肺臟病理生理學(xué)ye

1、葉俊麗Mail to yejunli126@126.com,肺病理生理學(xué)(Pulmonary Insufficiency),Department of pathophysiology,Contents,? Introduction?? Etiology and pathogenesis ??? Alterations of function and metabolism,? Introduction,,Normal ph

2、ysiological function of lung,External respiration Defensive function Filter function Metabolic function,Defensive function,,肺泡表面積80m2，接觸空氣15000L/天,Defensive function,非特異性：氣道異物的清除（顆粒、氣體）。,顆粒的清除：受氣道解剖、氣流速度、顆 粒大小影

3、響。,>5µm,沉積在上呼吸道1-5µm，沉積在小氣道0.1-1µm，沉積在肺泡<0.1µm，基本隨呼氣排出,氣體的清除：噴嚏、咳嗽。,,特異性防御機(jī)制--免疫反應(yīng)。,肺是重要的免疫系統(tǒng)。,淋巴組織、IgA、IgG、免疫反應(yīng)細(xì)胞等。,Defensive function,,,,,,,Filter function,arterial,,,(2010) IF= 47.05,Metab

4、olic function,肺組織參與糖、脂肪、蛋白質(zhì)的代謝。,Surfactant,,Metabolic function,,Metabolic function,,Metabolic function,,胺類：兒茶酚胺（CA）、5-HT、組胺等。,脂類：前列腺素、白三烯、PAF、乙酰膽堿等。,Metabolic function,,肽類：血管緊張素、緩激肽、血管活性腸肽、P物質(zhì)等。,,Pulmonary dysfunction,In

5、 the study ? ? ?,The respiration process in normal body,Respiratory failure,,ventilation,exchange,Case study,病史：患者男，45歲。因車禍致全身多發(fā)傷入院。手術(shù)搶救后次日（傷后23 h），患者呼吸困難加重，胸悶，口唇紫紺。 體檢：呼吸35-40次/ min，脈搏138次/ min，血壓97.5/45.0 mmHg，并且無(wú)尿

6、， 實(shí)驗(yàn)室檢查：SaO20.70-0.78,pH7.216；PaCO2 35.2mmHg，PaO2 39.0mmHg。拍X光片：右肺上葉不張，左肺下葉纖細(xì)陰影，間質(zhì)水腫，肺不張。,思考：患者的主要病理過(guò)程是什么?機(jī)制是什么？如何糾正該患者的缺氧問(wèn)題？,Conception of respiratory failure,,,外呼吸功能,,PaO2,,/ PaCO2,,病理過(guò)程,（呼吸衰竭）,,FiO2 ? 20%, RFI

7、≦ 300 ( RFI= PaO2 / FiO2 ),,PaO2 < 60mmHg,,PaCO2 > 50mmHg,Diagnosis of respiratory failure,,According to PaCO2,Classification of respiratory failure,Contents,? Introduction?? Etiology and pathogenesis ??? A

8、lterations of function and metabolism,外呼吸,Ventilatory disorder,Pathogenesis of Respiratory Failure,,Disorder of air exchange,肺通氣功能障礙,肺換氣功能障礙,,Alveolar ventilation（4L / min ),dead space,,Pulmonary ventilation（ 6L / min

9、 ),,,,,Normal respiratory movement,,,3,5,4,3,2,1,CenterMusclesChest wallAlveoliAirway,3,2,,Causes of impaired ventilation,,Restrictive hypoventilation,(限制性通氣不足),,（1） 呼吸肌麻痹,,,胸廓畸形,（2） 胸廓順應(yīng)性下降,,,,,,,,,,胸腔積液,,,,,（3）氣胸,

10、胸腔積液,,,,,,,,,,,,,（4）肺順應(yīng)性下降,肺纖維化,,Diffuse Fibrosis(white-tan tissue),,Caused by ARDS, hyperventilation and alveolar edema，etc.,,normal,Lack of surfactant,（4）肺順應(yīng)性下降,Causes of restrictive ventilatory disorder,,呼吸肌無(wú)力（Paraly

11、sis of respiratory muscles）,胸廓順應(yīng)性降低（Decreased compliance of chest wall）,肺順應(yīng)性降低（Decreased compliance of lung）,胸腔積液和氣胸（Hydrothorax or pneumothorax）,,Causes of impaired ventilation,,Restrictive hypoventilation (限制性通氣

