肺脏病理生理学培训课件

1、肺脏病理生理学肺脏病理生理学呼吸全过程Respiration肺通气pulmonaryventilation肺换气gasexchangein thelungs组织换气gasexchangein the tissues细胞氧化代谢cellularrespiration气体血液运输gas transportin the blood 外呼吸 external respiration 内呼吸 internal respiration肺脏病理生理学2呼吸全过程肺通气肺换气组织换气细胞氧化代谢气体血液 外呼吸 肺脏病理生理学3肺脏病理生理学3SymbolsP PressurePartial pressure

2、AAlveolaraarterialvvenousVVolume of gas / unit timeQVolume of blood/ unit time.肺脏病理生理学4SymbolsP Pressure.肺脏病理生理学4呼吸衰竭(Respiratory Failure) 外呼吸功能严重障碍 PaO2 ,伴有或不伴有PaCO2 的病理过程。判断标准：PaO2 50mmHg (正常：40 mmHg)呼吸功能不全(Respiratory Insufficiency)肺脏病理生理学5呼吸衰竭(Respiratory Failure) 外呼呼衰的类型Classification of Respir

3、atory failure1. 按PaCO2 是否升高： 低氧血症型（I型） 低氧血症伴高碳酸血症（II型）2. 按主要发病机制：通气障碍型 换气障碍型3. 按病变部位：中枢性和外周性肺脏病理生理学6呼衰的类型Classification of Respir一、呼衰的原因和发病机制 Respiratory Failure: The Causes and the Mechanisms.肺通气功能障碍 Disorders in Pulmonary Ventilation.肺换气功能障碍 Disorders in Gas Exchange of the Lungs 肺脏病理生理学7一、呼衰的原因和发

4、病机制肺脏病理生理学7 （一）肺通气功能障碍: Disorders in Pulmonary Ventilation限制性通气不足: 肺泡扩张受限2.阻塞性通气不足: 呼吸道阻塞或狭窄 气道阻力增加。肺脏病理生理学8 （一）肺通气功能障碍:限制性通气不足: 肺泡扩张受限肺脏病1.限制性通气不足（RestrictiveHypoventilation）：肺泡扩张受限中枢神经受损,周围神经受损,呼吸肌本身收缩功能障碍。 肺纤维化,肺泡表面活性物质减少。严重的胸廓畸形,肋骨骨折, 胸膜纤维化。呼吸肌活动障碍肺顺应性降低胸廓顺应降低胸腔积液和气胸肺脏病理生理学91.限制性通气不足（Restrictive

5、中枢神经受损,周气道阻力(正常人平静呼吸)：80%: 直径 2mm 气管 20%: 直径 2mm 气管病因：气管痉挛 肿胀 纤维化 渗出物 异物 肿瘤 气道内外压力改变2.阻塞性通气不足（Obstructive Hypoventilation): 呼吸道阻塞或狭窄 气道阻力增加。肺脏病理生理学10气道阻力(正常人平静呼吸)：2.阻塞性通气不足（Obst阻塞位于胸外，表现为吸气性呼吸困难 (Inspiratory Dyspnea)呼气吸气肺脏病理生理学11阻塞位于胸外，表现为吸气性呼吸困难 (Inspiratory阻塞位于胸内，表现为呼气性呼吸困难 (Exspiratory Dyspnea)呼气

6、吸气肺脏病理生理学12阻塞位于胸内，表现为呼气性呼吸困难 (Exspiratory用力呼气时等压点(isobaric point)移向小气道02520+353520202030正常人0152020+3525202020肺气肿慢性支气管炎0+3535152520202020肺脏病理生理学13用力呼气时等压点(isobaric point)移向小气道0问题 ： 呼吸衰竭? 限制性通气不足的定义及其发生原因? 阻塞性通气不足的定义?肺脏病理生理学14问题 ：肺脏病理生理学14（二）弥散障碍 Diffusion Impairment弥散面积减少2. 弥散膜厚度增加3. 弥散时间缩短肺脏病理生理学15（

7、二）弥散障碍弥散面积减少肺脏病理生理学15肺泡-毛细血管膜Alveolar-Capillary Membrane(弥散膜, diffusion membrane) 肺脏病理生理学16肺泡-毛细血管膜肺脏病理生理学161.弥散面积减少 (Decrease in the Surface Area of the Membrane)正常成人肺泡面积：70 m2静息时换气面积：40 m2弥散面积减少：肺不张，肺实变，肺叶切除等。肺脏病理生理学171.弥散面积减少 (Decrease in the Sur肺脏病理生理学18肺脏病理生理学182.弥散膜厚度增加(Increase in the Thickne

