Elastic Properties of the Chest Wall

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just as the lung is elastic, so is the thoracic cage. This can be illustrated by putting air into the intrapleural space (pneumothorax). Figure 7-10 shows that the normal pressure outside the lung is subatmospheric just as it is in the jar of Figure 7-3. When air is introduced into the intrapleural space, raising the pressure to atmospheric, the lung collapses inward, and the chest wall springs outward. This

Figure 7-10. The tendency of the lung to recoil to its deflated volume is balanced by the tendency of the chest cage to bow out. As a result, the intrapleural pressure is subatmospheric. Pneumothorax allows the lung to collapse and the thorax to spring out.

Airway pressure (cm water)

Figure 7-11. Relaxation pressure-volume curve of the lung and chest wall. The subject inspires (or expires} to a certain volume from the spirometer, the tap is closed, and the subject then relaxes his respiratory muscles. The curve for lung + chest wall can be explained by the addition of the individual lung and chest wall curves.

Airway pressure (cm water)

Figure 7-11. Relaxation pressure-volume curve of the lung and chest wall. The subject inspires (or expires} to a certain volume from the spirometer, the tap is closed, and the subject then relaxes his respiratory muscles. The curve for lung + chest wall can be explained by the addition of the individual lung and chest wall curves.

shows that under equilibrium conditions, the chest wall is pulled inward while the lung is pulled outward, the two pulls balancing each other.

These interactions can be seen more clearly if we plot a pressure-volume curve tor the lung and chest wall (Figure 7-11). For this, the subject inspires or expires from a spirometer and then relaxes the respiratory muscles while the airway pressure is measured ("relaxation pressure"). Incidentally, this is difficult for an untrained subject. Figure 7-11 shows that at functional residual capacity (FRC), the relaxation pressure of the lung and chest wall is atmospheric. Indeed, FRC is the equilibrium volume when the elastic recoil of the lung is balanced by die normal tendency for the chest wall to spring out. At volumes above this, the pressure is positive, and at smaller volumes, the pressure is subatmospheric.

Figure 7-11 also shows the curve for the lung alone. This is similar to that shown in Figure 7-3, except that for clarity no hysteresis is indicated and the pressures are positive instead of negative. They are the pressures that would be found from the experiment of Figure 7-3 if, after the lung had reached a certain volume, the line to the spirometer were clamped, the jar opened to the atmosphere (so that the lung relaxed against the closed airway), and the airway pressure measured. Note that at zero pressure the lung is at its minimal volume, which is below residual volume (RV).

The third curve is for the chest wail only. We can imagine this being measured on a subject with a normal chest wall and no lung! Note that at FRC the relaxation pressure is negative. In other words, at this volume the chest cage is tending to spring out. It is not until the volume is increased to about 75% of the vital capacity that the relaxation pressure is atmospheric, that is, that the chest wall has found its equilibrium position. At every volume, the relaxation pressure of the lung plus chest wall is the sum of the pressures for the lung and the chest wall measured separately. Because the pressure (at a given volume) is inversely proportional to compliance, this implies that the total compliance of the lung and chest wall is the sum of the reciprocals of the lung and chest wall compliances measured separately, or 1/CT = 1/CL + l/CCw-

Airway Resistance Airflow Through Tubes

If air flows through a tube (Figure 7-12), a difference of pressure exists between the ends. The pressure difference depends on the rate and pattern of flow. At low flow rates, the stream lines are parallel to the sides of the tube (A). This is known as laminar flow. As the flow rate is increased, unsteadiness develops, especially at branches. Here, separation of the stream lines from the wall may occur with the formation (if local eddies (B). At still higher flow rates, complete disorganization of the stream lines is seen; this is turbulence (C).

The pressure-flow characteristics for laminar flow were first described by the French physician Poiseuille. In straight circular tubes, the volume flow rate is given by

8nl where P is the driving pressure (AP in Figure 7-12A), r radius, n viscosity, and 1 length. It can be seen that driving pressure is proportional to flow rate, or P = KV.

