10 When intercostal muscles contract or relax, the volume of chest expand or recoil, then the volume of lungs expand or recoil. Why?
11 Pleural cavity is made up of two layers of pleura.One is visceral layer stick to the surface of lung and the other is parietal layer stick to thorax. There is only little liquid in the pleural cavity but not gas. The effect of this layer of liquid is : （ 1 ） The power between liquid molecules pastes two layers of pleura to make them tightly. （ 2 ） Lubrication effect between two layers of pleura.
12 Section B Pulmonary ventilation Pulmonary ventilation is the gas exchange process between lungs and environment.
13 Mechanics of Pulmonary Ventilation: Two factors: One is the power to push gas flowing. The other is resistance to prevent gas flowing. The former must overcome the latter, and then pulmonary ventilation can be completed.
14 Ⅰ the force that causesPulmonary Ventilation Ⅰ the force that causes Pulmonary Ventilation 1. Respiratory movement Thoracic expansion and contraction caused by respiratory muscles are named respiratory movement. (inspiration, expiration)
15 Muscles of inspiration : diaphragm and external intercostal muscles Muscles of expiration : internal intercostal muscles and abdominal muscles Eupnea deep breathing
16 The Process of eupnea: Inspiration: inspiration muscles contract thoraxes expand lungs expand lung volumes increase intrapulmonary pressure decreases gas enters lungs Expiration: diaphragm and external intercostal muscles relax thorax recoils lung recoils intrapulmonary pressure increases gas is removed.
19 patterns patterns : Abdominal breathing Thoracic breathing Eupnea deep breathing Normal quiet breathing is accomplished almost entirely by movement of the diaphragm. Breathing caused primarily by the movement of external intercostal muscles. Breathing at rest is calm. Respiratory movement is greatly enhanced.
20 2. intrapulmonary pressure Intrapulmonary pressure is the pressure in pulmonary alveoli. Intrapulmonary pressure is equal to atmospheric pressure when apnea, vocal cord is open.
21 At the first of inspiration, lung volume increases and intrapulmonary pressure decreases below atmospheric pressure. Air enters alveoli under the pressure difference. Intrapulmonary pressure increases as the increasing of gas in lung. At the last of inspiration, intrapulmonary pressure is equal to atmospheric pressure and the air flow stops.
22 At the first of expiration, lung volume decreases and intrapulmonary pressure increases until it exceeds atmospheric pressure. Air outflows lungs and intrapulmonary pressure decreases by and by. Intrapulmonary pressure is equal to atmospheric pressure at the last of expiration.
23 Artificial respiration: once respiration stops, intrapulmonary pressure can be changed factitiously. Pressure difference between intrapulmonary pressure and atmospheric pressure can be created to maintain pulmonary ventilation.
24 Intrapleural pressure is usually negative pressure. At the end of expiration of eupnea,the pressure is about -5~ -3mmHg. At the end of inpiration of eupnea, the pressure is about -10~ -5mmHg. 3. Intrapleural pressure
25 Intrapleural pressure ＝ intrapulmonary pressure － lungs recoil At the end of respiration or inspiration, intrapulmonary pressure equals atmospheric pressure intrapleural pressure= － lungs recoil
26 If pleura breaks, pleural cavity will be open to atmosphere and air will enter pleural cavity. This is called pneumothorax. At this time, two layers of pleura separate and lungs contract for the elastic recoil.
27 Power of Pulmonary Ventilation (Summary) Expansion and contraction of respiration muscles expansion and contraction of thoracic cage (lungs change with the moving of thoracic cage)lung volumes change pressure differences between lung volume and atmospheric pressure gas enters or is removed out of lungs.
28 Ⅱ Resistances to Pulmonary Ventilation one is elastic resistance (70 ％ ) （ the main resistance of eupnea ） elastic resistance of lung elastic resistance of thorax the other is non- elastic resistance( 30 ％ ) airway resistance inertial resistance viscous resistance of organization
29 1. Elastic Resistance and Compliance The ability of an elastic structure to resist stretching or distortion is named elastic resistance. Compliance is the expandability of elastic tissue when acted on by foreign forces. Relationship between compliance and elastic resistance C ＝ 1 / R ☆ ☆ ☆ Compliance is inversely proportional to elastic resistance, that is, the larger the compliance, the less elastic properties, and vice versa. E.g. an elastic band
30 （ 1 ） Elastic Resistance of Lungs and Compliance change of lung volume （△ V ） lungs compliance ＝ change of transpulmonary pressure （ △ P ） transpulmonary pressure is the difference between intrapulmonary pressure and pleural pressure. (L/cmH 2 O)
31 injector Water manometer Connect tracheal intubation Three-way tap
32 ① Lung static compliance diagram If curve slope is large, it means the compliance is large and the elastic resistance is small. If curve slope is small, it means the compliance is small and the elastic resistance is large. transpulmonary pressure(cmH 2 O) Lung volume change
34 ② Specific compliance Specific compliance = Measured lung compliance （ L/cmH 2 O ） / Total lung capacity （ L ） adult infant Lung compliance Total lung capacity Specific compliance Lung compliance is also influenced by the total capacity of the lung.
