病理生理學(xué)呼吸系統(tǒng)培訓(xùn)課程課件

1、病理生理學(xué)呼吸系統(tǒng)病理生理學(xué)呼吸系統(tǒng)病理生理學(xué)呼吸系統(tǒng)培訓(xùn)課程課件SymbolsP PressurePartial pressureAAlveolaraarterialvvenousVVolume of gas / unit timeQVolume of blood/ unit time.SymbolsP Pressure.呼吸衰竭(Respiratory Failure) 外呼吸功能嚴(yán)重障礙 PaO2 ,伴有或不伴有PaCO2 的病理過程。判斷標(biāo)準(zhǔn)：PaO2 50mmHg (正常：40 mmHg)呼吸功能不全(Respiratory Insufficiency)呼吸衰竭(Respirator

2、y Failure) 外呼呼衰的類型Classification of Respiratory failure1. 按PaCO2 是否升高： 低氧血癥型（I型） 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：中樞性和外周性呼衰的類型Classification of Respir一、呼衰的原因和發(fā)病機(jī)制 Respiratory Failure: The Causes and the Mechanisms.肺通氣功能障礙 Disorders in Pulmonary Ventilation.肺換氣功能障礙 Disorders in Gas Excha

3、nge of the Lungs 一、呼衰的原因和發(fā)病機(jī)制 （一）肺通氣功能障礙: Disorders in Pulmonary Ventilation限制性通氣不足: 肺泡擴(kuò)張受限2.阻塞性通氣不足: 呼吸道阻塞或狹窄 氣道阻力增加。 （一）肺通氣功能障礙:限制性通氣不足: 肺泡擴(kuò)張受限1.限制性通氣不足（RestrictiveHypoventilation）：肺泡擴(kuò)張受限中樞神經(jīng)受損,周圍神經(jīng)受損,呼吸肌本身 收縮功能障礙。 肺充血和嚴(yán)重肺纖維化,肺泡表面活性物 質(zhì)減少。 胸廓和胸膜本身病變。呼吸肌活動(dòng)障礙肺順應(yīng)性降低胸廓順應(yīng)降低胸腔積液和氣胸1.限制性通氣不足（Restrictive中樞

4、神經(jīng)受損,周氣道阻力(正常人平靜呼吸)：80%: 直徑 2mm 氣管 20%: 直徑 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）限制性通氣不足（Restrictive彌散膜厚度增加：肺水腫，肺泡透明膜形成，肺纖維化，肺泡毛細(xì)血管擴(kuò)張等。彌散面積減少 (Decrease in the Surface Area of the Membrane)(正常：100 mmHg)缺氧 肺小動(dòng)脈收縮 肺動(dòng)脈壓解剖分流 (anatomic shunt)又稱真性分流(true shunt): 生理?xiàng)l件下一部分靜脈血經(jīng)支氣管靜脈和極少的肺內(nèi)A-V吻合支

5、直接流入肺靜脈 ( 2%-3% 心輸出量).Oxygen and Carbon DioxideDissociation CurvesHis orthopedic injuries and burns were treated.and the Mechanisms一、呼衰的原因和發(fā)病機(jī)制阻塞位于胸內(nèi)，表現(xiàn)為呼氣性呼吸困難 (Exspiratory Dyspnea)呼氣吸氣呼衰的類型Classification of Respir用力呼氣時(shí)等壓點(diǎn)(isobaric point)移向小氣道02520+353520202030正常人0152020+3525202020肺氣腫慢性支氣管炎0+353515

6、2520202020用力呼氣時(shí)等壓點(diǎn)(isobaric point)移向小氣道0問題 ： 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?問題 ：（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（二）彌散障礙彌散面積減少毛細(xì)血管內(nèi)皮細(xì)胞肺泡I型細(xì)胞基膜紅細(xì)胞肺泡-毛細(xì)血管膜Alveolar-Capillary Membrane(彌散膜, diffusion membrane) 毛細(xì)血管內(nèi)皮細(xì)胞肺泡I型細(xì)胞基膜紅細(xì)胞肺泡-毛細(xì)血管膜1.彌散面積減少 (Decrease in the Surface Are

7、a 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。1.彌散面積減少 (Decrease in the Sur流量（Q): 5L彌散時(shí)間縮短: 心輸出量增加, 肺血流加快Changes in Central Nervous SystemDisorders in PulmonaryDisorders in Gas Exchange of the LungsDisorders in Pulmonary VentilationVA/Q: 0.(正常：100 mmHg)Hypoventilation): 呼吸道阻塞或狹窄