Laminar

Turbulent

Figure 7-12, Patterns of airflow in tubes. In A, the flow Is laminar; in B, transitional with eddy formation at branches; and in C, turbulent. Resistance is (Pn-P2)/flow.

Because flow resistance R is driving pressure divided by flow (compare p. 32), we have

irr'

Note the critical importance of tube radius; if the radius is halved, the resistance increases 16-fold! However, doubling the length only doubles resistance. Note also that the viscosity of the gas, but not its density, affects the pressure-flow relationship.

Another feature of laminar flow when it is fully developed is that the gas in the center of the tube moves twice as fast as the average velocity. Thus, a spike of rapidly moving gas travels down the axis of the tube (Figure 7-12A). This changing velocity across the diameter of the tube is known as the velocity profile.

Turbulent flow has different properties. Here pressure is not proportional to flow rate but, approximately, to its square: P - KV2. In addition, the viscosity of the gas becomes relatively unimportant,._but an increase in gas density increases the pressure drop for a given flow. Turbulent flow does not have the high axial flow velocity that is characteristic of laminar flow.

Whether flow will be laminar or turbulent depends to a large extent on the Reynolds number, Re. This is given by

2rvd where d is density, v average velocity, r radius, and n viscosity. Because density and velocity are in the numerator, and viscosity is in the denominator, the ex pression gives the ratio of inertial to viscous forces. In straight, smooth tubes, turbulence is probable when the Reynolds number exceeds 2000. The expression shows that turbulence is most likely to occur when the velocity of flow is high and the tube diameter is large (for a given velocity). Note also that a low-density gas like helium tends to produce less turbulence.

In such a complicated system of tubes as the bronchial tree with its many branches, changes in caliber, and irregular wall surfaces, the application of the above principles is difficult. In practice, for laminar flow to occur, the entrance conditions of the tube are critical. If eddy formation occurs upstream at a branch point, this disturbance is carried downstream some distance before it disappears. Thus, in a rapidly branching system like the lung, fully developed laminar flow (Figure 7-12A) probably only occurs in the very small airways where the Reynolds numbers are very low (approximately 1 in terminal bronchioles). In most of the bronchial tree, flow is transitional (B), while true turbulence may occur in the trachea, especially on exercise when flow velocities are high. In general, driving pressure is determined by both the flow rate and its square: P = K| V + K2Vr j 1

Laminar and Turbulent Flow

• In laminar flow, resistance is determined by the fourth power of the radius

• In laminar flow, the velocity profile shows a central spike of fast gas

• Turbulent flow is most likely to occur at high Reynolds numbers, that is when inertial forces dominate over viscous forces

Measurement of Airway Resistance

Airway resistance is the pressure difference between the alveoli and the mouth divided by a flow rate (Figure 7-12). Mouth pressure is easily measured with a manometer. Alveolar pressure can be deduced from measurements made in a body plethysmograph. More information on this technique is given on p. 152.

Pressures During the Breathing Cycle

Suppose we measure the pressures in the intrapleural and alveolar spaces during normal breathing.' Figure 7-13 shows that before inspiration begins, the intrapleural pressure is — 5 cm water because of the elastic recoil of the lung (compare Figures 7-3 and 7-10). Alveolar pressure is zero (atmospheric) because with no airflow, there is no pressure drop along the airways. However, for inspiratory flow to occur, the alveolar pressure falls, thus establishing the driving pressure (Figure 7-12). Indeed, the extent of the fall depends on the flow rate and the resistance of the airways. In normal subjects, the change in alveolar pressure is only 1-cm water or so, but in patients with airway obstruction, it may be many times that.

