The Respiratory System Part I. Dr. Adelina Vlad
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1 The Respiratory System Part I Dr. Adelina Vlad
2 The Respiratory Process Breathing automatic, rhythmic and centrally-regulated mechanical process by which the atmospheric gas moves into and out of the lungs Respiration the overall process of metabolites oxidation for the production of energy by living organisms; it includes breathing Respiratory process: External respiration + Internal (mitochondrial) respiration
3 The Respiratory Process External respiration - the exchange of O2 and CO2 between the atmosphere and the mitochondria A dual process of transporting - O2 from the atmosphere to the mitochondria - CO2 from the mitochondria to the atmosphere Internal respiration (oxidative phosphorylation) - the oxidation of carbon-containing compounds to form CO2 The lectures on respiratory physiology focus on external respiration
4 External Respiration Can be divided into four major functions: 1) Pulmonary ventilation 2) Diffusion of O2 and CO2 between the alveoli and the blood 3) Transport of O2 and CO2 in the blood and body fluids, to and from the body s tissue cells 4) Regulation of ventilation
5 Air pump Components of the Respiratory System delivers air to and removes air from the alveolar air spaces = alveolar ventilation consist of the lungs and the airways, the rib cage and the thoracic cavity with the muscles of respiration Surface for gas exchange represented by the alveoli Circulatory system internal convective system that delivers O2 to and removes CO2 from the tissues Mechanisms for carrying O2 and CO2 in the blood red blood cells are the main players Mechanisms for locally regulating the distribution of ventilation and perfusion complex feedback loops to regulate air flow and blood flow in the lungs Mechanisms for centrally regulating ventilation
6 The respiratory apparatus in humans
7 Nonrespiratory Roles of the Lungs Olfaction Ventilation is essential for delivering odorants to the olfactory epithelium Sniffing allows one to sample the chemicals in the air without the risk of bringing potential noxious agents deep into the lungs Left-ventricular reservoir The blood contained in the highly compliant pulmonary vessels is an important buffer for filling the left ventricle The left heart can sustain cardiac output for about two beats only with blood from pulmonary circulation
8 Filtering small emboli from the blood The pulmonary vasculature can trap microscopic emboli present in the venous blood (e.g., blood clots, fat, air bubbles) before they reach the left heart If the emboli are few and small, the affected alveoli can recover their function; if pulmonary emboli are large or frequent, they can cause serious symptoms or death Emboli made up of cancer cells may find a breeding ground for supporting metastatic disease Biochemical reactions The pulmonary capillary endothelium plays an important role in converting angiotensin I to angiotensin II, a reaction that is catalyzed by angiotensin converting enzyme (ACE), and selectively removes agents from the circulation (PGE1, PGE2, PGF2a, leukotrienes, serotonin, bradykinin)
9 Pulmonary Ventilation Pulmonary mechanics - is the physics of the lungs, airways and chest wall - explains how the body moves air in (inspiration) and out (expiration) of the lungs
10 The functional chest wall includes the rib cage, diaphragm, and abdomen
11 Inspiration Is an active process that implies contaction of: primary muscles of inspiration during a quiet breathing: diaphragm external intercostals secondary muscles of inspiration during a forced breathing: sternocleidomastoids anterior serrati scalenes
12 Expiration Is passive durig a quiet breathing Is active during a forced breathing and occurs by contracting the accessory muscle of expiration: internal intercostals rectus abdominis external obliques
13 Pressures That Cause the Movement of Air In and Out of the Lungs During inspiration and expiration the air moves in and out of the lungs due to variations of the: 1. Intrapleural pressure 2. Alveolar pressure 3. Transpulmonary pressure
14 Chest Wall Lung Interaction The lungs are elastic structures, kept distended inside the thoracic cavity due to their interaction with the chest wall This interaction occurs via the intrapleural space, which is a potential cavity between the visceral and parietal pleural membranes
15 Chest Wall Lung Interaction Elastic recoil of the lungs their tendency to collapse Elastic recoil of the chest wall its tendency to pull the thoracic cage outward The chest wall and the lungs pull away from each other relative vacuum between them that makes the pressure inside the intrapleural space lower than the barometric pressure (the intrapleural pressure is negative)