8、氣道阻力增加。Clinical CaseAbsence of congestive heart failure, 4.呼衰的類型Classification of Respiratory failure彌散距離：5 mMHis orthopedic injuries and burns were treated.一、呼衰的原因和發(fā)病機(jī)制Principals of the Prevention and限制性通氣不足（Restrictive5 l/min to 20 l/min.呼堿：I型呼衰 肺過度通氣 血 K+ , 血 Cl-2.彌散膜厚度增加(Increase in the Thicknes

9、s 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，肺纖維化，肺泡毛細(xì)血管擴(kuò)張等。流量（Q): 5L2.彌散膜厚度增加(Incre3.彌散時(shí)間縮短 (Shortening in the Diffusion Time)正常靜息狀態(tài)：血流通過毛細(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3.彌散時(shí)間縮短 (Shortening in the DSolubility Coefficient(vol/vol, 760 mmHg): O2: 0.024 CO2:0.57Solubility C

10、oefficient正常靜息狀態(tài)下：每分鐘肺泡通氣量（VA)： 4L 每分鐘肺血流量（Q): 5LVA/Q: 0.8.（三）肺泡通氣與血流比例失調(diào)Ventilation-Perfusion Imbalance正常靜息狀態(tài)下：.（三）肺泡通氣與血流比例失調(diào)VentVA.VA/Q 0.8 =0.8 0.8 0.8. 病肺 健肺 全肺PaO2PaCO2N1.部分肺泡通氣不足(Alveolar Ventilation Insufficiency)功能性分流 (functional shunt)靜脈血摻雜（venous admixture)VA.VA/Q 0.8 =0.8 血液氧和二氧化碳解離曲線Oxy

11、gen and Carbon DioxideDissociation Curves血液氧和二氧化碳解離曲線O2 transported as:O2: 1.5%Hb.O2: 98.5%CO2 transported as:CO2: 7%Hb.CO2: 23%HCO3-: 70%氧和二氧化碳血液中的運(yùn)輸Transport of O2 and CO2 in the BloodO2 transported as:CO2 transpor2.解剖分流增加(Increase in Anatomic Shunt)解剖分流 (anatomic shunt)又稱真性分流(true shunt): 生理?xiàng)l件下一部

12、分靜脈血經(jīng)支氣管靜脈和極少的肺內(nèi)A-V吻合支直接流入肺靜脈 ( 2%-3% 心輸出量).支氣管擴(kuò)張癥 支氣管血管擴(kuò)張，肺內(nèi)A-V短路開放 解剖分流 PaO2 .2.解剖分流增加(Increase in Anatomic20%: 直徑 2mm 氣管一、呼衰的原因和發(fā)病機(jī)制Airway pressure increased from 18 to 65 cm H2O.20%: 直徑 2mm 氣管中樞神經(jīng)受損,周圍神經(jīng)受損,呼吸肌本身Arterial blood gas measurements were: pH = 7.外呼吸功能嚴(yán)重障礙 PaO2 ,伴有或不伴有PaCO2 的病理過程。O2: 98

13、.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:彌散膜厚度增加：肺水腫，肺泡透明膜形成，肺纖維化，肺泡毛細(xì)血管擴(kuò)張等。按PaCO2 是否升高：靜脈血摻雜（venous admixture)Diffusion Impairment阻塞位于胸內(nèi)，表現(xiàn)為呼氣性呼吸困難 (Exspiratory Dyspnea)

14、20%: 直徑 0.8 0.8 0.83. 部分肺泡血流不足(Alveolar Perfusion Insufficiency)死腔樣通氣(dead space like ventilation）20%: 直徑 2mm 氣管Q.PaO2PaCO2NVA/血液氧和二氧化碳解離曲線Oxygen and Carbon DioxideDissociation Curves血液氧和二氧化碳解離曲線問題 ：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?問題 ：肺泡-毛細(xì)血管膜 (alveolar capillary membrane) 損傷引起的急性呼吸衰竭。病因：感染（肺

15、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 that pathologically and clinically is ARDS. Experts have speculated that the cause is from a corona virus that may be transmitt

