Respiratory Physiology PDF

Respiratory physiology 1  Respiratory System Body cell need Gas exchange: 200 ml O2/ min – O2 enters blood and CO2...

Respiratory physiology 1  Respiratory System Body cell need Gas exchange: 200 ml O2/ min – O2 enters blood and CO2 Upper respiratory leaves. Paranas system Regulation of blood pH: al sinuses – Altered by changing blood CO2 levels. Conducting Voice production: zone Lower – Movement of air through respiratory vocal folds makes sound and system speech. Olfaction: – Sense odor, when airborne Respiratory molecules drawn into nasal zone cavity. Protection: – Prevent entry and remove 2 microorganism.  Non respiratory functions 1. Provides route for water loss and heat elimination. 2. It enhance venous return. 3. Maintenance of acid base balance. 4. Enables various kinds of vocalization. 5. Defense against inhaled foreign matter. 3  Functional parts of Respiratory system Conducting zone Respiratory zone Series of interconnecting cavities Tissues within the lungs, and tubes both outside and within where gas exchange occurs. the lungs These include – Respiratory bronchioles, These include – Nose, – Alveolar ducts, – Pharynx, – Alveolar sacs, – Larynx, – Alveoli. (300 million) – Trachea, – Bronchi, – Bronchioles, The main sites of gas – Terminal bronchioles. exchange between air and blood. Their function is to filter, warm, Increased surface area (70 m2) moisten the air and conduct it into lungs. Volume is 5-6 lit. Volume is 150 ml. 4 Respiratory zone Begins as terminal bronchioles feed into respiratory bronchioles. Respiratory bronchioles lead to alveolar ducts, then to terminal clusters of alveolar sacs composed of alveoli. 150 - 300 million alveoli: Account for most of lung’s volume Each lobule of lung is wrapped in Elastic connective tissue, Lymphatic vessel, An arteriole, Venule and Branch of terminal bronchiole. 5  Alveoli Alveolus – Cup shaped outpouching lined by simple squamous epithelium and supported by a thin elastic basement membrane. 300 million alveoli, providing an immense surface area of 70 m 2 Alveolar sac – Consists of two or more alveoli that share a common opening. Two types of alveolar cells – Type I alveolar cells Continues lining of alveolar cell for Gas exchange – Type II alveolar cells Septal cells which Secrete alveolar fluid. (Surfactant: Phospholipids and lipoproteins) Reduce surface tension. (Reduces the tendency of alveoli to collapse). Third type cell is Alveolar macrophages (Dust cells). 6 Alveolus. It consist of four layers – A layer of Type I and type II alveolar cells and associated alveolar macrophages. Simple squamous epithelium. – An epithelial basement membrane underlying the alveolar wall. (Basal lamina) – A capillary basement membrane fused to epithelial basement membrane. – The capillary endothelium. 7  Three Basic Steps of Respiration Pulmonary ventilation: Gas exchange between atmosphere and lungs. Physical movement of air into and out of lungs. External respiration Gas exchange between lungs and blood (O2 loading and CO2 unloading). 1.Gas diffusion. 2. Transport of respiratory gases –via movement of blood, O2 from lungs is transported to cell and tissues. Internal respiration Gas exchange between capillaries and tissues (O2 unloading and CO2 loading). 8  Pulmonary Ventilation A mechanical process that depends on volume change in thoracic cavity Volume change lead to pressure change. – Pressure and volume are inversely related. Which leads to flow Boyle’s law of gases to equalize 9 pressure.  Pulmonary ventilation Air flows between atmosphere and alveoli of lungs. Due to pressure differences created by contraction and relaxation of respiratory muscles. Pressure differences in caused by changes in lung volume by respiratory muscles. – Inspiration – Air flows into the lungs (Inhalation). Volume of lung increased – Pressure became decreased. – Expiration – Gases exit the lungs (Exhalation). Volume of lung decreased – Pressure will increased. 