mechanics of respiration inspiration and expiration.pptx

Mechanics of breathing inspiration and expiration

1. Mechanics of Respiration

2. Mechanism of breathing Inspiration refers to inflow of atmospheric air into the lungs. This obviously occurs when the intrapulmonary pressure falls below the atmospheric air pressure . Expiration refers to outflow of air from the lungs into the atmosphere. This obviously occurs when the intrapulmonary pressure rises above the atmospheric air pressure . Changes in the intrapulmonary pressure which govern the respiratory cycle of inspiration and expiration are related to changes in the intrapleural pressure.

3. Changes in the intrapleural pressure are brought about by changes in the size of the thoracic cavity. Expansion of the thoracic cage leads to fall in intrapleural pressure and decrease in the size of the thoracic cavity leads to rise in the intrapleural pressure . Changes in the size of the thoracic cavity are brought about by the actions of respiratory muscles

4. Muscles of normal tidal inspiration are diaphragm and external intercostal muscles. Accessory muscles of inspiration are scaleni , sternomastoid and serratus anterior, and alae nasi . Muscles of expiration are internal intercostal muscles and abdominal muscles (abdominal recti muscles, transverse abdominis muscles and internal oblique muscles).

5. Inspiration Inspiration is an active process, normally produced by contraction of the inspiratory muscles (negative-pressure breathing). During tidal inspiration (quiet breathing), the diaphragm and external intercostal muscles contract and cause an increase in all the three dimensions of the thoracic cavity .

6. Role of Diaphragm The diaphragm is a dome-shaped, musculotendinous partition between thorax and abdomen . The convexity of this dome is directed towards the thorax. When the diaphragm contracts, the following changes occur : The dome becomes flattened and the level of diaphragm is lowered, thereby increasing the vertical diameter of the thoracic cavity.

7. During quiet breathing , the descent of diaphragm is about 1.5 cm, and during forced inspiration, it increases to 7 cm. In tidal inspiration (quiet breathing ), 70-75% of expansion of chest is caused due to contraction of diaphragm.

8. Role of External Intercostal Muscles The fibres of external intercostal muscles slope downwards and forwards. They are attached close to the vertebral ends of the upper ribs than the lower ribs. From a pivot-like joint with the vertebrae, the ribs slope obliquely downwards and forwards. So , when the external intercostal muscles contract (because of the lever effect), the ribs are elevated, causing lateral and anteroposterior enlargement of thoracic cavity due to the so-called bucket handle and pump handle effects, respectively.

9. Role of Laryngeal Muscles The abductor muscles of the larynx contract during inspiration, pulling the vocal cords apart. Expiration Expiration in quiet breathing is largely a passive phenomenon and is brought about by the following : Elastic recoil of the lungs Decrease in size of the thoracic cavity due to relaxation of diaphragm and external intercostal muscles

10. Mechanism of Forced Inspiration 1 . Forceful contraction of diaphragm leading to a descent of diaphragm by 7-10 cm as compared to 1-1.5 cm during quiet inspiration . 2 . Forceful contraction of external intercostal muscles causing more elevation of ribs, leading to more increase in transverse and anteroposterior diameters of thoracic cavity . 3 . Contraction of accessory muscles of inspiration, which causes the Sternomastoid muscles contract and lift the sternum upwards. Anterior serrati muscles contract and lift most of the ribs upwards. Scaleni muscles contract and lift the first two ribs

11. Forced Expiration Forced expiration is required when respiration is increased during exercise or in the presence of severe respiratory disease. It is an active process caused by the following : 1 . Contraction of abdominal muscles causes the following : Downward pull on the lower ribs, thus decreasing the anteroposterior diameter of the thoracic cavity. 2 . Contraction of the internal intercostal muscles causes the effect which is just opposite to that of the external intercostal muscles. This is because of the leverage mechanism of the direction of the muscle fibres , which slope downwards and backwards.

12. Hence, their contraction tends to pull all the ribs downwards, thereby reducing the anteroposterior diameter (because of falling of the pump handle effect) as well as the transverse diameter (because of action of ribs like the falling of the bucket handle) of the thoracic cavity.