Intrapleural pressure falls during inspiration for two reasons. First, as the lung expands, its elastic recoil increases (Figure 7-3). This alone would cause the in-

Figure 7-13. Pressures during the breathing cycle. If there were no airway resistance, alveolar pressure would remain at zero, and intrapleural pressure would follow the broken line ABC, which is determined by the elastic recoil of the lung. Airway (and tissue) resistance contributes the hatched portion of intrapleural pressure (see text).

Figure 7-13. Pressures during the breathing cycle. If there were no airway resistance, alveolar pressure would remain at zero, and intrapleural pressure would follow the broken line ABC, which is determined by the elastic recoil of the lung. Airway (and tissue) resistance contributes the hatched portion of intrapleural pressure (see text).

trapleural pressure to move along the broken line ABC. In addition, however, the pressure drop along the airway is associated with a further fall in intrapleural pressure,' represented by the hatched area, so that the actual path is AB'C. Thus, the vertical distance between lines ABC and AB'C reflects the alveolar pressure at any instant. As an equation of pressures, (mouth — intrapleural) = (mouth — alveolar) + (alveolar — intrapleural).

On expiration, similar changes occur. Now intrapleural pressure is ¡ess negative than it would be in the absence of airway resistance because alveolar pressure is positive. Indeed, with a forced expiration, intrapleural pressure goes above zero.

Note that the shape of the alveolar pressure tracing is similar to that of flow. Indeed, they would be identical if the airway resistance remained constant during the cycle. Also, the intrapleural pressure curve ABC would have the same shape as the volume tracing if the lung compliance remained constant.

' There is also a contribution made by tissue resistance, which is considered later in this chapter.

Br m

Chief Site of Airway Resistance

As the airways penetrate toward the periphery of the lung, they become more numerous but much narrower (see Figures 1-3 and 1-5). Based on Poiseuille's equation with its (radius)4 term, it would be natural to think that the major part of the resistance lies in the very narrow airways. Indeed, this was thought to be the case for many years. However, it has now been shown by direct measurements of the pressure drop along the bronchial tree that the major site of resistance is the medium-sized bronchi and that the very small bronchioles contribute relatively little resistance. Figure 7-14 shows that most of the pressure drop occurs in the airways up to the seventh generation. Less than 20% can be attributed to airways less than 2 mm in diameter (about generation 8). The reason for this apparent paradox is the prodigious number of small airways.

The fact that the peripheral airways contribute so little resistance is important in the detection of early airway disease. Because they constitute a "silent zone," it is probable that considerable small airway disease can be present before the usual measurements of airway resistance can detect an abnormality. This issue is considered in more detail in Chapter 10.

x cu ec

Segmental bronchi

Terminal bronchioles

Airway generation

Figure 7-14. Location of the chief site of airway resistance. Note that the intermediate-sized bronchi contribute most of the resistance and that relatively little is located in the very small airways.

Lung volume (I)

Figure 7-15, Variation of airway resistance (AWR) with lung volume. If the reciprocal of airway resistance (conductance) is plotted, the graph is a straight line.

Lung volume (I)

Figure 7-15, Variation of airway resistance (AWR) with lung volume. If the reciprocal of airway resistance (conductance) is plotted, the graph is a straight line.

Factors Determining Airway Resistance

Lung volume has an important effect on airway resistance. Like the extra-alveolar blood vessels (Figure 4-2), the bronchi are supported by the radial traction of the surrounding lung tissue, and their caliber is increased as the lung expands (compare Figure 4-6). Figure 7-15 shows that as lung volume is reduced, airway resistance rises rapidly. If the reciprocal of resistance (conductance) is plotted against lung volume, an approximately linear relationship is obtained.

At very low lung volumes, the smalt airways may close completely, especially at the bottom of the lung, where the lung is less well expanded (Figure 7-9). Patients who have increased airway resistance often breathe at high lung volumes; this helps to reduce their airway resistance.

