病理生理學(xué)呼吸系統(tǒng)

1、病理生理學(xué)系Department of Pathophysiology高遠(yuǎn)生,呼吸衰竭Respiratory Failure,,Symbols,,呼吸衰竭(Respiratory Failure),,呼吸功能不全(Respiratory Insufficiency),,呼衰的類型Classification of Respiratory failure,1. 按PaCO2 是否升高： 低氧血癥型（I型）

2、 低氧血癥伴高碳酸血癥（II型）2. 按主要發(fā)病機(jī)制：通氣障礙型 換氣障礙型3. 按病變部位：中樞性和外周性,,一、呼衰的原因和發(fā)病機(jī)制 Respiratory Failure: The Causes a

3、nd the Mechanisms,.肺通氣功能障礙 Disorders in Pulmonary Ventilation.肺換氣功能障礙 Disorders in Gas Exchange of the Lungs,,（一）肺通氣功能障礙: Disorders in Pulmonary Ventilation,,氣道阻力(正常人平靜呼吸)：

4、80%: 直徑 >2mm 氣管 20%: 直徑 <2mm 氣管病因：氣管痙攣` 腫脹` 纖維化` 滲出物` 異物` 腫瘤` 氣道內(nèi)外壓力改變,2.阻塞性通氣不足（Obstructive Hypoventilation): 呼吸道阻塞或狹窄 氣道阻力增加。,,,阻塞位于胸外，表現(xiàn)為吸氣性呼吸困難 (Inspiratory Dyspnea),,阻塞位于胸內(nèi)，表現(xiàn)為呼氣性呼吸困難 (Exspi

5、ratory Dyspnea),,用力呼氣時(shí)等壓點(diǎn)(isobaric point)移向小氣道,,問(wèn)題 ： 呼吸衰竭? 限制性通氣不足的定義及其發(fā)生原因? 胸內(nèi)、胸外氣道阻塞在呼吸中的差異?,（二）彌散障礙 Diffusion Impairment,彌散面積減少2. 彌散膜厚度增加3. 彌散時(shí)間縮短,,,肺泡-毛細(xì)血管膜Alveolar-Capillary Membrane(彌散膜, diffusion me

6、mbrane),1.彌散面積減少 (Decrease in the Surface Area of the Membrane),正常成人肺泡面積：70 m2靜息時(shí)換氣面積：40 m2彌散面積減少：肺不張，肺實(shí)變，肺葉切除等。,,2.彌散膜厚度增加(Increase in the Thickness of the Membrane),肺泡膜厚度：1 mM彌散距離：5 mM彌散膜厚度增加：肺水腫，肺泡透明膜形成，

7、肺纖維化，肺泡毛細(xì)血管擴(kuò)張等。,,3.彌散時(shí)間縮短 (Shortening in the Diffusion Time),正常靜息狀態(tài)：血流通過(guò)毛細(xì)血管時(shí)間: 0.75 s 彌散時(shí)間： 0.25 s彌散時(shí)間縮短: 心輸出量增加, 肺血流加快,,,VA/Q 0.8 =0.8 >0.8 <0.8,1.部分肺泡通氣不足(Alveolar Ven

8、tilation Insufficiency)功能性分流 (functional shunt)靜脈血摻雜（venous admixture),,血液氧和二氧化碳解離曲線Oxygen and Carbon DioxideDissociation Curves,,氧和二氧化碳血液中的運(yùn)輸Transport of O2 and CO2 in the Blood,,2.解剖分流增加(Increase in Anatomic

9、 Shunt),,,,,3. 部分肺泡血流不足(Alveolar Perfusion Insufficiency)死腔樣通氣(dead space like ventilation）,,血液氧和二氧化碳解離曲線Oxygen and Carbon DioxideDissociation Curves,,問(wèn)題 ：彌散障礙的發(fā)生機(jī)制?功能性分流,靜脈血摻雜?解剖分流, 真性分流?死腔樣通氣?,,肺泡-毛細(xì)血管膜 (alveol

