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The goals of respiration are to provide oxygen to the tissues and to remove carbon dioxide. To achieve these goals, respiration can be divided into four major functions: (1) pulmonary ventilation, which means the inflow and outflow of air between the atmosphere and the lung alveoli; (2) diffusion of oxygen and carbon dioxide 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, and the subsequent five chapters cover other respiratory functions plus the physiology of special respiratory abnormalities.
Mechanics of Pulmonary Ventilation
Mechanics of Pulmonary Ventilation
Muscles That Cause Lung Expansion and Contraction
The lungs can be expanded and contracted in two ways: (1) by downward and upward movement of the diaphragm to lengthen or shorten the chest cavity, and (2) by elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity. Figure 37-1 shows these two methods.
Normal quiet breathing is accomplished almost entirely by the first method, that is, 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 that 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. This expands the lungs because, in the natural resting position, the ribs slant downward, as shown on the left side of Figure 37-1, thus allowing the sternum to fall backward toward the vertebral column. But when the rib cage is elevated, the ribs project almost directly forward, so that the sternum also moves forward, away from the spine, making the anteroposterior thickness of the chest about 20 per cent greater during maximum inspiration than during expiration. Therefore, all the muscles that elevate the chest cage are classified as muscles of inspiration, and those 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 (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 (1) 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) internal intercostals.
Figure 37-1 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.
Figure 37-1 also shows the mechanism by which 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, and this causes leverage on the ribs to raise them upward, thereby causing inspiration. The internal intercostals function exactly in the opposite manner, functioning as expiratory muscles because they angle between the ribs in the opposite direction and cause opposite leverage.
Movement of Air In and Out of the Lungs and the Pressures That Cause the Movement
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 the walls of the chest cage, except where it is suspended at its hilum from the mediastinum. 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. Further, 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
Figure 37-2 Changes in lung volume, alveolar pressure, pleural pressure, and transpulmonary pressure during normal breathing.
Figure 37-3 Compliance diagram in a healthy person. This diagram shows compliance of the lungs alone
The lungs can be expanded and contracted in two ways: (1) by downward and upward movement of the diaphragm to lengthen or shorten the chest cavity, and (2) by elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity. Figure 37-1 shows these two methods.
Normal quiet breathing is accomplished almost entirely by the first method, that is, 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 that 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. This expands the lungs because, in the natural resting position, the ribs slant downward, as shown on the left side of Figure 37-1, thus allowing the sternum to fall backward toward the vertebral column. But when the rib cage is elevated, the ribs project almost directly forward, so that the sternum also moves forward, away from the spine, making the anteroposterior thickness of the chest about 20 per cent greater during maximum inspiration than during expiration. Therefore, all the muscles that elevate the chest cage are classified as muscles of inspiration, and those 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 (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 (1) 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) internal intercostals.
Figure 37-1 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.
Figure 37-1 also shows the mechanism by which 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, and this causes leverage on the ribs to raise them upward, thereby causing inspiration. The internal intercostals function exactly in the opposite manner, functioning as expiratory muscles because they angle between the ribs in the opposite direction and cause opposite leverage.
Movement of Air In and Out of the Lungs and the Pressures That Cause the Movement
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 the walls of the chest cage, except where it is suspended at its hilum from the mediastinum. 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. Further, 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
Figure 37-2 Changes in lung volume, alveolar pressure, pleural pressure, and transpulmonary pressure during normal breathing.
Pleural pressure is the pressure of the fluid in the thin space between the lung pleura and the chest wall pleura. As noted earlier, this 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, which is the amount of suction required to hold the lungs open to their resting level. Then, 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 centimeters of water.
These relationships between pleural pressure and changing lung volume are demonstrated in Figure 37-2, showing in the lower panel the increasing negativity of the pleural pressure from -5 to -7.5 during inspiration and in the upper panel an increase in lung volume of 0.5 liter. Then, during expiration, the events are essentially reversed.
Alveolar Pressure
Alveolar pressure is the pressure of the air 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 centimeters water 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 37-2 demonstrates that during normal inspiration, alveolar pressure decreases to about -1 centimeter of water. 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, opposite pressures occur: The alveolar pressure rises to about +1 centimeter of water, and this forces the 0.5 liter of inspired air out of the lungs during the 2 to 3 seconds of expiration.
Transpulmonary Pressure. Finally, note in Figure 37-2 the difference between the alveolar pressure and the pleural pressure. This is called the transpulmonary pressure. It is the pressure difference between that in the alveoli and that on the outer surfaces of the lungs, and 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 human being averages about 200 milliliters of air per centimeter of water transpulmonary pressure. That is, every time the transpulmonary pressure increases 1 centimeter of water, the lung volume, after 10 to 20 seconds, will expand 200 milliliters.
These relationships between pleural pressure and changing lung volume are demonstrated in Figure 37-2, showing in the lower panel the increasing negativity of the pleural pressure from -5 to -7.5 during inspiration and in the upper panel an increase in lung volume of 0.5 liter. Then, during expiration, the events are essentially reversed.