10  Inhalation and exhalation Lungs can be expanded and contracted in two ways. By downward and upward movement of diaphragm to lengthen or shorten the chest cavity. By elevation and depression of ribs to increase and decrease the anteroposterior diameter of chest cavity. Two types of pulmonary ventilation 11 1. Normal quit breathing. Muscle involved in ventilation 12  Inhalation The lungs must expand, which increases lung volume leads to decreases alveolar pressure in lungs to below atm pressure. – It is otherwise called as negative pressure breathing. Inhalation mainly due to contraction of two muscles. Diaphram (innervated by phrenic nerves) – Pulls lower surfaces of lungs downward. – Which increase vertical dimension of thoracic cavity. – Responsible for 75% air to come inside the lungs External intercoastal muscles. (innervated by intercoastal nerves) – Elevate ribs and sternum – Which increase anterioposterior and lateral diameter of chest 13 cavity.  Exhalation Normal exhalation is a passive process because no muscular contractions are involved. Instead, exhalation results from elastic recoil of chest wall and lungs. Two inwardly directed forces contribute to elastic recoil. 1. Recoil of elastic fibers that were stretched during inhalation. 2. Inward pull of surface tension due to the film of alveolar fluid. The pressure in the lungs is greater than the atmospheric pressure. 14  Pulmonary Pressure Normal atmosphere pressure is 760 mmHg Lungs concern with four types of pressure Interpleural pressure. – Pressure of fluid in thin space between lung pleura and chest wall pleura. – Normal pleural pressure at beginning of inspiration is 756 mm Hg. – Expansion of chest cage pulls outward on lungs with greater force and creates more negative pressure, of about 754 mm Hg. Alveolar pressure – Pressure of the air inside the lung alveoli. – Pressure in all pulmonary tree is equal to atmospheric pressure (760 mm Hg). – During normal inspiration, alveolar pressure decreases to about 758 mm Hg. – During expiration, alveolar pressure rises to about 762 mmHg. Transpulmonary pressure – Difference between the alveolar pressure and pleural pressure. Recoil pressure – Measure the elastic forces in lungs that tend to collapse the lungs at each instant of respiration. 15  Pressure change in Pulmonary inhalation 16  Pressure change in Pulmonary exhalation Diaphragm relaxes due to elasticity. External intercoastal muscle and ribs depressed. Decrease the size of thoracic cavity. Alveolar pressure raised to 762 mmHg. The air flow from area of higher pressure in alveoli to low pressure in atmosphere. 17  Three types of breathing Eupnea (Quit breathing) – Diaphragm, external and internal intercostal muscles involved. – During inspiration Contraction of diaphragm pulls the lower surfaces of lungs downward. – During expiration The diaphragm simply relaxes and elastic recoil of lungs, Chest wall and abdominal structures compresses the lungs and expels the air. Hyperpnea (Forced breathing) – Involvement of Accessory muscles. Apnea – No breathing 18  Factors affecting pulmonary ventilation 1. Surface tension of alveolar fluid (inward direct force) – During breathing, surface tension must be overcome to expand lungs during inhalation. – Decreases the size of alveoli during exhalation. – Lung surfactant reduce surface tension. (phospholipids and lipoproteins) 2. Compliance of lung (Elasticity of lungs) – Effort required to stretch the lungs. – High compliance lung expand easily. – Low compliance lung resist expansion. 3. Air way resistance – If diameter of bronchioles increases, resistance will decrease. Increased signal from sympathetic division – If diameter of bronchioles decreased, resistance increases. Asthma and emphysema increase air way resistance due to obstruction. Increased signal from parasympathetic division. 