Thorax

The bony thorax protects the lungs, heart, and great vessels but also allows the lungs to change volume from a minimum of 1.5 to 2.0 L to a maximum of 6 to 8 L. This large expansion is made possible by the articulation of the ribs with the spine and the sternum, the arrangement of the muscles, and the motion of the diaphragm. The ribs articulate with the transverse processes of the thoracic vertebrae and have flexible cartilaginous connections with the sternum. The ribs angle down, both from back to front and from midline to side, so that as they elevate, both the anteroposterior and the transverse dimensions of the thorax increase (Figure 3-1). The external intercostal muscles that angle down from posterior to anterior (Figure 3-2) are well situated to elevate the ribs. With deep inspiratory efforts, the first and second ribs are elevated and stabilized by the accessory muscles of respiration in the neck. If the upper extremities are fixed, the pectoralis muscles also can act to raise the ribs (e.g., leaning onto a chair back or against a wall when out of breath). Expiration normally is passive, driven by the elastic recoil of the lung, but can be assisted by the internal intercostal muscles. Forced expiration or a cough requires the abdominal muscles to force the diaphragm upward.

Figure 3-1 Frontal (left) and lateral (right) views of thorax movement. With rib elevation, both the transverse and anteroposterior dimensions increase.

Figure 3-2 Action of the major respiratory muscle groups—intercostals, accessories, diaphragm, and abdominals.

The diaphragm is dome-shaped in its relaxed position and can be pulled flatter by muscle contraction. The diaphragm most often is described as fixed at the periphery so that its action pulls down the center of the dome, lengthening the lungs. However, if it is fixed centrally by the pressure of the abdominal contents, the peripheral attachments will lift the ribs, which swing outward when elevated, increasing the transverse diameter of the chest. In addition, the increase in abdominal pressure associated with descent of the diaphragm acts on the lower ribs in the so-called zone of apposition to impart an outward force. The actual action of the diaphragm is a combination of these mechanisms in a proportion that varies with position and abdominal wall tension.

The intercostal muscles are innervated from the thoracic spine at their own level, and the abdominal muscles are innervated from lower thoracic and lumbar level, but the diaphragm is served by the phrenic nerves, which originate at the cervical level (C3 to C5). Thus, the diaphragm remains functional in patients who have spinal injuries below the midcervical level. The long course of each phrenic nerve along the mediastinum, however, makes it vulnerable to both transient and permanent interruptions by disease, injury, or surgery. Occasionally, local irritation of a phrenic nerve leads to intractable singultus (i.e., hiccups). The respiratory muscles are more fully discussed in Chapter 6.

Pleural Space

The lungs are covered by a thin visceral pleura, which is invaginated into the lobar fissures. The inner aspect of each hemithorax, including the top of the diaphragm and the mediastinal surface, is lined with the parietal pleura, which joins the visceral pleura on each side at the lung hilum. The pleural space extends deeply into the posterior and lateral costophrenic recesses and is a potential space, normally containing only a few milliliters of fluid to serve a lubricating function.

The inspiratory force of the chest wall and diaphragm is transmitted to the lung by creation of a more negative pressure in this potential space. In pathologic states, pleural effusions may form and necessarily make the lung volume smaller by occupying part of the intrathoracic space. Penetration of the chest wall or rupture of the lung surface can allow air to enter the pleural space, creating a pneumothorax.

Airways

The upper respiratory passages (nasal cavities and pharynx) conduct, warm, and moisten air as it moves into the lungs. The respiratory system develops as an offshoot from the digestive system and, like the digestive system, has an absorptive function. The entire system is continuously exposed to particulate and infective agents and accordingly is protected by a well-developed lymphoid barrier and, more superficially, a mucous barrier. The upper respiratory passages contain the olfactory areas and also conduct and help shape the sounds that produce speech.

