Respiratory #1, Pulmonary Ventilation - Physiology

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Respiratory #1, Pulmonary Ventilation - Physiology

  1. 1. Chapter 24: Physiology of the Respiratory System 1
  2. 2. RESPIRATORY PHYSIOLOGY • Definition: complex, coordinated processes that help maintain homeostasis (Figure 24-1) • 4 major functions: 1. External respiration • Pulmonary ventilation (breathing) • Pulmonary gas exchange 1. Transport of gases by the blood 2. Internal respiration • Systemic tissue gas exchange • Cellular respiration 1. Regulation of respiration 2
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  4. 4. PULMONARY VENTILATION • Respiratory cycle (ventilation, breathing) – Inspiration: movement of air into the lungs – Expiration: movement of air out of the lungs • Mechanism of pulmonary ventilation – The pulmonary ventilation mechanism must establish two gas pressure gradients (Figures 24-2 and 24-3) • One in which the pressure within the alveoli (Pₐ) of the lungs is lower than atmospheric pressure (Pb) to produce inspiration • One in which the pressure in the alveoli (Pₐ) of the lungs is higher than atmospheric pressure (Pb) to produce expiration 4
  5. 5. Surface Tension • Force exerted by fluid in alveoli to resist distension. • Lungs secrete and absorb fluid, leaving a very thin film of fluid. – This film of fluid causes surface tension. • H20 molecules at the surface are attracted to other H20 molecules by attractive forces. – Force is directed inward, raising pressure in alveoli.
  6. 6. Surfactant • Phospholipid produced by alveolar type II cells. • Lowers surface tension. Insert fig. 16.12 – Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules. • As alveoli radius decreases, surfactant’s ability to lower surface tension increases. Figure 16.12
  7. 7. Surfactant is a substance produce by type II alveolar epithelial cells (~ 10% of the surface area of the alveoli) which reduce the surface tension of the fluid in the inner surface of the alveoli it is a mixture of phospholipids, proteins, and ions, the most important component is phospholipid dipalmitoyl phosphatidylcholine which is responsible for reducing the surface tension (formed of 2 parts, hydrophilic part dissolves in the water lining the alveoli and hydrophobic part directed toward the air) the alveolar collapse pressure in an average-sized alveolus with radius of about 100µm and lined with surfactant, is about 4cm of H2O, but if it is lined with pure water is about 18cm of H2O  important of surfactant in reducing the amount of transpulmonary pressure required to keep
  8. 8. Boyle’s Law • Changes in intrapulmonary pressure occur as a result of changes in lung volume. – Pressure of gas is inversely proportional to its volume. • Increase in lung volume decreases intrapulmonary pressure. – Air goes in. • Decrease in lung volume, raises intrapulmonary pressure above atmosphere. – Air goes out.
  9. 9. Quiet Inspiration • Active process: – Contraction of diaphragm, increases thoracic volume vertically. – Contraction of parasternal and internal intercostals, increases thoracic volume laterally. – Increase in lung volume decreases pressure in alveoli, and air rushes in. • Pressure changes: – Alveolar changes from 0 to –3 mm Hg. – Intrapleural changes from –4 to –6 mm Hg. – Transpulmonary pressure = +3 mm Hg.
  10. 10. Expiration • Quiet expiration is a passive process. – After being stretched, lungs recoil. – Decrease in lung volume raises the pressure within alveoli above atmosphere, and pushes air out. • Pressure changes: – Intrapulmonary pressure changes from –3 to +3 mm Hg. – Intrapleural pressure changes from –6 to –3 mm Hg. – Transpulmonary pressure = +6 mm Hg.
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  13. 13. PULMONARY VENTILATION: MECHANISM – Pressure gradients are established by changes in the size of the thoracic cavity that are produced by contraction and relaxation of muscles (Figures 24-4 and 24-5) – Boyle’s law: the volume of gas varies inversely with pressure at a constant temperature – Inspiration: contraction of the diaphragm and external intercostals produces inspiration; as they contract, the thoracic cavity becomes larger (Figures 24-6 and 24-7) • Expansion of the thorax results in decreased intrapleural pressure, leading to decreased alveolar pressure • Air moves into the lungs when alveolar pressure drops below atmospheric pressure • Compliance: ability of pulmonary tissues to stretch, thus making inspiration possible 13
