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1、病理生理学呼吸系统,病理生理学呼吸系统,病理生理学呼吸系统培训课程课件,Symbols,SymbolsP Pressure.,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),呼吸衰竭(Respiratory Failure) 外呼,呼衰的类型Classification of Respiratory failure,1. 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、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,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,一、呼衰的原因和发病机制,（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
3、.阻塞性通气不足: 呼吸道阻塞或狭窄 气道阻力增加。,（一）肺通气功能障碍:限制性通气不足: 肺泡扩张受限,1.限制性通气不足（RestrictiveHypoventilation）：肺泡扩张受限,1.限制性通气不足（Restrictive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。,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
4、现为吸气性呼吸困难 (Inspiratory Dyspnea),阻塞位于胸外，表现为吸气性呼吸困难 (Inspiratory,呼衰的类型Classification of Respiratory failurePartial pressure长期缺氧 肺血管平滑肌增殖 管壁增厚纠正水、电解质及酸碱平衡紊乱,保 护重要器官功能Hypoventilation): 呼吸道阻塞或狭窄 气道阻力增加。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）限制性通气不足（Restrictive弥散膜厚度增加：肺水肿，肺泡透明膜形成，肺纤维化，
5、肺泡毛细血管扩张等。弥散面积减少 (Decrease in the Surface Area of the Membrane)(正常：100 mmHg)缺氧 肺小动脉收缩 肺动脉压解剖分流 (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).Oxygen and Carbon DioxideDissociation CurvesHis orthopedic injuries and burns were treated.and the Mechanisms一、呼衰的原因和发
6、病机制,阻塞位于胸内，表现为呼气性呼吸困难 (Exspiratory Dyspnea),呼衰的类型Classification of Respir,用力呼气时等压点(isobaric point)移向小气道,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? 胸内、胸外气道阻塞在呼吸中的差异?,问题 ：,（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,（二）弥散障碍弥散面积减少,肺泡-毛细血管膜Alveolar-Capillary Membrane(弥散膜, dif
7、fusion membrane),毛细血管内皮细胞肺泡I型细胞基膜红细胞肺泡-毛细血管膜,1.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。,1.弥散面积减少 (Decrease in the Sur,流量（Q): 5L弥散时间缩短: 心输出量增加, 肺血流加快Changes in Central Nervous SystemDisorders in PulmonaryDisorders in Gas Exchange of the Lu
8、ngsDisorders in Pulmonary VentilationVA/Q: 0.(正常：100 mmHg)Hypoventilation): 呼吸道阻塞或狭窄 气道阻力增加。Clinical CaseAbsence of congestive heart failure, 4.呼衰的类型Classification of Respiratory failure弥散距离：5 mMHis orthopedic injuries and burns were treated.一、呼衰的原因和发病机制Principals of the Prevention and限制性通气不足（Restri
9、ctive5 l/min to 20 l/min.呼碱：I型呼衰 肺过度通气 血 K+ , 血 Cl-,2.弥散膜厚度增加(Increase in the Thickness 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。,流量（Q): 5L2.弥散膜厚度增加(Incre,3.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,3.弥散时间缩短 (S
10、hortening in the D,Solubility Coefficient(vol/vol, 760 mmHg): O2: 0.024 CO2:0.57,Solubility Coefficient,正常静息状态下：.（三）肺泡通气与血流比例失调Vent,VA/Q 0.8 =0.8 0.8 0.8,病肺 健肺 全肺,PaO2,1.部分肺泡通气不足(Alveolar Ventilation Insufficiency)功能性分流 (functional shunt)静脉血掺杂（venous admixture),VA.VA/Q 0.8 =0.8,血液氧和二氧化碳解离曲线Oxygen an
11、d Carbon DioxideDissociation Curves,血液氧和二氧化碳解离曲线,氧和二氧化碳血液中的运输Transport of O2 and CO2 in the Blood,O2 transported as:CO2 transpor,2.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 .,2.解剖分
12、流增加(Increase in Anatomic,20%: 直径 2mm 气管一、呼衰的原因和发病机制Airway pressure increased from 18 to 65 cm H2O.20%: 直径 2mm 气管中枢神经受损,周围神经受损,呼吸肌本身Arterial blood gas measurements were: pH = 7.外呼吸功能严重障碍 PaO2 ,伴有或不伴有PaCO2 的病理过程。O2: 98.A previously healthy 23-year-old male sustained numerous traumatic crush, burn, and
13、 smoke inhalation injuries during a landing accident in an airplane.CO2 transported as: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。按PaCO2 是否升高：静脉血掺杂（venous admixture)Diffusion Impairment阻塞位于胸内，表现为呼气性呼吸困难 (Exspiratory Dyspnea)20%: 直径 2mm 气管阻塞性通气不足（Obstructive弥散时间缩短 (Shortening in the Diffusion Time)Diffusion
14、Impairment阻塞位于胸外，表现为吸气性呼吸困难 (Inspiratory Dyspnea)Partial pressure,PaO2,3. 部分肺泡血流不足(Alveolar Perfusion Insufficiency)死腔样通气(dead space like ventilation）,20%: 直径 2mm 气管Q.PaO2PaCO2NVA/,血液氧和二氧化碳解离曲线Oxygen and Carbon DioxideDissociation Curves,血液氧和二氧化碳解离曲线,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?,问题 ：,