The larynx opens off the lowest part of the pharynx. During swallowing, the larynx is closed off from both the pharynx above and the esophagus posteriorly by the epiglottis. The trachea begins at the lower border of the cricoid cartilage of the larynx, at the level of the sixth cervical vertebra. The lumen of the trachea is held open by incomplete, C-shaped cartilaginous rings. The posterior membranous portion contains smooth muscle. When the intrathoracic pressure exceeds the intraluminal pressure, as during a cough, the membranous portion becomes invaginated, the ends of the rings may overlap, and the lumen is greatly narrowed. Smooth muscle contraction narrows the lumen but increases its rigidity. With deep inspiration, the trachea enlarges and lengthens. The trachea bifurcates into the main bronchi, which become in turn lobar, segmental, and then subsegmental bronchi, and end in bronchioles, which lack cartilage and are approximately 1 mm in diameter. Beyond these are the respiratory bronchioles, alveolar ducts, sacs, and alveoli, which make up the respiratory zone in which gas exchange and other functions take place.

The intraparenchymal bronchi are invested with overlapping helical bands of smooth muscle wound in clockwise and counterclockwise fashion. The amount of smooth muscle increases proportionately in the smaller bronchioles to occupy approximately 20% of the wall thickness. Elastic fibers are present at every level of the respiratory system and become a rich component of the connective tissue in the smaller bronchi and bronchioles. They stretch when the lungs are expanded in inspiration, and their recoil helps to return the lungs to their end-exhalation volume. Although the smooth muscle stops at the portals of the respiratory zone, elastin and collagen contribute to the alveolar wall and form an irregular, wide-meshed net of delicate, interlacing fibers.

The number of airway generations required to reach the respiratory zone varies with pathway length, so that areas near the hilum may be reached in 15 generations, whereas those in the periphery may require 25 generations. Although the size of individual airways becomes smaller, the number of airways approximately doubles with each new generation, so that the total cross-sectional area of the combined air path increases. This is especially so in the smaller bronchi and bronchioles, where the “daughters” of each division are only slightly smaller than the “parent.” The rapidly increasing total cross-sectional area of small airways, shown diagrammatically in Figure 3-3, means that their contribution to airflow resistance in the lungs is small. Thus, diseases that affect these peripheral airways may be functionally silent until they reach an advanced state.

Figure 3-3 Total cross-sectional area of the airways. The aggregate luminal area increases greatly from approximately 2.5 cm² in the trachea and major airways to more than 100 cm² at the level of the terminal bronchioles.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006; data from Weibel ER: Morphometry of the human lung, New York, Springer-Verlag, 1963.)

There is further dramatic expansion in the gas-exchanging respiratory zone as the airways terminate in an estimated 480 million alveoli with a surface area of 130 m².

Interdependence in the Lung

Because the lung parenchyma is made up of interconnected alveolar walls, interstitial tissues, and fibers, any local distortion must be opposed by the surrounding tissue. That is, if a small zone of alveoli within a lobe begins to collapse, the surrounding tissue is stretched and thus tends to pull the alveoli back open. This property, termed structural interdependence, in concert with surfactant and the presence of collateral air pathways, helps to prevent alveolar collapse, even when small bronchioles become plugged. When collapsed areas of lung cannot expand despite distention of the surrounding alveoli, lung injury may develop as a result of extremely large stretching forces that are generated at the interface. These forces contribute to the ventilator-induced lung injury seen with mechanical ventilation at high tidal volumes and the more overt barotrauma that may result when high levels of end-expiratory pressure are applied. Because the bronchi and blood vessels travel through, and have attachments to, the lung parenchyma, they too are affected by the surrounding tissue. As the lung expands, the caliber of these channels also increases, and at low lung volumes, airway closure may occur.

Lung Volumes

The total gas-containing capacity of the lungs can be divided into a series of “volumes,” as shown in Figure 3-4, which, in combination, give lung “capacities.” The largest amount of air that can be held in the lungs at full inspiration is the total lung capacity (TLC). After a complete forced exhalation, the lungs are not empty but contain a residual volume (RV). The difference between TLC and RV—that is, the greatest volume of air that can be inhaled or exhaled—is the vital capacity (VC). The vital capacity can be affected by factors that either limit expansion of the lung (restrictive processes) or limit lung emptying (airflow obstruction).

Figure 3-4 The normal spirogram and subdivisions of lung volume. By convention, volume is used to describe the smallest subdivisions that do not overlap (residual volume, expiratory reserve volume, tidal volume, and inspiratory reserve volume), and capacity is used to describe combinations of these volumes (functional residual capacity, inspiratory capacity, vital capacity, and total lung capacity).

