1、病理生理学呼吸系统SymbolsP P PressurePressurePartial pressurePartial pressureA AAlveolarAlveolara aarterialarterialv vvenousvenousV VVolume of gas/unit timeVolume of gas/unit timeQ QVolume of blood/unit timeVolume of blood/unit time.呼吸衰竭呼吸衰竭(Respiratory Failure)(Respiratory Failure)外呼吸功能严重障碍外呼吸功能严重障碍 PaOPaO2
2、 ,2 ,伴伴有或不伴有有或不伴有PaCOPaCO2 2 的病理过程。的病理过程。判断标准：判断标准：PaOPaO2 2 60mmHg 50mmHg 50mmHg (正常：正常：40 mmHg)40 mmHg)呼吸功能不全呼吸功能不全(Respiratory Insufficiency)(Respiratory Insufficiency)呼衰的类型呼衰的类型Classification of Classification of Respiratory failureRespiratory failure1.1.按按PaCOPaCO2 2 是否升高：是否升高：低氧血症型（低氧血症型（I I型）
3、型）低氧血症伴高碳酸血症（低氧血症伴高碳酸血症（IIII型）型）2.2.按主要发病机制：通气障碍型按主要发病机制：通气障碍型 换气障碍型换气障碍型3.3.按病变部位：中枢性和外周性按病变部位：中枢性和外周性Respiratory Failure:The Causes and the Mechanisms功能功能功能功能功能功能肺泡扩张受限肺泡扩张受限呼吸道阻呼吸道阻塞或狭窄塞或狭窄 气道阻力增加。气道阻力增加。RestrictiveHypoventilation肺泡扩张受限肺泡扩张受限 中枢神经受损中枢神经受损,周围神经受损周围神经受损,呼吸肌本身呼吸肌本身 收缩功能障碍。收缩功能障碍。肺充血
4、和严重肺纤维化肺充血和严重肺纤维化,肺泡表面活性物肺泡表面活性物 质减少。质减少。胸廓和胸膜本身病变。胸廓和胸膜本身病变。A previously healthy 23-year-old male sustained numerous traumatic crush,burn,and smoke inhalation injuries during a landing accident in an airplane.病肺 健肺 全肺Experts have speculated that the cause is from a corona virus that may be transmit
5、ted via respiratory secretions and develops after 2-11 days of a febrile illness.O2 transported as:阻塞位于胸内，表现为呼气性呼吸困难(Exspiratory Dyspnea)肺源性心脏病发生机制?Ventilation-Perfusion ImbalanceArterial blood gas measurements were:pH=7.按PaCO2 是否升高：限制性通气不足（RestrictiveCO2:7%弥散时间：0.（四）急性呼吸窘迫综合征按PaCO2 是否升高：弥散面积减少(Decr
6、ease in the Surface Area of the Membrane)80%:直径 2mm 气管Hypoxemia,2.ARDS发生机制(Pathogenesis)气道阻力气道阻力(正常人平静呼吸正常人平静呼吸)：80%:80%:直径直径 2mm 2mm 气管气管 20%:20%:直径直径 2mm 2mm 气管气管病因：气管痉挛病因：气管痉挛 肿胀肿胀 纤维化纤维化 渗出渗出物物 异物异物 肿瘤肿瘤 气道内外压力改变气道内外压力改变Hypoventilation呼吸道阻塞或呼吸道阻塞或狭窄狭窄 气道阻力增加。气道阻力增加。阻塞位于胸外，表现为吸气性呼吸困难阻塞位于胸外，表现为吸气性
7、呼吸困难 (Inspiratory Dyspnea)呼气呼气吸气吸气阻塞位于胸内，表现为呼气性呼吸困难阻塞位于胸内，表现为呼气性呼吸困难 (Exspiratory Dyspnea)呼气呼气吸气吸气用力呼气时等压点用力呼气时等压点(isobaric(isobaric point)point)移向小气道移向小气道02520+353520202030正常人正常人0152020+3525202020肺气肿肺气肿慢性支气管炎慢性支气管炎0+3535152520202020问题问题 ：呼吸衰竭呼吸衰竭?限制性通气不足的定义及其发生原因限制性通气不足的定义及其发生原因?胸内胸内、胸外气道阻塞在呼吸中的差异胸