19  Role of surface tension In inner surface of alveoli, water surface also contract. Force the air out of alveoli through bronchi and collapse alveoli. Net effect cause an elastic contractile force of the entire lungs. – Which is called the surface tension elastic force. Role of surfactant – Surface active agent in water to reduce surface tension. – Secreted by type II alveolar epithelial cells. Composed of – Phospholipid – Surfactant apoproteins. – Calcium ions. 20  Role of Diameter of alveoli When air way of alveoli is blocked, surface tension will increased. Increased surface tension will collapse the lung. The amount of pressure generated in this way in an alveolus can be calculated by 21  Effect of Alveolar Radius Surface tension in alveoli is inversely affect the radius of alveolus. – Smaller the alveolar radius, greater the alveolar pressure caused by surface tension. – When the alveoli have half the normal radius, alveolar pressures will doubled. Small premature babies, surfactant not secreted until 7 month of gestation, their lungs have an extreme tendency to collapse. This condition is called respiratory distress syndrome of newborn. 22 Spirometry Record changes in Pulmonary Volume. Record the volume movement of air into and out of the lungs. When one breathes into and out of chamber, the drum rises and falls, and an appropriate recording is made on a moving sheet of paper. Lung have four volume and four capacities. 23  Pulmonary volume Tidal volume (-------ml). – Volume of air inspired or expired during normal breath. – The amount of air moved in single cycle of inspiration and expiration. – The single cycle is called respiratory cycle. Inspiratory reserve volume. – Extra volume of air that can be inspired above the normal tidal volume. Expiratory reserve volume. – Maximum extra volume of air that can be expired by forceful expiration after the end of normal tidal expiration. Residual volume. – Volume of air remaining in the lungs after the most forceful expiration. – Lungs do not completely empty after with each expiration. 24 Spirogram of lung volumes and capacities 25  Lung volumes Minute ventilation. – Total volume of air inhaled and exhaled each minute. – Respiratory rate multiplied by tidal volume. – Normal respiratory rate is 12 breaths/min. MV = 12 breaths/min × 500 ml/breath. = 6 liters/min Alveolar ventilation rate is – 12 breaths/min × 350 ml/breath. = 4200 ml/min. 26  Pulmonary Capacities Inspiratory capacity (------ml) – Tidal volume plus the inspiratory reserve volume. Distending the lungs to the maximum amount. Functional residual capacity (------ml) – Expiratory reserve volume plus the residual volume. Air that remains in lungs at the end of normal expiration Vital capacity (------ml) – Inspiratory reserve volume plus tidal volume plus expiratory reserve volume. – Maximum amount of air a person can expel from lungs after first filling the lungs to their maximum extent. Total lung capacity (-------milliliters) – Maximum volume to which the lungs can be expanded with the greatest possible effort. 27 Restrictive VS Obstructive Lung disease Restricted lungs disease – Both TLC and RV reduced – Lung cannot expand to a normal maximum volume. – Fibrotic diseases like tuberculosis, and chest cage diseases. Airway obstruction – More difficult to expire than to inspire. – Air tends to enter the lung easily but trapped in lungs. – Increases both TLC and RV. – Maximum expiratory flow rate is greatly reduced. – Asthma and Emphysema. 28 FVC vs FEV Total volume changes of FVCs are not greatly different. Major difference in the amounts of air that these persons can expire each second. – The % of FVC, expired in first second divided by the total FVC is 80 per cent. – But in airway obstruction the total FVC is 47% – In severe acute asthma, it is reduced to 20%. 29  Dead space air During respiration, the air present in nose, pharynx and trachea is called dead space air. The normal dead space air in a young adult man is about 150 ml. – This increases slightly with age. 30  Nervous stimulation Bronchial tree is very much exposed to norepinephrine and epinephrine Released into blood by sympathetic stimulation of adrenal glands. – Cause greater stimulation of beta-adrenergic receptors leads to dilation of the bronchial tree. Parasympathetic nerve derived from vagus nerves penetrate lung parenchyma. It was activated by noxious gases, dust, cigarette smoke or bronchial infection. Secrete acetylcholine cause vasoconstriction. – Administration of atropine block release acetylcholine cause relieve the obstruction. 