Physiology of Respiration Lec 3 PDF
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Uploaded by IllustriousPlumTree
Jabir Ibn Hayyan Medical University
2024
Dr.Zainab Ali Altufailie
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This document appears to be lecture notes on the Physiology of Respiration, likely for a medical or life science undergraduate course. It covers topics such as pulmonary ventilation, lung mechanics, and pressures related to respiration.
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Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 Lung Physiology Page|1 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 By the end of lecture 3 ;y...
Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 Lung Physiology Page|1 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 By the end of lecture 3 ;you will be able to: ◆ define the muscles of respiration and explain their role in pulmonary ventilation ◆ explain the changes in intra-pleural and intra-alveolar pressures during respiration ◆ define lung compliance and its related variables Pulmonary Ventilation 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. (4) Regulation of 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. (2) By elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity 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. Page|2 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 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, 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 (3) scalene, 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. (2) internal intercostals. Page|3 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 Page|4 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 Pressures that Cause the Movement of Air In and Out of the Lungs 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. Pleural Pressure and Its Changes during Respiration Pleural pressure is the pressure of the fluid in the thin space between the lung pleura and the chest wall pleura. There 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. 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). 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. The difference between the alveolar pressure and the pleural pressure 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. Page|5 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 Compliance of the Lungs The extent to which the lungs will expand for each unit increase in transpulmonary pressure 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. Compliance Diagram of the Lungs 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 (2) elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces. Page|6 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 The elastic forces of the lung tissue are determined mainly by elastin and collagen fibers interwoven among the lung parenchyma. The elastic forces caused by surface tension are much more complex. 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 operative in the saline solution–filled lung. The 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. Page|7 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 Surfactant, Surface Tension, and Collapse of the Alveoli ◆ Surfactant and Its Effect on Surface Tension 1. Surfactant is a surface active agent in water, which means that it greatly reduces the surface tension of water. 2. 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. 3. It 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. 4. In quantitative terms, 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 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 = 2 x 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 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 Page|8 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 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. Page|9 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 A re u e o plian e is An in rease o plian e ause by o urs in pul onary brosis. pul onary e physe a 2 Al eolar e e a Atele tasis. nor al aging lung. 4 e o pneu o thora Page|10 Physiology of Respiration.LEC.3 Dr.Zainab Ali Altufailie \2024 **Home work: Q:In case of emphysema , lung compliance increased ;mention the pathophysiological explanation? References: Good luck Page|11