16、ed via respiratory secretions and develops after 2-11 days of a febrile illness. 肺泡-毛細(xì)血管膜 (alveolar capillary m病理生理學(xué)呼吸系統(tǒng)培訓(xùn)課程課件ARDS發(fā)生機(jī)制(Pathogenesis)肺泡膜內(nèi)皮細(xì)胞損傷致病因子釋放中性粒細(xì)胞趨化因子中性粒細(xì)胞聚集，釋放氧自由基、蛋白酶、炎癥介質(zhì)肺水腫死腔樣通氣肺泡型上皮細(xì)胞損傷表面活性物質(zhì)合成支氣管痙攣血管收縮微血栓肺泡膜通透性肺不張功能性分流PaO2PaCO2ARDS發(fā)生機(jī)制(Pathogenesis)肺泡膜致病釋放中 A previously h

17、ealthy 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

18、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 mmHg, and PO2 of 62 mmHg

19、.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 H2O. Repeat arterial blood gas measurement of PO2 indica

20、ted 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

21、 (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 when these signs and symptoms are linked with diffuse alveolar damage.Clinical Case The diagnosis of ARD急性呼吸窘迫綜合征(ARDS)的概念

22、及發(fā)生機(jī)制?問題 ：急性呼吸窘迫綜合征(ARDS)的概念及發(fā)生機(jī)制?問題 ：二、呼衰時(shí)機(jī)體功能和代謝變化 Functional and Metabolic Change in Respiratory Failure （一）酸堿平衡紊亂(acid-base balance disturbance)和電解質(zhì)變化呼酸: 型呼衰 CO2潴留 血 K+ , 血 Cl- 呼堿：I型呼衰 肺過度通氣 血 K+ , 血 Cl-代酸：嚴(yán)重缺氧 無氧代謝 乳酸二、呼衰時(shí)機(jī)體功能和代謝變化（一）酸堿平衡紊亂(acid-b（二）呼吸系統(tǒng)的變化(Changes in Respiratory System)呼吸調(diào)節(jié)(Re

23、gulation 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PaO250 mmHgPaO280 mmHg（二）呼吸系統(tǒng)的變化(Changes in Respirat（三）循環(huán)系統(tǒng)變化(Changes in Circulation System) 輕度PaO2 和 PaCO2 可興奮心血管運(yùn)動(dòng)中樞 嚴(yán)重PaO2 和 PaCO2 抑制心血管運(yùn)動(dòng)中樞 （三）循環(huán)系統(tǒng)變化(Changes in Circulat缺氧 肺小動(dòng)脈收縮 肺動(dòng)脈壓 右心后負(fù)荷長(zhǎng)期缺氧 肺血管平滑肌增殖 管壁增厚長(zhǎng)期缺氧 紅細(xì)胞增多 血液粘度 心負(fù)荷缺氧、酸中毒 心肌舒縮功能呼吸衰

24、竭 右心衰竭 肺源性心臟病 (cor pulmonale)缺氧 肺小動(dòng)脈收縮 肺動(dòng)脈壓 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 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 SystemPaO2: 60 mmHg 智力，視力輕度減退（四）肺性腦病發(fā)

25、生機(jī)制Pathogenesis of pulmonary encephalopathy-氨基丁酸腦脊液 pH溶酶體酶釋放中樞抑制磷脂酶活性神經(jīng)損傷顱內(nèi)壓PO2PaCO2血管內(nèi)皮損傷血管通透性腦水腫腦血管擴(kuò)張腦充血肺性腦病發(fā)生機(jī)制-氨基丁酸腦脊液 pH溶酶體中樞抑制磷問題：呼吸衰竭時(shí)呼吸調(diào)節(jié)的變化？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？問題：支氣管擴(kuò)張癥 支氣管血管擴(kuò)張，肺內(nèi)A-V短路開放 解剖分流 PaO2 .In the ER he was intubated and had no signs of pneumothorax.嚴(yán)重PaO2 和 PaCO2 抑制心血管運(yùn)動(dòng)中樞肺泡膜厚度：1 mMHis initial B.In the ER he was intubated and had no signs of pneumothorax.彌散膜厚度增加：肺水腫，肺泡透明膜形成，肺纖維化，肺泡毛細(xì)血管擴(kuò)張等。肺泡膜厚度：1 mM阻塞性通氣不足（Obstructive呼吸衰竭時(shí)呼吸調(diào)節(jié)的變化？嚴(yán)重PaO2 和 PaCO2 抑制心血管運(yùn)動(dòng)中樞肺充血和嚴(yán)重肺纖維化,肺泡表面活性物Hypoventilation）：肺泡擴(kuò)張受限VA/Q: 0.氧和二氧化碳血液中的運(yùn)輸Diffusion ImpairmentCO2 transpor