31  Airway resistance Sympathetic motor neurons – Epinephrine - Bronchodilation Decrease airway resistance – increase air flow Parasympathetic motor neurons – Histamine Nicotine - Bronchoconstriction Increase airway resistance – decrease air flow. Two substance released in lung tissues by mast cells. – Heparin. – Slow reactive substance of anaphylaxis. Cause airway obstruction occurs in allergic asthma. 32  Gas exchange Gas exchange across respiratory membrane is efficient due to – Difference in partial pressure. – Small diffusion distance. – Lipid soluble gases. – Large surface area of alveoli. – Coordination of blood flow and air flow. 33  Basic laws of gas exchange Daltons law – The partial pressure of each gas is directly proportional to its percentage in the mixture. Henry’s law – When a mixture of gases is in contact with a liquid, each gas will dissolve in liquid in proportion to its partial pressure and its solubility coefficient. Various gases in air have different solubility. – Carbon dioxide is the most soluble. – Oxygen is 1/20th as soluble as carbon dioxide. – Nitrogen is practically insoluble in plasma. 34  Alveolar gas exchange The pressure of a specific gas in a mixture is called partial pressure (Px). – Atmospheric pressure is sum of pressures of all gases. (atm pressure is 760 mmHg) – N2- 78.6 %; O2- 20.9 %; CO2 - 0.04 %; H2O - 0.04 %; other gases - 0.06 %. Partial pressures determine the movement of O2 and CO2 between the atmosphere and lungs. Gas always diffuses from the area of high partial pressure to the area of low partial pressure. 35  Gas exchange in body External respiration or pulmonary gas exchange. – As blood flows through pulmonary capillaries. – Blood picks up O2 from alveolar air and unloads CO2 into alveolar air. Internal respiration or systemic gas exchange – The exchange of O2 and CO2 between systemic capillaries and tissue cells. 36  Pulmonary gas exchange Blood leaving the pulmonary capillaries near alveolar air spaces mixes with a small volume of blood that has flowed through conducting portions of the Venous blood for respiratory system Gas analysis Arterial Blood Gas - ABGs 37 Systemic gas exchange 38  Transport of oxygen In resting human being, 250 ml of O2 utilized/min. 100 ml of oxygenated blood - 20 ml of O2. – 1.5% (0.3ml) dissolved in plasma – 98.5% (19.7 ml) bound to Hb in RBC. Heme portion of Hb have 4 Fe2+ bind 4O2. The higher H the PO2, more O2 combines+with H Hb. + 39  Pulmonary gas exchange 15ml/dl 20ml/dl 40 Transport of oxygen 41 H2CO3 = Carbonic acid  Transport of O2 and CO2 Movement of gas is based on partial pressure difference form one point to another. O2 diffuses from alveoli into pulmonary capillary blood. Higher pO2 in capillary blood than in the tissues causes O2 to diffuse into surrounding cells. Intracellular pCO2 rises causes CO2 to diffuse into the tissue capillaries. pCO2 in pulmonary capillary blood is greater than that in the alveoli to diffuse into alveoli. 42  Factor affecting the dissociation of O2 1. Acidity (pH). – When acidity increased, the affinity of Hb for O 2 decreases. – Metabolically active tissues have lactic acid and H 2CO3 2. Partial pressure of CO2. – As PCO2 rises, Hb releases O2 more readily. 3. Temperature. – If temperature increases, the amount of O 2 released from Hb also increased. 4. 2,3- Bisphosphoglycerate (BPG) – Greater the level of BPG, the more O 2 is unloaded from Hb. 43  Transport of CO2 In resting human being, 200 ml of CO2 produced / min. 100 ml of deoxygenated blood contains 53 ml of CO2. which is transported in blood in three main forms. 1. Dissolved CO2 - 7% dissolved in plasma. – When reaches lungs, diffuses into alveolar air and exhaled. 