内科呼吸全册配套完整课件3

内科呼吸全册配套完整课件3ChronicObstructivePulmonaryDisease(COPD)

慢性阻塞性肺疾病CharacterofCOPDChronicbronchitis

andemphysemaChronicObstructivePulmonaryDisease(chronic,cough,sputum,dyspnea)

CharacterofCOPDChronicbronchitis慢支+emphysema肺气肿1.notfullyreversible

airflowlimitation不完全可逆气道阻塞2.anabnormalinflammatoryresponse(Includerespiratoryandsystemic)异常炎症反应

RelationshipofCOPDandChronicbronchitis,AsthmaorEmphysemaNewDefinitionCOPDisapreventableandtreatablediseasestatecharacterizedbyairflowlimitationthatisnotfullyreversible气流受限不完全可逆.Theairflowlimitationisusuallyprogressive进行性andisassociatedwithanabnormalinflammatoryresponse异常炎症反应

ofthelungstonoxiousparticlesorgases,primarilycausedbycigarettesmoking.AlthoughCOPDaffectsthelungs,italsoproducessignificantsystemicconsequences全身并发症.GOLD2006慢性阻塞性肺疾病是一种可预防、可治疗的常见疾病特征为持续存在的气流受限气流受限呈进行性发展，伴有气道和肺对有害颗粒或气体所致慢性炎症反应的增加急性加重和合并症影响患者整体疾病的严重程度GOLD2011

COPD的定义（GOLD2011)7肺充气过度肺泡附着丧失气道弹性回缩能力丧失支气管平滑肌收缩力增加气流受限COPD是一种以炎症为核心的

多因素构成的疾病杯状细胞增生/化生粘液腺肥大支气管平滑肌增多气道纤维化肺泡破坏结构改变炎症细胞的数量/活性增加:

-CD8+T淋巴细胞

-中性粒细胞

-血液单核细胞肺泡巨噬细胞

-肥大细胞炎症介质增多:

-IL-8

-TNF-

蛋白酶/抗蛋白酶失衡气道炎症营养不良体重减轻骨骼肌受累骨质疏松因心血管疾病死亡全身效应粘液纤毛功能障碍气道粘膜损伤粘液产生过多粘液清除减少肺部炎症全身炎症靶器官

肺部炎症通过全身炎症，

引起全身效应WhyCOPDisImportant?COPDistheonlychronicdiseasethatisshowingprogressiveupwardtrendinbothmortalityandmorbidityItisexpectedtobethethirdleadingcauseofdeathby2020Approximately8%Chineseabove15arecurrentlysufferingformCOPD*PercentChangeinAge-AdjustedDeathRates,U.S.,1965-199800.51.01.52.02.53.0Proportionof1965Rate1965-19981965-19981965-19981965-19981965-1998–59%–64%–35%+163%–7%CoronaryHeartDiseaseStrokeOtherCVDCOPDAllOtherCausesDefinition:Inflammationofbronchiandthesurroundingtissue.Feature:

chronicmucushypersecretion粘液分泌亢进andcough咳嗽.ChronicBronchitis慢性支气管炎Etiology病因

Exposure外因Tobaccosmoke吸烟Occupationaldustsandchemicals职业Infections感染Socio-economicstatus经济HostFactors内因Genes基因Hyper-responsiveness高反应性Lunggrowthanddefensemechanism肺发育smokerslung–NormalLungClinicalmanifestation

symptomsCharacter特征:chroniconset,recurrentattackandlongcourseofdiseaseMainsymptoms主要症状:

cough咳:chronic,longterm,repeated

expectoration痰:mucoidsputum,purulentsputumwheninfection

wheezing喘:seeninsomepatientsClinicalmanifestation

Sign体征:

1.noobvioussigninearlystage2.sometimesmoistrales湿罗音andrhonchi(sonorous)干罗音beheard,orwheezing哮鸣

