Mechanical Aspects of the Lungs and Chest Wall

The discussion of pulmonary physiology begins with an introduction to a few concepts about the mechanical properties of the respiratory system, which have important implications for assessment of pulmonary function and its derangement in disease states.

The lungs and chest wall have elastic properties. They have a particular resting size (or volume) they would assume if no internal or external pressure were exerted on them, and any deviation from this volume requires some additional influencing force. If the lungs were removed from the chest and no longer had the external influences of the chest wall and pleural space acting on them, they would collapse to the point of being almost airless; they would have a much lower volume than they have within the thoracic cage. To expand these lungs, positive pressure would have to be exerted on the air spaces, as could be done by putting positive pressure through the airway. (Similarly, a balloon is essentially airless unless positive pressure is exerted on the opening to distend the elastic wall and fill it with air.)

Alternatively, instead of positive pressure exerted on alveoli through the airways, negative pressure could be applied outside the lungs to cause their expansion. Thus, what increases the volume of the isolated lungs from the resting, essentially airless, state is application of a positive transpulmonary pressure—the pressure inside the lungs relative to the pressure outside. Internal pressure can be made positive, or external pressure can be made negative; the net effect is the same. With the lungs inside the chest wall, the internal pressure is alveolar pressure, whereas external pressure is the pressure within the pleural space (Fig. 1-2). Therefore, transpulmonary pressure is defined as alveolar pressure (P_alv) minus pleural pressure (P_pl). For air to be present in the lungs, pleural pressure must be relatively negative compared with alveolar pressure.

The relationship between transpulmonary pressure and lung volume can be described for a range of transpulmonary pressures. The plot of this relationship is the compliance curve of the lung (Fig. 1-3, A). As transpulmonary pressure increases, lung volume naturally increases. However, the relationship is not linear but curvilinear. At relatively high volumes, the lungs reach their limit of distensibility, and even rather large increases in transpulmonary pressure do not result in significant increases in lung volume.

Switching from the lungs to the chest wall, if the lungs were removed from the chest, the chest wall would expand to a larger size when no external or internal pressures were exerted on it. Thus the chest wall has a springlike character. The resting volume is relatively high, and distortion to either a smaller or larger volume requires alteration of either the external or internal pressures acting on it. The pressure across the chest wall is akin to the transpulmonary pressure. Again, with the lungs back inside the chest wall, the pressure across the chest wall is the pleural pressure (internal pressure) minus the external pressure surrounding the chest wall (atmospheric pressure).

The compliance curve of the chest wall relates the volume enclosed by the chest wall to the pressure across the chest wall (Fig. 1-3, B). The curve becomes relatively flat at low lung volumes at which the chest wall becomes stiff. Further changes in pressure across the chest wall cause little further decrement in volume.

To examine how the lungs and chest wall behave in situ, remember that the elastic properties of each are acting in opposite directions. At the normal resting end-expiratory position of the respiratory system (functional residual capacity [FRC]), the lung is expanded to a volume greater than the resting volume it would have in isolation, whereas the chest wall is contracted to a volume smaller than it would have in isolation. However, at FRC the tendency of the lung to become smaller (the inward or elastic recoil of the lung) is exactly balanced by the tendency of the chest wall to expand (the outward recoil of the chest wall). The transpulmonary pressure at FRC is equal in magnitude to the pressure across the chest wall but acts in an opposite direction (Fig. 1-3, C). Therefore pleural pressure is negative, a consequence of the inward recoil of the lungs and the outward recoil of the chest wall.

The chest wall and the lungs can be considered as a unit, the respiratory system. The respiratory system has its own compliance curve, which is essentially a combination of the individual compliance curves of the lungs and chest wall (see Fig. 1-3, C). The transrespiratory system pressure, again defined as internal pressure minus external pressure, is airway pressure minus atmospheric pressure. At a transrespiratory system pressure of 0, the respiratory system is at its normal resting end-expiratory position, and the volume within the lungs is FRC.

Two additional lung volumes can be defined, as can the factors that determine each of them. Total lung capacity (TLC) is the volume of gas within the lungs at the end of a maximal inhalation. At this point the lungs are stretched well above their resting position, and even the chest wall is stretched beyond its resting position. We are able to distort both the lungs and chest wall so far from FRC by using our inspiratory muscles, which exert an outward force to counterbalance the inward elastic recoil of the lung and, at TLC, the chest wall. However, at TLC it is primarily the extreme stiffness of the lungs that prevents even further expansion by inspiratory muscle action. Therefore, the primary determinants of TLC are the expanding action of the inspiratory musculature balanced by the inward elastic recoil of the lung.

At the other extreme, when we exhale as much as possible, we reach residual volume (RV). At this point a significant amount of gas still is present within the lungs—that is, we can never exhale enough to empty the lungs entirely of gas. Again, the reason can be seen by looking at the compliance curves in Figure 1-3, C. The chest wall becomes so stiff at low volumes that additional effort by the expiratory muscles is unable to decrease the volume any further. Therefore, RV is determined primarily by the balance of the outward recoil of the chest wall and the contracting action of the expiratory musculature. However, this simple model for RV applies only to the young individual with normal lungs and airways. With age or airway disease, further expulsion of gas during expiration is limited not only by the outward recoil of the chest wall but also by the tendency for airways to close during expiration and for gas to be trapped behind the closed airways.