35 ③ Source of lungs elastic resistance a. The elastic recoil power of lungs elastic recoil power surface tension bead liquid layer Alveolar surface tension b. The recoil power caused by surface tension between the liquid layer of inner alveoli and gas in alveoli.
36 Retraction force can be calculated by Formula Laplace. Retraction force P = 2T / r T ： surface tension dyn/cm r ： alveoli radius （ cm ）
37 (2) Pulmonary Surfactant DPPC DPPC is an important pulmonary surfactant in the the liquid layer of inner alveoli, DPPC binding to apolipoprotein exist as lipoprotein. liquid layer Alveolar surface tension
38 DPPC is synthesised by Ⅱ alveoli cells.
39 physiological effect of pulmonary surfactant （ 1 ） Lower alveolar surface tension and reduce inspiration resistance. （ 2 ） Accommodate surface tension and stable alveolar pressure. （ 3 ） The effect of suction is reduced. Reduce the producing of alveolar liquid and prevent pulmonary edema.
40 development of Pulmonary surfactant occurent from cyesising 25 － 30 weeks at the high point in cyesising 40 weeks Premature may get respiratory distress syndrome even to death for deficiency of pulmonary surfactant and formation of pulmonary atelectasis.
41 2. non-elasrtic resistance Learn by yourself.
42 Ⅲ Pulmonary Volume and Capacities
43 Tidal Volume(TV) : amount of air inhaled or exhaled in one quiet breathing. 500mL Inspiratory reserve volume (IRV) : the maximum extra volume of air that can be inspired over and above the normal tidal volume. 1500-2000mL 1. Pulmonary Volume
44 ● Expiratory reserve volume (ERV ): the maximum extra volume of air that can be exspired by forceful expiraton after the end of a normal tidal expiraton. 900-1200mL ● RV(residual volume): amount of air remaining in the lungs after maximum expiraton. 1000-1500mL
45 2. pulmonary capacities ● Inspiratory Capacity (IC):maximum amount of air that can be inhaled after a normal tidal expiration. = TV + IRV 2000 － 2500 mL ● Functional residual capacity (FRC): amount of air remaining in the lungs after a normal tidal expiration. = RV+ERV 2500 mL
46 vital capacity (VC ): amount of air that can be exhaled with maximum effort after maximum inspiration. = TV+ IRV +ERV ♀ 2500 ♂ 3500mL total lung capacity (TLC): maximum amount of air that lungs can contain.=RV+VC 3500 － 5000 mL
48 timed vital capacity (TVC) expired 80% of all vital capacity at the first second expired 96% of all vital capacity at the second second expired 99% of all vital capacity at the third second
53 respiratory rate （ time/min ） tidal volume （ ml ） （ ml ） ventilation volume （ ml/min ） （ ml/min ） alveolar ventilation （ ml/min ） （ ml/min ） 165008000 5600 810008000 6800 32 250 80003200 If tidal volume decreases half, respiratory rate increases double. Minute ventilation volume keeps constant, but alveolar ventilation will decrease greatly. Considering as ventilation efficiency of slow and deep respiration is higher than fast and light respiration.
54 Section C Gas exchange
55 Ⅰ principle of gas exchange gas diffusion: Gas molecules move freely among one another. The result is gas molecules diffuse from high-pressure area toward low-pressure area. The process is called gas diffusion. Exchange of gas in alveoli and tissues are physical diffusion processes.
56 The volume of gas diffusion in unit time is called diffusion rate. It is effected by the following factors D∝D∝ △ P*T*A*S d*√MW △ P is the pressure difference between the two ends of the diffusion pathway, T is the temperature, A represents the cross-sectional area of the pathway, S is the solubility of the gas, d is the distance of diffusion, MW stands for the molecular weight of the gas.