Examination

Chestx-rayimagingExamination

Pulmonaryfunctiontest肺功能:maybenormalinearlystage.FEV75%decreasedwhensmallairwayobstruction.Graduallyobstructiveairwayfunctionappeared.Bloodroutine血常规:elevatedneutrophiloreosinophilSputumexamination痰检:bacterialcultureguideantibiotictreatmentDiagnosis诊断标准Persistenceofcoughandexcessivemucussecretionformostdaysoutof3monthsinatleast2successiveyears（≥3m/yⅹ2y）,excludingotherchroniclungdiseases(TB,Bronchiectasis)NotenoughcourseofdiseasebutdefinitechestimagingorlungfunctionType分型Typing:1、simple：cough,sputum2、wheezing：withwheezing(actuallyChronicbronchitisplusasthma)PartiallyobstructionofbronchiallumenEasilyinhaledduetoenlargementoflumenwheninspiredHardtoexhaleduetomorenarrowingoflumenwhenexspiredDilationofterminalairwayduetohigherPressureChronicbronchitisemphysemaContributingfactor

协同因素Poorlynutritionofalveoliorrespiratorybronchioleduetodecreasedbloodsupplybecauseofoppressionofhighairwaypressure血供减少Damagedbronchialcartilageandleadtothelossofsupportingfunction软骨损伤Increasedproteinaseduetochronicairwayinflammationorsmoking炎症蛋白酶Others:Alpha1-AntitrypsinDeficiencyCigarettesmokeAlveolarmacrophageNeutrophilPROTEASESAlveolarwalldestruction(Emphysema)Mucushypersecretion(Chronicbronchitis)PROTEASEINHIBITORSNeutrophilchemotacticfactors

CELLULARMECHANISMSOFCOPD

NeutrophilelastaseCathepsinsMatrixmetalloproteinasesCytokines(IL-8)Mediators(LTB4)4))?CD8+lymphocyte-MCP-1

NeutrophilelastaseCathepsinsMMP-1,MMP-9,MMP12Granzymes,perforinsOthers……..PROTEASE-ANTIPROTEASEIMBALANCEINCOPD

1-AntitrypsinSLPIElafinTIMPsPathologyfeature

Alveolarwallbecamethinness肺泡壁薄Alveolarsacenlargement肺泡扩大ruptureofalveoliandformationofbleb肺泡破裂融合PathologicalCategorize

病理类型PanlobularEmphysema全小叶型Centrilobularemphysema小叶中央型Inpanlobularemphysema,theenlargementanddestructionofairspaceinvolvetheacinusmoreorlessuniformly.Incentrilobularemphysema,respiratorybronchiolesareselectivelyanddominantlyinvolved.DefinitionofCOPDcharacterisedbyairflowlimitationthatisnotfullyreversible.TheairflowlimitationisusuallyprogressiveSomedefinitedisease(cysticfibrosisordiffusepanbronchiolitis)haveairflowlimitationbutisnotCOPDChronicsimplebronchitisorasthmaevensomeemphysemawithoutairflowlimitationisnotCOPDCOPDPathophysiology

病生机制Airflowobstruction/airwaynarrowingmucuspluggingairwayinflammation,edema,fibrosisairwaycollapsibilityduetoalveolarwalldestructionbronchospasmHyperinflationGasexchangedefectsMild-moderatedisease

PaO2Severedisease

PaCO2COPDPathophysiologyDynamiclungfunctionairflowobstruction

FEV1,

FEV1/FVChyperreactivity 15-20%prevalenceStaticlungfunctionhyperinflation

TLC,FRCgas-trapping

RVGasexchangeandtheratioofventilation-perfusionmild-modCOPD hypoxaemiasevere(FEV1<1L) hypercapniaemphysema

DLco

ClinicalmanifestationSymptom1.cough,sputumand/orwheezing咳,痰,喘2.graduallyprogressivedyspneaorshortnessofbreath进行性加重的呼吸困难3.Chestpainortightness胸痛或紧缩感ClinicalmanifestationSign:1.notobviousinearlystage2.typicalsign:barrelchest桶状胸,decreasedchestmovement胸廓运动下降,diminishedtactilefremitus触觉语音下降,Hyperresonance过清音,decreasedvesicularbreathsound肺泡呼吸音下降andprolongexpiration呼气延长orwheeze哮鸣音examination