15、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Acute 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
16、 that the cause is from a corona virus that may be transmitted via respiratory secretions and develops after 2-11 days of a febrile illness.,肺泡-毛细血管膜 (alveolar capillary m,病理生理学呼吸系统培训课程课件,ARDS发生机制(Pathogenesis)肺泡膜致病释放中,A previously healthy 23-year-old male sustained numerous traumatic crush, burn, a
17、nd smoke inhalation injuries during a landing accident in an airplane. His initial B.P. was 80/50 mmHg, and he 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 plac
18、ed on the assist-control mode with the initial settings of inspired O2 concentration at 40%, respiration rate 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,A previously health,24 hrs. after admission, the pa
19、tient becomes agitated and his respiration rate increased to 30/min. His minute ventilation also increased 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 wh
20、ite out pattern.,Clinical Case,24 hrs. after admiss,The diagnosis of ARDS is contingent upon 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. Appropriat
21、e antecedent history. Currently, there are no specific laboratory tests for ARDS. A definitive diagnosis is made when these signs and symptoms are linked with diffuse alveolar damage.,Clinical Case,The diagnosis of ARD,急性呼吸窘迫综合征(ARDS)的概念及发生机制?,问题 ：,急性呼吸窘迫综合征(ARDS)的概念及发生机制?问题 ：,二、呼衰时机体功能和代谢变化 Functio
22、nal and Metabolic Change in Respiratory Failure,（一）酸碱平衡紊乱(acid-base balance 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,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
23、枢,（二）呼吸系统的变化(Changes in Respirat,（三）循环系统变化(Changes 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,（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),缺氧 肺小动脉收缩 肺动脉压,PaO2: 60 mmHg 智力，视力轻度减退40-
24、50 mmHg 神经精神症状20 mmHg 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,PaO2: 60 mmHg 智力，视力轻度减退（四）,肺性脑病发生机制Pathogenesis of pulmonary encephalopathy,肺性脑病发生机制-氨基丁酸脑脊液 pH溶酶体中
25、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？,问题：,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 .In the ER he was intubated and had no signs of pneumothorax.严重PaO2 和 PaCO2 抑制心血管运动中枢肺泡膜厚度：1 mMHis initial B.In the ER he was intubated and had no signs of pneumothorax.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。肺泡膜厚度：1 mM阻
26、塞性通气不足（Obstructive呼吸衰竭时呼吸调节的变化？严重PaO2 和 PaCO2 抑制心血管运动中枢肺充血和严重肺纤维化,肺泡表面活性物Hypoventilation）：肺泡扩张受限VA/Q: 0.氧和二氧化碳血液中的运输Diffusion ImpairmentCO2 transported as:5 l/min to 20 l/min.按主要发病机制：通气障碍型氧和二氧化碳血液中的运输,A previously healthy 23-year-old male sustained numerous traumatic crush, burn, and smoke inhalatio
27、n injuries during a landing accident in an airplane.Decreased lung compliance (effective static compliance 25-35 ml/cm H2O), and 5.Decreased lung compliance (effective static compliance 25-35 ml/cm H2O), and 5.限制性通气不足: 肺泡扩张受限肺性脑病的定义及发生机制？Airway pressure increased from 18 to 65 cm H2O.中枢神经受损,周围神经受损,呼
28、吸肌本身Appropriate antecedent history.阻塞性通气不足（Obstructive用力呼气时等压点(isobaric point)移向小气道Partial pressure通气量（VA)： 4L(正常：100 mmHg)Absence of congestive heart failure, 4.长期缺氧 肺血管平滑肌增殖 管壁增厚纠正水、电解质及酸碱平衡紊乱,保 护重要器官功能（三）循环系统变化(Changes in Circulation System)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 .弥散时间缩短: 心输出量增加, 肺血流加
29、快Diffusion ImpairmentChanges in Central Nervous System,长期缺氧 肺血管平滑肌增殖 管壁增厚Appropriate antecedent history.（三）循环系统变化(Changes in Circulation System)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）长期缺氧 肺血管平滑肌增殖 管壁增厚急性呼吸窘迫综合征(ARDS)的概念及发生机制?病肺 健肺 全肺(正常：100 mmHg)氧和二氧化碳血液中的运输Clinical CaseAcute Res
30、piratory Distress Syndrome (ARDS)阻塞性通气不足（Obstructive按病变部位：中枢性和外周性肺充血和严重肺纤维化,肺泡表面活性物流量（Q): 5L静脉血掺杂（venous admixture)Diffusion Impairment限制性通气不足: 肺泡扩张受限呼衰的类型Classification of Respiratory failure,（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 Prevention and Treatment of Respiratory Failure,支气管扩张症 支气管血管扩张，肺内A-V短路开放,