57 1. Gas partial pressure difference: gas partial pressure difference is larger—diffuses faster 2. Gas molecular weight and solubility: when solubility is high, it diffuses fast when molecular weight is large,it diffuses slowly.
58 3. Diffusion area of alveolar membrane : when diffusion area of alveolar membrane is large,it diffuses fast ★ diffusion area of alveolar membrane is 40m 2 in normal quiet state. ★ diffusion area of alveolar membrane is 70m 2 during sports.
60 4. Diffusion distance—thickness of alveolar membrane(inverse ratio relationship) ★ Pulmonary fibrosis ★ Pulmonary edema 5. Temperature of fluid increases Solubility increases—Diffuses fast Averages 0.6 μm
61 Ventilation/perfusion ratio is the rate between alveolar ventilation and pulmonary blood flow. V A : alveolar ventilation per minute Q : pulmonary perfusion per minute V A /Q (value of normal quiet state) ＝ 4.2L/5L ＝ 0.84 If blood flow decreases and gas exchange are normal--the exchange total amount decreases. So alveolar ventilation and blood flow must keep an appropriate ratio. 6. Ventilation /Perfusion Ratio(V A /Q )
62 ★ ventilation /perfusion ratio increases:it means partial alveolar gas can not exchange fully with the blood =physiological dead space increases. ★ ventilation /perfusion ratio decreases:it means partial blood flow through hypoventilation alveoli. They can not get fully exchange. And it equals functional arteriovenous shunt.
63 When normal adult is standing, every part of lung V A / Q is not well-distributed Apex of lung : V A descent/Q descent, Q descenting is more obvious. ratio rises(more than 3) Base of lung: V A descents/Q rises, ratio descents(0.6).
64 7. pulmonary diffusion capacity When all kinds of gas is under unit partial pressure difference,the gas volume(ml) passing through respiratory membrane per minute is called pulmonary diffusion capacity. It is the physiological index to test the diffusion ability of respiratory membrane. DLDL V PAPA PBPB
65 CO 2 diffusibility/ O 2 diffusibility= √O 2 molecular weight/ √CO 2 molecular weight=√32/√44 ＝ 5.6/6.6 But because CO 2 solubility/ O 2 solubility= 0.592/0.0244=24.3/1.0(Herry’s law ） CO 2 diffusion velocity/ O 2 diffusion velocity = （ 5.6/6.6 ） × （ 0.592/0.0244)=20.6/1.0 From all above,we know that the diffusion velocity of CO 2 is much more than that of O 2. There is no diffusion disturbance of CO 2 in clinical.
66 Ⅱ Pulmonary gas exchange P O 2 of mixed venous blood is 5.32 kPa （ 40mmHg ） is lower than 13.82 kPa （ 104mmHg ） of alveolar gas. O 2 in alveolar gas diffuses to blood. P O 2 in blood rises gradually until it is almost equal to P O 2 in alveolar gas.
67 P CO 2 of mixed venous blood is 6.12kPa （ 46mmHg ） It is higher than 5.32 kPa （ 40mmHg) of alveolar gas. CO 2 in blood diffuses to alveolar gas. P CO 2 in blood descents gradually until it is almost equal to P CO 2 in alveolar gas.
69 Ⅲ Tissues Gas Exchange
72 Section D Gas Transport Ⅰ Existing forms of O 2 and CO 2 in the blood chemical combination(primary) physical dissolution(medium) two forms O2O2 physical dissolution combination physical dissolutionO2O2 lung tissue CO 2 physical dissolutioncombination physical dissolution
75 Maximum capacity of hemoglobin binding with O 2 (in every 100ml blood ) is named oxygen capacity. When normal Hb is in 15g/100ml blood, 1g Hb binds with 1.34ml O 2. Oxygen capacity= 15×1.34 ＝ 20ml The volume of hemoglobin binding with oxygen (in fact or really) is called oxygen content. arterial blood: 20ml O 2 venous blood: 15ml O 2
76 The percentage of oxygen content to oxygen capacity is called oxygen saturation. oxygen content oxygen capacity In arterial blood, oxygen content equals 20ml and oxygen saturation is 100%. In venous blood, oxygen content equals 15ml and oxygen saturation is 75%. ×100%)(=
77 form O 2 partial pressure is higher(lung) Hb ＋ O 2 HbO 2 O 2 partial pressure is lower(tissues) reduction 、 royal blue oxygenation 、 red break relaxation tension （一）
78 character 1. Reversible binding. Without enzyme. Fast. Effected by PO 2. 2. O 2 binds with Fe 2+ of hemoglobin. The iron value is permanent. So the process is called oxygenation but not oxidation. PO 2 ↑ PO 2 ↓ HbO 2 Hb + O 2
79 3. Globin of hemoglobin is made up of two αpeptide chains and two β peptide chains. There is a protoheme molecular on each peptide chain including a Fe 2+. Each Fe 2+ binds with an O 2. So each hemoglobin can bind with four O 2. Fe
80 4. O 2 can facilitate binding or releasing. In lungs, increasing of P O 2 promotes combination. In tissues, decreasing of P O 2 promotes releasing. PO 2 ↑ PO 2 ↓ HbO 2 Hb + O 2
81 5. The binding or releasing curves of Hb and O 2 appear S form.This is related to the allosterism effect of Hb. Hb binds with O 2 —salt bond breaks, R form Hb releasing with O 2 —salt bond forms,T form The affinity of T form to O 2 is smaller. The affinity of R form to O 2 is larger. relaxation tension HbHbO 2
82 （二） oxygen dissociation curve The curve reacts the relationship of PO 2 and saturation of oxygenation Hb.
