Respiratory Physiology PDF

Respiratory physiology: Pulmonary Ventilation 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, and (2) by elevation and depression of the ribs to increase and decrease the anteroposterior diameter...

Respiratory physiology: Pulmonary Ventilation 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, and (2) by elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity. Mechanics of Pulmonary Ventilation In normal quiet breathing, inspiration is an active process due to contraction of inspiratory muscles, but expiration is a passive process. Mechanics of Inspiration :( Figure 43). The normal resting inspiration is brought about by contraction of the main muscles of inspiration as: 1. The Diaphragm: When it contracts, the abdominal contents are forced downward and forward, and the vertical dimension of the chest cavity is increased. In addition, the lower rib margins are lifted and moved out, causing an increase in the transverse diameter of the thorax. 1  Figure 1: Contraction of diaphragm during normal quiet (A) and forced (B) inspiration. 2. The external intercostal muscles: When they contract, the ribs are pulled upward like a bucket handle (increasing the transverse diameter of the thorax), and outward pushing the sternum upward and forward like pump handle (increasing the anteroposterior diameter of the thorax). (Figure 44). 2  3. By contraction of the diaphragm and external intercostals, the chest cavity is expanded in all dimensions, leading to expansion of the lungs as well. The pressure inside the lungs falls down, and air is drawn into the lung (inspiration). Forced inspiration: In addition to contraction of the diaphragm and external intercostal muscles, other accessory muscles of inspiration come into action as: a- Scalene muscles which elevate the first two ribs. b- Sternomastoid muscles which Figure 2:Bucket handle motion of the ribs (a) and pump handle motion of the sternum (b) as a result of contraction of external raise the sternum. intercostals muscles. c- Anterior serrati which lift many of the ribs. Expiration: Normal quiet expiration is passive. During expiration, the inspiratory muscles simply relax. The elastic recoil of the lungs, chest wall, and abdominal structures, as well as the drop of the thoracic cage by its weight compress the lungs and expel the air outside. The thorax returns back to the resting expiratory level (mid thoracic position). 3 Forced expiration, as during exercise or voluntary hyperventilation, is active. The elastic forces are not powerful enough to cause the necessary rapid expiration, so that extra force is achieved, mainly by contraction of the expiratory muscles. The most important muscles of expiration are: (Figure 45) 1. The abdominal wall muscles as the rectus abdominus, internal and external oblique, and transversus abdominus. When these muscles contract intra-abdominal pressure is raised and the diaphragm is pushed upward thereby compressing the lungs, increasing the pressure inside and pushing air forcefully out. 2. The internal intercostals which run downward and backward contract. They pull the ribs downward and inward thus decreasing thoracic volume. 4  A B Figure 3:Comparison between inspiration (A) and forced expiration (B). PRESSURE CHANGES DURING RESPIRATORY CYCLE &COMPLIANCE There are three pressures responsible for movement of air in and out of the lungs. These pressures are Intrapleural pressure (IPP) Intra-alveolar or intrapulmonary pressure (IAP) Transpulmonary or distending pressure. Intra-pleural pressure (IPP): 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 5 mucoid fluid (pleural fluid) that lubricates movement of the lungs within the cavity. Furthermore, continual suction of excess fluid into lymphatic channels maintains a slight suction between the visceral and the parietal pleural surfaces. Therefore, the lungs slide easily on the chest wall, but resist being pulled away from it, in the same way that two moist pieces of glass slide on each other but resist separation. (Figure 46). Figure 4:Pleural sac is a closed sac containing thin film of fluid surrounding the lung. Definition of IPP: it is the pressure in the “potential space” between the lungs and chest wall (pleural space). It is a negative pressure (sub-atmospheric). Normal values of IPP During normal quiet breathing: IPP is about -5 cm H2O (compared to atmospheric pressure) at the beginning of inspiration. During normal inspiration, the chest cage pulls the 6 surface of the lung with a great force, the diaphragm contracts it enlarges the thoracic cavity and creates a more negative pressure. The IPP becomes -7.5 cm H2O at end of normal inspiration. This causes more pulling of the lung i.e. increasing lung volume, leading to a decrease in the pressure inside the lung and drawing of air inside. At the beginning of expiration, IPP is -7.5 cm H2O.The negativity decreases during expiration; it becomes -5 cm H2O at end of normal expiration. (Figure 47). Figure 5:Changes in IPP, IAP and lung volume during normal quiet breathing. Causes of the negative intra-pleural pressure: 1. Lack of air in the pleural cavity (thin layer of fluid). 