical ventilation.


Resistance is the pressure required to produce a flow of 1 L/s into or out of the lung. The units are centimeters of water per liter per second, (cm H2O per liter per second). This general concept is illustrated in Figure 7-1, in which the pertinent driving pressure (AP) is the pressure difference between the ends of the tubes. The pressure required to produce a flow of 1 L/s in a large tube is less than that in a small tube. Hence, the resistance (R) of the small tube is much higher than that of the large tube.

In the lung, measurement of the resistance of the entire system is of interest. Figure 7-2 illustrates how this can be obtained. Flow at the mouth can be measured with a flowmeter. The pressure driving the flow can be measured in either of two ways. Pleural pressure (Ppl) can be measured from a small balloon-catheter unit placed in the lower third of the esophagus and attached to a pressure transducer. Pressure changes in the esophagus have been shown to reflect those in the pleural cavity. The difference between Ppl and Pao (the pressure at the mouth) is the driving pressure, which divided by flow (V) is defined as the pulmonary resistance (Rpulm). Rpulm includes airway resistance plus a small component due to the resistance of the lung tissue.

FIG. 7-1. Measurement of resistance (R) through a large tube (A) and small tube (B). Flow (V) is measured by the flowmeter, and driving pressure (AP) is measured by a differential pressure transducer. To drive the same flow, the decrease in pressure is greater in tube B and hence the resistance (R) of tube B is higher than that of tube A.

The other and much more common resistance measurement is obtained by measuring alveolar pressure (Palv) and relating this to Pao. Palv can be measured in a body plethysmograph and does not require swallowing an esophageal balloon. In this method, the driving pressure is Palv minus Pao. This result is divided by flow to determine the airway resistance, Raw. Raw is slightly lower than Rpulm because of the absence of tissue resistance. Both Rpulm and Raw can be measured during either inspiration or expiration, or as an average of both. Figure 7-3 describes how Raw is measured.

Average resistance in normal adults is 1 to 3 cm H2O/L per second. It is higher in the small lungs of children because the airways are smaller. Occasionally, the term conductance is used. Conductance is a term borrowed from the electrical engineering field and is the reciprocal of resistance, its units being liters per second per centimeter of water, L/s per cm H2O. Thus, a high resistance means a low conductance—flow is not ''conducted'' well.

FIG. 7-2. Model illustrating how pulmonary resistance (Rpulm) and airway resistance (Raw) are measured. An esophageal balloon is required to measure pleural pressure (Ppl). Palv, alveolar pressure; Pao, pressure at the mouth; V, flow.

FIG. 7-3. The equipment used to measure lung volume by the body plethysmograph (see Fig. 3-6, page 34) has been modified by inserting a flowmeter between the patient's mouth and the pressure gauge and valve. The flowmeter measures airflow (V). The subject is instructed to pant shallowly through the system with the valve open. This provides a measure of plethsymographic pressure as a function of flow, that is, Ppleth/V. With the subject still panting, the valve is closed. This provides a measure of alveolar pressure as a function of plethysmographic pressure, that is, Palv/Ppleth. As shown, airway resistance (Raw) is obtained by multiplying these two ratios.

FIG. 7-4. Resistance is a hyperbolic function of lung volume. When its reciprocal, conductance, is plotted, a straight line results. Note that the conductance line intersects the volume axis at 1 liter, which is the residual volume in this example. At the same time, resistance is becoming infinitely high.

Resistance varies inversely with lung volume (Figure 7-4). At high lung volumes, the airways are wider and the resistance is lower. To standardize for this effect, resistance is typically measured during breathing at functional residual capacity.

Resistance is increased when the airways are narrowed. Narrowing may be due to bronchoconstriction of inflamed airways in asthma, mucus and thickened bronchi in chronic bronchitis, or floppy airways in emphysema.

