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Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 Respiratory physiology The study of respiratory physiology is important to medicine, because many of the respiratory diseases (e.g., cystic fibrosis, asthma, emphysema, pulmonary hypertension, and pneumonia) impact many of the subspecialties, from pediatrics, to internal medicine, to surgery, and to geriatrics. The human lungs are so efficiently designed that gas exchange can increase >20-fold to remove carbon dioxide and to supply oxygen to tissues in order to meet the body’s energy demands. Lecture Outline Functional anatomy Ventilation Gas exchange Gas transport in blood Regulation of ventilation Functional anatomy The respiratory system is composed of the conducting airways and the respiratory airways. Figure: respiratory system Conducting and Respiratory Airways 1 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 The conducting airways include the nose, mouth, pharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles. As their name suggests, these airways conduct air to the respiratory airways; they do not participate in gas exchange. The bronchi are > 1 mm in diameter and have cartilaginous rings that protect them from collapsing during expiration. They are not embedded in the lung parenchyma, so their diameter is not dependent on lung volume. The bronchi branch to form bronchioles that are smaller in diameter and have no supporting cartilage. They are embedded within lung parenchyma, and their diameter expands and contracts with lung volume. Figure: conductive zone Innervation: Smooth muscles innervated by autonomic nervous system: - parasympathetic - muscarinic - bronchoconstriction - sympathetic - beta2 - receptors – bronchodilation -mainly to adrenalin The respiratory airways include the respiratory bronchioles (i.e., bronchioles with alveoli in their walls; and alveolar ducts. Alveoli: There are ~300 million alveoli in adult lungs, each being ~250μm in diameter. Their walls are composed of a simple squamous epithelium, 2 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 primarily type I pneumocytes. Each alveolus is encased by pulmonary capillaries, which are sandwiched between the lumens of adjacent alveoli. The total surface area available for gas exchange is ~150 m2. Alveoli first begin to appear on the respiratory bronchioles, marking the start of the respiratory portion of the lung. These alveoli are isolated initially, then become more numerous and are collected into sacs. Each sac has a central open space, or alveolar duct, that is continuous with the lumen of its respiratory bronchiole. The alveolar walls are composed of squamous epithelium and are in direct contact with the pulmonary capillaries for gas exchange to occur. Connective tissue with abundant elastic fibers is found throughout the branches of the bronchial tree and the alveoli. These contribute substantially to the elastic recoil of the lungs during expiration. Figure: respiratory zone Removal of Inhaled Particles With its surface area of 50 to 100 square meters, the lung presents the largest surface of the body to an increasingly hostile environment. Various mechanisms for dealing with inhaled particles have been developed. Large particles are filtered out in the nose. Smaller particles that deposit in the conducting airways are removed by a moving staircase of mucus that 3 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 continually sweeps debris up to the epiglottis, where it is swallowed. The mucus, secreted by mucous glands and also by goblet cells in the bronchial walls, is propelled by millions of tiny cilia, which move rhythmically under normal conditions but are paralyzed by some inhaled toxins. The alveoli have no cilia, and particles that deposit there are engulfed by large wandering cells called macrophages. The foreign material is then removed from the lung via the lymphatics or the blood flow. Blood cells such as leukocytes also participate in the defense reaction to foreign material. Pressures in the lungs To understand the mechanics of ventilation and airflow during breathing, it is necessary to review the pressure in the lungs. – Intra-pleural pressure is the pressure in the intra-pleural space. – Alveolar pressure is the pressure within the alveoli. – Trans-pulmonary pressure is alveolar pressure minus intra-pleural pressure. Intra-pleural pressure is always less than alveolar pressure; therefore, transpulmonary pressure is always positive. It is the positive trans-pulmonary pressure that keeps the lungs inflated (like a balloon) against the chest wall. Pleural Pressure and Its Changes Pleural pressure is the pressure of the fluid in the thin space between the lung pleura and the chest wall pleura. 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. 4 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 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). 