8、外气道阻塞在呼吸中的差异?毛细血管内皮细胞毛细血管内皮细胞肺泡肺泡I I型细胞型细胞基膜基膜红细胞红细胞肺泡肺泡-毛细血管膜毛细血管膜Alveolar-Capillary MembraneAlveolar-Capillary Membrane(弥散膜弥散膜,diffusion membrane)diffusion membrane)限制性通气不足:肺泡扩张受限缺氧 肺小动脉收缩 肺动脉压（一）酸碱平衡紊乱(acid-base balance disturbance)和电解质变化and the MechanismsCO2:23%24 hrs.Disorders in Pulmonary Vent
9、ilationHypoxemia,2.In the ER he was intubated and had no signs of pneumothorax.Decreased lung compliance(effective static compliance 25-35 ml/cm H2O),and 5.Functional and Metabolic Change in Respiratory FailureRespiratory Failure:The CausesTransport of O2 and CO2 in the Blood(弥散膜,diffusion membrane)
10、Solubility Coefficient阻塞性通气不足（Obstructive呼衰的类型Classification of Respiratory failure（一）一般原则(General Principals)外呼吸功能严重障碍 PaO2 ,伴有或不伴有PaCO2 的病理过程。Severe acute respiratory syndrome(SARS)is a good example of a probable infectious pneumonia that pathologically and clinically is ARDS.1.1.弥散面积减少弥散面积减少 (Dec
11、rease in(Decrease in the Surface Area of the the Surface Area of the Membrane)Membrane)正常成人肺泡面积：正常成人肺泡面积：70 m2静息时换气面积：静息时换气面积：40 m2弥散面积减少：肺不张，肺实变，弥散面积减少：肺不张，肺实变，肺叶切除等。肺叶切除等。弥散膜厚度增加弥散膜厚度增加(Increase in the(Increase in the Thickness of the Membrane)Thickness of the Membrane)肺泡膜厚度：肺泡膜厚度：1 1 m mM M弥散距离：弥
12、散距离：5 5 m mM M弥散膜厚度增加：弥散膜厚度增加：肺水肿，肺泡肺水肿，肺泡透明膜形成，肺纤维化，肺泡毛细透明膜形成，肺纤维化，肺泡毛细血管扩张等。血管扩张等。正常静息状态：正常静息状态：血流通过毛细血管时间血流通过毛细血管时间:Solubility CoefficientSolubility Coefficient(vol/vol,760 mmHg):(vol/vol,760 mmHg):O O2 2:0.0240.024 CO CO2 2:0.570.57.Ventilation-Perfusion ImbalanceV VA A.病肺病肺 健肺健肺 全肺全肺2 22 2N N1.
13、1.部分肺泡通气不足部分肺泡通气不足(Alveolar(Alveolar Ventilation Insufficiency)Ventilation Insufficiency)功能性分流功能性分流 (functional shunt)(functional shunt)静脉血掺杂（静脉血掺杂（venous admixture)venous admixture)血液氧和二氧化碳解离曲线血液氧和二氧化碳解离曲线Oxygen and Carbon DioxideDissociation CurvesO O2 2 transported as:transported as:O O2 2:1.5%:1
14、.5%HbHb.O O2 2:98.5%:98.5%COCO2 2 transported as:transported as:COCO2 2:7%7%HbHb.COCO2 2:23%:23%HCOHCO3 3-:70%:70%氧和二氧化碳血液中的运输氧和二氧化碳血液中的运输Transport of O2 and CO2 in the Blood2.2.解剖分流增加解剖分流增加(Increase in(Increase in Anatomic Shunt)Anatomic Shunt)解剖分流解剖分流 (anatomic shunt)(anatomic shunt)又称真性又称真性分流分流(t
15、rue shunt):(true shunt):生理条件下一部分静生理条件下一部分静脉血经支气管静脉和极少的肺内脉血经支气管静脉和极少的肺内A-VA-V吻合支吻合支直接流入肺静脉直接流入肺静脉 (2%-3%2%-3%心输出量心输出量).).支气管扩张症支气管扩张症 支气管血管扩张，肺支气管血管扩张，肺内内A-VA-V短路开放短路开放 解剖分流解剖分流 P Pa aO O2 2 .Q Q.2 22 2N N.病肺病肺 健肺健肺 全肺全肺3.3.部分肺泡血流不足部分肺泡血流不足(Alveolar(Alveolar Perfusion Insufficiency)Perfusion Insuffic