12、不足),Obstructive hypoventilation (阻塞性通氣不足),Factors influencing the airway resistance,,80% of the airway resistance comes from central airway (>2mm), 20% from peripheral small airway (<2mm).,,,Obstruction of cen

13、tral airway (中央性氣道阻塞）,Obstruction of peripheral airway (外周性氣道阻塞),Causes of obstructive ventilatory disorder,Inspiration,Obstruction of extrathoracic airway,Obstruction of intrathoracic airway,,,,,,,,,,,,,,,

14、,Intra-thoracic pressure,,,,,,,,,,,,,,,Intra-thoracic pressure,,,,,,Expiration,,Inspiration,Intraairway pressure,Intraairway pressure,,Obstruction of central airway (中央性氣道阻塞）,Obstruction of peripheral airway

15、 (外周性氣道阻塞),Causes of obstructive ventilatory disorder,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,Obstruction of peripheral airway,Intra-thoracic pressure,Intra-thoracic pressure,Expiration,Inspiration,Intraairway pressure,

16、Intraairway pressure,,,normal,COPD,Equal pressure point shifts up leading to airway closure caused by forced expiration,Atmosphere pressure,Intrathoracic pressure,Intraairway pressure,,Changes of blood gas in alveolar hy

17、poventilation,,Alveolar hypoventilation,,,Changes of blood gas in alveolar hypoventilation,,2. PaCO2 is the best index of alveolar ventilation of total lung,1. The ratio of the increased value of to the decreased value

18、of is equal to the respiratory quotient,Ventilatory disorder (肺通氣功能障礙),Causes of Respiratory Failure,,Disorder of air exchange (肺換氣功能障礙 ),,Normal gas exchange,Causes of disorder of air exchange,,Impaired Gas

19、Diffusion （彌散障礙）,Ventilation- Perfusion Imbalance （通氣/血流比例失調(diào)）,Increased anatomic shunt （解剖分流增加）,Impaired Gas Diffusion （彌散障礙）,Factors influencing gas diffusion speed,,thickness：<1-5 µmT

20、otal area：about 70-80 m2 at rest 40 m2,Normal structure of diffusion membrane,Diffusion speed ∝,Etiologies and mechanisms of impaired diffusion,,Surface area of diffusion membrane↓

21、 (肺泡膜面積減少),Thickness of diffusion membrane↑ (肺泡膜厚度增加 ),Shorten of diffusion time (彌散時(shí)間縮短 ),,,,pO2（kPa）,Artery,Capillary,Vein,,,,,,,,,,,,,,13.310.78.005.332.67 0,0 0.25 0.50

22、 0.75,,The changes of the diffusion time （1）At rest （2）Physical load increase,Time（S）,,Changes of blood gas in diffusion disorder,,D

23、iffusion disorder,The dissolubility of CO2 in water and its diffusion index is greater than that of O2. PaCO2 is the best index of alveolar ventilation of total lung.,？,,,,,,,,HbO2,,,,H2CO3,,,,,,,,,,,,,,1

24、00 80 60 40 20 0,20 40 60 80 100 120 140,動(dòng)脈血氧分壓(mmHg),,,,,,,靜脈血 動(dòng)脈血,O2解離曲線,,病變部位,非病變部位,,,,,,Causes of disorder of air exchange

25、,Ventilation- Perfusion Imbalance （通氣/血流比例失調(diào)）,Impaired Gas Diffusion （彌散障礙）,,,Most common and important mechanism of RF caused by pulmonary diseases.,Normal physiological VA/Q mismatch,Ventilation/Perfusio

26、n Imbalance,,,Partial alveolar hypoventilation,Partial alveolar hypoperfusion,Classification of Ventilation- Perfusion Imbalance,,A,C,B,A：V/Q normalB：V/Q ↓（perfusion, no ventilation）C：V/Q ↑（ ventilation, no perfusion

27、 ）,部分肺泡阻塞性或限制性通氣不足,病變部肺泡通氣明顯減少，血流未相應(yīng)減少,,,VA/Q 顯著降低(?0.8)，氣少血多,,,病變部位靜脈血未經(jīng)充分動(dòng)脈化,,類似于動(dòng) - 靜脈短路,Partial alveolar hypoventilation( functional shunt),Functional shunt,,Physiological shunt：3% of pulmonary