83 oxygen dissociation curve character 1. Superior segment of curve: PO 2 60 － 100mmHg. Slope is flat. Partial pressure of oxygen changes greatly. But oxygen saturation changes little— even PO 2 of environment or alveoli descents, oxygenation saturation will maintain high level.
84 Significance: Hemoglobin amortization function: even blood itself of environment oxygen change greatly, tissue PO 2 still remain in normal range. PO 2 descents in plateau
85 2. Middle segment of curve PO 2 60 － 40mmHg is the part that HbO 2 releases O 2. e.g. venous blood PO 2 level
86 3. Inferior segment of curve. PO 2 10 － 40mmHg. The slope is steep. PO 2 descents a little. It makes oxygen saturation descent greatly. This is benefit to supplying oxygen for tissue activity.
87 （三） factors effect oxygen dissociation curve T increases, the concentration of H +, CO 2, 2 ， 3-DPG rises, pH descents. Curve move to right. Oxygen saturation descents and dissociation increases. And vice versa.
88 2 ， 3 － DPG is a kind of organophosphate in RBC. 缺氧、贫血 hypoxia, anemia 长时间运动 long time sports RBC 2 ， 3DPG increases
89 factors effect oxygen dissociation curve
90 Ⅲ Transportation of CO 2 transportation of CO 2 physical dissolution （ 5% ） combination （ 95% ） bicarbonate （ 88% ） Carbaminohemoglobin （ 7% ）
92 （一） Transport in bicarbonate pattern character: 1. Reaction is reversible. But it need the help of enzyme(CA). 2. Conjugation or dissociation is decided by partial pressure difference of CO 2. 3. There is the transfer of Cl － in the reaction.
93 （二） Transport in carbaminohemoglobin pattern in tissues HbNH 2 +CO 2 HbNHCOOH lung HbNHCOO － ＋ H ＋
94 character 1. Reaction is reversible and need not the help of enzyme. 2. Conjugation or dissociation is decided by the oxygenation effect of Hb. Much Deoxy Hb binds with CO 2. Little Hb binds dissociation is much. 3. The effect of partial pressure difference is not obvious. in tissues HbNH 2 +CO 2 HbNHCOOH lung HbNHCOO - ＋ H + carbaminohemoglobin
95 Section E Regulation of Respiration
96 Ⅰ respiratory center Respiratory center is composed of several groups of nerve cells which produce and regulate respiratory movement in central nervous system.
97 Lumsden experiment in year 1923 Cross-cut site Patterns of respiration Patterns of respiratory movement after cutting vagus nerve Between pons Normal Deeper and slower and midbrain In the middle Deeper and slower Apneusis of pons Between Pons Anomalo-respiration Pant respiration and medulla Between medulla Respiration arrests Respiration arrests and spinal cord
98 Conclusion: Superior part of pons -- pneumotaxic respiratory center medulla --basic respiratory center spinal cord--primary respiratory center
99 Regulation of Cerebral Cortex to Respiration 1. Liberty Regulation and Creation of respiration Conditioned reflex. 2. Coordination with the process of language activity. Clinical: Descending pass of spinal cord pro-Lateral funiculus is damaged.---Autonomous breathing arrests. Regulate through voluntary breathing. Use breathing machine during sleeping. Oden’s curse
100 Ⅱ Formation of Respiratory Rhythm vagi
101 Reversion inhibition theory(part neuronal circuit feedback and controling theory) 1 ） Central inspiratory activity 2 ） inspiratory off-switch mechanism central inspiratory activity inspiration-initiative process expiration-passive -process
102 3 ） The mechanism of changing from expiratory phase to inspiration—there are probably a group of cutting off expiratory neurs. Imagining the process of expiration phase is probably controled by a mechanism of inhibiting inspiration ability during respiration phase. The ability degree of this mechanism is getting weaker during the expiration phase.once reaching the critical level, the inhibition of inspiration ability is relieved and the next inspiration will begin.
