Physiology of Respiration PDF
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Ain Shams University
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Summary
These notes provide a comprehensive overview of human respiration. The document discusses the functional anatomy of the respiratory system, its functions, ventilation, mechanics of breathing, gas transport, hypoxia, cyanosis and the regulation of respiration. It contains diagrams that show the processes described.
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Physiology of respiration Lecture objectives By the end of this lecture you should be able to:- 1. Describe functional anatomy of the respiratory system. 2. Recognize the functions of the respiratory system. 3. Discuss alveolar ventilation. 4. Discuss mechanics of breathing 5. Give...
Physiology of respiration Lecture objectives By the end of this lecture you should be able to:- 1. Describe functional anatomy of the respiratory system. 2. Recognize the functions of the respiratory system. 3. Discuss alveolar ventilation. 4. Discuss mechanics of breathing 5. Give a brief account on gas transport and O₂-hemo- globin dissociation curve. 6. Define hypoxia and compare between its different types. 7. Define cyanosis. 8. Discuss regulation of respiration. Components Of The Respiratory System Upper air passages & Conducting Respiratory zone of lower zone of lower air passages air passages (Air conditioning ) (Gas exchange) Functional structure Of The Respiratory System Air passages are divided into:- 1. Upper air passages – The nose – Pharynx – Larynx 2. Lower air passages are divided into:- – Conducting zone : Tracheobronchial tree. It extends from the trachea to the terminal bronchioles. – Respiratory zone: Respiratory bronchioles & alveoli Conducting zone Respiratory zone Components Trachea & bronchial tree Respiratory bronchioles Lung alveoli Function 1. Conduct air to the Exchange of gases respiratory zone 2. Defensive function due to presence of:- Mucus Cilia phagocytes 3. Warming of air 4. Add water vapor to inspired air. 5. phonation Functions of the respiratory system 1. Gas exchange: respiratory system extracts O₂ from the atmospheric air and eliminates Co₂ produced by body during its metabolism. 2. Help venous return. 3. Metabolic function: a. Synthesis of SURFACTANT to be used by the lung. b. Conversion of ANGIOTENSIN- I to ANGIOTENSIN –II which is a strong vasoconstrictor substance and is involved in regulation of arterial blood pressure. c. Rich in FIBRINOLYTIC SYSTEM which would dissolve any blood clot in the venous blood pumped to the lung. What is Respiration? 1. External respiration:- It is the exchange of gases between the body and the external environment. This exchange involves the following steps:- a. Ventilation: exchange of gases between atmosphere and alveoli. b. Diffusion of gases : exchange of gases between the alveolar air and blood in the pulmonary capillaries. c. Transport of gas by the blood from lung to tissues by the cardiovascular system. d. Diffusion of gas between the blood in systemic capillaries and the tissues across capillary wall. 2. Internal respiration:- Itis the use of O₂ by mitochondria in various metabolic processes to produce energy ( ATP ) and the production of CO₂ as a waste product. What is Respiration? Respiration is the exchange of gases What is Ventilation? Inspired air is rich in oxygen and poor in carbon dioxide. Alveolar air is poor in oxygen ( it diffuses continuously from the alveolar air to the blood in pulmonary capillaries) and is rich in carbon dioxide (it diffuses continuously from the blood in pulmonary capillaries to the alveolar air). Ventilation is the process by which alveolar air is renewed (.i.e. partially replaced ) by the atmospheric air. If there is no ventilation, there will be no replenishment of oxygen and no removal of CO₂.Thus alveolar PaO₂ will fall and alveolar PaCO₂ will rise towards the venous blood PO₂ and PCO₂ values. Ventilation is the mass movement of air between the atmosphere & the alveoli. Air tends to move from a region of higher pressure to a region of lower pressure. Alveolar air Atmospheric pressure: It is constant all the time. Atmospheric pressure Intrapulmonary pressure: It is the pressure inside the alveoli. It increases with decreased lung volume and decrease with increased lung volumes. However it always equilibrates with the atmospheric pressure because they are communicating with each other Intrapleural pressure: it is the pressure in the pleural sac. It is always negative. Thus, it stretches the lung alveoli. Mechanics of Breathing A. During inspiration The muscles of inspiration contract (mainly the diaphragm). Thus , the thoracic cage and the lung expand, intrapulmonary pressure decrease and air moves from outside to inside the lung till the intrapulmonary pressure equilibrate with atmospheric pressure. B. During expiration The muscles of inspiration are relaxed , the lungs recoil pulling the chest wall backwards, the intrapulmonary pressure increase and air moves from inside the lung to the outside till the intra-pulmonary pressure equilibrates with atmospheric pressure. Muscles of expiration are contract only in deep forceful expiration. NORMAL RESTING EXPIRASTION IS PASSIVE Why the lung is elastic? The lung is elastic because : A. It is rich in elastic fibers. B. Surface tension of the fluid film lining the alveoli. Lung alveoli are lined by thin layer of water molecules (thin fluid film). These water molecules have attraction forces in between which make them try to get closer to each other so as to minimize their surface area with air. While trying to get closer to each other, the water molecules would pull on the alveolar wall causing it to get smaller and smaller until it finally collapses. Elastic force of the lung is important for the normal expiration to be passive. However, if it was not moderated , it may lead to lung collapse. SURFACTANT IS THE MODERATOR OF THIS FORCE The fluid film lining the alveoli Elastic lung tissue Elastic forces of the lung decrease the ability of the lung to expand and increase lung tendency to collapse The fluid film lining the alveoli Lung surfactant is a lipid molecule synthesized by lung alveolar cells that decrease surface tension of the fluid lining the alveoli Elastic lung tissue Surfactant decrease surface tension of the fluid lining the alveoli, thus preventing lung collapse and helps easy lung expansion. It is deficient premature babies , a condition called infantile respiratory distress syndrome (IRDS). CO₂ O₂ CO₂ CO₂ Transport of Gases O₂ Transport of Oxygen & Transport of carbon dioxide O₂ O₂ CO₂ 1-Oxygen Transport Oxygen delivery system in the body consists of: 1. The lungs 2. The CVS To reach the tissues, an oxygen molecule should: 1. be introduced into the alveoli. 2. cross the alveolocapillary membrane. 3. bind hemoglobin in RBCs. 4. circulate with the blood. 5. dissociate from hemoglobin to be taken by tissue cells. Any obstacle in in this journey will result in decreased O2 tension at the tissues.i.e. Hypoxia. Diffusion of O2 across the alveolocapillary membrane is:- 1. directly proportional to r P (.i.e. pressure gradient) 2. directly proportional to the surface area of the alveolocapillary membrane. 3. inversely proportional to thickness of alveolocapillary membrane O₂ Transport in blood O₂ is transported in blood in two forms:- 1. Physically dissolved O₂. It represent a small fraction ( 1.5%). 2. Chemically bound to hemoglobin. It is the most important form (98.5%). Hemoglobin is formed of 4 subunits, each subunit contains a ferrous ion that binds reversibly with O₂, so the reaction is called oxygenation and not oxidation. HbO₂ ↔O₂+ Hb Hemoglobin Molecule O2 O2 O2 O2 Lung O2 O2 O2 O2 Physically dissolved O₂ Chemically bound O₂ O₂ content in blood=amount of O₂ in chemical combination with hemoglobin. It depends on hemoglobin content in the blood. O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 % HB saturation in venous blood is 75% Because PO₂ is decreased. O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 Hypoxia It is decreased O₂ tension at tissues. Decreased O₂ tension in blood is termed hypoxemia Types of hypoxia are:- 1. Hypoxic hypoxia 2. Anemic hypoxia 3. Stagnant hypoxia 4. Histotxic hypoxia Hypoxia Cause Hypoxic 1. Decreased oxygen tension in atmospheric air hypoxia as in high altitudes or badly ventilated areas. 2. ↓alveolar ventilation due to lung disease or respiratory center depression. 3. Decreased O₂ diffusion across alveolo-capillary membrane due to lung fibrosis. Anemic Anemia hypoxia Stagnant Decreased blood flow to tissues hypoxia Histotoxic Tissues are unable to use O₂ hypoxia Cyanosis It is bluish discoloration of the skin &mucous membranes.This color appears when the amount of reduced Hb exceeds 5 gm/ 100 ml blood. It appears in hypoxic hypoxia & stagnant hypoxia. In cyanosis , reduced HB is > 5gm/ 100 ml O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 Regulation of respiration Normal respiratory movements are involuntary (they are carried out without conscious control ). Respiration is controlled by:- 1. Medullary respiratory center :Medullary respiratory neurons have intrinsic ability to discharge nerve impulses spontaneously and rhythmically to the muscles of respiration (.i.e. they have automaticity). There are two defined groups of medullary respiratory neurons:- –I neurons which discharge during inspiration. They innervate muscles of inspiration producing inspiration. –E neurons which inhibit I neurons, thus initiate expiration by relaxation of inspiratory muscles. 2. Pontine respiratory centers: They play role in switching between inspiration and expiration. Regulation of respiratory center activity 1-Chemical regulation Activity of the medullary respiratory center is affected by arterial levels of O₂. Co₂ & pH. These changes are sensed by :- – Peripheral chemoreceptors: They are located in the aortic arch & carotid arteries. They are sensitive to changes in PaO₂. PaCO₂ & H⁺ – Central chemoreceptors: They are located in medulla oblongata close to the respiratory center. They are sensitive to PaCO₂ and H⁺ in cerebrospinal fluid. Increased H⁺level in arterial blood doesn’t stimulate these receptors because H⁺ can't cross the blood brain barrier 1. Changes in arterial PCO₂ ( the most potent). Increased arterial PCO₂ → stimulation of the central and peripheral chemoreceptors→ strong stimulation of the respiratory center → increased rate & depth of breathing →↑ alveolar ventilation → washout of Co₂ → ↓arterial PCO₂ 2. Changes in arterial PO₂. Decreased arterial PO₂ below 60 mmHg →stimulation of the peripheral chemoreceptors→ stimulation of the respiratory center→ increased rate and depth of breathing→↑ alveolar ventilation→↑alveolar PO₂ →↑arterial PO₂ 3. Changes in blood pH. Decreased arterial pH → stimulation of the peripheral chemoreceptors→ stimulation of the respiratory center→ increased rate & depth of breathing→↑ alveolar ventilation →↓arterial PCO₂ →↓ formation of carbonic acid →↓Hydrogen ion concentration. Regulation of respiratory center activity 2-Non -Chemical regulation 1. Signals from the cerebral cortex: The cerebral cortex can voluntarily stimulate respiration causing voluntary tackypnea (.i.e. increased respiratory rate), or it can depress respiration causing voluntary apnea (.i.e. stop of breathing). Voluntary control of respiration can not overcome the influence of changes in blood gases on the respiratory center. 2. Signals from the lung: The lung contain receptors that send signals to the respiratory center.e.g. stretch receptors to modulate respiratory center activity. References 1. Sherwood L. 2012. Fundamentals of human physiology 4th ed. United states. Brooks/Cole, Cengage Learning. Chapters 12 (p 345-377).