28、perfusion,PathoPhysiological shunt ：30-50% of pulmonary perfusion,Local hypoventilation,,Functional shunt（venous admixture）,,,,,,airway,,Pulmonary vein,Pulmonary artery,,capillary,,,,alveoli,,,肺動(dòng)

29、脈拴塞、炎癥、收縮或DIC,病變部肺泡血流明顯減少，通氣未相應(yīng)減少,Partial alveolar hypoperfusion (dead space like ventilation),,,VA/Q 顯著升高(〉0.8)，氣多血少,,,病變部位肺泡通氣不能充分被利用,,肺泡死腔增大,Dead space like ventilation,,Physiological：30% of alveolar ventilation,Patho

30、physiological：60-70%,Local hypoperfusion,,dead space like ventilation,,,,normal,,,,,,,,,,,,,,,,,,,,,,,changes of blood gas in Ventilation-Perfusion Imbalance,,Ventilation-Perfusion Imbalance,,,,,Abnormal,Normal,,,Total l

31、ung,,,氣少血多,氣多血少,（depend on compensatory degree）,changes of blood gas in functional shunt,,,氧離曲線決定,CO2解離曲線決定,,,,,,,,代償過(guò)度， PaCO2降低,代償不足， PaCO2升高,代償適度， PaCO2正常,changes of blood gas in functional shunt,,,,,,,,HbO2,,,,H2CO3,,

32、,,,,,,Abnormal,Normal,Total,,氣少血多,氣多血少,（取決于代償程度）,（hypoventilation）,（hyperventilation）,changes of blood gas in functional shunt,abnormal,normal,total,,氣少血多,氣多血少,,,,changes of blood gas in VDf,,病變肺,健側(cè)肺,全肺,,氣少血多,氣多血少,（取決于代償

33、程度）,（ hypoventilation ）,（ hyperventilation ）,changes of blood gas in VDf,肺換氣功能障礙的基本原因,,彌散障礙 (Impaired Gas Diffusion),通氣血流比例失調(diào)(Ventilation- Perfusion Imbalance),解剖分流增加(Increased anatomic shunt),解剖分流(anatom

34、ic shunt),,,anatomic shunt,,airway,,,,,,,,,,,Pulmonary artery,,Pulmonary veins,解剖分流增加,,,,,,,,,,,,,,功能性分流,功能性分流（VA= 0）,解剖分流,,,,No gas exchange,,,真性分流,,真正分流,功能性分流,解剖上不允許氣體交換，吸入純氧無(wú)效,部分肺泡氣體交換減少，吸入純氧有效,如何鑒別功能性分流與真正分流,,,,肺泡通氣與

35、血流比例失調(diào),氣道,肺動(dòng)脈,肺靜脈,肺泡,毛細(xì)血管,1. 正常,2. 解剖分流,3. 功能分流,4. 死腔樣通氣,分流,低氧,通氣不足,血流不足,低氧,低氧,,,,,,,,,,,,返回,Acute respiratory distress syndrome, ARDS（急性呼吸窘迫綜合征）,----------Acute respiratory failure caused by acute lung injury,1992年歐美AR

36、DS聯(lián)席會(huì)議認(rèn)為，ARDS不是一個(gè)獨(dú)立的疾病而是一個(gè)連續(xù)的病理過(guò)程。 *早期為急性肺損傷（ALI）,重度ALI即為ARDS,,ARDSEpidemiology,Incidence:5 – 71 per 100,000Financial cost:$5,000,000,000 per annumFatality: 40%-60%,,ARDSEtiology,,,ARDS--------Etiology,,AR

37、DSPathophysiology,肺間質(zhì)/肺泡水腫進(jìn)行性缺氧due to intra-pulmonary shunt (V/Q = 0)shunt ~ 25% - 50%氣道阻力增加,,,病因,,直接損傷,,急性肺泡毛細(xì)血管膜損傷,,間接激活炎癥細(xì)胞,,,急性呼吸衰竭,?,,Causes and mechanisms of ARDS,Mechanism of cell injury and repair,? 炎癥細(xì)胞

