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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 Ca
2、uses 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）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
3、加。,阻塞位于胸外，表现为吸气性呼吸困难 (Inspiratory 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
4、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。,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
5、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 Ventilation 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 Dioxide Dissociation 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 Per
6、fusion Insufficiency) 死腔样通气(dead space like ventilation）,血液氧和二氧化碳解离曲线 Oxygen and Carbon Dioxide Dissociation 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 (A
7、RDS),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 il
8、lness.,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
9、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 at 12/min, and tidal volume at 900 ml. Arterial blood gas measurements were: pH = 7.47, PCO2 of 33 mmH
10、g, and PO2 of 62 mmHg.,Clinical Case,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 H2O. Repeat arterial blood gas measurement of PO2 indi
11、cated 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: 1. Hypoxemia, 2. Diffuse pulmonary infiltrates on radiography, 3. Absence of congestive heart failure, 4. Decreased lung compliance (effective stat
12、ic 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 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 Function
13、al 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 Ci
14、rculation 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 encephalopath
15、y,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 the Prevention and Treatment of Respiratory Failure,1 I 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50 2. 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 mm
16、Hg,（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 impairment ( ) functional shunt ( ) venous admixture ( ) anatomic shunt ( ); true shunt( ) dead space like ventilation ( ) ventilation-perfusion ratio ( ) acute respiratory distress syndrome (ARDS) (