2. Carbamino compounds – 23% bind with Hb. CO2 bind to amino acids in globin chain 3. Bicarbonate ions – 70% in blood plasma as HCO-3. CA - Carbonic anhydras 44 Systemic gas exchange Amount of CO2 Amount of CO2 53ml/dl 48ml/dl 45  Transport of CO2 The lower the amount of oxyhemoglobin (Hb–O2), the higher the CO 2 46 carrying capacity of the blood, a relationship known as the Haldane Transport of Carbon Dioxide 47  Diffusion of Carbon Dioxide Due high tissue cell Pco2, carbon dioxide diffuses from the cells into the tissue capillaries and is then carried by the blood to the lungs. CO2 diffuses exactly opposite to diffusion of O2. CO2 can diffuse about 20 times as rapidly as O2. 5 mm Hg pressure difference causes all the required CO2 diffusion out of the pulmonary capillaries to alveoli. 48  Factors affecting gas exchange Partial pressure difference of the gases. – Larger the partial pressure difference, greater the rate of gas diffusion. Surface area available for gas exchange – The rate of gas exchange is directly proportional with surface area in respiratory membranes. – (Emphysema – surface area decreased). Diffusion distance – Increase the diffusion distance, slower the gas exchange – pulmonary edema increase diffusion distance. Molecular weight and solubility of gases – O diffuse 1.2 times more than CO due low Molecular 2 2 Weight. – Solubility of CO - 20 times more than O. 2 2 – Net outward CO diffusion occurs 20 times more rapidly than 2 net inward O2 diffusion. 49 Reversible combination of oxygen Fetal Hb have higher affinity than adult Hb 50 Combination of oxygen with Hb 100 ml blood contains 15 g of Hb. 1g of Hb binds 1.34 ml of O2. 15 g of Hb binds 20.1 ml of O2. This is expressed as 20 volumes %. 51  Factors associated with dissociation of O2 from Hb 52  Factors associated with dissociation of O2 from Hb Acidity of blood – Blood became slightly acidic from 7.4 to 7.2. – O -Hb dissociation curve shifts, on 15% to right. 2 Increase in CO concentration. 2 – Increase CO2 leads to increase in H CO in blood which 2 3 increase the H ion concentration. (Bohr effect) + Increase in blood temperature. Increase in 2,3 Bisphosphoglycerate (Byproduct of glycolysis) – Normal BPG shift O -Hb curve to right. 2 – During Hypoxia, BPG increases shift O -Hb curve further to 2 right. During exercise. – Shift O2-Hb curve to right – Deliver extra amount of O2. 53 Effect of carbon monoxide CO combines Hb in the same position. It binds 250 times much tenacity as O2. a CO pressure of only 0.6 mm Hg can be lethal. In CO poisoning Feedback mechanism to stimulate respiration may absent. Brain is the first organ affected and became disoriented and unconscious. O2 at high partial pressure is used for treatment. Administration of 5% CO2, strongly stimulates the respiratory center.54  Respiratory acidosis and alklosis When problem involved in lungs Respiratory acidosis Hypoventilation Increase CO2 – Increase H2CO3 – H+ and HCO3- pH below blood pH (7.35- 7.45) pH – 7.2 – Hypercapnia Respiratory alkolosis Hyperventilation Decrease CO2 – decrease H2CO3 – H+ and HCO3- pH above blood pH (7.35- 7.45) pH – 7.6 – Hypocapnia 55  Metabolic acidosis and alkolosis Metabolic acidosis Accumulation of any acid other than CO2 Accumulation of lactic, uric acids and keto acids. Metabolic alkalosis Vomitting of gastric juice Loss of H+ from body 56  Regulation of Respiration Involuntary control of respiration. Voluntary control of respiration Regulation of respiration rate depends upon – 1. Conscious and unconscious thoughts. – 2. Emotional state. – 3. Anticipation. Respiratory muscles alter the size of thorax by impulse from nerves in brain and relax in absence of impulse. – These nerve impulses sent from clusters of neurons located bilaterally in medulla oblongata and pons of brain stem. – These neurons are collectively called respiratory center. 57  Respiration center which sent nerve impulse to respiratory muscle. The stimulated respiratory muscles, alter the size of thoracic cavity for respiration. Three levels to control the activity of respiration. – 1. Central control of breathing in brain stem. – 2. Chemoreceptors for CO2, H+, O2. Central chemoreceptors in the medulla oblongata. Peripheral chemoreceptors in carotid and aortic bodies. – 3.Inflation reflex. 