Spirometry肺量计DiagnosisAssessingseverityAssessingprognosisMonitoringprogressionFEV1/FVC,FEV1%predicted

toestimateobstructionandseverity。BronchodilatorReversibilityTesting:todetectthereversibility,afterbronchodilator,

FEV1/FVC<70%，FEV1%predicted<80%，representnottotallyreversible。Others:RV、TLC

andRV/TLCChestX-ray：ECG：Bloodgas：todetectrespiratoryfailure.Bloodroutineandsputumexamination：IntercostalspacewideningDepressionandflatteningofthediaphragmBluntingofthecostophrenicangleIrregularradiolucencyofthelungfieldShadowoftheheartnarrowingPlainchestradiograph胸部平片low,flatdiaphragms,retrosternalairspace↑,hyperlucencyDiagnosis

evidence：1、smokingforlongtime2、chronicbronchitis+graduallyprogressivedyspnea3、sign：emphysema4、PFT:airwayflowlimitationCOPDclassificationbasedonspirometry肺功能分级

GOLDSPIROMETRYisnottosubstituteforclinicaljudgmentintheevaluationoftheseverityofdiseaseinindividualpatients.SeverityPostbronchodilatorFEV1/FVCPostbronchodilatorFEV1%predictedMildCOPD<0.7>80ModerateCOPD<0.750-80SevereCOPD<0.730-50VerysevereCOPD<0.7<30ClinicalFeaturesofCOPDPatientsMildCOPD:noabnormalsigns,smokerscough,littleornobreathlessnessModerateCOPD:breathlessnesswith/withoutwheezing,coughwith/withoutsputumSevereCOPD:breathlessnessonanyexertion/atrest,wheezeandcoughprominent,lunginflationusual,cyanosis,peripheraledema,andpolycythemiainadvanceddisease评估方法的改变GOLD2006:COPD严重程度是根据肺功能来分级缺陷：肺功能级别不同的患者发生急性加重的频率、住院率及病死率是不一样的，但对于特定的个体，肺功能并不是衡量患者呼吸困难、运动耐力和健康状态的可靠指标。GOLD2011修订版：使用分期（grade）保留COPD的肺功能分级系统，因为FEV1仍是预测未来风险的重要因素。加入症状、风险等综合评估。43症状（mMRCorCAT评分）如果mMRC0-1orCAT<10

较少症状(AorC)如果mMRC>2orCAT>10

较多症状(BorD)STEP1：评估症状(C)(D)(A)(B)mMRC0-1CAT<10mMRC>2CAT>

10GOLD201144CAT（COPD评估测试）我从不咳嗽○1○2○3○4○5我一直咳嗽我一点痰也没有○1○2○3○4○5我有很多很多痰我一点也没有胸闷的感觉○1○2○3○4○5我有很重的胸闷的感觉当我爬坡或爬一层楼时，我并不感到喘不过气来○1○2○3○4○5当我爬坡或爬一层楼时，我感觉非常喘不过气来我在家里的任何劳动都不受慢阻肺的影响○1○2○3○4○5我在家里的任何活动都很受慢阻肺的影响每当我外出时就外出○1○2○3○4○5因为我有慢阻肺，我所以从来没有外出过我睡眠非常好○1○2○3○4○5因为我有慢阻肺，我的睡眠非常不好我精力旺盛○1○2○3○4○5我一点精力都没有评分＞3020＜评分≤3010＜评分≤20＜10分疾病状态非常严重严重中等病情轻微45呼吸困难指数（mMRC）46Risk