Alveolar Pressure
Alveolar pressure is the pressure of the air 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 centimeters water 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 37-2 demonstrates that during normal inspiration, alveolar pressure decreases to about -1 centimeter of water. 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, opposite pressures occur: The alveolar pressure rises to about +1 centimeter of water, and this forces the 0.5 liter of inspired air out of the lungs during the 2 to 3 seconds of expiration.
Transpulmonary Pressure. Finally, note in Figure 37-2 the difference between the alveolar pressure and the pleural pressure. This is called the transpulmonary pressure. It is the pressure difference between that in the alveoli and that on the outer surfaces of the lungs, and 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 human being averages about 200 milliliters of air per centimeter of water transpulmonary pressure. That is, every time the transpulmonary pressure increases 1 centimeter of water, the lung volume, after 10 to 20 seconds, will expand 200 milliliters.
Figure 37-3 Compliance diagram in a healthy person. This diagram shows compliance of the lungs alone
Compliance Diagram of the Lungs. Figure 37-3 is a diagram relating lung volume changes to changes in transpulmonary pressure. Note that the relation is different for inspiration and expiration. Each curve is recorded by changing the transpulmonary 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.
The characteristics of the compliance diagram are determined by the elastic forces of the lungs. These can be divided into two parts: (1) elastic forces of the lung tissue itself 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 37-4, 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 the case of the saline solution-filled lungs, there is no air-fluid interface; therefore, the surface tension effect is not present-only tissue elastic forces are o
perative in the saline solution-filled lung.
Figure 37-4 Comparison of the compliance diagrams of saline-filled and air-filled lungs when the alveolar pressure is maintained at atmospheric pressure (0 cm H2O) and pleural pressure is changed.
The characteristics of the compliance diagram are determined by the elastic forces of the lungs. These can be divided into two parts: (1) elastic forces of the lung tissue itself 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 37-4, 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 the case of the saline solution-filled lungs, there is no air-fluid interface; therefore, the surface tension effect is not present-only tissue elastic forces are o
perative in the saline solution-filled lung.Figure 37-4 Comparison of the compliance diagrams of saline-filled and air-filled lungs when the alveolar pressure is maintained at atmospheric pressure (0 cm H2O) and pleural pressure is changed.
Note that transpleural pressures required to expand air-filled lungs are about three times as great as those required to expand saline solution-filled lungs. 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. Let us now discuss surfactant and its relation to the surface tension forces.
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: that is, there is 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 results in an attempt to force the 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 per cent 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 dipalmitoylphosphatidylcholine, surfactant apoproteins, and calcium ions. The dipalmitoylphosphatidylcholine, along with several less important phospholipids, is responsible for reducing the surface tension. It does this 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.
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 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:
For the average-sized alveolus with a radius of about 100 micrometers and lined with normal surfactant, this calculates to be about 4 centimeters of water pressure (3 mm Hg). If the alveoli were lined with pure water without any surfactant, the pressure would calculate to be about 18 centimeters of water pressure, 4.5 times as great. Thus, one sees how important surfactant is in reducing alveolar surface tension and therefore also reducing the effort required by the respiratory muscles to expand the lungs.
Effect of Alveolar Radius on the Pressure Caused by Surface Tension. Note from the preceding formula that the pressure generated as a result of surface tension in the alveoli is inversely affected by the radius of the alveolus, which means 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 is especially significant in small premature babies, many of whom have alveoli with radii less than one quarter that of an adult person. Further, 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 than that. Therefore, many premature babies have little or no surfactant in the alveoli when they are born, and their lungs have an extreme tendency to collapse, sometimes as great as six to eight times that in a normal adult person. This causes the condition called respiratory distress syndrome of the newborn. It is fatal if not treated with strong measures, especially properly applied continuous positive pressure breathing.
Source : Guyton & Hall
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. Let us now discuss surfactant and its relation to the surface tension forces.
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: that is, there is 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 results in an attempt to force the 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 per cent 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 dipalmitoylphosphatidylcholine, surfactant apoproteins, and calcium ions. The dipalmitoylphosphatidylcholine, along with several less important phospholipids, is responsible for reducing the surface tension. It does this 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.
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 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:
For the average-sized alveolus with a radius of about 100 micrometers and lined with normal surfactant, this calculates to be about 4 centimeters of water pressure (3 mm Hg). If the alveoli were lined with pure water without any surfactant, the pressure would calculate to be about 18 centimeters of water pressure, 4.5 times as great. Thus, one sees how important surfactant is in reducing alveolar surface tension and therefore also reducing the effort required by the respiratory muscles to expand the lungs. Effect of Alveolar Radius on the Pressure Caused by Surface Tension. Note from the preceding formula that the pressure generated as a result of surface tension in the alveoli is inversely affected by the radius of the alveolus, which means 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 is especially significant in small premature babies, many of whom have alveoli with radii less than one quarter that of an adult person. Further, 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 than that. Therefore, many premature babies have little or no surfactant in the alveoli when they are born, and their lungs have an extreme tendency to collapse, sometimes as great as six to eight times that in a normal adult person. This causes the condition called respiratory distress syndrome of the newborn. It is fatal if not treated with strong measures, especially properly applied continuous positive pressure breathing.
Source : Guyton & Hall
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