(From Pulmonary terms and symbols: a report of the ACCP-ATS Joint Committee on Pulmonary Nomenclature, Chest 67:583–593, 1975.)

A normal breath has a tidal volume (VT) that is only a small portion of the vital capacity (approximately 10%), and even during strenuous exercise, VT increases to only 50% to 60% of VC. Increases in VT occur by extending into the inspiratory reserve and expiratory reserve volumes as shown in Figure 3-4. At the end of a relaxed tidal exhalation, the lungs and chest wall return to a resting position, which normally is approximately 50% of TLC. The volume contained in the lungs at this end-tidal position is the functional residual capacity (FRC), and the volume that can be inhaled from this point is the inspiratory capacity (IC).

The Lung–Chest Wall System

To understand the process of normal breathing, special maneuvers such as coughing, and the effects of positive-pressure ventilators requires knowledge of the mechanical properties of the thorax. Three primary forces are involved:

In combination, these forces result in changes in lung (and thorax) volume, in alveolar pressure (PA), and in intrapleural pressure (Ppl).

Volumes of Elastic Structures

The recoil tendency of a spring can be expressed in terms of its unstressed or resting length and its length-tension relationship. Similarly, for expandable volumetric structures, the relevant properties are the unstressed volume and the relationship between volume and the transmural pressure required to achieve that volume (Figure 3-5). By convention, transmural pressures are expressed as the difference between the pressure inside and the pressure outside the structure (Pin – Pout). It is convenient to think of this as the distending pressure required to achieve a certain volume. In addition, this distending pressure also represents the recoil pressure, or the tendency of the structure to return to its unstressed volume (where transmural pressure is zero). A positive recoil pressure indicates a tendency to become smaller. A structure distorted to a volume below its unstressed volume has a negative recoil pressure, which indicates its tendency to become larger.

Figure 3-5 Elastic recoil of an expandable structure. The transmural pressure (Pin – Pout) associated with each volume indicates the tendency to return to the unstressed volume. Positive pressure and negative pressure inflation are equivalent.

Elastic Properties of the Lung

The lungs are elastic structures with a tendency to recoil to a small “unstressed volume” (usually slightly less than RV). To maintain any lung volume larger than this unstressed volume requires a force that distends the lungs; this force is the difference between the alveolar pressure (PA) and the pressure surrounding the lungs, the intrapleural pressure (Ppl). The elastic properties of the lungs and their tendency to recoil are represented by a plot of the relationship between lung volume and transmural pressure (Figure 3-6). Such graphs apply to an excised lung being inflated by a pump, an in vivo lung inflated by a ventilator, or the more physiologic normal lung inflated by expanding the chest (to create a more negative pleural pressure). In each case, the curve of volume versus the transpulmonary pressure difference (PA − Ppl) is the same.

Figure 3-6 Normal pressure-volume curve of the lung. The elastic recoil pressure of the lung was obtained during a very slow expiration from total lung capacity (the curve on inspiration is somewhat different). PA, alveolar pressure; Ppl, intrapleural pressure.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006.)

The slope of this pressure-volume curve represents the compliance of the lungs (CL), as represented by Equation 1.

The CL varies with volume, decreasing as the lungs near the limit of their distensibility at TLC. Usually, CL is measured just above FRC in the tidal breathing range. Because it normally is expressed in absolute volume units (e.g., L/cm H₂O), CL is strongly dependent on the lung size. A single lung, for example, undergoes only half the volume change that would result from the same pressure change in two lungs. A small child’s normal CL is considerably lower than that of an adult. For this reason, CL often is divided by lung volume to give the volume-independent specific compliance.

Elastic Properties of the Chest Wall

The chest wall has elastic properties that can be expressed in the same way as for those of the lung (Figure 3-7). The chest wall differs from many common elastic structures in that its unstressed volume (where recoil pressure = 0) normally is quite high. When expanded above its unstressed volume, it recoils inward, but if the chest wall is “distorted” to a smaller volume, its tendency is to recoil outward. Recoil pressure for the relaxed chest wall is Ppl − Patm, or simply Ppl, because Patm is taken to be zero (Figure 3-8; Table 3-1). The compliance of the chest wall is similar to that of the lungs in the midvolume range; of note, however, at TLC, the chest wall remains as distensible as it is at FRC. At low thoracic volumes, the chest wall compliance becomes very low, resisting further exhalation, and this is the mechanism determining residual volume in children and young adults. By middle age, losses in the elasticity of the tissue attachments supporting small airways cause airway closure to be the mechanism limiting further active exhalation.