2. Elastic recoil forces of the lung which tend to decrease the lung volume i.e. pull the visceral pleura inward. Causes of elastic recoil forces of the lung: 1/3 of the elastic recoil is due to elastic fibers of the lung tissue which are continuously stretched and always tend to recoil. 7  2/3 of the elastic recoil is due to the surface tension of the fluid lining the alveoli causing intermolecular attraction between the surface molecules of the fluid lining the alveoli so the alveoli tend to collapse. 3. Elastic properties of the chest wall which tend to expand the thoracic cage thus it pulls the parietal pleura outwards. The two opposing forces result in continuous pulling of the two pleural layers apart from each other creating a negative pressure in the pleural cavity. (Figure 48) As the parietal pleura is in contact with other intrathoracic structure. It creates negative pressure in the thoracic cavity, therefore intrathoracic pressure is also normally negative pressure and almost equal to IPP. 8 Figure 6:The development of negative IPP is due to inward recoil force of the lungs and outward recoil force of the chest wall. Significances of negative IPP: 4. It maintains the lung inflated and prevents its collapse. 5. It helps expansion of the lung during inspiration. 6. It helps venous return. 7. It helps lymphatic drainage through thoracic duct. Alveolar pressure (intrapulmonary pressure): Definition: It is the pressure of air inside the lung alveoli. When the glottis is opened and no air is flowing into or out of the lungs, alveolar pressure is equal to atmospheric pressure (zero cm H2O). 9 During inspiration, the increased volume of alveoli as a result of lung expansion decreases the intra alveolar pressure to a value below atmospheric pressure about - 1 cm H2O. This slight negative pressure is enough to move 500 ml of air into the Figure 7: Changes in IAP during normal quiet breathing. lungs in 2 seconds required for inspiration. At the end of inspiration, the alveolar pressure returns to atmospheric pressure (zero cm H2O). During expiration, opposite changes occur. The lung alveoli collapse before air is expelled from them. The alveolar pressure rises to about +1 cm H2O. This forces the 500 ml of inspired air out of the lung during 2-3 seconds of expiration. By the end of expiration, the pressure drops gradually and becomes atmospheric again. (Figure 49). Transpulmonary pressure Figure 8: Transpulmonary pressure (PALV-PPL) and its relation to the size of alveoli (right). Definition: It is the pressure difference between that in the alveoli (P ALV) and that on the outer surfaces of the lungs (P PL). It determines of the degree 10 of distension of the alveoli, so it is also called distending pressure. (Figure 50) Transpulmonary pressure = (P ALV. –P PL) REGULATION OF RESPIRATION It includes: I- Neural (Non Chemical) regulation of respiration. II- Chemical regulation of respiration. III- Other factors I- Neural regulation of respiration. Respiratory Center: The respiratory center is composed of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem. 1. Medullary centers: (Figure 62) a- Dorsal respiratory group (DRG): Site: They are bilateral groups of inspiratory neurons located in the dorsal part of medulla oblongata. 11 Function: They are inspiratory neurons that continuously send excitatory impulses to the contralateral inspiratory muscles (diaphragm-external intercostals). b- Ventral respiratory group of neurons (VRG): Site: They are located in the ventral part of the medulla lateral to DRG. Figure 9: Medullary respiratory center (DRG) and (VRG). Function: They contain both inspiratory and expiratory neurons. The neurons of the ventral respiratory group remain almost totally inactive during normal quiet respiration. They are especially important in providing the powerful expiratory signals to the expiratory muscles during heavy expiration as during muscular exercise. c- The pre-BÖtzinger complex (pre-BOTC): Site: a small group of pacemaker cells on either side of the medulla Function: These neurons Figure 10: Pacemaker cells in the pre-BÖtzinger complex produce rhythmic discharges in phrenic motor neurons, they are the generator neurons for the respiratory 12 rhythm. Therefore, the basic rhythm of respiration is generated mainly in the DRG and pre-BÖtzinger complex. (Figure 63). 