58  Central control of Respiration center Central control of breathing in brain stem has three sites. Pons 1. Medullary rhythmicity area in medulla oblongata. – Dorsal respiratory group – Ventral respiratory group 2 sec 2. Apneustic center in 3 sec pons. Medulla oblongata 3. Pneumotaxic centre in Phrenicpons. and Intercoastal nerves 59  Medullary Rhythmicity Area Control the basic rhythm of respiration. There are inspiratory and expiratory areas within the medullary rhythmicity area. 1. Dorsal respiratory group – Inspiratory area – Pacemaker of respiratory system. – Input to respiratory centre: Vagus nerves and Glossopharyngeal nerves from peripheral chemoreceptors in lung. – Output from respiratory centre: Phrenic nerves to the diaphragm. (C3, C4 and C5) Intercostal nerves to the external intercostal muscles. 2. Ventral respiratory group – Expiratory area. – Ventrolateral part of medulla, involved in expiration. – Not activated during normal breathing (Passive process). – Activated during exercise. 60  Medullary Respiration Center The neurons of expiratory area remain Inhalation lasts for 2 seconds inactive during quiet breathing. and exhalation lasts for 3 However, during forceful breathing nerve seconds. impulses from inspiratory area activate 61 expiratory area  Function of Pneumotaxic center Located dorsally in nucleus parabrachialis of upper pons. Transmits signals to inspiratory area. When the pneumotaxic signal is strong, inspiration might last for 0.5 second. When the pneumotaxic signal is weak, inspiration might continue for 5 seconds. Thus filling the lungs with a great excess of air. – Main function is Primarily to limit inspiration. – Second function is increase the rate of breathing. 62  The Pneumotaxic center – Superior portion of pons, controls rate and depth of breathing. – Transmits inhibitory impulses to inspiratory area. – Turnoff inspiratory area before lung became too full of air. – Regulates respiratory volume and respiratory rate. – If pneumotaxic area more active, breathing rate is more rapid. Neurons located within the nucleus of tractus solitarius. Nucleus have sensory termination of both vagus and glossopharyngeal nerves. Receive impulse from – 1. Peripheral Chemoreceptor – 2. Baroreceptor – 3. Receptor from lungs. 63  Apneustic center (lower Pons) Stimulate inspiration. Producing deep and prolonged inspiratory gasp. The result is a long, deep inhalation. When pneumotaxic area is active, it overrides signals from apneustic area. 64  Cortical Influences on Respiration Cerebral cortex has connections with respiratory center. Cerebral cortex – Voluntary control of Respiration. – Person can voluntarily hyperventilate and hypoventilate. Voluntary control is protective because it enables us to prevent water or irritating gases from entering the lungs. – When pCO2 and H+ ion increase, the inspiratory area is strongly stimulated, nerve impulses sent to phrenic and intercostal nerves to inspiratory muscles and breathing resumes. – Nerve impulses from hypothalamus and limbic system also stimulate respiratory center, allow emotional stimuli to alter respirations. for example, in laughing and crying. 65  Chemoreceptors Sensory neurons that are responsive to chemicals. Present in two locations monitor levels of CO 2, H, and O2 and provide input to respiratory center. – Central chemoreceptors in medulla oblongata. Respond to changes in H concentration or PCO2. – Peripheral chemoreceptors in carotid and aortic bodies. Part of peripheral nervous system and sensitive to changes in pO2, H+ and pCO2 in blood. Sensory neurons from aortic bodies are part of vagus (X) nerves. The carotid bodies are part of right and left glossopharyngeal (IX) nerves. 66  Chemical Control of Respiration The goal of respiration is to maintain proper concentrations of O2, CO2, and H+ ions in tissues. Excess CO2 or H+ ions in blood act directly on the respiratory center regulate inspiratory and the expiratory motor signals to respiratory muscles. – O2 not directly control respiratory center of brain in controlling respiration It act only on peripheral chemoreceptors located in the carotid and aortic bodies. 