(GOLDClassificationofAirflowLimitation)Risk

(Exacerbationhistory)>21

0(C)(D)(A)(B)4321

Symptoms(mMRC，CAT)低风险（AorB）气流受限1or20或1次急性加重/年高风险(CorD)气流受限3or4≥2次急性加重/年只要出现一次由急性加重导致的住院即可被视为高风险STEP2：评估急性加重GOLD201347Stageofdisease分期AcuteExacerbations急性加重期Stable

stage稳定期COPD急性加重（AECOPD)GOLD2011

AECOPD是一次急性事件，特征是COPD患者呼吸系统症状的恶化，而且是超出每日正常的变化，导致用药方案的改变定义降低患者的生活质量症状和肺功能的恢复延迟数周加剧了肺功能的下降速度与死亡增加有关，尤其是需要住院的患者加重社会经济负担重要性4980%感染因素所致细菌感染40-60%病毒感染30%非典型病原体5-10%20%非感染因素所致环境因素服药依从性差80%20%HoussetBetal.InterJAntimicrobialAgents.2007;29(suppl1):s11-s16.AECOPD的病因50致病菌平均值(%)范围(%)流感嗜血杆菌352-69卡他莫拉菌162-33肺炎链球菌164-38铜绿假单胞菌92-35汇总结果来自54项使用抗菌药物治疗AECOPD的研究MartinezFJetal.ExpertRev.AntiInfect.Ther.2006;4:101–124流感嗜血杆菌是最常见的致病菌51组别病原微生物抗菌药物I级及Ⅱ级COPD急性加重流感嗜血杆菌、肺炎链球菌、卡他莫拉菌青霉素、β-内酰胺酶/酶抑制剂、大环内酯类、第1/2代头孢菌素、多西环素、左氧氟沙星等，一般可口服Ⅲ级及Ⅳ级COPD急性加重；无铜绿假单孢菌感染危险因素流感嗜血杆菌、肺炎链球菌、卡他莫拉菌、肺炎克雷伯菌、大肠杆菌、肠杆菌属

-内酰胺类／酶抑制剂、第2/3代头孢菌素、氟喹诺酮类(莫西沙星，左氧氟沙星及加替沙星)Ⅲ级及Ⅳ级COPD急性加重；有铜绿假单孢菌感染危险因素以上细菌及铜绿假单胞菌第3代头孢菌素、亚胺培南、美洛培南等，也可联合用氨基糖苷类、氟喹诺酮类(环丙沙星)中华医学会呼吸病学分会慢性阻塞性肺疾病学组.2007年(修订版)中华医学会呼吸病学会AECOPD推荐用药52ComplicationsofCOPD

并发症CorPulmonale

肺心病syncope,hypoxia,pedaledema,passivehepaticcongestion,anddeath.AcuteExacerbations急性加重Chronicrespiratoryfailure呼吸衰竭Polycythemia

–hypoxia红细胞增多症Pneumothorax气胸Differentialdiagnosis

鉴别诊断Bronchialasthma哮喘:reversibilityoftheairflowBronchiectasis支扩:especiallymildpatients,chroniccoughandmucussputumPulmonaryTB肺结核：positiveanti-fastsmearBronchogeniccarcinoma肺癌：Emphysemaduetoothercause其它肺气肿:forcompensationorelder

ManagementofCOPDPreventdeclineinFEV1

延缓FEV1下降Reducemortality降低死亡率Improvequalityoflife改善生存质量

symptoms

exercisetolerance

exacerbations Minimalside-effectsGoals治疗目标

缓解症状提高运动耐力

改善健康状况

预防疾病进展预防和治疗急性加重降低死亡率GOLD

2013缓解症状降低风险GOLD提出稳定期COPD的治疗目标原则：根据患者症状严重程度、急性加重风险、药物可获得性及患者对药物疗效反应进行个体化治疗56Non-pharmacologicTherapies

非药物治疗AdjustmentTherapy&Education教育AvoidanceofTobacco&Pollution戒烟Vaccination疫苗Nutrition营养LungVolumeReductionorTransplantExercise&Rehabilitation康复COPDSmokingcessation戒烟Physicianinterventioncritical最关键干预措施MultidisciplinaryapproachWithdrawal anxiety,irritability,difficulty concentrating,sleepdisruption, fatigue,drowsiness,depressionNicotinereplacement

withdrawalsymptomsnicotinegum(2mg=cigarette)transdermalnicotinepatchesx8wks20-40%/6mosvs5-20%/6moswithplaceboFEV1AgeFletcherCandPetoR,BMJ1977;1:1645-1648.ImagerycourtesyO’DonnellD非药物治疗康复治疗：改善活动耐力，乏力和呼吸困难症状。长期家庭氧疗：流量1-2L/min,>15小时/天，适用于极重度伴有慢性呼衰的患者，能够改善生存率。GOLD