38、通過(guò)炎癥介質(zhì)的損傷作用 ? 缺血缺氧的基因調(diào)節(jié)反應(yīng) ? 應(yīng)急蛋白的產(chǎn)生與激活 ? 生長(zhǎng)因子的作用 ? 細(xì)胞骨架與小管結(jié)構(gòu)的損傷與重建,,單核－巨噬細(xì)胞 ARDS發(fā)病6～24ｈ，肺巨噬細(xì)胞數(shù)量速增，且持續(xù)時(shí)間長(zhǎng)。肺巨噬細(xì)胞來(lái)自骨髓單核細(xì)胞，是肺的正常細(xì)胞成分。分為４型：肺泡巨噬細(xì)胞（AM）：其數(shù)量為肺泡常駐細(xì)胞80％；肺間質(zhì)巨噬細(xì)胞；樹(shù)突狀細(xì)胞（dendritic c

39、ell）；肺血管內(nèi)巨噬細(xì)胞（pulmonary intravascular macro－ phage， PIM）,Pathophysiology of ARDS,,Bello證實(shí)，支氣管肺泡灌注液，PMNs凋 亡延遲: * 粘細(xì)胞-巨噬細(xì)胞集落刺激因子（GM-CSF） * 粘細(xì)胞集落刺激因子（G-CSF） * TNF-2、IL-1β、IL-6 ①延長(zhǎng)PM

40、Ns生命周期 ②維持了白細(xì)胞的多種功能。,3. NF-κB活性顯著增高, 促進(jìn)蛋白質(zhì)轉(zhuǎn)錄。,,4. 在炎性介質(zhì)作用下,中性粒細(xì)胞流變學(xué)特性的改變（如變形性降低、體積增加,聚集）,肺循環(huán)低灌注壓、大容量、分枝少，肺血管中性粒細(xì)胞含量較其他部位大血管高40~80倍。 中性粒細(xì)胞通過(guò)肺毛細(xì)血管時(shí)間延長(zhǎng)：26s(2~120s)，紅細(xì)胞1~2s。,2.多形核中性粒細(xì)胞（PMNs）凋亡延遲或抑制的調(diào)控作用,Pathophysiol

41、ogy of ARDS,Drost用細(xì)胞通過(guò)分析儀研究膿毒血癥病人中性粒細(xì)胞流變學(xué)特性 ，這些細(xì)胞通過(guò)直徑為8um，長(zhǎng)為20um微管。* 移動(dòng)方式：跳躍式快速移動(dòng)與停頓，變形，在<5.3 μm毛細(xì)血管變形時(shí)間延長(zhǎng)。硬化(rinidity)，變形性降低，體積增大20~100%。 （Na+/H+)* 粘附形成雙聯(lián)體。幼稚粒細(xì)胞增加。,Normal Cell,Apoptotic cell,Cell undergoing ap

42、optosis,5.血小板： 釋放AAM、5-羥色胺（5-HT）,血小板激活因子（PAF）,表皮生長(zhǎng)因子（EGF）、轉(zhuǎn)化生長(zhǎng)因子（TGF）等。,,Pathophysiology of ARDS,6. 血管內(nèi)皮細(xì)胞： 可選擇性地代謝生物活性物質(zhì)，如5-HT、去甲腎上腺素、緩激肽、血管緊張素Ⅰ等；可釋放氧自由基、花生四烯酸、前炎癥因子和生長(zhǎng)因子；也可表達(dá)某些粘附分子。,,,,,7. 肺泡上皮細(xì)胞 分為Ⅰ型肺泡細(xì)胞（pneu

43、mocyte typeⅠ，PC-Ⅰ）和Ⅱ型肺泡細(xì)胞（PC-Ⅱ）。它們?cè)贏RDS發(fā)病中的變化，包括直接受損和PC-Ⅱ表面活性物質(zhì)（PS）代謝異常兩個(gè)方面。,,Pathophysiology of ARDS,ARDS Acute Exudative Phase,ARDSProliferative Phase,Type II pneumocyteproliferatedifferentiate into Type I cellsre

44、line alveolar wallsFibroblast proliferationinterstitial/alveolar fibrosis,ARDSFibrotic Phase,Characterized by:local fibrosisvascular obliterationRepair process:resolution vs fibrosis,,,RDS,呼吸窘迫綜合征：肺泡腔內(nèi)蛋白性液體滲出，并

45、在肺泡管和肺泡表面形成膜狀物,肺泡萎陷,NRDS：小支氣管內(nèi)可見(jiàn)吸入的羊水成分（胎便小體和角化物質(zhì)）,NRDS：肺泡內(nèi)可見(jiàn)吸入的角化物質(zhì),RDS,早產(chǎn)兒呼吸窘迫綜合征（II－III度） 肺透亮度明顯降低、細(xì)顆粒、網(wǎng)狀陰影，支氣管充氣正常,“ 白肺”（IV度）,*ARDS發(fā)病的三個(gè)階段 局部炎癥反應(yīng)階段： 有限全身炎癥反應(yīng)階段：介質(zhì)入血