67  Central Chemoreceptor in Medulla Oblongata Sensitive to the pH of Cerebrospinal fluid (CSF). Decrease the pH of CSF stimulate hyperventilation. – CO2 from arterial blood diffuse into CSF. – CO2 is lipid soluble easily cross blood brain barrier. – In CSF CO2 combine with H2O to produce H2CO3 – H2CO3 dissociate as H+ and HCO-3. Increase in pCO2 cause increase H+ leads to hyperventilation. (Hypercapnia) Decrease in pCO2 cause decrease H+ leads to hypoventilation. (Hypocapnia) 68 Direct Chemical Control of Respiratory Center A chemosensitive area located 0.2 mm beneath the ventral surface of medulla. This area is highly sensitive to changes in either blood pCO2 or H+ ion concentration. Sensor neurons are excited by H+ ion. H+ ions directly stimulate the ions but not cross the blood brain barrier. Changes in H+ concentration in blood have less effect in stimulating the chemosensitive neurons than do changes in blood CO2. 69  Ventilatory response to CO2 Normally PCO2 in arterial blood is 40 mmHg. Increase in PCO2 is called Hypercapnia – Central chemoreceptrs stimulated due to increase in H+ – Peripheral chemoreceptors stimulated by increase in PCO2 and H+. Decrease in PCO2 is called hypocapnia – The central and peripheral chemoreceptors are not stimulated. – The inspiratory center is strongly stimulated when PCO2 is rising above normal than when PO2 is fall below normal. 70  Peripheral Chemoreceptor Important for detecting changes in O2 in blood. Respond lesser extent to changes in CO2 and H+ ion concentrations. Present in carotid bodies, aortic bodies and very few in other arteries of the thoracic and abdominal regions. When O2 concentration in arterial blood falls below normal, chemoreceptors become strongly stimulated. The impulse rate is particularly sensitive to changes in arterial pO2 in range of 60 to 30 mm Hg. Peripheral chemoreceptors sensitive five times as rapidly as central stimulation. 71 Factors stimulating Peripheral Chemoreceptors Carotid bodies and Aortic bodies. Decrease arterial pO2 – When PO2 decrease to less than 60 mmHg, – Hypoxemia Increases breathing rate Increase in arterial pCO2 – Stimulate chemoreceptors and increase breathing. – Pheripheral chemoreceptor is less importance than central chemoreceptor in brain. Increases in arterial (H+). – Stimulate carotid bodies directly. – Metabolic acidosis increases 72 breathing rate. Ventilatory response to CO2 73  Inflation reflex The walls of bronchioles, have stretch-sensitive receptors called baroreceptors or stretch receptors. – Baroreceptors stretched during over inflation of lungs. – Nerve impulses sent by vagus nerves to inspiratory and apneustic area. – Inspiratory and apnueustic area is inhibited, as a result, exhalation begins to deflate the lungs. This reflex called as inflation (Hering–Breuer) reflex. – It is a protective mechanism for preventing excessive inflation of lungs. 74 Resuscitator The apparatus forces air through the mask or endotracheal tube into the lungs. Resuscitators now have adjustable positive-pressure limits that are commonly set at 12 to 15 cm H2O pressure for normal 75 lungs. Tank Respirator (The “Iron-Lung”). Leather diaphragm moves inward, positive pressure develops around the body and causes expiration. – Positive pressure rises to 0 to +5 cmH2O. Diaphragm moves outward, negative pressure causes inspiration. – Negative pressure that causes inspiration falls to -10 to -20 cm H2O. 76  Ageing Efficiency of respiratory system decrease with ageing – The chest wall becomes more rigid as well. Elastic tissue deteriorates cause lower lung compliance and vital capacity. – The airways and tissues of respiratory tract, including alveoli, become less elastic and more rigid. – Chest movements are restricted by arthritic changes. – Some degree of emphysema normally occurs. – A decrease in blood level of O , decreased activity of alveolar 2 macrophages and diminished ciliary action of epithelium lining the respiratory tract. Elder people are more susceptible to pneumonia, bronchitis, emphysema and other pulmonary disorders. 77 The End 78