病理生理学 呼吸系统课件.ppt

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1、病理生理学系Department of Pathophysiology高远生,呼吸衰竭Respiratory Failure,Symbols,呼吸衰竭(Respiratory Failure),呼吸功能不全(Respiratory Insufficiency),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.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,一、呼衰的原因和发病机制 Respiratory Failure:The Causes and the

2、 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）肺通气功能障碍:Disorders in Pulmonary Ventilation,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。,阻塞位于胸外，表现为吸气性呼吸困难(In

3、spiratory Dyspnea),阻塞位于胸内，表现为呼气性呼吸困难(Exspiratory Dyspnea),用力呼气时等压点(isobaric point)移向小气道,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?,（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,肺泡-毛细血管膜Alveolar-Capillary Membrane(弥散膜,diffusion membrane),1.弥散面积减少(Decrease in the Surface Area of the Membrane),正

4、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。,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。,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,VA/Q 0.8=0.8 0.8 0.8,1.部分肺泡通气不足(Alveolar Vent

5、ilation Insufficiency)功能性分流(functional shunt)静脉血掺杂（venous admixture),血液氧和二氧化碳解离曲线Oxygen and Carbon DioxideDissociation Curves,氧和二氧化碳血液中的运输Transport of O2 and CO2 in the Blood,2.解剖分流增加(Increase in Anatomic Shunt),3.部分肺泡血流不足(Alveolar Perfusion Insufficiency)死腔样通气(dead space like ventilation）,血液氧和二氧化碳解

6、离曲线Oxygen and Carbon DioxideDissociation Curves,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 inf

7、ectious 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.,A previously healthy 23-year-old male sustained numerous traumatic crush,bu

8、rn,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

9、 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,24 hrs.after admission,the patient becomes agitated and his r

10、espiration 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 white out pattern.,Clinical Case,The

11、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.Appropriate antecedent history.Currently,there are no specific laboratory tes

12、ts for ARDS.A definitive diagnosis is made when these signs and symptoms are linked with diffuse alveolar damage.,Clinical Case,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 CO2潴留 血 K+,血 Cl-呼碱：I

13、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,（三）循环系统变化(Changes in Circulation System),PaO2:60 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

14、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,肺性脑病发生机制Pathogenesis of pulmonary encephalopathy,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？,（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

15、 the Prevention and Treatment of Respiratory Failure,1I 型呼衰只有缺O2而无CO2潴留，可吸入较高浓度O2，一般不超过502.II型呼衰有CO2潴留,应持续低浓度低流量吸氧，如30，12L/min，使PaO2上升到 60 mmHg,（二）吸氧(Oxygen Inhalation),问题：II型呼吸衰竭吸氧的原则？,respiratory failure(respiratory insufficiency()restrictive hypoventilation()obstructive hypoventilation()diffusion

16、 impairment()functional shunt()venous admixture()anatomic shunt();true shunt()dead space like ventilation()ventilation-perfusion ratio()acute respiratory distress syndrome(ARDS)()cor pulmonale()pulmonary encephalopathy(),respiratory failure(呼吸衰竭)respiratory insufficiency(呼吸功能不全)restrictive hypoventi

17、lation(限制性通气不足)obstructive hypoventilation(阻塞性通气不足)diffusion impairment(弥散障碍)functional shunt(功能性分流)venous admixture(静脉血掺杂)anatomic shunt(解剖分流);true shunt(真性分流)dead space like ventilation(死腔样通气)ventilation-perfusion ratio(肺泡通气与血流比例)acute respiratory distress syndrome(ARDS)(急性呼吸窘迫综合征)cor pulmonale(肺源性心脏病)pulmonary encephalopathy(肺性脑病),Vocabulary,