103 Ⅲ Reflex Control of Breathing Respiratory movement can be regulated, accelerated or inhibited by all kinds of stimulus to the body.
104 （一） Chemical Control of Breathing 1. Chemoreceptor （ 1 ） peripheral chemoreceptor Carotid body and aortic body: stimulated when P CO 2 in blood increases, P O 2 in blood decrease, H + Concentration in blood increase.
105 (2) central chemoreceptor
106 Abdomen Lateral of central chemoreceptor feel the stimulation of H + change in the Cerebra Spinal Fluid. character a. Not feel the stimulation of deficiency of O 2. b. H + in the blood has no effect to it. For it is difficult to pass the blood brain barrier.
107 c. The sensibitity to CO 2 is higher than that to peripheral chemoreceptor. But the latent period of reaction to sudden change of P CO 2 in the arterial blood is longer than that of the peripheral chemoreceptor. d. Utility stimulant is not CO 2 itself but the increase of H + caused by CO 2.
109 2. Regulation of CO 2 、 H + 、 O 2 to respiration （ 1 ） Influence of CO 2 to respiration a. Act indirectly to central chemoreceptor(main pathway) b. Act directly to peripheral chemoreceptor. The sensibitity of central chemoreceptor to H ＋ is about 25 times of that of peripheral chemoreceptor.
110 air P CO 2 Arterial P CO 2 peripheral chemoreceptor diffuses across blood-brain barrier Brain extracellular fluid P CO 2 Brain extracellular fluid [H + ] ( CO 2 +H 2 O H 2 CO 3 HCO 3 - + H + ) CA central chemoreceptor Medullary inspiratory neurons Ventilation increases 80% + + + + “+”: exciting
111 （ 2 ） Effect of O 2 to respiration 1 ） character a. Hypoxia stimulation act through peripheral chemoreceptor. If the inputing of peripheral chemoreceptor is cut, the stimulation effect disappear. b. The direct effect of hypoxia to center is light inhibition.
112 2 ） The pathway of hypoxia regulating respiration The main pathway is acting directly on peripheral chemoreceptor and inputting impulse.respiration center is excited.
113 （ 3 ） Effect of H + to respiration 1 ） Increasing H + or decreasing pH can faster respiration. It is the effective stimulator to chemoreceptor. 2 ） Pathway of H + regulating respiration a. H + in blood increases—excites peripheral chemoreceptor mainly b. H + in Cerebra Spinal Fluid increases-- excites central chemoreceptor. Because H + is very difficult to diffuses across the blood-brain barrier, so brain extracellular fluid [H + ] increased very little.
115 （ 4 ） Interface of PCO 2 、 H + and PO 2 effect respiration 1 ） P CO 2 does main role in normal respiration regulation. 2 ） When any of the three factor changes,it can induce the continued change of the other factors.and it can change the respiration effect of the first factor changing. 3 ） Hypoxia and increasing of H + concentration can strengthen the stimulation effect of P CO 2 increasing to respiration.
116 150 2500 150 350 the end of inspiration the end of exspiration 500 150 350 inspirationexspiration
117 the alveolar ventilation reaction of changing any of the factors of P CO 2 ， P O 2 ， PH in Arterial blood but not controling the other two factors
118 PCO 2 PO 2 summary central chemoreceptor peripheral chemoreceptor
119 Ⅳ Pulmonary Stretch Reflex Inflation of the lungs caused inhibition of inspiration, while collapse of the lungs enhanced inspiration. This reflex is termed Pulmonary Stretch Reflex.
122 Pulmonary Pulmonary inflation reflex deflation reflex Part of sensor Smooth muscle of bronchus and bronchiole Stimulation property dilatate diminish Effect relax(expiration) Shrink(inspiration) Significance Urge inspiration urge expiration change change into expiration into inspiration promptly, promptly,inhibit too deep inhibit too expiration. or too long inspiration.