Pulmonary Ventilation - Clinical Tree

The main functions of respiration are to provide oxygen to the tissues and remove carbon dioxide. The four major components of respiration are the following: (1) pulmonary ventilation , which means the inflow and outflow of air between the atmosphere and the lung alveoli; (2) diffusion of oxygen (O ₂ ) and carbon dioxide (CO ₂ ) between the alveoli and the blood ; (3) transport of oxygen and carbon dioxide in the blood and body fluids to and from the body’s tissue cells; and (4) regulation of ventilation and other facets of respiration. This chapter is a discussion of pulmonary ventilation; the subsequent five chapters cover other respiratory functions plus the physiology of special respiratory abnormalities.

Mechanics of Pulmonary Ventilation

Muscles That Cause Lung Expansion and Contraction

The lungs can be expanded and contracted in two ways: (1) by downward or upward movement of the diaphragm to lengthen or shorten the chest cavity; and (2) by elevation or depression of the ribs to increase or decrease the anteroposterior diameter of the chest cavity. Figure 38-1 shows these two methods.

Figure 38-1, Contraction and expansion of the thoracic cage during expiration and inspiration, demonstrating diaphragmatic contraction, function of the intercostal muscles, and elevation and depression of the rib cage. AP, Anteroposterior.

Normal quiet breathing is accomplished almost entirely by movement of the diaphragm. During inspiration, contraction of the diaphragm pulls the lower surfaces of the lungs downward. Then, during expiration, the diaphragm simply relaxes, and the elastic recoil of the lungs, chest wall, and abdominal structures compresses the lungs and expels the air. During heavy breathing, however, the elastic forces are not powerful enough to cause the necessary rapid expiration, so extra force is achieved mainly by contraction of the abdominal muscles , which pushes the abdominal contents upward against the bottom of the diaphragm, thereby compressing the lungs.

The second method for expanding the lungs is to raise the rib cage. Raising the rib cage expands the lungs because, in the natural resting position, the ribs slant downward, as shown on the left side of Figure 38-1 , thus allowing the sternum to fall backward toward the vertebral column. When the rib cage is elevated, however, the ribs project almost directly forward, so the sternum also moves forward, away from the spine, making the anteroposterior thickness of the chest about 20% greater during maximum inspiration than during expiration. Therefore, all the muscles that elevate the chest cage are classified as muscles of inspiration, and the muscles that depress the chest cage are classified as muscles of expiration .

The most important muscles that raise the rib cage are the external intercostals , but others that help are the following: (1) sternocleidomastoid muscles, which lift upward on the sternum; (2) anterior serrati , which lift many of the ribs; and (3) scaleni , which lift the first two ribs.

The muscles that pull the rib cage downward during expiration are mainly the following: (1) the abdominal recti , which have the powerful effect of pulling downward on the lower ribs at the same time that they and other abdominal muscles also compress the abdominal contents upward against the diaphragm; and (2) the internal intercostals .

Figure 38-1 also shows the mechanism whereby the external and internal intercostals act to cause inspiration and expiration. To the left, the ribs during expiration are angled downward, and the external intercostals are elongated forward and downward. As they contract, they pull the upper ribs forward in relation to the lower ribs, which causes leverage on the ribs to raise them upward, thereby causing inspiration. The internal intercostals function in the opposite manner, functioning as expiratory muscles because they angle between the ribs in the opposite direction and cause opposite leverage.

Pressures That Cause Movement of air in and out of the Lungs

See . The lung is an elastic structure that collapses like a balloon and expels all its air through the trachea whenever there is no force to keep it inflated. Also, there are no attachments between the lung and walls of the chest cage, except where it is suspended at its hilum from the mediastinum , the middle section of the chest cavity. Instead, the lung “floats” in the thoracic cavity, surrounded by a thin layer of pleural fluid that lubricates movement of the lungs within the cavity. Furthermore, continual suction of excess fluid into lymphatic channels maintains a slight suction between the visceral surface of the lung pleura and the parietal pleural surface of the thoracic cavity. Therefore, the lungs are held to the thoracic wall as if glued there, except that they are well lubricated and can slide freely as the chest expands and contracts.

Pleural Pressure and Its Changes During Respiration

Pleural pressure is the pressure of the fluid in the thin space between the lung pleura and chest wall pleura. This pressure is normally a slight suction, which means a slightly negative pressure. The normal pleural pressure at the beginning of inspiration is about −5 centimeters of water (cm H ₂ O), which is the amount of suction required to hold the lungs open to their resting level. During normal inspiration, expansion of the chest cage pulls outward on the lungs with greater force and creates more negative pressure to an average of about −7.5 cm H ₂ O.