Contraction of bronchial smooth muscle narrows the airways and increases airway resistance. This may occur reflexly through the stimulation of receptors in the trachea and large bronchi by irritants such as cigarette smoke. Motor innervation is by the vagus nerve. The tone of the smooth muscle is under the control of the autonomic nervous system. Stimulation of adrenergic receptors causes bronchodi la ration as do epinephrine and isoproterenol.

(J-Adrenergic receptors are of two types: pi receptors occur principally in the heart, while [3? receptors relax smooth muscle in the bronchi, blood vessels, and uterus. Selective Pj-adrenergic agonists are now extensively used in the treatments of asthma.

Parasympathetic activity causes bronchoconstriction, as does acetylcholine. A fall of Pco2 in alveolar gas causes an increase in airway resistance, apparently as a result of a direct action on bronchiolar smooth muscle. The injection ot his-

Airway Resistance

• Highest in the medium-sized bronchi; low in very small airways

• Decreases as lung volume rises because the airways are then pulled open

• Bronchial smooth muscle is controlled by the autonomic nervous system; stimulation of p-adrenergic receptors causes bronchodilatation

• Breathing a dense gas as in diving increases resistance taminc into the pulmonary artery causes constriction of smooth muscle located in the alveolar ducts.

The tJensif)' and viscosity of the inspired gas affect the resistance offered to flow. The resistance is increased during a deep dive because the increased pressure raises gas density, but it is reduced when a helium-O? mixture is breathed. The fact that changes in density rather than viscosity have such an influence on resistance is evidence that flow is not purely laminar in the medium-sized airways, where the main site of resistance ties (Figure 7-14)-

Dynamic Compression of Airways

Suppose a subject inspires to total lung capacity and then exhales as hard as possible to residual volume. We can record a flow- volume curve like A in Figure 7-16, which shows that flow rises very rapidly to a high value but then declines over most of expiration, A remarkable feature of this flow-volume envelope is that it is virtually impossible to penetrate it. For example, no matter whether we start exhaling slowly and then accelerate, as in B, or make a less forceful expiration, as in C, the descending portion of the flow-volume curve takes virtually the same path.

Volume

Figure 7-16. Flow-volume curves. In A, a maximal inspiration was followed by a forced expiration. In 6, expiration was initially slow and then forced. In C, expiratory effortwas submaximal. In all three, the descending portions of the curves are almost superimposed.

Volume

Figure 7-16. Flow-volume curves. In A, a maximal inspiration was followed by a forced expiration. In 6, expiration was initially slow and then forced. In C, expiratory effortwas submaximal. In all three, the descending portions of the curves are almost superimposed.

Figure 7-17. Isovolume pressure-flow curves drawn forthree lung volumes. Each of these was obtained from a series of forced expirations and inspirations (see text), Note that at the high lung volume, a rise in intrapleural pressure (obtained by increasing expiratory effort) results in a greater expiratory flow. However, at mid and low volumes, flow becomes independent of effort after a certain intrapleural pressure has been exceeded.

Figure 7-17. Isovolume pressure-flow curves drawn forthree lung volumes. Each of these was obtained from a series of forced expirations and inspirations (see text), Note that at the high lung volume, a rise in intrapleural pressure (obtained by increasing expiratory effort) results in a greater expiratory flow. However, at mid and low volumes, flow becomes independent of effort after a certain intrapleural pressure has been exceeded.

Thus, something powerful is limiting expiratory flow, and over most of the lung volume, flow rate is independent of effort.

We can get more information about this curious state of affairs by plotting the data in another way, as shown in Figure 7-17. For this, the subject takes a series of maximal inspirations (or expirations) and then exhales (or inhales) fully with varying degrees of effort. If the flow rates and intrapleural pressures are plotted at the same lung volume for each expiration and inspiration, so-called isovolume pressure'fknv curves can be obtained. It can be seen that at high lung volumes, the expiratory flow rate continues to increase with effort, as might be expected. However, at mid or low volumes, the flow rate reaches a plateau and cannot be increased with further increase in intrapleural pressure. Under these conditions, flow is therefore effort independent.