Ventilation

To maintain normal gas exchange to the tissues, an adequate volume of air must pass through the lungs for provision of O₂ to and removal of CO₂ from the blood. A normal person at rest typically breathes approximately 500 mL of air per breath at a frequency of 12 to 16 times per minute, resulting in a ventilation of 6 to 8 L/min (minute ventilation []).* The volume of each breath (tidal volume [VT]) is not used entirely for gas exchange; a portion stays in the conducting airways and does not reach the distal part of the lung capable of gas exchange. The portion of the tidal volume that is “wasted” (in the sense of gas exchange) is termed the volume of dead space (VD), and the volume that reaches the gas-exchanging portion of the lung is the alveolar volume (VA). The anatomic dead space, which includes the larynx, trachea, and bronchi down to the level of the terminal bronchioles, is approximately 150 mL in a normal person; thus, 30% of a tidal volume of 500 mL is wasted.

As for CO₂ elimination by the lung, alveolar ventilation (), which is equal to the breathing frequency (f) multiplied by VA, bears a direct relationship to the amount of CO₂ removed from the body. In fact, the partial pressure of CO₂ in arterial blood (PaCO₂) is inversely proportional to ; as increases, PaCO₂ decreases. Additionally, PaCO₂ is affected by the body’s rate of CO₂ production (); if increases without any change in , PaCO₂ shows a proportional increase. Thus, it is easy to understand the relationship given in Equation 1-1:

As mentioned earlier, the dead space comprises that amount of each breath going to parts of the tracheobronchial tree not involved in gas exchange. The anatomic dead space consists of the conducting airways. In disease states, however, areas of lung that normally participate in gas exchange (parts of the terminal respiratory unit) may not receive normal blood flow, even though they continue to be ventilated. In these areas, some of the ventilation is wasted; such regions contribute additional volume to the dead space.

Hence, a more useful clinical concept than anatomic dead space is physiologic dead space, which takes into account the volume of each breath not involved in gas exchange, whether at the level of the conducting airways or the terminal respiratory units. Primarily in certain disease states, in which there may be areas with normal ventilation but decreased or no perfusion, the physiologic dead space is larger than the anatomic dead space.

Quantitation of the physiologic dead space or, more precisely, the fraction of the tidal volume represented by the dead space (VD/VT), can be made by measuring PCO₂ in arterial blood (PaCO₂) and expired gas (PECO₂) and by using Equation 1-2, known as the Bohr equation for physiologic dead space:

Consider the two extremes. If the expired gas came entirely from perfused alveoli, PECO₂ would equal PaCO₂, and according to the equation, VD/VT would equal 0. On the other hand, if expired gas came totally from the dead space, it would contain no CO₂, PECO₂ would equal 0, and VD/VT would equal 1. In practice, this equation is used in situations between these two extremes, and it quantifies the proportion of expired gas coming from alveolar gas (PCO₂ = PaCO₂) versus dead space gas (PCO₂ = 0).

In summary, each normal or tidal volume breath can be divided into alveolar volume and dead space, just as the total minute ventilation can be divided into alveolar ventilation and wasted (or dead space) ventilation. Elimination of CO₂ by the lungs is proportional to alveolar ventilation; therefore, PaCO₂ is inversely proportional to alveolar ventilation and not to minute ventilation. The wasted ventilation can be quantified by the Bohr equation, with use of the principle that increasing amounts of dead space ventilation augment the difference between PCO₂ in arterial blood and expired gas.

Circulation

Because the entire cardiac output flows from the right ventricle to the lungs and back to the left side of the heart, the pulmonary circulation handles a blood flow of approximately 5 L/min. If the pulmonary vasculature were similar in structure to the systemic vasculature, large pressures would have to be generated because of the thick walls and high resistance offered by systemic-type arteries. However, pulmonary arteries are quite different in structure from systemic arteries, with thin walls that provide much less resistance to flow. Thus, despite equal right and left ventricular outputs, the normal mean pulmonary artery pressure of 15 mm Hg is much lower than the normal mean aortic pressure of approximately 95 mm Hg.

One important feature of blood flow in the pulmonary capillary bed is the distribution of flow in different areas of the lung. The pattern of flow is explained to a large degree by the effect of gravity and the necessity for blood to be pumped “uphill” to reach the apices of the lungs. In the upright person, the apex of each lung is approximately 25 cm higher than the base, so the pressure in pulmonary vessels at the apex is 25 cm H₂O (19 mm Hg) lower than in pulmonary vessels at the bases. Because flow through these vessels depends on the perfusion pressure, the capillary network at the bases receives much more flow than the capillaries at the apices. In fact, flow at the lung apices falls to 0 during the part of the cardiac cycle when pulmonary artery pressure is insufficient to pump blood up to the apices.

West developed a model of pulmonary blood flow that divides the lung into zones, based on the relationships among pulmonary arterial, venous, and alveolar pressures (Fig. 1-4). As stated earlier, the vascular pressures—that is, pulmonary arterial and venous—depend in part on the vertical location of the vessels in the lung because of the hydrostatic effect. Apical vessels have much lower pressure than basilar vessels, the difference being the vertical distance between them (divided by a correction factor of 1.3 to convert from cm H₂O to mm Hg).

At the apex of the lung (zone 1 in Fig. 1-4

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