8、ss of the Membrane)肺泡膜厚度：1 mM弥散距离：5 mM弥散膜厚度增加：肺水肿，肺泡透明膜形成，肺纤维化，肺泡毛细血管扩张等。肺脏病理生理学192.弥散膜厚度增加(Increase in the Thi3.弥散时间缩短 (Shortening in the Diffusion Time)正常静息状态：血流通过毛细血管时间: 0.75 s 弥散时间： 0.25 s弥散时间缩短: 心输出量增加, 肺血流加快肺脏病理生理学203.弥散时间缩短 (Shortening in the DSolubility Coefficient(vol/vol, 760 mmHg): O2: 0.

9、024 CO2:0.57肺脏病理生理学21Solubility Coefficient肺脏病理生理学2正常静息状态下：每分钟肺泡通气量（VA)： 4L 每分钟肺血流量（Q): 5LVA/Q: 0.8.（三）肺泡通气与血流比例失调Ventilation-Perfusion Imbalance肺脏病理生理学22正常静息状态下：.（三）肺泡通气与血流比例失调VentVA.VA/Q 0.8 =0.8 0.8 0.8. 病肺 健肺 全肺PaO2PaCO2N1.部分肺泡通气不足(Alveolar Ventilation Insufficiency)功能性分流 (functional shunt)静脉血掺杂

10、（venous admixture)肺脏病理生理学23VA.VA/Q 0.8 =0.8 血液氧和二氧化碳解离曲线Oxygen and Carbon DioxideDissociation Curves肺脏病理生理学24血液氧和二氧化碳解离曲线肺脏病理生理学24O2 transported as:O2: 1.5%Hb.O2: 98.5%CO2 transported as:CO2: 7%Hb.CO2: 23%HCO3-: 70%氧和二氧化碳血液中的运输Transport of O2 and CO2 in the Blood肺脏病理生理学25O2 transported as:CO2 transp

11、or2.解剖分流增加(Increase in Anatomic Shunt)解剖分流 (anatomic shunt)又称真性分流(true shunt): 生理条件下一部分静脉血经支气管静脉和极少的肺内A-V吻合支直接流入肺静脉 ( 2%-3% 心输出量).支气管扩张症 支气管血管扩张，肺内A-V短路开放 解剖分流 PaO2 .肺脏病理生理学262.解剖分流增加(Increase in AnatomicQ.PaO2PaCO2NVA/Q.病肺 健肺 全肺0.8 0.8 0.83. 部分肺泡血流不足(Alveolar Perfusion Insufficiency)死腔样通气(dead spac

12、e like ventilation）肺脏病理生理学27Q.PaO2PaCO2NVA/Q.病肺 健肺 血液氧和二氧化碳解离曲线Oxygen and Carbon DioxideDissociation Curves肺脏病理生理学28血液氧和二氧化碳解离曲线肺脏病理生理学28问题 ：弥散障碍的发生机制?功能性分流,静脉血掺杂?解剖分流, 真性分流?死腔样通气?肺脏病理生理学29问题 ：肺脏病理生理学29肺泡-毛细血管膜 (alveolar capillary membrane) 损伤引起的急性呼吸衰竭。病因：感染（肺炎，败血症等），休克，严重创伤，吸入毒物或胃酸等。（四）急性呼吸窘迫综合征Acu

13、te Respiratory Distress Syndrome (ARDS)Severe acute respiratory syndrome (SARS) is a good example of a probable infectious pneumonia that pathologically and clinically is ARDS. Experts have speculated that the cause is from a corona virus that may be transmitted via respiratory secretions and develo

14、ps after 2-11 days of a febrile illness. 肺脏病理生理学30肺泡-毛细血管膜 (alveolar capillary m肺脏病理生理学31肺脏病理生理学31肺脏病理生理学培训课件 A previously healthy 23-year-old male sustained numerous traumatic crush, burn, and smoke inhalation injuries during a landing accident in an airplane. His initial B.P. was 80/50 mmHg, and h

15、e was immediately infused with saline at the maximal rate. In the ER he was intubated and had no signs of pneumothorax. His orthopedic injuries and burns were treated. The ventilator was placed on the assist-control mode with the initial settings of inspired O2 concentration at 40%, respiration rate