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. Trans-pulmonary 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. Figure: change in pressure during inspiration and expiration 5 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 Ventilation Ventilation (breathing) is the process by which air enters and exits the lungs. Respiration is the overall term for ventilation, gas exchange, and utilization in cells. Mechanics of Ventilation Ventilation occurs in a cyclical manner with alternating inspiratory and expiratory phases. Inspiration Inspiration is an active process and is principally mediated by the diaphragm during quiet breathing. – Contraction of the diaphragm enlarges the chest cavity, reducing intra-pleural pressure. This increases the trans-pulmonary pressure and expands the lungs . Minimal movement of the diaphragm (a few centimeters) is sufficient to move several liters of gas. – The external intercostal and accessory muscles are not necessary for resting respiration, but they contribute substantially to deep respiration during exercise and respiratory distress. When the diaphragm moves to the inspiratory position, the ribs are elevated by the intercostal muscles (chiefly the external intercostals) and scalene muscles. Because the ribs are curved and directed obliquely downward, elevation of the ribs expands the chest transversely (toward the flanks) and anteriorly. Meanwhile, the diaphragm leaflets are lowered by muscle contraction causing the chest to expand inferiorly. These processes result in overall expansion of the thoracic volume. Expiration Expiration is a passive process during quiet breathing. When the diaphragm relaxes, air is expelled from the lungs due to the elastic recoil of the lung–chest wall system. Active expiration (using muscles of expiration) occurs during exercise or in obstructive lung disease. 6 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 When the diaphragm moves to the expiratory position , the chest becomes smaller in all dimensions, and the thoracic volume is decreased. This process does not require additional muscular energy. The muscles that are active during inspiration are relaxed, and the lung contracts as the elastic fibers in the lung tissue that were stretched on inspiration release their stored energy, causing elastic recoil. For forcible expiration, however, the muscles that assist expiration (mainly the internal intercostal muscles) can actively lower the rib cage more rapidly and to a greater extent than is possible by passive recoil alone. 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. Muscles of respiration: 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. 7 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 External Respiration Internal Respiration Physical Properties of the Lungs 1.Compliance. 2.Elasticity. 3.Surface tension. 1.Compliance of the respiratory system Lung Compliance Lung compliance expresses the dispensability of the lungs, that is, how easily the lungs expand when trans-pulmonary pressure increases. It is expressed by the following equation: C = ΔV/ΔP 8 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 where C = lung compliance ΔV = increase in lung volume (mL) ΔP = increase in trans-pulmonary pressure (mm Hg). – Compliance is inversely related to stiffness. – Compliance is inversely related to the elastic recoil, or elastance, of the lung. Recoil causes the lungs to return to their previous volume when stretching ceases following an increase in trans-pulmonary pressure. It is mediated by surface tension in the alveoli and by elastic fibers in the lung connective tissue. Changes in lung compliance in disease states – Lung compliance is decreased in pulmonary fibrosis because the interstitium surrounding the alveoli becomes infiltrated with inelastic collagen. – Lung compliance is increased in emphysema because many small alveoli are replaced by fewer but larger coalesced air spaces that have less elastic recoil. – Lung compliance is normal in asthma. 2.Elasticity: It means tendency to return to initial size after distension. This occurs due to the high content of elastin proteins present in the lung walls which is very elastic and resist distension. Elastic tension increases during inspiration and is reduced by recoil during expiration. most of elastin proteins present in the lung walls which is very elastic and resist distension. Elastic tension increases during inspiration and is reduced by recoil during expiration. 3.Surface Tension in the Alveoli Surface tension is due to the cohesive forces between water molecules at the air–water interface in the alveoli of lungs. It acts to contract the alveoli and is a major contributor to the force of elastic recoil of the lung. 9 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 If there were no opposing force, surface tension would cause the alveoli to collapse (atelectasis). However, the collapsing force is opposed by trans-pulmonary pressure, which is always positive, allowing the alveoli to remain open. However, surface tension is reduced by pulmonary surfactant, and the reduction is greater in small alveoli than in larger ones because small alveoli concentrate the surfactant. Thus, the increased tendency to collapse because of small radius is just balanced by a greater reduction in surface tension. Surfactant Surfactant is a complex substance, consisting of proteins and phospholipids (mainly dipalmitoyl lecithin), that is produced in type II pneumocytes. It lines alveoli and lowers surface tension by the same mechanism as detergents and soaps (i.e., it coats the water surface and reduces cohesive interactions between water molecules). As an extension of its role in lowering surface tension, surfactant also produces the following effects: – It increases compliance at all lung volumes, which allows for easier lung inflation and greatly decreases the work of breathing. – It reduces the otherwise highly negative pressure in the interstitial space, which reduces the rate of filtration from pulmonary capillaries. This assists in maintaining lungs without excessive water. Failure of surfactant