These relationships between pleural pressure and changing lung volume are demonstrated in Figure 38-2 ; in the lower panel shows the increasing negativity of the pleural pressure from −5 to −7.5 cm H ₂ O during inspiration and in the upper panel an increase in lung volume of 0.5 liter. Then, during expiration, the events are essentially reversed.

Figure 38-2, Changes in lung volume, alveolar pressure, pleural pressure, and transpulmonary pressure during normal breathing.

Alveolar Pressure—Air Pressure Inside the Lung Alveoli

When the glottis is open and no air is flowing into or out of the lungs, the pressures in all parts of the respiratory tree, all the way to the alveoli, are equal to atmospheric pressure, which is considered to be zero reference pressure in the airways—that is, 0 cm H ₂ O pressure. To cause inward flow of air into the alveoli during inspiration, the pressure in the alveoli must fall to a value slightly below atmospheric pressure (below 0). The second curve (labeled “alveolar pressure”) of Figure 38-2 demonstrates that during normal inspiration, alveolar pressure decreases to about −1 cm H ₂ O. This slight negative pressure is enough to pull 0.5 liter of air into the lungs in the 2 seconds required for normal quiet inspiration.

During expiration, alveolar pressure rises to about +1 cm H ₂ O, which forces the 0.5 liter of inspired air out of the lungs during the 2 to 3 seconds of expiration.

Transpulmonary Pressure—Difference between Alveolar and Pleural Pressures

Note in Figure 38-2 that the transpulmonary pressure is the pressure difference between that in the alveoli and that on the outer surfaces of the lungs (pleural pressure); it is a measure of the elastic forces in the lungs that tend to collapse the lungs at each instant of respiration, called the recoil pressure .

Compliance of the Lungs

The extent to which the lungs will expand for each unit increase in transpulmonary pressure (if enough time is allowed to reach equilibrium) is called the lung compliance . The total compliance of both lungs together in the normal adult averages about 200 ml of air/cm H ₂ O transpulmonary pressure. That is, every time the transpulmonary pressure increases by 1 cm H ₂ O, the lung volume, after 10 to 20 seconds, will expand 200 ml.

Compliance Diagram of the Lungs

Figure 38-3 is a diagram relating lung volume changes to changes in pleural pressure, which, in turn, alters transpulmonary pressure. Note that the relationship is different for inspiration and expiration. Each curve is recorded by changing the pleural pressure in small steps and allowing the lung volume to come to a steady level between successive steps. The two curves are called, respectively, the inspiratory compliance curve and the expiratory compliance curve , and the entire diagram is called the compliance diagram of the lungs .

Figure 38-3, Compliance diagram in a healthy person. This diagram shows changes in lung volume during changes in transpulmonary pressure (alveolar pressure minus pleural pressure).

The characteristics of the compliance diagram are determined by the elastic forces of the lungs. These forces can be divided into two parts: (1) elastic forces of the lung tissue; and (2) elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces.

The elastic forces of the lung tissue are determined mainly by elastin and collagen fibers interwoven among the lung parenchyma. In deflated lungs, these fibers are in an elastically contracted and kinked state; then, when the lungs expand, the fibers become stretched and unkinked, thereby elongating and exerting even more elastic force.

The elastic forces caused by surface tension are much more complex. The significance of surface tension is shown in Figure 38-4 , which compares the compliance diagram of the lungs when filled with saline solution and when filled with air. When the lungs are filled with air, there is an interface between the alveolar fluid and the air in the alveoli. In lungs filled with saline solution, there is no air-fluid interface and, therefore, the surface tension effect is not present; only tissue elastic forces are operative in the lung filled with saline solution.

Figure 38-4, Comparison of the compliance diagrams of saline-filled and air-filled lungs when the alveolar pressure is maintained at atmospheric pressure (0 cm H 2 O) and pleural pressure is changed to change the transpulmonary pressure.

Note that transpleural pressures required to expand air-filled lungs are about three times as great as those required to expand lungs filled with saline solution. Thus, one can conclude that the tissue elastic forces tending to cause collapse of the air-filled lung represent only about one-third of the total lung elasticity, whereas the fluid-air surface tension forces in the alveoli represent about two-thirds .

The fluid-air surface tension elastic forces of the lungs also increase tremendously when the substance called surfactant is not present in the alveolar fluid.