The reason for this remarkable behavior is compression of the airways by intrathoracic pressure. Figure 7-18 shows schematically the forces acting across an airway within the lung. The pressure outside the airway is shown as intrapleural, although this is an oversimplification. In A, before inspiration has begun, airway pressure is everywhere zero (no flow), and because intrapleural pressure is —5 cm water, there is a pressure of 5 cm water holding the airway open. As inspiration

A. Preinspiraîion
B. During inspiration

BLJ!

C. End-inspiration
D. Forced expiration

Figure 7-18. Scheme showing why airways are compressed during forced expiration. Note that the pressure difference across the airway is holding it open, except during a forced expiration. See text for details.

b starts (B), both intrapleural and alveolar pressure fall by 2 cm water (same lung volume as A and tissue resistance is neglected), and flow begins. Because of the pressure drop along the airway, the pressure inside is — 1 cm water, and there is a pressure of 6 cm water holding the airway open. At end-inspiration (C), again flow is zero, and there is an airway transmural pressure of 8 cm water.

Finally, at the onset of forced expiration (D), both intrapleural pressure and alveolar pressure increase by 38 cm water (same lung volume as C). Because of the pressure drop along the airway as flow begins, there is now a pressure of 11 cm water, tending to close the airway. Airway compression occurs, and the downstream pressure limiting flow becomes the pressure outside the airway, or intrapleural pressure. Thus, the effective driving pressure becomes alveolar minus intrapleural pressure. This is the same Starling resistor mechanism that limits the blood flow in zone 2 of the lung, where venous pressure becomes unimportant just as mouth pressure does here (Figures 4-8 and 4-9). Note that if intrapleural pressure is raised further by increased muscular effort in an attempt to expel gas, the effective driving pressure is unaltered. Thus, flow is independent of effort.

Maximal flow decreases with lung volume (Figure 7-16) because the difference between alveolar and intrapleural pressure decreases and the airways become narrower. Note also that flow is independent of the resistance of the airways downstream of the point of collapse, called the equal pressure point. As expiration progresses, the equal pressure point moves distally, deeper into the lung. This occurs because the resistance of the airways rises as lung volume falls,

Dynamic Compression of Airways

* Limits air flow in normal subjects during a forced expiration

I * May occur in diseased lungs at relatively low expiratory flow rates thus re- j ducing exercise ability

• During dynamic compression flow is determined by alveolar pressure minus I j pleural pressure (not mouth pressure)

j • Is exaggerated in some lung diseases by reduced lung elastic recoil and loss of radial traction on airways and therefore the pressure within the airways falls more rapidly with distance from the alveoli.

Several factors exaggerate this flow-limiting mechanism. One is any increase in resistance of the peripheral airways because that, magnifies the pressure drop along them and thus decreases the intrabronchial pressure during expiration (19 cm water in D). Another is a low lung volume because that reduces the driving pressure (alveolar-intrapleural). This driving pressure is also reduced if recoil pressure is reduced, as in emphysema. Also in this disease, radial traction on the airways is reduced and they are compressed more readily. Indeed, while this type of flow limitation is only seen during forced expiration in normal subjects, it may occur during the expirations of normal breathing in patients with severe lung disease.

In the pulmonary function laboratory, the flow rate during a maximal expiration is often determined from the forced expiratory volume or FEVj_o which is the volume of gas that can be exhaled in 1 second after a maximal inspiration. Another popular measurement is the forced expiratory flow or FEF25_7g% which is the average flow rate measured over the middle half (by volume) of the expiration. More information about these tests can be found in Chapter 10.

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Responses

  • BENJAMIN BOHM
    Why chest wall pressure is subatmospheric?
    3 years ago
  • melanie
    Why intrapleural pressure is subatmospheric?
    3 years ago
  • mario
    Is chest wall elastic?
    9 months ago
  • tiziana
    What can alter chest wall elasticity?
    4 months ago

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