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  18. 18. PULMONARY VENTILATION: MECHANISM (cont.) – Expiration: a passive process that begins when the inspiratory muscles are relaxed, which decreases the size of the thorax (Figures 24-8 and 24-9) • Decreasing thoracic volume increases the intrapleural pressure and thus increases alveolar pressure above the atmospheric pressure • Air moves out of the lungs when alveolar pressure exceeds the atmospheric pressure • The pressure between parietal and visceral pleura is always less than alveolar pressure and less than atmospheric pressure; the difference between intrapleural pressure and alveolar pressure is called transpulmonary pressure, always negative to avoid “collapse tendency of the lungs” • Elastic recoil: tendency of pulmonary tissues to return to a smaller size after having been stretched; occurs passively during expiration 18
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  20. 20. Quiet Inspiration • Active process: – Contraction of diaphragm, increases thoracic volume vertically. – Contraction of parasternal and internal intercostals, increases thoracic volume laterally. – Increase in lung volume decreases pressure in alveoli, and air rushes in. • Pressure changes: – Alveolar changes from 0 to –3 mm Hg. – Intrapleural changes from –4 to –6 mm Hg. – Transpulmonary pressure = +3 mm Hg.
  21. 21. Expiration • Quiet expiration is a passive process. – After being stretched, lungs recoil. – Decrease in lung volume raises the pressure within alveoli above atmosphere, and pushes air out. • Pressure changes: – Intrapulmonary pressure changes from –3 to +3 mm Hg. – Intrapleural pressure changes from –6 to –3 mm Hg. – Transpulmonary pressure = +6 mm Hg.
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  23. 23. PULMONARY VENTILATION • Pulmonary volumes: we must have normal volumes of air moving in and out as well as remaining in the lungs for normal exchange of oxygen and carbon dioxide to occur (Figure 24-11) – Spirometer: instrument used to measure the volume of air (Figure 24-10) – Tidal volume (TV): amount of air exhaled after normal inspiration, 500 ml – Expiratory reserve volume (ERV): largest volume of additional air that can be forcibly exhaled past the TV(1000-1200 ml is normal ERV) – Inspiratory reserve volume (IRV): amount of air that can be forcibly inhaled after normal inspiration (normal IRV is 3300ml) – Residual volume: amount of air that cannot be forcibly exhaled (1200 ml) 23
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  26. 26. PULMONARY VENTILATION (cont.) • Pulmonary capacities: the sum of two or more pulmonary volumes – Vital capacity (VC): the largest volume of air that can be moved in and out of the lungs; IRV + TV + ERV • A person’s VC depends on many factors, including the size of the thoracic cavity and posture – Functional residual capacity (FRC): the amount of air at the end of a normal respiration; ERV + RV – Total lung capacity (TLC): the sum of all four lung volumes; the total amount of air a lung can hold – Inspiratory capacity (IC): the maximal amount of air an individual can inspire after a normal expiration; TV + IRV – Alveolar ventilation: volume of inspired air that reaches the alveoli – Anatomical dead space: air in passageways that do not participate in gas exchange (Figure 24-6) – Physiological dead space: anatomic dead space plus the volume of any nonfunctioning alveoli (as in pulmonary disease) – Alveoli must be properly ventilated for adequate gas exchange 26
  27. 27. PULMONARY VENTILATION (cont.) • Pulmonary air flow: rates of air flow into and out of the pulmonary airways – Total minute volume: volume moved per minute (ml/min); TV x RR; 6000ml – Forced expiratory volume (FEV) or forced vital capacity (FVC): volume of air expired per second during forced expiration (as a percentage of VC) (Figure 24-12) – Flow-volume loop: graph that shows flow (vertically) and volume (horizontally), with the top of the loop representing expiratory flow volume and the bottom of the loop representing inspiratory flow volume relations (Figure 24-13) 27
  28. 28. • Restrictive disorder: – Vital capacity is reduced. – FVC is normal. • Obstructive disorder: – VC is normal. – FEV1 is < 80%. 28
  29. 29. TIDAL BREATHING FORCED EXPIRATION NORMAL FEV1 FEV1 FEV1 = 3.0L FVC = 4.2L FEV1/FVC = 80% OBSTRUCTIVE FEV1 = 0.9L FVC = 2.3L FEV1/FVC = 40% RESTRICTIVE FEV1 1 SECOND FEV1 =1.8L FVC = 2.3L FEV1/FVC = 90%
  30. 30. Pulmonary Disorders • Dyspnea: – Shortness of breath. • COPD (chronic obstructive pulmonary disease): – Asthma: • Obstructive air flow through bronchioles. – Caused by inflammation and mucus secretion. » Inflammation contributes to increased airway responsiveness to agents that promote bronchial constriction. » IgE, exercise.
  31. 31. Pulmonary Disorders (continued) – Emphysema: • Alveolar tissue is destroyed. • Chronic progressive condition that reduces surface area for gas exchange. – Decreases ability of bronchioles to remain open during expiration. » Cigarette smoking stimulates macrophages and leukocytes to secrete protein digesting enzymes that destroy tissue. • Pulmonary fibrosis: – Normal structure of lungs disrupted by accumulation of fibrous connective tissue proteins. • Anthracosis.

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