13. Pressure and Volume Changes During Respiratory Cycle Intrapulmonary Pressure Changes during Respiratory Cycle The movement of air in and out of the lungs depends primarily on the pressure gradient between the alveoli and the atmosphere (i.e. transairway pressure). Intrapulmonary or alveolar pressure is the air pressure inside the lung alveoli. At the End Expiration and End Inspiration, i.e. when the glottis is open and there is no movement of air, the pressures in all parts of the respiratory tree are equal to atmospheric pressure; the intrapulmonary pressure is considered to be 0 mm Hg (760 mmHg)

14. During inspiration in quiet breathing, the pressure in the alveoli decreases to about - 1 mm Hg (759 mm Hg), which is sufficient to suck in about 500 mL of air into the lungs within 2-second period of inspiration. At the end of inspiration , the intrapulmonary pressure again becomes zero . During forced inspiration against a closed glottis, the intrapulmonary pressure may be as low as -80 mm Hg below the atmospheric pressure .

15. During expiration in quiet breathing, the elastic recoil of the lungs causes the intrapulmonary pressure to swing slightly to the positive side (+1 mm Hg (761 mm Hg)), which forces the 500 mL of inspired air out of the lungs during 2-3 seconds of expiration. At the end of expiration, once again the alveolar pressure regains the atmospheric pressure (0 mm Hg ). Forceful expiration against the closed glottis may produce intrapulmonary pressure of as much as 100 mm Hg.

16. Intrapleural (Pleural) Pressure Pleural pressure is the pressure of fluid in the space between the visceral pleura and parietal pleura . Normal Pleural Pressure when the respiratory muscles are completely relaxed and the airways are open is about -2.5 mm Hg . The negative pleural pressure (-2.5 mm Hg) is the amount of suction required to hold the lungs at their equilibrium volume or the functional residual capacity

17. Lung volumes and capacities Static lung volumes and capacities Lung volumes The maximum volume to which a lung can be expanded has been divided into four nonoverlaping volumes. 1. Tidal volume (TV). It is the volume of air inspired or expired with each breath during normal quiet breathing. It is approximately 500 ml in a normal adult male . 2. Inspiratory reserve volume (IRV). It is the extra volume of air that can be inhaled by a maximum inspiratory effort over and beyond the normal tidal volume. It is about 3000 ml in a normal adult male.

18. 3 . Expiratory reserve volume (ERV). It is the extra volume of air that can be exhaled by maximum forceful expiration over and beyond the normal tidal volume, (i.e. after the end of normal passive expiration). It is approximately 1100 ml in a normal adult male. 4. Residual volume (RV). It is the volume of the air that still remains in the lungs after the most forceful expiration. It is about 1200 ml in a normal adult male.

19. Lung capacities Lung capacities are combination of two or more pulmonary volumes : 1 . Inspiratory capacity (IC). This is the maximum volume of the air that can be inspired after normal tidal expiration. Therefore , it equals the tidal volume plus inspiratory reserve volume (TV + IRV) and is approximately 3500 ml in a normal adult male. 2 . Expiratory capacity. It is the maximum volume of air that can be expired after normal tidal inspiration. It equals tidal volume plus expiratory reserve volume (TV + ERV) and is approximately about 1600 ml in a normal adult male.

20. 3. Functional residual capacity (FRC). It is the volume of the air remaining in the lungs after normal tidal expiration. Therefore , it equals the expiratory reserve volume plus the residual volume (ERV + RV) and is about 2300 ml in a normal adult male. Significance of FRC. The FRC (RV + ERV) of about 2300 ml represents the air that remains in the lungs most of the times. Even after the most forceful expiration about 1200 ml (residual volume) air is always present in the lungs. This has several advantages:

21. i. Continuous exchange of gases ii. Breath holding iii. Dilution of toxic inhaled gases Factors affecting FRC. Hyperinflation of the lungs seen in following conditions may be associated with increased FRC: Old age due to loss of elasticity of lungs, Emphysema , Bronchial asthma.

22. 4. Vital capacity (VC). This is the maximum amount of air a person can expel from the lungs after the deepest possible inspiration. Therefore , it equals the tidal volume plus the inspiratory reserve volume plus the expiratory reserve volume (TV + IRV + ERV) and is about 4600 ml in a normal adult male . Significance of vital capacity Estimation of VC allows the assessment of the strength of respiratory muscles. VC also provides useful information about other aspects of pulmonary functions through FEV

23. 5. Total lung capacity (TLC). It is the volume of air present in the lungs after the maximal inspiration. It equals the vital capacity plus the residual volume (VC + RV) and is about 5800 ml in a normal adult male.