Figure 3-7 Pressure-volume curves of the combined thoracic system. The relaxed chest wall has a relatively high unstressed volume. The recoil of the combined respiratory system is the sum of the recoil of the chest wall plus that of the lung.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006; data from Rahn H, Otis AB, Chadwich LE, Fenn WO: The pressure-volume diagram of the thorax and lung, Am J Physiol 146:161–178, 1946.)

Figure 3-8 Balance of pressures and forces at functional residual capacity. The opposing recoils of lung and chest wall create a negative intrapleural pressure.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006.)

Table 3-1 Recoil Pressures of the Lungs, Chest Wall, and Respiratory System, Measured as the Transmural Pressure Difference*

* For example, pressure inside minus pressure outside.

Lung and Chest Wall: The Respiratory System

In the intact thorax, the lungs and chest wall must move together. The muscular effort required to inspire a volume of air, or the pressure that must be developed by a ventilator to achieve the same volume change, is determined by the pressure-volume curve of the combined respiratory system, shown by the red line in Figure 3-7. The lungs and chest wall normally contain the same volume of air, so that only points at the same horizontal level in Figure 3-7 can coexist. Because both the lungs and the chest wall are expanded together, the distending pressure for the respiratory system is the sum of the distending pressures required by the lungs and chest wall. The transmural pressure for the respiratory system is PA – Patm (see Table 3-1). Figure 3-7 shows that a greater pressure change is required to add volume to the respiratory system than to either of its components alone, and thus the compliance of the respiratory system is lower than that of either lungs or chest wall at the same volume. This may at first seem paradoxical, because the tendency of the chest wall to expand might be thought to help lung expansion; however, as the system volume is increased, the outward recoil of the chest wall decreases, and this force must be replaced by additional work.

The third mechanical factor, muscle force, is not considered in Figure 3-7. Thus, the pressure difference across the lung, which has no muscle, can always be taken from its curve, but the pressure across the chest wall (and diaphragm) may reflect muscle tension and is described by this curve only during complete relaxation. Similarly, the curve for the respiratory system shows the pressure that would be measured by a manometer held tightly in the mouth after the subject has inhaled or exhaled to a particular volume and then relaxed all muscle effort.

At the resting end-tidal position of the respiratory system (FRC), no active muscular forces are applied, and PA = Patm (distending pressure = 0). The lung is distended above its low unstressed volume, and the chest wall is held below its relatively high unstressed volume. The relaxed FRC is the volume at which the opposing tendencies of the lungs to recoil inward and the chest wall to recoil outward are evenly balanced. Any change in the unstressed volume or the compliance of either lungs or chest wall results in a new FRC. For example, obesity reduces the unstressed volume of the chest wall and thus also reduces the FRC (and expiratory reserve volume) (see Chapter 62). Emphysema increases both compliance and unstressed volume of the lung, which results in a higher FRC and a “shift to the left” of the respiratory system pressure-volume curve.

The opposing forces of lung and chest wall create a subatmospheric (negative) pressure in the intrapleural space at the FRC (see Figure 3-8). Because the lungs and chest wall are not directly linked, it is actually the intrapleural pressure that opposes lung recoil and chest wall recoil. Thus, at a relaxed FRC, it must have the same magnitude as each of these recoil forces. The average pleural pressure normally is approximately −5 cm H₂O at FRC.

Respiratory Muscle Effort

The maximum inspiratory and expiratory pressures measure the maximal efforts of the respiratory muscles (Figure 3-9). That is, with an inhalational effort against a closed pressure manometer, the maximum negative pressure that can be generated at the mouth is approximately 100 cm H₂O at a low lung volume. At TLC, no negative pressure can be generated, so no more air can be drawn into the chest. Maximum expiratory pressures are somewhat greater, measuring 150 to 200 cm H₂O at high lung volume, and fall to zero at RV.