16 Intrapleural Pressure, PIP Is the pressure of the fluid inside the intrapleural space and has negative values Gravity and the respiratory movements influence PIP values: By pulling the lungs downward gravity makes PIP more negative to the apex compared to the base of the thoracic cavity of an upright subject At the beginning of inspiration, PIP is about 5 cm H2O; at the end of a quiet inspiration, PIP decreases to an average of about 7.5 cm H2O Upright subject
17 PIP and the Pleural Fluid Pleural fluid - transudat with mucoid characteristic, favoring slippage of the lungs during ventilation The pumping of the fluid from the intrapleural space by the lymphatics into the mediastinum, the superior surface of the diaphragm, and the lateral surfaces of the parietal pleura maintains a negative PIP
18 Alveolar Pressure, PA Is the pressure of the air inside the alveoli When the glottis is open and no air flows into or out of the lungs, the pressures in all parts of the respiratory tree, including the alveoli (PA), are equal to atmospheric pressure (PB) PA PB governs the gas exchange between the lungs and the atmosphere; the alveolar pressure, PA, is a dynamic element, directly involved in producing air flow
19 Transpulmonary Pressure (PTP) Is the force responsible for keeping the alveoli open, expressed as the pressure gradient across the alveolar wall: PTP = PA PIP PA should be always > PIP (PTP > 0) in order to maintain the lungs expanded in the thoracic cavity PTP is a static parameter which does not cause airflow, but determines lung volume (VL) PIP has a static component (-PTP) that determines lung volume and a dynamic component (PA) that determines air flow
20 PIP, PA and PTP During Quiet Breathing PIP is the pressure directly controlled by the activity of the respiratory muscles; PA and PTP flow from PIP The negative shift in PIP occurring during inspiration has two effects: PA becomes more negative and PTP is made more positive
21 Static Compliance of the Lungs Is the extent to which the lungs will expand for each unit increase in transpulmonary pressure (a measure of how easy it is to inflate the lungs): C=DVL/DPTP Static compliance - determined at a steady state, when the glottis was open and the breathing movements were stopped, allowing no airflow Elastance the compliance reciprocal, a measure of the elastic recoil of the lungs: E=1/C The characteristics of static compliance are determined by the elastic forces of the lungs, represented by: (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
22 Static Pressure-Volume Curves for Lungs in Health and Disease The compliance decreases at high lung volumes due to anatomic and viscous limitations Fibrosis: stiff lungs due to fibrous tissue deposition, with decreased compliance (elastic recoil is much greater) Emphysema: floppy lungs as a result of elastin destruction, with increased compliance (much less elastic recoil)
23 Compliance Diagram in a Healthy Person This diagram shows compliance of the lungs alone 1. Stable VL at low lung volumes it is difficult to pop open an almost completely collapsed airway; rising PTP has little effect on VL 2. Opening of airways the first increases in VL reflect the popping open of the proximal airways, followed by their expansion and recruitment of others 3. Linear expansion of open airways when all the airways are open, making PIP more negative by chest wall expansion inflates the lungs and increases VL in a linear fashion 4. Limit of airway inflation at high VL lungs compliance decreases
24 Hysteresis Defines the difference between the inflation and deflation compliance paths It exists because a greater pressure difference is required to open a previously closed (or narrowed) airway than to keep an open airway from closing
25 Surface Tension When water forms a surface with air, the water molecules on the surface of the water have a strong attraction for one another the water surface is always attempting to contract On the inner surfaces of the alveoli the water surface is also attempting to contract (surface water molecules tend to dive into the bulk, decreasing the area of the airwater interface), causing an elastic contractile force of the entire lungs, called the surface tension elastic force the surface tension contributes to the elastic recoil
26 Effect of Surface Tension on Compliance Lungs inflated with saline solution (= no air-water interface and null surface tension) have an up to three times higher compliance, proving that the surface tension at the air-water interface accounts for about two thirds of the elastic recoil of the lungs (von Neergaard, 1929) surface tension decreases lung compliance In lungs inflated with saline solution hysteresis is much smaller as well Laplace s equation:
27 Effect of Surface Tension on Total Alveolar Surface Area The pressure generated as a result of surface tension in occluded alveoli is inversely affected by the radius of the alveolus (Laplace s equation): the smaller the alveolus radius, the higher the pressure needed to keep it open as alveoli have different sizes and are interconnected, smaller alveoli would tend to collapse in bigger ones, decreasing the total alveolar surface area (gas exchange area)
28 Pulmonary Surfactant Surfactant is a surface active agent in water = reduces the surface tension of water (e.g. pressure generated in occluded alveoli of identical size is 18 cm H2O without and 4 cm H2O with surfactant) Due to its components with both hydrophobic and hydrophilic properties, the surfactant gets into the surface of the air-water interface and decreases here the density of water molecules
29 The most important components of the pulmonary surfactant are the phospholipid dipalmitoylphosphatidylcholine, surfactant apoproteins, and calcium ions It is secreted by type II alveolar epithelial cells starting the 6 th and 7 th month of gestation respiratory distress syndrome of the newborn in underdeveloped infants due to insufficient secretion of surfactant By reducing alveolar surface tension, the surfactant reduces the elastic forces of the lung and increases compliance
30 Chest Wall Compliance The thoracic cage has its own elastic and viscous characteristics The compliance of the entire pulmonary system (the lungs and thoracic cage together) is measured while expanding the lungs of a totally relaxed person The compliance of the combined lung-thorax system is almost one half that of the lungs alone When the lungs are expanded to high volumes or compressed to low volumes the limitations of the chest wall become extreme and the compliance of the combined lung-thorax system can be less than one fifth that of the lungs alone
31 Work of Breathing Under resting conditions, the respiratory muscles perform work to cause inspiration, and not expiration The work of inspiration can be divided into three fractions: (1) Work required to expand the lungs against the lung and chest elastic forces, called compliance work or elastic work (2) Work required to overcome the viscosity of the lung and chest wall structures, called tissue resistance work (3) Work required to overcome airway resistance to movement of air into the lungs, called airway resistance work
32 Lung Volumes and Capacities VC = IRV + TV + ERV VC = IC + ERV TLC = VC + RV TLC = IC + FRC FRC = ERV + RV IRV = Inspiratory reserve volume TV = Tidal volume ERV = Expiratory reserve volume RV = Residual volume TLC = Total lung capacity IC = Inspiratory capacity FRC = Functional residual capacity VC = Vital Capacity L L L L L L L L
33 The magnitude of IRV depends on Lung compliance any disorder causing a decrease in compliance is decreasing IRV Muscle strength IRV decreases if the respiratory muscles are weak or if their innervation is compromised Comfort pain limits the ability to perform a maximal inspiration Flexibility of skeleton IRV is decreased by joint stiffness (arthritis, kyphoscoliosis) Posture IRV is lower in a recumbent position because the movement of the diaphragm downward is more difficult without the help of the gravity The magnitude of ERV depends on the same factors, plus the strength of the accessory expiratory muscles
34 Functional Residual Capacity FRC the volume of air that remains in the lungs at the end of each normal expiration To measure FRC the spirometer is used in an indirect manner, e.g. by determining the degree of dilution of the helium after the subject has breathed, starting from the end of a normal expiration, air mixed with He at a known initial concentration: Knowing FRC, one can calculate RV and TLC as well:
35 Alveolar Ventilation The scope of pulmonary ventilation is the renewal of the air in the gas exchange areas: the alveoli, alveolar sacs, alveolar ducts, and respiratory bronchioles Alveolar ventilation is the rate at which new air reaches gas exchange areas Alveolar ventilation is one of the major factors determining the concentrations of oxygen and carbon dioxide in the alveoli Anatomic dead space respiratory passages where gas exchange does not occur; the air from the dead space just fills the proximal (conducting) airways, and never reaches exchange areas it is not used for refreshing the alveolar air
36 Physiologic dead space - on occasion, some of the alveoli themselves are nonfunctional or only partially functional because of absent or poor blood flow through the adjacent pulmonary capillaries = alveolar dead space - When the alveolar dead space is included in the total measurement of dead space, this is called the physiologic dead space The rate of alveolar ventilation: where VT is the tidal volume, and VD is the physiologic dead space volume., Normally, alveolar ventilation would equal 12 x ( ) = 4200 ml/min
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