16、 at 12/min, and tidal volume at 900 ml. Arterial blood gas measurements were: pH = 7.47, PCO2 of 33 mmHg, and PO2 of 62 mmHg.Clinical Case 肺脏病理生理学33 A previously health 24 hrs. after admission, the patient becomes agitated and his respiration rate increased to 30/min. His minute ventilation also inc

17、reased from 8.5 l/min to 20 l/min. Airway pressure increased from 18 to 65 cm H2O. Repeat arterial blood gas measurement of PO2 indicated 35 mmHg and chest x-ray now showed diffuse infiltrates in a white out pattern.Clinical Case 肺脏病理生理学34 24 hrs. after admiss The diagnosis of ARDS is contingent upo

18、n 5 factors: 1. Hypoxemia, 2. Diffuse pulmonary infiltrates on radiography, 3. Absence of congestive heart failure, 4. Decreased lung compliance (effective static compliance 25-35 ml/cm H2O), and 5. Appropriate antecedent history. Currently, there are no specific laboratory tests for ARDS. A definit

19、ive diagnosis is made when these signs and symptoms are linked with diffuse alveolar damage.Clinical Case 肺脏病理生理学35 The diagnosis of ARD急性呼吸窘迫综合征(ARDS)的概念及发生机制?问题 ：肺脏病理生理学36急性呼吸窘迫综合征(ARDS)的概念及发生机制?问题 ：肺脏二、呼衰时机体功能和代谢变化 Functional and Metabolic Change in Respiratory Failure （一）酸碱平衡紊乱(acid-base balance

20、 disturbance)和电解质变化呼酸: 型呼衰 CO2潴留 血 K+ , 血 Cl- 呼碱：I型呼衰 肺过度通气 血 K+ , 血 Cl-代酸：严重缺氧 无氧代谢 乳酸肺脏病理生理学37二、呼衰时机体功能和代谢变化（一）酸碱平衡紊乱(acid-b（二）呼吸系统的变化(Changes in Respiratory System)呼吸调节(Regulation of Respiration) 的变化外周化学感受器中枢化学感受器呼吸加深加快抑制呼吸中枢PaO250 mmHgPaO280 mmHg肺脏病理生理学38（二）呼吸系统的变化(Changes in Respirat（三）循环系统变化(C

21、hanges in Circulation System) 轻度PaO2 和 PaCO2 可兴奋心血管运动中枢 严重PaO2 和 PaCO2 抑制心血管运动中枢 肺脏病理生理学39（三）循环系统变化(Changes in Circulat缺氧 肺小动脉收缩 肺动脉压 右心后负荷长期缺氧 肺血管平滑肌增殖 管壁增厚长期缺氧 红细胞增多 血液粘度 心负荷缺氧、酸中毒 心肌舒缩功能呼吸衰竭 右心衰竭 肺源性心脏病 (cor pulmonale)肺脏病理生理学40缺氧 肺小动脉收缩 肺动脉压 肺脏病理生理学40PaO2: 60 mmHg 智力，视力轻度减退40-50 mmHg 神经精神症状20 mmH

22、g 神经细胞不可逆损坏(慢性呼衰PaO2 20 mmHg神志仍可清醒）PaCO2 80 mmHg CO2麻醉(头痛,头昏,嗜睡，精神错乱, 扑翼样震颤, 抽搐, 及昏迷等中枢神经系统症状）肺性脑病(pulmonary encephalopathy):呼衰引起的脑功能障碍（四）中枢神经系统变化Changes in Central Nervous System肺脏病理生理学41PaO2: 60 mmHg 智力，视力轻度减退（四）肺性脑病发生机制Pathogenesis of pulmonary encephalopathy-氨基丁酸脑脊液 pH溶酶体酶释放中枢抑制磷脂酶活性神经损伤颅内压PO2PaCO2血管内皮损伤血管通透性脑水肿脑血管扩张脑充血肺脏病理生理学42肺性脑病发生机制-氨基丁酸脑脊液 pH溶酶体中枢抑制磷问题：呼吸衰竭时呼吸调节的变化？肺源性心脏病发生机制?肺性脑病的定义及发生机制？肺脏病理生理学43问题：肺脏病理生理学43（一）一般原则 (General Principals) 1. 防治原发病 2. 防止或去除诱因 3. 改善肺通气 4. 纠正水、电解质及酸碱平衡紊乱,保 护重要器官功能五、呼衰的防治原则 Principals of the Preven