24. B. Dynamic Ling Volumes and Capacities 1 . Timed vital capacity (TVC) or Forced vital capacity (FVC) - maximum volume of air which can be breathed out as forcefully and rapidly as possible following a maximal inspiration . FEV₁, (forced expiratory volume in 1 sec) Volume of FVC expired in 1st second of exhalation . Normal : 80% of FVC . ( ii) FEV₂ (forced expiratory volume in 2 secs ) Volume of FVC expired in first two seconds of exhalation . Normal : 95% of FVC . ( iii) FEV₃ (forced expiratory volume in 3 secs ) Volume of FVC expired in first three seconds of exhalation . Normal : 98-100% of FVC.

25. 2. Forced expiratory flow during 25-75% of expiration (FEF25-75%) mean expiratory flow rate during middle 50% of FVC. Therefore, also called maximum mid expiratory flow rate (MMEFR ) Normal : 300 L/min . Significance : Sensitive indicator of small airway disease where most of chronic obstructive pulmonary diseases like bronchial asthma, emphysema starts.

26. 3. Minute or pulmonary ventilation (MV or PV) Volume of air expired or inspired by the lungs in one minute. Normal : 6L/min. TV (500 ml) x RR (12/min ) 4 . Peak expiratory flow rate (PEFR) - expiratory flow rate during the peak of FVC . Normal : 400-450 L/min . Significance : markedly ↓s in obstructive airway diseases . 5 . Maximum breathing capacity (MBC) or Maximum voluntary ventilation (MVV) - Largest volume of air that can be moved into and out of the lungs in one minute by maximum voluntary effort . Normal : 90-170 L/min.

27. 6. Pulmonary reserve (PR) or breathing reserve (BR) maximum amount of air above the pulmonary ventilation, which can be breathed in and out of the lungs in one minute (i.e., MVV - PV ). % PR = ( MVV - PV ) x 100/MVV, also called dyspnoeic index . Normal : ≥ 60-70%; if <60%, dyspnoea (difficulty in breathing) is usually present.

28. Alveolar Surface Tension It is the inward directed force and tries to reduce the surface area and collapses the lungs . Cause : Due to intermolecular attraction between the surface molecules . Surfactant 1 . Mixture of protein-lipid complexes ( Dipalmitoyl phosphatidyl choline - DPCC) present inside the alveoli; produced by granular pneumocytes (type II cells ). 2 . Actions ( i) ↓s surface tension (by 7-14 times) by forming a layer between the fluid lining the alveoli and alveolar air .

29. (ii) Adjusts surface tension during breathing; surface tension is inversely related to the concentration of surfactant per unit area . ( iii) Keeps the alveoli dry and thus helps in exchange of gases. Mechanism : Low pulmonary capillary hydrostatic pressure (normal: 10 mmHg) tends to pull fluid from the alveoli into pulmonary capillaries (with oncotic pressure: 25 mmHg) → keeps the alveolar surface free of fluid.

30. Note : decrease in surfactant will leads to increase in surface tension in the alveoli will leads to draw the fluid from pulmonary capillaries into alveoli leads to pulmonary oedema . Factors affecting surfactant Decreases 1. inhalation of 100% O₂ 2. occlusion of main bronchus or pulmonary artery 3. cigarette smoking 4. cutting both the vagi .

31. Increases 1. thyroid hormones. 2. glucocorticoids Hyaline membrane disease or Infant respiratory distress syndrome ( IRDS ) Serious disease of infants due to deficiency of surfactant. Increase in surface tension in the lungs Collapse of alveoli Pulmonary oedema Pulmonary insufficiancy death

32. Compliance Change in lung volume (AV) per unit change in airway pressure (AP ). Significance : It is a measure of distensibility (i.e., compliance) of the lungs and the chest wall and is expressed in L/cm H2O . Compliance of the lungs and the thoracic wall i.e., lungs inside the thorax . Normal : 0.13/cm H2O . 2 . Compliance of the lungs only i.e., lungs outside the chest wall. Normal : 0.22 L/cm H2O.

33. Exchange of gases The gas exchange is the process of delivering the oxygen from the lungs to the blood circulation and eliminating carbon dioxide from the bloodstream to the lungs. This process takes place in the lungs; between the alveoli and a network of tiny blood vessels called capillaries, which are located in the walls of the alveoli. The basic principle of gas : Diffusion is a process in which a concentration gradient transport. Gas molecules move from an area of high concentration to an area of low concentration. Blood, which has a low concentration of oxygen and high concentration of carbon dioxide, is subject to gas exchange with air in the lungs.

