Chapter 3 Respiratory Mechanics
This chapter describes the physical properties of the lungs and chest wall involved in the cyclic processes of ventilation supporting the metabolic needs of the body. The contribution of respiratory muscles to these processes is reviewed here; their function is described more fully in Chapter 6. Clinical measurements of some of these mechanical properties are an important part of pulmonary function testing, as discussed in Chapter 9.
Structure of the Thorax and Lungs
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.
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.
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.
The properties of the lung and chest that affect and effect the movement of air into and out of the lungs are central to understanding both normal and abnormal lung function.
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:
• Elastic recoil properties of the lung
• Elastic recoil properties of the chest wall
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.
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.