Surfactant, Surface Tension, and Collapse of the Alveoli

Principle of Surface Tension

When water forms a surface with air, the water molecules on the surface of the water have an especially strong attraction for one another. As a result, the water surface is always attempting to contract. This is what holds raindrops together—a tight contractile membrane of water molecules around the entire surface of the raindrop. Now, let us reverse these principles and see what happens on the inner surfaces of the alveoli. Here, the water surface is also attempting to contract. This tends to force air out of the alveoli through the bronchi and, in doing so, causes the alveoli to try to collapse. The net effect is to cause an elastic contractile force of the entire lungs, which is called the surface tension elastic force .

Surfactant and Its Effect on Surface Tension

Surfactant is a surface-active agent in water , which means that it greatly reduces the surface tension of water. It is secreted by special surfactant-secreting epithelial cells called type II alveolar epithelial cells , which constitute about 10% of the surface area of the alveoli. These cells are granular, containing lipid inclusions that are secreted in the surfactant into the alveoli.

Surfactant is a complex mixture of several phospholipids, proteins, and ions. The most important components are the phospholipid dipalmitoyl phosphatidylcholine, surfactant apoproteins , and calcium ions . The dipalmitoyl phosphatidylcholine and several less important phospholipids are responsible for reducing the surface tension. They perform this function by not dissolving uniformly in the fluid lining the alveolar surface. Instead, part of the molecule dissolves while the remainder spreads over the surface of the water in the alveoli. This surface has from one-twelfth to one-half the surface tension of a pure water surface.

Quantitatively, the surface tension of different water fluids is approximately the following: pure water, 72 dynes/cm; normal fluids lining the alveoli but without surfactant, 50 dynes/cm; normal fluids lining the alveoli and with normal amounts of surfactant included, between 5 and 30 dynes/cm.

Pressure in Occluded Alveoli Caused by Surface Tension

If the air passages leading from the alveoli of the lungs are blocked, the surface tension in the alveoli tends to collapse the alveoli. This collapse creates positive pressure in the alveoli, attempting to push the air out. The amount of pressure generated in this way in an alveolus can be calculated from the following formula:

Pressure = \frac{2 \times Surface tension}{Radius of alveolus}

$Pressure = \frac{2 \times Surface tension}{Radius of alveolus}$

For the average-sized alveolus with a radius of about 100 micrometers and lined with normal surfactant , this calculates to be about 4 cm H ₂ O pressure (3 mm Hg). If the alveoli were lined with pure water without any surfactant, the pressure would be calculated as about 18 cm H ₂ O pressure—4.5 times as great. Thus, one sees the importance of surfactant in reducing alveolar surface tension and therefore also reducing the effort required by the respiratory muscles to expand the lungs.

Pressure Caused by Surface Tension Is Inversely Related to Alveolar Radius

Note from the preceding formula that the smaller the alveolus, the greater the alveolar pressure caused by the surface tension. Thus, when the alveoli have half the normal radius (50 instead of 100 micrometers), the pressures noted earlier are doubled. This phenomenon is especially significant in small premature infants, many of whom have alveoli with radii less than 25% that of an adult person. Furthermore, surfactant does not normally begin to be secreted into the alveoli until between the sixth and seventh months of gestation and, in some cases, even later. Therefore, many premature infants have little or no surfactant in the alveoli when they are born, and their lungs have an extreme tendency to collapse, sometimes as much as six to eight times that in a normal adult person. This situation causes respiratory distress syndrome of the newborn . It is fatal if not treated with strong measures, especially properly applied continuous positive pressure breathing.

Effect of the Thoracic Cage on Lung Expansibility

Thus far, we have discussed the expansibility of the lungs alone, without considering the thoracic cage. The thoracic cage has its own elastic and viscous characteristics and, even if the lungs were not present in the thorax, muscular effort would still be required to expand the thoracic cage.

Compliance of Thorax and Lungs Together

The compliance of the entire pulmonary system (the lungs and thoracic cage together) is measured while expanding the lungs of a totally relaxed or paralyzed subject. To measure compliance, air is forced into the lungs a little at a time while recording lung pressures and volumes. To inflate this total pulmonary system, almost twice as much pressure is required compared with the same lungs after removal from the chest cage. Therefore, the compliance of the combined lung-thorax system is almost exactly half that of the lungs alone—110 ml/cm H ₂ O pressure for the combined system, compared with 200 ml/cm H ₂ O for the lungs alone. Furthermore, when the lungs are expanded to high volumes or compressed to low volumes, the limitations of the chest become extreme. When near these limits, the compliance of the combined lung-thorax system can be less than 20% of that of the lungs alone.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here