16、iency)死腔样通气死腔样通气(dead space like(dead space like ventilationventilation）血液氧和二氧化碳解离曲线血液氧和二氧化碳解离曲线Oxygen and Carbon DioxideDissociation Curves问题问题：弥散障碍的发生机制弥散障碍的发生机制?功能性分流功能性分流,静脉血掺杂静脉血掺杂?解剖分流解剖分流,真性分流真性分流?死腔样通气死腔样通气?肺泡肺泡-毛细血管膜毛细血管膜(alveolar capillary membrane)损伤引起的急性呼吸衰竭。损伤引起的急性呼吸衰竭。病因：感染（病因：感染（肺炎，败血
17、症等）肺炎，败血症等），休克，休克，严重创伤，严重创伤，吸入毒物或胃酸等。吸入毒物或胃酸等。急性呼吸窘迫综合征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 viru
18、s that may be transmitted via respiratory secretions and develops after 2-11 days of a febrile illness.弥散面积减少：肺不张，肺实变，肺叶切除等。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 .限制性通气不足的定义及其发生原因?二、呼衰时机体功能和代谢变化Transport of O2 and CO2 in the Blood弥散面积减少(Decrease in the Surface Area of the Membrane)病因：气管痉挛 肿胀 纤维化 渗出物 异物
19、 肿瘤 气道内外压力改变缺氧 肺小动脉收缩 肺动脉压(cor pulmonale)弥散时间缩短:心输出量增加,肺血流加快限制性通气不足:肺泡扩张受限Arterial blood gas measurements were:pH=7.判断标准：PaO2 60mmHg静息时换气面积：40 m2按PaCO2 是否升高：弥散面积减少：肺不张，肺实变，肺叶切除等。外呼吸功能严重障碍 PaO2 ,伴有或不伴有PaCO2 的病理过程。静脉血掺杂（venous admixture)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
20、吻合支直接流入肺静脉(2%-3%心输出量).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 membrane)损伤引起的急性呼吸衰竭。ARDSARDS发生机制发生机制(Pathogenesis)肺泡膜肺泡膜内皮细胞损伤内皮细胞损伤致病致病因子因子释放中性粒释放中性粒
21、细胞趋化因子细胞趋化因子中性粒细胞聚中性粒细胞聚集，释放氧自集，释放氧自由基、蛋白酶、由基、蛋白酶、炎症介质炎症介质肺肺水肿水肿死腔样死腔样通气通气肺泡肺泡型型上皮细胞上皮细胞损伤损伤表面活表面活性物质性物质合成合成支气管支气管痉挛痉挛血管收缩血管收缩微血栓微血栓肺泡膜肺泡膜通透性通透性肺不张肺不张功能性功能性分流分流PaOPaO2 2PaCOPaCO2 2 A previously healthy 23-year-old male sustained numerous traumatic crush,burn,and smoke inhalation injuries during a la
22、nding 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
23、 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 24 hrs.after admission,the patient becomes agitated and his respiration rate increased to 30/min.His minut
24、e 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 white out pattern.Clinical Case The diagnosis of ARDS is contingent upon 5 factors
25、: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 definitive diagnosis is made whe