Figure 3-9 Maximum inspiratory and expiratory forces. The normal maximum force generated by inspiratory muscles is greatest at low lung volume, and the expiratory force is greatest at high lung volume.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006.)

Surface Tension

At the surface of a liquid, the intermolecular forces are not balanced by the more widely spaced molecules of the gas phase, which creates a surface tension. The surface tension of the air-liquid interface that lines the alveoli contributes an important part of the elastic properties of the lung shown by the pressure-volume curve. If a lung is filled with liquid, surface forces are abolished, and the resultant pressure-volume curve (Figure 3-10) reflects only the tissue properties of the lung. This liquid-filled curve is shifted to the left, indicating that the lung can be distended with much less pressure. The air-filled lung, in addition to requiring greater pressures, demonstrates marked hysteresis; that is, the pressure-volume curve during inflation is different from that during deflation.

Figure 3-10 Effect of surface tension on recoil force. Pressure-volume curves obtained on inflation and deflation of a normal air-filled lung and the same lung when filled with saline. The horizontal difference between the curves reflects the effect of surface tension, which is greater on inspiration than expiration and abolished when the lung is liquid filled.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006; data from Bachofen H, Hildebrandt J, Bachofen M: Pressure-volume curves of air- and liquid-filled excised lungs—surface tension in situ, J Appl Physiol 29:422–431, 1970.)

The air-filled deflation curve approaches the liquid-filled curve at low lung volume, indicating that the pressure from surface tension becomes small at this volume. Given no other parameters, however, the prediction would be that pressure from surface forces should increase as alveoli become smaller. Laplace’s law relates the pressure within a sphere to wall tension (T) and radius (r), P = 2T/r, whereas for a cylinder, P = T/r. If the surface tension remains constant as “r” decreases (smaller alveoli or airway), the pressure from the surface tension should rise. This situation is avoided in the lung by the presence of a unique surface-lining material, surfactant, which not only reduces surface tension but does so in a volume-dependent manner. As lung volume and surface area decrease, the lining layer compresses, and surface tension decreases until it is nearly abolished at RV. This property has important beneficial consequences in the lung, including the following:

Pulmonary surfactant is produced in alveolar type II cells in the form of lamellar bodies, appears in the alveolar lining liquid as tubular myelin, and then spreads as a monolayer at the air-liquid interface. The major component, and the component that is primarily responsible for the surface tension–lowering effects, is dipalmitoyl phosphatidylcholine (DPPC). DPPC has a nonpolar end, made up of two saturated fatty acid chains, and a polar end that tends to have a positive charge. At the air-liquid interface, the molecules orient with the hydrophilic polar end in the liquid and the fatty acid chains projecting into the air (Figure 3-11). Both ends have similar cross-sectional area allowing them to pack closely together. The molecules may also adsorb directly to the epithelial surface, which tends to have a negative charge, in areas where a liquid subphase is absent.

Figure 3-11 Pulmonary surfactant at the air-liquid interface in an alveolus. The nonpolar fatty acid chains project into the alveolar gas phase, whereas the hydrophilic polar end lies within the surface of the liquid phase or may be able to bond directly to the epithelium. The close arrangement of the molecules facilitates their surface tension–lowering properties. The fluid hypophase tends to fill alveolar corners and surface irregularities.

Flow Resistance

Airflow between the atmosphere and alveolar gas depends on the driving pressure (i.e., alveolar – atmospheric) and the airway resistance, as shown in Equation 2.

Airflow resistance (Raw) is affected by the following factors:

Thus, a doubling of length doubles resistance, but a halving of caliber causes a 16-fold increase in resistance. Factors affecting airway caliber include the following:

All of these factors are similar during both inspiration and expiration, except the last. During inspiration, the intrathoracic pressure that surrounds the airways is more negative than the intraluminal pressure, so airways tend to be distended (Figure 3-12). During passive exhalation, the magnitude of the airway distending force is lower, so airflow resistance is somewhat higher. With active expiratory efforts, the pleural pressure becomes positive, and with the addition of lung recoil, the pressure in the alveoli is even higher. However, the intraluminal pressure decreases progressively in airways mouthward of the alveoli, reflecting both frictional losses and a decrease in lateral pressure through the Bernoulli effect, because the decreasing cross-sectional area of the composite airway requires a marked increase in velocity of air movement (convective acceleration). Because their cartilaginous structure is incomplete, airways are compressed under such forces, and calculated resistance is much higher.