46、 SIRS/CARS失衡階段： 瀑布樣釋放炎癥擴(kuò)散，失控。 細(xì)胞因子，保護(hù)?自身破壞。,Pathophysiology of ARDS,,Causes,Inflammatory response,,,,,,,,,,,,,,,,,,,,,,,,MODS,Primary inflammation,SIRS,CARS,抗炎因子大量釋放,致炎因子大量釋

47、放,Balance,Anti-inflammatory response,,Secondary mediators,,,,agents（chemical, physical or biological） inflammationPulmonary edema atelectasis bronchospasm vasoconstriction thrombosisDiffusio

48、n disorder shunt dead space like ventialtion hypoxia,,Type I RF,ARDSClinical Phases,I. Injury PhaseII. Latent/Lag PhaseIII. ARF PhaseIV. Recuperative/Terminal Phase,ALI的診斷標(biāo)準(zhǔn):

49、 1.急性起?。?2.氧合指數(shù)PaO2/FIO2≤300mmHg（ 40kPa ） 3.正位胸片兩肺斑片狀陰影； 4.PAWP≤18mmHg（2.4kPa），或無(wú)左房壓力增高,ARDS的診斷標(biāo)準(zhǔn): ALI診斷標(biāo)準(zhǔn)基礎(chǔ)+氧合指數(shù)≤200mmHg（26.67kPa）,1.血清表面活性蛋白-A (S

50、P-A),ARDS早期預(yù)測(cè),ARDS病人支氣管肺泡灌洗液（BALF） 中(SP-A)水平降低，而血清水平明顯增高。因此，血清SP-A可以作為預(yù)測(cè)ARDS發(fā)生的高危因素。,2. 抗IL-8/IL-8復(fù)合物,具有ARDS高危因素的病人中，BALF抗IL-8/IL-8復(fù)合物含量越高，發(fā)生ARDS的幾率越大，死亡率也越高。與PMNs在肺泡的濃度呈正相關(guān)。,3. HT156,ALI發(fā)病機(jī)理中，肺泡上皮屏障的損傷處于中心位置，HT156是人類I

51、型肺泡上皮細(xì)胞膜蛋白成分。ALI病人肺水腫液及血漿中含量數(shù)倍于正常人，表明HT156可以作為肺泡上皮損傷的生化標(biāo)記物，有助于預(yù)測(cè)ALI的發(fā)生。,,目前正在進(jìn)行的治療探索,抗氧化劑： N－乙酰半胱氨酸（NAC），谷胱甘肽、VitE、VitC高頻通氣ß腎上腺素能受體興奮劑蛋白酶抑制劑中心粒細(xì)胞－內(nèi)皮黏附抑制劑補(bǔ)體抑制劑、彈性蛋白酶抑制劑IL－10、布洛酚持續(xù)大流量CVVH的作用,,,,,,Chronic obstru

52、ctive pulmonary disease (COPD),,Chronic bronchitis,Emphysema,,Chronic airway obstruction（diameter<2mm）,COPD 患病率（1990年）,India4.383.44China26.2023.70Other Asia 2.891.79Sub-Saharan Africa4.412.49Latin Americ

53、a and Caribbean3.362.72Middle Eastern Crescent2.692.83World9.347.33*From Murray & Lopez, 1996,男/1000,女/1000,,,中國(guó)城市十大死亡原因 (2003),中國(guó)農(nóng)村十大死亡原因 (2003),WHO和中國(guó)呼吸界關(guān)注COPD,世界COPD日：11月世界戒煙日：5月31日GOLD:Global Initiativ

54、e for Chronic Obstructive Lung Disease(2002,2004,2009)中國(guó)《COPD診治規(guī)范》（1997）中國(guó)《慢性阻塞性肺疾病診治指南》（2002年-2009版）,2010 - The Year of the Lung: Measure your lung health – Ask your doctor about a simple breathing test called spirom

55、etry,Symptoms,When it’s hard to breathe, it’s hard to do anythingPeople with COPD:avoid activities that they used to do more easilylimit activity to accommodate shortness of breath and other symptoms. Some activitie