34. The air in the lungs has a higher concentration of oxygen and lower concentration of carbon dioxide . This concentration gradient enables gas exchange during breathing. Mechanism of respiration Diffusion of gases occurs into and out of the alveoli through the respiratory membrane ( external respiration ) and the capillary membranes in the tissue ( internal respiration ). External respiration Venous blood that enters the lungs through the pulmonary artery has passed from all tissues within the body and consists of high levels of co2 and low levels of o2. Co2 diffuses from venous blood via its concentration gradient in the direction of the alveoli until equilibrium with the alveolar air is reached. In the same way, oxygen diffuses from the alveoli into the blood.

35. Internal respiration: It is the gas exchange by diffusion between the blood in the capillaries and the body cells. O2 diffuses from the bloodstream through the capillary wall into the tissue. Co2 diffuses from cells into the extracellular fluid and then into the bloodstream to the venous end of the capillary. Partial pressures in gas exchange: Diffusion of O₂ The normal alveolar pressure po₂ is 104 mm Hg, where as the blood entering the pulmonary capillary normally has po₂ is 40 mm Hg. Diffusion of CO₂ The average pco₂ in the pulmonary capillary blood is 46mm Hg and in the alveoli is 40 mm Hg.

36. Transport of Respiratory Gases : Transport of Oxygen - Oxygen is transported from alveoli to the tissues by blood in 2 forms; 1) As Simple physical solution 2) In combination with Hemoglobin As Simple Solution - Oxygen dissolves in the water of plasma and is transported in this physical form. Amount of oxygen transported is very neglisible , it forms only 3% of total oxygen in blood, still transport of oxygen in this form becomes important during muscular exercise to meet the excess demand of oxygewn by the tissues. In combination with Hemoglobin - Oxygen combines with hemoglobin in blood and is transported as Oxyhemoglobin . Transport of oxygen in this form is maximum amount 97% of oxygen is trasported by this method.

37. Oxygen Dissociation Curve - It demonstrates the relationship between partial pressue of oxygen and the percentage saturation of hemoglobin with oxygen. When the partial pressure of oxygen is more, hemoglobin accepts oxygen and when the partial pressure of oxygen is less, Hemoglobin release oxygen. Under normal condition, oxygen- hemoglobin dissociation curve is ‘S’ shaped or Sigmoid shaped. Lower part of the curve indictes dissociation of oxygen from hemoglobin. Upper part of the curve indicates the uptake of oxygen by hemoglobin dependin upon partial pressure of oxygen. P 50 - Is the partial pressure of oxygen at which hemoglobin saturation with oxygen is 50%. When the partial pressure of oxygen is 25 to 27mmHg, the hemoglobin is saturated to about 50%. That is, the blood contains 50% of oxygen. At 40mmHg of partial pressure of oxygen, the saturation is 75%. It becomes 95% when the partial pressure of oxygen is 100mmHg.

38. When Oxygen dissociation curve shift to Left indicates - Acceptance (Association) of oxygen by hemoglobin. When Oxygen dissociation curve shift to Right indicates - Dissociation of oxygen from hemoglobin. Shift to Right : Decreased affinity for O2 Decrease in partial pressure of oxygen. Incvrease in partial pressure of Carbon dioxide. Increase in H+ ion concentration and decrease in pH. Increased body temperature. Increase 2,3-DPG Shift to Left : Increased affinity for O2 In fetal blood because, fetal hemoglobin has got more affinity for oxygen than the adult hemoglobin. Decrease in H+ ion concentration and increase in pH. Decrease PCO2 Decrease temperature Decrease 2,3-DPG

39. Transport of Carbon dioxide - CO2 is transported by the blood from cells to the alveoli. Carbon dioxide is transported in the blood in 4 ways: As dissolved form (7%) As Carbonicacid (Negligible) As Bicarbonate (63%) As Carbamino compounds (30%) Carbon dioxide dissociation curve - CO2 is transported in blood as physical solution and in combination with water, plasma proteins and hemoglobin. The amount of carbon dioxide combining with blood depends upon the partial pressure of CO2. Norma; Carbon dioxide dissociatrion curve shows that the CO2 content in te blood is 48 mL% when the partial pressure of CO2 is 40 mmHg and it is 52 mL% when the partial pressure of CO2 is 48 mmHg. CO2 content is becomes 70 mL% when the partial pressure is about 100 mmHg.