Figure 3-12 Dynamic compression. Comparison of intrathoracic and intraluminal pressures during inspiration, passive expiration, and forced expiration. In each case, the lung volume is the same, with a recoil pressure of 10 cm H₂O. During inspiration, the intrathoracic airways tend to be distended, which lowers airway resistance. In passive expiration, although intrapleural pressure may remain slightly negative, a positive alveolar pressure is generated by lung elastic recoil. Central airways are less distended than during inspiration. In forced expiration, high intrapleural pressure, plus lung recoil, creates a large, positive alveolar pressure to drive flow but also compresses central airways. Flow is limited once dynamic compression begins downstream from the point where intraluminal pressure falls below pleural pressure (the so-called equal pressure point). Further effort increases alveolar driving pressure but also increases compression. Airway resistance becomes high and varies with the degree of effort.

Maximum airflow rates are evaluated by having the subject take a full inspiration to TLC and blow the air out as forcefully and completely (to RV) as possible. With use of a spirometer, this forced vital capacity (FVC) is recorded as an expiratory spirogram (volume versus time), or if the flow rate is directly measured, the same information can be recorded as a maximum expiratory flow versus volume curve (Figure 3-13). A remarkable feature of this maneuver is that the maximum flow rate for any volume, except the higher lung volumes near the beginning of the exhalation, is achieved with submaximal effort and cannot be exceeded with further effort. This flow limitation, or “effort independence,” is demonstrated in Figure 3-14 and is a consequence of the dynamic compression noted previously. The mechanism of this flow limitation is related to the rate of propagation of a pressure wave through a compliant tube, but the result can be understood with a simpler conceptual model of dynamic compression. Because this compression begins just beyond the point at which intraairway pressure falls to equal pleural pressure, the effective pressure driving flow from the alveoli to this point becomes PA − Ppl (i.e., in Figure 3-12, for forced expiration, 30 − 20 = 10 cm H₂O). This is the same as the elastic recoil pressure of the lung and is a function of lung volume, not effort. If, in the example of Figure 3-12, a greater expiratory effort is made and the pleural pressure is raised to 40 cm H₂O at the same lung volume, the alveolar pressure becomes 50 cm H₂O and the effective driving pressure = (50 − 40) = 10 cm H₂O, so the resultant flow rate remains unchanged.

Figure 3-13 Forced vital capacity maneuver. This common breathing test can be displayed as an expiratory spirogram or as a flow-volume curve. Volume axes show percentage of vital capacity expired.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006.)

Figure 3-14 Effort-independent flow. The top curve represents a maximum expiratory effort, and the lower curves show the flow that results from progressively less effort. At lower lung volumes, the maximum flow rate is relatively independent of effort.

(Modified from Bates DV, Macklem PT, Christie RV: Respiratory function in disease, ed 2, Philadelphia, WB Saunders, 1971, pp 10–95.)

This mechanism may have its major physiologic significance in normal persons during a cough. Although overall airflow rate (L/second) out of the lungs is not increased by the high pleural pressure generated, the airflow velocity (m/second) through the narrowed major airways is greatly increased, which aids in the removal of secretions and foreign material.

Work of Breathing

The muscle effort required to raise lung volume above the FRC during inspiration is a form of work. Part of this is the elastic work used to stretch the tissues and the surface lining of the lung, whereas another part is the frictional work required to overcome airflow resistance in the airways. The elastic work stored in stretched fibers on inspiration then provides the energy needed to push air out on the subsequent passive exhalation. With active expiratory efforts, additional muscle work is done on expiration as well.

The elastic and frictional components of respiratory work are affected differently by lung volume. At low lung volume, airways are narrower, and resistance (and thus frictional work) increases rapidly (R is proportional to 1/r⁴). At higher lung volumes, the airways are larger, but muscles must do more elastic work to keep the lungs stretched. The relaxed FRC is the volume at which the static recoil forces of the lung and chest wall are balanced, but Figure 3-15 shows that FRC also is the volume at which work of breathing is least. If either the elastic or frictional contributions to work of breathing change, FRC may change rapidly or chronically.