26、n these signs and symptoms are linked with diffuse alveolar damage.Clinical Case 急性呼吸窘迫急性呼吸窘迫综合征综合征(ARDS)(ARDS)的概念及发生的概念及发生机制机制?问题问题：呼衰时机体功能和代谢变化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（一）酸碱平衡紊乱(acid-base(acid-base balance disturbance)balance disturbance)和电解质变化和电解
27、质变化呼酸呼酸:型型呼衰呼衰 COCO2 2潴留潴留 血血 K K+,血血 ClCl-呼碱：呼碱：I I型呼衰型呼衰 肺过度通气肺过度通气 血血 K K+,血血 ClCl-代酸：严重缺氧代酸：严重缺氧 无氧代谢无氧代谢 乳酸乳酸（二）呼吸系统的变化（二）呼吸系统的变化(Changes in(Changes in Respiratory System)Respiratory System)?呼吸调节呼吸调节(Regulation of Respiration)(Regulation of Respiration)?的变化的变化外周化学外周化学感受器感受器中枢化学中枢化学感受器感受器呼吸呼吸加深加
28、快加深加快抑制抑制呼吸中枢呼吸中枢PaOPaO2 260 mmHg50 mmHg50 mmHgPaOPaO2 230 mmHg80 mmHg80 mmHg（三）（三）循环系统变化循环系统变化(Changes in(Changes in Circulation System)Circulation System)轻度轻度PaOPaO2 2 和和 PaCOPaCO2 2 可兴奋心可兴奋心血管运动中枢血管运动中枢 严重严重PaOPaO2 2 和和 PaCOPaCO2 2 抑制心血抑制心血管运动中枢管运动中枢 缺氧缺氧 肺小动脉收缩肺小动脉收缩 肺动脉压肺动脉压 右心后负荷右心后负荷长期缺氧长期缺氧
29、肺血管平滑肌增殖肺血管平滑肌增殖 管壁增厚管壁增厚长期缺氧长期缺氧 红细胞增多红细胞增多 血液粘度血液粘度 心负荷心负荷缺氧、酸中毒缺氧、酸中毒 心肌舒缩功能心肌舒缩功能呼吸衰竭呼吸衰竭 右心衰竭右心衰竭 肺源性心脏病肺源性心脏病 (cor pulmonale)(cor pulmonale)PaOPaO2 2:60 mmHg :60 mmHg 智力，视力轻度减退智力，视力轻度减退40-50 mmHg 40-50 mmHg 神经精神症状神经精神症状20 mmHg 20 mmHg 神经细胞不可逆损坏神经细胞不可逆损坏(慢性呼衰慢性呼衰PaOPaO2 2 20 mmHg20 mmHg神志仍可清醒）神
30、志仍可清醒）PaCOPaCO2 2 80 mmHg CO80 mmHg CO2 2麻醉麻醉(头痛头痛,头昏头昏,嗜睡，嗜睡，精神错乱精神错乱,扑翼样震颤扑翼样震颤,抽搐抽搐,及昏迷等及昏迷等中枢神经系统症状）中枢神经系统症状）肺性脑病肺性脑病(pulmonary encephalopathy):(pulmonary encephalopathy):呼衰呼衰引起的脑功能障碍引起的脑功能障碍（四）中枢神经系统变化（四）中枢神经系统变化Changes in Central Nervous SystemChanges in Central Nervous SystemHypoxemia,2.ARDS发
31、生机制(Pathogenesis)Solubility Coefficient正常成人肺泡面积：70 m2解剖分流,真性分流?（四）中枢神经系统变化弥散面积减少(Decrease in the Surface Area of the Membrane)换气障碍型血液氧和二氧化碳解离曲线病因：感染（肺炎，败血症等），休克，严重创伤，吸入毒物或胃酸等。静息时换气面积：40 m2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and the Mechanisms（四）急性呼吸窘迫综合征阻塞性通气不足（Obstructive（一）一般原则(General Principals)静息时
32、换气面积：40 m2PaCO2 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）肺性脑病发生机制肺性脑病发生机制Pathogenesis of pulmonaryPathogenesis of pulmonary encephalopathy encephalopathy-氨基丁酸氨基丁酸脑脊液脑脊液 pHpH溶酶体溶酶体酶释放酶释放中枢抑制中枢抑制磷脂酶磷脂酶活性活性神经神经损伤损伤颅内压颅内压POPO2 2PaCOPaCO2 2血管内皮损伤血管内皮损伤血管血管通透性通透性脑脑水肿水肿脑血管脑血管扩张扩张脑充血脑充血问题：问题：呼吸衰竭时呼吸调呼吸衰竭时呼吸调节的变化？节的变化？肺源性心脏病发生肺源性心脏病发生机制机制?肺性脑病的定义及肺性脑病的定义及发生机制？发生机制？（一）一般原则（一）一般原则 (General Principals)(General Principals)1.1.防治原发病防治原发病 2.2.防止或去除诱因防止或去除诱因 3.3.改善肺通气改善肺通气 4.4.纠正水、电解质及酸碱平衡紊乱纠正水、电解质及酸碱平衡紊乱,保保 护重要器官功能护重要器官功能