There is a strong negative correlation between resistance and maximal expiratory flow. A high resistance is associated with decreased flows, EV1denced by decreases in the forced expiratory volume in 1 second (FEV1) and forced expiratory flow rate over the middle 50% of the forced vital capacity (FEF25-75). There are, however, a few exceptions to this relationship. One is illustrated in Figure 7-5. This type of maximal expiratory flow-volume curve is occasionally seen in the elderly. Resistance in this case is normal, but flow low in the vital capacity, such as the FEF25-75, is decreased. The converse also can occur, namely, normal forced flows and an increased resistance.

FIG. 7-5. Flow-volume curve showing normal flow at high lung volumes but abnormally low flows over the lower 50% of the vital capacity. In this case, resistance is often normal, but the forced expiratory flow rate over the middle 50% of the forced vital capacity is low.

PEARL: A patient with a variable obstructing lesion in the extrathoracic trachea (see Fig. 2-7D, page 19) may have a considerable increase in resistance but normal maximal expiratory flow. The increased resistance reflects the markedly decreased inspiratory flows caused by the high inspiratory resistance.


Compliance is a measure of the lungs' elasticity. Compliance of the lungs (Cl) is defined as the change in lung volume resulting from a change of 1 cm H2O in the elastic pressure of the lungs. Figure 7-6 is similar to Figure 7-2, but a spirometer is added to measure volume (V). When the lung is not moving (that is, airflow is zero), the Ppl is negative (subatmospheric). The lungs are elastic and always tend to collapse. This is resisted by the chest wall, so the Ppl when volume is not changing reflects the static elastic pressure or recoil of the lung at that volume. If lung volume is increased by a known amount (AV) and volume is again held constant, the new Ppl is more negative (the recoil of the lung is greater). This AV divided by the difference in the two static Ppl values (∆Ppl) defines the lung compliance, Cl = ∆V/∆Ppl (L/cm H2O) at that volume. In addition, it is common practice to measure the elastic recoil pressure with the subject holding his or her breath at total lung capacity (TLC); this is termed the PTLC (recoil pressure at TLC). The measurement of lung compliance requires the introduction of an esophageal balloon (to measure Ppl).

FIG. 7-6. Model demonstrating the measurement of compliance. An esophageal balloon is required. Cl, compliance of the lungs; Pao, pressure at the mouth; Ppl, pleural pressure.

Compliance measured when there is no airflow, as in the above discussion, is termed static compliance (CLstat). Compliance is often measured during quiet breathing, also with an esophageal balloon-catheter system. During a breath, there are two times when airflow is zero. These occur at the end of inspiration and the end of expiration. The difference in Ppl at these two times also defines a change in elastic recoil pressure. This APpl divided into the volume change is called the dynamic compliance of the lung (CLdyn).

In normal adult subjects, CLstat and CLdyn are nearly the same and range from 0.150 to 0.250 L/cm H2O. Cl varies directly with lung size, compliance being lower in subjects with small lungs.

Compliance is reduced in subjects with pulmonary fibrosis, often to values as low as 0.050 L/cm H2O, reflecting the fact that these lungs are very stiff. Large changes in pressure produce only small changes in volume. Again, static and dynamic compliance are similar.

The situation in chronic obstructive pulmonary disease (COPD), especially emphysema, is different. Static compliance is much increased, to values often more than 0.500 L/cm H2O. This high compliance reflects the floppy, inelastic lungs. However, CLdyn is much lower, often in the normal range. The explanation for this apparent paradox relates to the very nonuniform ventilation of the lungs in COPD, as discussed in Chapter 8. In essence, during breathing in COPD, air preferentially flows into and out of the more normal regions of the lung. Because the elasticity of these regions is not as severely impaired, CLdyn is nearer normal values. This difference between CLstat and CLdyn is referred to as frequency dependence of compliance. It is important to remember that a low CLdyn in COPD does not mean that the lung is stiff or fibrotic.