production and/or excessive surfactant breakdown occurs in neonatal respiratory distress syndrome (RDS). Effect of Alveolar Radius on the Pressure Caused by Surface Tension 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, 10 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 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. The work of inspiration can be divided into three fractions: (1) that required to expand the lungs against the lung and chest elastic forces, called compliance work or elastic work; (2) that required to overcome the viscosity of the lung and chest wall structures, called tissue resistance work; and (3) that required to overcome airway resistance to movement of air into the lungs, called airway resistance work. Airway Resistance Resistance is inversely proportional to the airway radius to the fourth power, small changes in diameter cause large changes in resistance. – The large airways offer little resistance to airflow. The small airways individually have high resistance, but their enormous number in parallel reduces their combined resistance to a small value. Therefore, the sites of highest resistance in the bronchial tree are normally in the medium airways. Regulation of Airway Resistance: Airway resistance is primarily regulated by modulation of airway radius by the parasympathetic and sympathetic nervous systems. 11 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 – Parasympathetic nervous system: Vagal stimulation releases acetylcholine that acts on muscarinic (M3) receptors in the lungs, leading to bronchoconstriction. This increases the resistance to airflow. – Sympathetic nervous system: Postganglionic sympathetic nerves release norepinephrine that act on β2 receptors, leading to broncho-dilation. This decreases the resistance to airflow Lung Volumes and Capacities – Lung volumes are a way to functionally divide volumes of air that occur during different phases of the breathing cycle. They are all measured by spirometry, except for residual volume.They vary with height, sex, and age. – Lung capacities are the sums of two or more lung volumes. – Tidal, inspiratory, and expiratory reserve volumes and inspirational and vital capacities are used in basic pulmonary function tests. Lung Volumes – Tidal volume (TV) is the volume of air that moves in or out of the lungs during one normal, resting inspiration or expiration. – Inspiratory reserve volume (IRV) is the volume of air that can be inspired beyond a normal inspiration. – Expiratory reserve volume (ERV) is the volume of air that can be expired beyond a normal expiration. – Residual volume (RV) is the volume of air left in the lungs and airways after maximal expiration. Lung Capacities – Inspirational capacity (IC) is the maximum volume of air that can be inspired with a deep breath following a normal expiration. It is the sum of TV and IRV. 12 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 – Functional residual capacity (FRC) is the volume of the lungs after passive expiration with relaxed respiratory muscles. It is the sum of ERV and RV. – Vital capacity (VC) or forced vital capacity (FVC): is the maximum volume of air that can be expired in one breath after deep inspiration. It is the sum of TV, IRV, and ERV. – Total lung capacity (TLC) is the total volume of air that can be contained in the lungs and airways after a deep inspiration. It is the sum of all four lung volumes: TV, IRV, ERV, and RV. Note: TLC and FRC cannot be measured by spirometry because residual volume is needed for their calculation. Forced Expiratory Volume (FEV1) is the volume of air that can be forcibly expired in the first second following a deep breath. It is usually > 70% of the FVC (FEV1/FVC > 70%). – In obstructive lung disease (e.g., asthma and COPD), FEV1 is reduced proportionally more than FVC; therefore, FEV1 /FVC < 70%. – In restrictive lung disease (e.g., fibrosis), both FEV1 and FVC are reduced. This means that FEV1 /FVC is normal or increased. Figure: old spirometry technique 13 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 Figure: lung volumes and capacities Dead Space Dead space is volume within the bronchial tree that is ventilated but does not participate in gas exchange. – Anatomical dead space is the volume of the conducting airways (pharynx, trachea, and bronchi) that do not contain alveoli and therefore cannot participate in gas exchange. It is ~150 to 200 mL. – Physiological dead space is the total volume of the bronchial tree that is ventilated but does not participate in gas exchange. The total volume exhaled is the forced vital capacity (FVC), and the volume exhaled in the first second is the forced expiratory volume (FEV1). 14 Respiratory System Physiology Dr. Amjed Hassan Al-Juboory lecture 1 – In healthy lungs, physiological dead space is approximately equal to anatomical dead space. However, physiological dead space may be increased in lung diseases where there are mismatches between ventilation (V) and perfusion (pulmonary blood flow [Q]). – Physiological dead space can be calculated using Bohr’s equation. This calculation assumes that the partial pressure of CO2 (Paco2) in the alveoli is the same as that in systemic arterial blood. Ventilation Rate Minute ventilation refers to the total ventilation per minute. It is expressed as Minute ventilation = TV × breaths/min Alveolar ventilation refers to ventilation of alveoli that participate in gas exchange per minute. It is expressed as Alveolar ventilation = (TV – physiological dead space) × breaths/min. 15