2. Pontine centers: Although the rhythmic discharge of medullary neurons concerned with respiration is spontaneous, it is modified by neurons in the pons and afferents in the vagus from receptors in the airways and lungs. (Figure 64) a. Apneustic center (AP): Site: It is located in the lower part of the pons. Function: These neurons send continuous excitatory nerve impulses to DRG producing deep and prolonged inspiration and decrease respiratory rate. The apneustic center is inhibited by: Impulses from the vagus nerve. Impulses from the pneumotaxic center. b. Pneumotaxic center (PC): Figure 11: Pontine centers (pneumotaxic and apneustic). Site: PC is located dorsally in the upper part of the pons Function: It limits inspiration i.e. it controls the duration of inspiration. It sends inhibitory inputs which make the discharges from the apneustic center to DRG intermittent rather than tonic i.e. switching off inspiration. Thus creating the normal breathing rhythm. PC shortens inspiration and prevents over inflation of the lung. 13  II- Chemical Regulation of Respiration Breathing patterns are sensitive to chemicals in the blood through activation of chemoreceptors. Central chemoreceptors: They are located on the ventral surface of the medulla oblongata. They are bathed in the cerebrospinal fluid and separated from the blood by blood-brain barrier (BBB) which is formed of the meninges and the wall of blood vessels. BBB is relatively impermeable to H+, but CO2 molecules can diffuse through it easily because they are small lipid soluble uncharged molecules. When the PaCO2 rises, CO2 diffuses into the CSF and reacts with H2O forming H2CO3 which dissociates to HCO3- and H+. Central chemoreceptors are highly sensitive to Figure 12: stimulation of the central chemoreceptors by excess CSF H+ changes in CSF hydrogen ion concentration. Increased H+ stimulates the receptors à ↑ ventilation à wash out of excess CO2 à decrease PCO2. (Figure 65,66). Characters of the central chemoreceptors: The central chemoreceptors are stimulated at Figure 13: Environment of the central chemoreceptors. PaCO2 higher than 35 mmHg. Therefore, They are bathed in brain extracellular fluid (ECF) through which CO2 easily diffuses from blood vessels to cerebrospinal fluid (CSF). The CO2 reduces the CSF pH, during rest, the normal arterial PCO2 (40 thus stimulating the chemoreceptors 14  mmHg) stimulates and maintains normal breathing i.e. normal PaCO2 is the main drive of ventilation in quiet breathing. The central chemoreceptors do not adapt to constant H+ level in the CSF as that created by the steady arterial PCO2. The sensitivity of the central chemoreceptors to arterial PCO2 is reduced during sleep, anesthesia, CO2 narcosis and by some drugs as morphine. The central chemoreceptors are not affected by H+ in the blood (as acidosis due to diabetes) because H+ cannot pass BBB. The stimulatory effect of ↑ PaCO2 on the central chemoreceptors appears after 1-2 minutes and reaches the final steady state after 5-10 minutes 2. Peripheral chemoreceptors: (Figure 67). a) The Carotid bodies: They are located bilaterally at the bifurcation of the common carotid artery. They are sensitive to hypoxia, less sensitive to acidosis and least sensitive to hypercapnia (increased PaCO2).Carotid bodies are predominant in humans. b) The Aortic bodies: Figure 14: peripheral chemoreceptors They are located close to the aortic arch. The sensitivity of the aortic bodies is less than the carotid bodies and their ventilation responses are much weaker. Importance of the peripheral chemoreceptors: 15  They are the only mechanism in the body that detects changes in O2 tension in the body fluid. They rapidly increase their firing rate as the arterial O2 tension falls below 55 mmHg i.e. detect hypoxemia. They respond to CO2 excess more rapidly but less effectively than the central chemoreceptors. The response to CO2 excess is important, when the central chemoreceptors are depressed. They respond to increased H+ concentration in the blood which is caused by excess CO2 or fixed acids as lactic acid or acetoacetic acid. Ventilatory responses to changes in PaCO2 A. Increased PaCO2 (hypercapnia): Arterial P CO2 is the major chemical regulator of respiration. 1- Acute increase in PaCO2: When PaCO2 rises, the respiratory center is stimulated therefore, breathing increases in depth and rate à increase CO2 washout until PaCO2 returns to the normal level. B. Decrease PaCO2 (Hypocapnia): It Results from hyperventilation. Hypocapnia is a strong inhibitor of breathing and it could produce apnea. When the PaCO2 decreases, H+ also decreases causing alkalosis 16