The compliance of the entire respiratory system (Crs) can also be measured. It requires that the respiratory muscles be relaxed. This measurement is most often made when a patient is on a ventilator. The patient's lungs are inflated, the airway is occluded, and the occluded airway pressure is measured. The lungs are allowed to deflate a measured amount, and a second occlusion pressure is obtained. Crs is the change in volume divided by the difference in the two pressures. Because the lungs and chest wall are in series, Crs includes both lung (CLstat) and chest wall (Ccw) compliance. Because the reciprocals of the compliances are added, the equation describing this relationship is as follows:

(Eq. 1)

Thus, a decrease in Crs may be due to a decrease in either lung or chest wall compliance (or both), a fact that is sometimes overlooked.


The basics of lung mechanics have been presented. This section details the mechanical handicaps associated with obstructive and restrictive lung diseases.

FIG. 7-7. Lung static elastic recoil pressure (Pst) is plotted against absolute lung volume for three typical subjects: a patient with emphysema (E), a normal subject (N), and a patient with pulmonary fibrosis (F).

Lung Static Elastic Recoil Pressure

We noted prEV1ously that the Ppl measured when the lung is not moving is the static elastic recoil pressure of the lung, which we now define as Pst. This pressure is measured from a small balloon placed in the lower esophagus.

In Figure 7-7, Pst is plotted during deflation of the lung from total lung capacity to residual volume. Three cases are shown: a normal subject (N); a patient with emphysema, an obstructive disorder (E); and a patient with pulmonary fibrosis, a restrictive disease (F). The curves are plotted as a function of absolute lung volume. Note the loss of lung recoil and hyperinflation in emphysema (E). This contrasts with the reduced lung volume and increased lung recoil in pulmonary fibrosis (F).

The E curve emphasizes two problems faced by the patient with emphysema and by most patients with COPD. First, the loss of recoil pressure means that the lung parenchyma cannot distend the airways as much as in the normal case (see the tethering springs in Fig. 2-2, page 8). Second, as shown in Figure 9-2 (page 94), the ability of the inspiratory muscles to generate force is reduced because of the hyperinflation.

In the curve, representing the subject with pulmonary fibrosis, the ability of the expiratory muscles to develop force is reduced (see Fig. 9-2, page 94) because of the reduced lung volume. In addition, the increased recoil of the fibrotic lung requires the respiratory muscles to exert greater than normal force to expand the lung.

PEARL: You might think that the Pst derives from the elastic and collagen fibers in the lung. However, the major contribution to the elastic recoil comes from surface tension forces acting at the air-fluid interface in the alveoli. This is demonstrated in Figure 7-8, in which are plotted static inflation and deflation airway pressures in a lung containing air (the normal situation) and the same lung inflated and deflated with saline after the air has been removed. With saline filling, the alveolar air-fluid interface is abolished, as is the surface tension. Note how little recoil pressure remains in the saline lung, and what does remain reflects the relatively small tissue contribution. The markedly different inflation and deflation curves, especially in the air-filled lung, represent hysteresis—a common property of biologic tissues.

FIG. 7-8. Plot of static airway pressure versus lung volume in an excised lung first inflated and deflated with air. The arrows indicate the inflation and deflation paths. The lung is then degassed (all the air is removed) and inflated and deflated with saline. The marked shift to the left of the saline curve reflects the loss of recoil when surface tension at the alveolar air-fluid interface is abolished. The difference between the inflation-deflation curves is called hysteresis.

Work of Breathing

Figure 7-9 illustrates the effects of the alterations in Pst and in airflow resistance on the work of breathing required of the respiratory muscles. The static curves of Figure 7-7 have been replotted; the Ppl during inspiration has been added to each curve. Work is a product of pressure and volume. In each case, the hatched area between the inspiratory loop (identified by the arrows) and the static curve represents the resistive work of that breath. It is much increased in the E curve. The area between the static curve and the zero pressure axis reflects the work required to keep the lung inflated, that is, the elastic work. Compared with the normal curve, the subject with emphysema has large increases in work due to increased airflow resistance, whereas the subject with fibrosis has large increases in elastic work due to the stiffness of the lung. Although the total inspiratory work loop is less in emphysema than in fibrosis, more work is required during expiration. In addition, the hyperinflation in emphysema puts the system at a distinct mechanical disadvantage.

