病理生理学呼吸系统培训课程课件

单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,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,P Pressure,Partial pressure,AAlveolar,aarterial,vvenous,VVolume of gas / unit time,QVolume of blood/ unit time,.,.,SymbolsP Pressure.,呼吸衰竭(Respiratory Failure),外呼吸功能严重障碍 PaO,2 ,伴有或不伴有PaCO,2,的病理过程。,判断标准：PaO,2, 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PaCO,2,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,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 Mechanism,s,.,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.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,（,Restrictive,Hypoventilation,）,：,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。,肺充血和严重肺纤维化,肺泡表面活性物,质减少。,胸廓和胸膜本身病变。,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,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 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，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 Curves,His orthopedic injuries and burns were treated.,and the Mechanisms,一、呼衰的原因和发病机制,阻塞位于胸内，表现为呼气性呼吸困难,(Exspiratory Dyspnea),呼气,吸气,呼衰的类型Classification of Respir,用力呼气时等压点(isobaric point)移向小气道,0,25,20,+35,35,20,20,20,30,正常人,0,15,20,20,+35,25,20,20,20,肺气肿,慢性支气管炎,0,+35,35,15,25,20,20,20,20,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,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,Alveolar-Capillary Membrane,(,弥散膜,diffusion 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,m,2,静息时换气面积：,40 m,2,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 System,Disorders in Pulmonary,Disorders in Gas Exchange of the Lungs,Disorders in Pulmonary Ventilation,VA/Q: 0.,(正常：100 mmHg),Hypoventilation): 呼吸道阻塞或狭窄 气道阻力增加。,Clinical Case,Absence of congestive heart failure, 4.,呼衰的类型Classification of Respiratory failure,弥散距离：5 mM,His 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（Restrictive,5 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,m,M,弥散距离：5,m,M,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 (Shortening in the D,Solubility Coefficient,(vol/vol, 760 mmHg):,O,2,: 0.024,CO,2,:0.57,Solubility Coefficient,正常静息状态下：,每分钟肺泡,通气量（V,A,)：,4L,每分钟肺血,流量（Q):,5L,V,A,/Q: 0.8,.,.,.,.,（三）肺泡通气与血流比例失调,Ventilation-Perfusion Imbalance,正常静息状态下：.（三）肺泡通气与血流比例失调Vent,V,A,.,V,A,/Q,0.8 =0.8 0.8 0.8,.,.,病肺 健肺 全肺,PaO,2,PaCO,2,N,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 and Carbon DioxideDissociation Curves,血液氧和二氧化碳解离曲线,O,2,transported as:,O,2,: 1.5%,Hb,.,O,2,: 98.5%,CO,2,transported as:,CO,2,: 7%,Hb,.,CO,2,: 23%,HCO,3,-,: 70%,氧和二氧化碳血液中的运输,Transport of O,2,and CO,2,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 P,a,O,2,.,2.解剖分流增加(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 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 0.8 0.8 0.8,3. 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 ：,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 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,内皮细胞损伤,致病,因子,释放中性粒,细胞趋化因子,中性粒细胞聚,集，释放氧自,由基、蛋白酶、,炎症介质,肺,水肿,死腔样,通气,肺泡型,上皮细胞,损伤,表面活,性物质,合成,支气管,痉挛,血管收缩,微血栓,肺泡膜,通透性,肺不张,功能性,分流,PaO,2,PaCO,2,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, and 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 placed on the assist-control mode with the initial settings of inspired O,2,concentration at 40%, respiration rate at 12/min, and tidal volume at 900 ml. Arterial blood gas measurements were: pH = 7.47, PCO,2,of 33 mmHg, and PO,2,of 62 mmHg.,Clinical Case,A previously health,24 hrs. after admission, the patient 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 H,2,O. Repeat arterial blood gas measurement of PO,2,indicated 35 mmHg and chest x-ray now showed diffuse infiltrates in a white 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 H,2,O), and 5. Appropriate 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,Functional 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,CO,2,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,呼吸中枢,PaO,2,50 mmHg,PaO,2,80 mmHg,（二）呼吸系统的变化(Changes in Respirat,（三）循环系统变化(Changes in Circulation System),轻度PaO,2,和 PaCO,2,可兴奋心血管运动中枢,严重PaO,2,和 PaCO,2,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,PaO,2,: 60 mmHg 智力，视力轻度减退,40-50 mmHg 神经精神症状,20 mmHg 神经细胞不可逆损坏,(慢性呼衰PaO,2,20 mmHg神志仍可清醒）,PaCO,2,80 mmHg CO,2,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,-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,PO,2,PaCO,2,血管内皮损伤,血管,通透性,脑,水肿,脑血管,扩张,脑充血,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？,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 mM,His 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 Impairment,CO2 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 inhalation 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 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 Case,Acute Respiratory 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,