Figure 3-15 Work of breathing. The combined work of lung and chest wall expansion (elastic) and airflow resistance (frictional) is normally lowest near functional residual capacity.

(Modified from Culver BH, editor: The respiratory system, Seattle, University of Washington Publication Services, 2006.)

The narrowed airways in obstructive disease increase frictional work and the volume at which work is the least increases. The accompanying shift of the tidal breathing range to a higher volume may occur quite suddenly in an asthma attack or may develop slowly with chronic obstructive disease. When airflow rates increase, frictional work becomes relatively more important, so that patients who have obstructive disease may shift to a higher end-expiratory volume during exercise or voluntary hyperventilation.

Restrictive disease processes reduce lung compliance (CL). Accordingly, the force the muscles must generate to stretch the lung increases. The elastic work required to breathe at any lung volume is higher, and this shifts the volume for least work lower. Increased CL, as with emphysema, has the opposite effect. Figure 3-7 shows that the static forces predict the same changes in FRC (greater lung recoil results in lower FRC volume and vice versa).

Normally, the energy consumed by breathing is very small. In metabolic terms, less than 1 mL/minute of oxygen consumption is required for each liter per minute of ventilation, or only a few percent of total body oxygen consumption at rest. Derangements of respiratory mechanics may increase the work of breathing significantly, contributing to the common symptom of dyspnea. With severe airflow obstruction, the energy cost of breathing becomes much higher. Increases in respiratory frequency associated with activity may cause COPD patients to shift their tidal ventilation to a higher end-expiratory lung volume whereby the increased airway caliber allows the tidal breath to be exhaled within the shorter expiratory time available. This dynamic hyperinflation places the inspiratory muscles at further mechanical disadvantage and is a major contributor to exertional dyspnea and exercise limitation. If the expiratory time does not allow the alveolar pressure to fully equilibrate to atmospheric pressure, then the residual positive end-expiratory alveolar pressure (termed auto-PEEP) must be overcome by additional inspiratory effort before inspiratory airflow can begin. The same phenomenon also is seen during mechanical ventilation of patients with airflow obstruction and may have hemodynamic consequences, as well as impairing their ability to initiate breaths.

Distribution of Ventilation

The incoming air of each tidal breath is not distributed evenly to all alveoli in the lung. Pleural pressure is not the same throughout the chest but has a vertical gradient of several centimeters of water because of the effects of gravity, the configuration of the chest and diaphragm, the presence of the heart and mediastinal structures, and the need for the lung to fit within the thorax irrespective of the shape of either the lung or the thorax. At FRC measured with the patient in the upright position, −5 cm H₂O is an average value at chest midlevel; near the apices, however, the pressure outside the lung might be −8 cm H₂O, whereas near the bases it might be only −2 cm H₂O. Because alveoli throughout the lung seem to have similar maximum volume and pressure–volume relationships, and because alveolar pressure is everywhere the same, those alveoli near the top of the lung are held at larger volume (distending pressure of 8 cm H₂O) than those near the bottom (distending pressure of 2 cm H₂O). This places the lower alveoli on a steeper (more compliant) portion of their pressure-volume curve. In addition, the proximity of the basal alveoli to the motion of the diaphragm exposes them to a greater increase in distending pressure with inspiration. These two factors combine to give the lower portion of the normal lung a relatively greater proportion of the tidal ventilation than that distributed to the apices.

A second consequence of the higher (i.e., less negative) pleural pressure in the basal portions of the lung is that the distending pressure of the small airways also is less. At low lung volume, airways may close, and the dependent portions of the lung reach this “closing volume” first, whereas higher portions of the lung are still partially distended. Thus, in a patient who breathes at very low lung volumes, near residual volume (e.g., with obesity), basal airway closure may occur, with consequent poor ventilation of the lung bases.

In summary, respiratory units in the basal portion of the lung contain less gas but receive more ventilation so long as they remain open. However, they are more susceptible to airway closure and loss of ventilation at low lung volume.