10、ar capillary membrane) 損傷引起的急性呼吸衰竭。病因：感染（肺炎，敗血癥等），休克，嚴(yán)重創(chuàng)傷，吸入毒物或胃酸等。,（四）急性呼吸窘迫綜合征Acute Respiratory Distress Syndrome (ARDS),,Severe acute respiratory syndrome (SARS) is a good example of a probable infectious pneumonia

11、 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 previousl

12、y 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

13、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 O2

14、 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 bec

15、omes 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 i

16、ndicated 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 rad

17、iography, 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 labor

18、atory tests for ARDS. A definitive diagnosis is made when these signs and symptoms are linked with diffuse alveolar damage.,Clinical Case,,急性呼吸窘迫綜合征(ARDS)的概念及發(fā)生機(jī)制?,問(wèn)題 ：,二、呼衰時(shí)機(jī)體功能和代謝變化 Functional and Metabolic Change in

19、Respiratory Failure,（一）酸堿平衡紊亂(acid-base balance disturbance)和電解質(zhì)變化呼酸: Ⅱ型呼衰 CO2潴留 血 K+ , 血 Cl- 呼堿：I型呼衰 肺過(guò)度通氣 血 K+ , 血 Cl-代酸：嚴(yán)重缺氧 無(wú)氧代謝 乳酸,,（二）呼吸系統(tǒng)的變化(Changes in Respiratory System),呼吸調(diào)節(jié)(Regulation

20、 of Respiration) 的變化,,,外周化學(xué)感受器,中樞化學(xué)感受器,呼吸加深加快,抑制呼吸中樞,,,,,,,,（三）循環(huán)系統(tǒng)變化(Changes in Circulation System),,,,,,PaO2: 60 mmHg 智力，視力輕度減退40-50 mmHg 神經(jīng)精神癥狀20 mmHg 神經(jīng)細(xì)胞不可逆損壞(慢性呼衰PaO2 20 mmHg神志仍可清醒）PaCO2

21、>80 mmHg CO2麻醉(頭痛,頭昏,嗜睡，精神錯(cuò)亂, 撲翼樣震顫, 抽搐, 及昏迷等中樞神經(jīng)系統(tǒng)癥狀）肺性腦病(pulmonary encephalopathy):呼衰引起的腦功能障礙,（四）中樞神經(jīng)系統(tǒng)變化Changes in Central Nervous System,,肺性腦病發(fā)生機(jī)制Pathogenesis of pulmonary encephalopathy,問(wèn)題：呼吸衰竭時(shí)呼吸調(diào)節(jié)的變化？

22、肺源性心臟病發(fā)生機(jī)制?肺性腦病的定義及發(fā)生機(jī)制？,（一）一般原則 (General Principals) 1. 防治原發(fā)病 2. 防止或去除誘因 3. 改善肺通氣 4. 糾正水、電解質(zhì)及酸堿平衡紊亂,保 護(hù)重要器官功能,五、呼衰的防治原則 Principals of the Prevention and Treatment of Respiratory Failure,,1．I 型呼衰只有缺

23、O2而無(wú)CO2潴留，可吸入較高濃度O2，一般不超過(guò)50％2. II型呼衰有CO2潴留, 應(yīng)持續(xù)低濃度低流量吸氧，如30％，1～2L/min，使PaO2上升到 60 mmHg,（二）吸氧(Oxygen Inhalation),,問(wèn)題：II型呼吸衰竭吸氧的原則？,respiratory failure (respiratory insufficiency ( )restrictive hypoventilation ( )obs

24、tructive hypoventilation ( )diffusion impairment ( )functional shunt ( )venous admixture ( ) anatomic shunt ( ); true shunt( ) dead space like ventilation ( )ventilation-perfusion ratio ( )acute respiratory

25、 distress syndrome (ARDS) ( )cor pulmonale ( )pulmonary encephalopathy ( ),respiratory failure (呼吸衰竭)respiratory insufficiency (呼吸功能不全)restrictive hypoventilation (限制性通氣不足)obstructive hypoventilation (阻塞性通氣不足)diffu

26、sion impairment (彌散障礙)functional shunt (功能性分流)venous admixture (靜脈血摻雜) anatomic shunt (解剖分流); true shunt(真性分流) dead space like ventilation (死腔樣通氣)ventilation-perfusion ratio (肺泡通氣與血流比例)acute respiratory dis