56、s include:Take elevator instead of stairs.Park close by instead of walking.Avoid shopping or other similar day-to-day tasks. Stay home rather than go out with friends.,COPD的定義以及病情危重度的分級(jí),不可逆的氣流受限的疾病支氣管擴(kuò)張癥囊性纖維化肺結(jié)核

57、支氣管哮喘 除非與COPD重疊的部分外均不屬于COPD的范疇,發(fā) 病 機(jī) 制,COPD的發(fā)病機(jī)制尚未完全明了。炎癥機(jī)制:目前普遍認(rèn)為COPD以氣道、肺實(shí)質(zhì)和肺血管的慢性炎癥為特征，在肺的不同部位有肺泡巨噬細(xì)胞、T淋巴細(xì)胞（尤其是CD8＋）和中性粒細(xì)胞增加。 激活的炎癥細(xì)胞釋放多種介質(zhì)，包括白三烯B4（LTB4）、白介素8（IL－8）、腫瘤壞死因子а（TNF－а）和其他介質(zhì)。這些介質(zhì)能破壞肺的結(jié)構(gòu)和（或）促進(jìn)中性粒細(xì)胞炎癥反應(yīng)。

58、肺部的蛋白酶和抗蛋白酶失衡機(jī)制。氧化與抗氧化失衡機(jī)制。,炎癥/免疫與COPD,,炎癥/免疫與COPD,肺部的蛋白酶和抗蛋白酶失衡？,antitrypsin與COPD,ROS與COPD,Chun-zhen Zhao et al. Respiratory Medicine (2010) 104, 1391-1395.,COPD的定義以及病情危重度的分級(jí)-- COPD嚴(yán)重度的分級(jí),分級(jí),特征,分級(jí),特征,0：危險(xiǎn)狀態(tài),肺功能正常慢性癥狀

59、(咳嗽、咳痰),:輕度COPD,FEV1/FVC<70%FEV1≥80%的預(yù)計(jì)值有或沒(méi)有慢性癥狀(咳嗽、咳痰),:中度COPD,FEV1/FVC<70%30%<FEV1<80%的預(yù)計(jì)值（ⅡA：50%≤FEV1<80%的預(yù)計(jì)值ⅡB：30%≤FEV1<50%的預(yù)計(jì)值）有或無(wú)慢性癥狀(咳嗽咳痰、呼吸困難),:重度COPD,FEV1/FVC<70%FEV1<30%的預(yù)計(jì)值或FEV1&

60、lt;50%的預(yù)計(jì)值伴有呼吸衰竭或右心衰的臨床表現(xiàn),COPD,Airway obstruction, constriction or EPP Shift up,,Obstructive hypoventilation,,,,,Lack of surfactant，dysfunction of respiratory muscles,Diffision memembrane area ↓,,V/Q imbalance,,,,Restri

61、ctive hypoventilation,Diffusion disorder,,,,Functional shunt or dead space like ventilation,Pathophysiology of COPD-induced RF,§ 3Alterations of function and metabolism,外呼吸障礙,,血?dú)猱惓?,酸堿、電解質(zhì)異常,各系統(tǒng)器官反應(yīng),,,代償,失代償,總體變化趨

62、勢(shì),Acid-base imbalance and electrolyte disturbances,,呼吸衰竭,,缺 氧,CO2潴留,,,代酸,呼酸,呼堿,代堿,Effects on respiratory system,,,呼吸運(yùn)動(dòng)的變化,,,,Effects on cardiovascular system,,Mechanism of Pulmonary heart disease,,,,Respiratory failure,

63、,肺心病：右心壁增厚，右心腔擴(kuò)張,Cor pulmonale,Cor pulmonale,肺源性心臟病的熱點(diǎn)問(wèn)題,,,,,,檢索詞：pulmonary hypertension 2010 review hypoxia,,,Effects on central nervous system,,,呼吸衰竭,肺性腦病(pulmonary encephalopathy),,+,,Pulmonary encephalopathy is de

64、fined as the neuropsychiatric syndrome caused by respiratory failure,Effects on kidney,,功能性腎衰,,器質(zhì)性腎衰,,RF,,,,,Effects on digestive system,,,呼吸衰竭,,胃腸粘膜出血、糜爛、潰瘍形成,,§ 4Principles of Treatment of Respiratory Insufficie