FIG. 7-9. The pleural pressure generated during an inspiratory breath is plotted for a normal subject (N), a patient with emphysema (E), and a patient with fibrosis (F). The inspiratory loops are plotted on the static recoil curves of Figure 7-7. The hatched areas reflect the work of breathing required to overcome the resistance to airflow (RS). The areas between the static curve and the zero-pressure line reflect the work required to keep the lung inflated, the elastic work (EL). See text for further discussion.

Static Lung Recoil Pressure and Maximal Expiratory Flow

In section 2B (page 6) and Figure 2-2 (page 8), we noted that lung elasticity, specifically Pst, is the pressure that drives maximal expiratory flow. It is informative to evaluate the relationship between maximal expiratory flow and Pst. Figure 7-10A shows how this relationship is obtained, and Figure 7-10B shows its behavior in normal and diseased lungs.

In Figure 7-10A, flow-volume and static lung recoil curves for a normal subject and a patient with pure emphysema are plotted on the common vertical axis of absolute lung volume. Thus, at any lung volume corresponding to the decreasing portion of the flow-volume curve, it is possible to measure simultaneous values of maximal expiratory flow (Vmax) and Pst.

FIG. 7-10. Relationships between maximal expiratory flow (Vmax) and lung static elastic recoil pressure (Pst). A. Vmax and Pst are plotted on a common vertical absolute volume axis for a normal subject and a patient with pure emphysema.

B. Corresponding values of Vmax and Pst obtained at various lung volumes are plotted with Vmax as a function of Pst. This is called a maximal flow static recoil curve. In the case of chronic bronchitis, the flow-volume and Pst-volume curves are not shown. See text for further discussion.

In Figure 7-10B, Pst is plotted against Vmax at various lung volumes. Such a graph is called a maximal flow static recoil (MFSR) curve. The normal range of values is shown by the two dashed lines. Values obtained from the normal curve in Figure 7-10A are connected by the solid line. The same has been done for the case of pure emphysema. Because the subject has no airway disease, the values fall within the normal range. This indicates that the decrease in maximal flow is mainly due to loss of lung recoil. However, if there is significant chronic bronchitis, the MFSR curve is shifted down and to the right, indicating that although there may be some loss of recoil pressure, this does not explain the decrease in flow, which is largely due to airway disease and associated increased airway resistance. The MFSR curve is useful in that it stresses the fact that maximal expiratory flow may be reduced by a loss of recoil pressure or significant airway disease or by both.


This procedure has been used for more than 40 years and has had a rebirth because of improved instrumentation. Briefly, the patient breathes quietly on a closed system. Small (~1 cm H2O) oscillations of pressure are superimposed on the patient's breathing. Measurement of airway pressure and flow and application of electric circuit analysis allow total respiratory resistance (that of the lung and the thorax) to be computed and related to the frequency of the oscillation. Because the thorax is a relatively small and stable component, the technique can provide much information about pulmonary resistance.

The advantages of the forced oscillation technique are many. It is the only noninvasive way to estimate pulmonary resistance—an esophageal balloon or body plethysmograph is not needed. It can be used in infants and children—no special breathing maneuvers are used. It can be used in sleep studies and in the intensive care unit. It also may prove to be the simplest and best way to test for airway hyperreactivity. It does not require a deep inhalation, which can alter bronchomotor tone (see Case 32, page 226), nor forced expiratory maneuvers, which can be tiring and may alter bronchial tone. We expect use of the forced oscillation technique to increase.

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