201360COPD:Pharmacology

药物治疗Bronchodilators支气管扩张剂:

2-agonistbronchodilators激动剂Theophylline茶碱Corticosteroids激素Longtermoxygentherapy长期氧疗ManagementofCOPDexacerbations急性发作期处理COPD:Pharmacology

2-agonistbronchodilators

激动剂Rapid-acting2-agonists速效salbutamol,terbutalinesymptomaticrelief pre-exertional2puffs4-6x/dprn minimalriskLongacting

2-agonists长效salmeterol,formoterolregulartherapy1-2puffsbid benefit:

activity/exertion,QOLCOPD:PharmacologyAnticholinergicbronchodilators抗胆碱类BenefitsvsRisksRegulartherapySymptomaticbenefit?

exacerbationsMinimals/e drymouth,urinaryretentionAgentsIpratropium/Atrovent 4-6puffsqidTiotropium/Spiriva 1puffQDCOPD:PharmacologyTheophylline茶碱Multipleeffectsbronchodilation,respiratorystimulant,improvedcardiovascularfunction,improveddiaphragmfunctionLimitedrolebecauseofnarrowtherapeuticwindows/e GI,CNS,cardiacOD-biddosingwithlong-actingpreparationsCOPD:PharmacologyInhaledSteroids吸入糖皮质激素SymptomaticCOPDpatientswith“asthmatic”tendency(20%)FEV1<50%predictedandrepeatedexacerbationsrequiringantibioticsand/ororalglucocorticosteroids(EvidenceB)?OralsteroidrespondersExacerbationsperyear

0CAT<10mMRC0-1

GOLD4

CAT>

10mMRC>

2GOLD3GOLD2GOLD1SAMAprnor

SABAprnLABAor

LAMAICS+LABAorLAMACOPD稳定期药物治疗-首选ABDCICS+LABAand/or

LAMA©2014GlobalInitiativeforChronicObstructiveLungDisease2ormore

or

>1leadingtohospitaladmission1(notleadingtohospitaladmission)66COPD:ExacerbationsManagement急性加重处理Identifycause明确诱因Infection----最常见但不是唯一的诱因“Infectious”bronchitiscommoncauseMostcommonlyviralBacteria-S.pneumonia,H.influenzae,M. catarrhalisAntibioticsif2of3:

dyspnea,

sputum volume,or

purulenceAgents Clavulan,cefuroxime, macrolides,FQsAECOPD治疗-氧疗

氧疗是AECOPD住院患者的基础治疗吸入氧浓度不宜过高,需注意可能发生潜在的CO2潴留及呼吸性酸中毒。氧疗30min后应复查动脉血气，以确认氧合满意，且未引起CO2

潴留和(或)呼吸性酸中毒在有给氧设施情况下,吸入雾化液最好在氧流量6~8L/min的条件下给予雾化吸入AECOPD诊治中国专家共识（2014年修订版）.国际呼吸杂志,2014,34(1):1-11.GOLD201468AECOPD治疗-支气管扩张剂首选短效支气管扩张剂为β2受体激动剂,若效果不显著,建议加用抗胆碱能药物长效支气管扩张剂合并/不合并吸入糖皮质激素在急性加重时的治疗效果不确定。患者接受机械通气治疗时,可通过特殊接合器进行吸入治疗。由于药物颗粒可沉淀在呼吸机管道内,因此所需药量为正常的2~4倍。静脉使用甲基黄嘌呤类药物(茶碱或氨茶碱)为二线用药,适用于对短效支气管扩张剂疗效不佳以及某些较为严重的AECOPD患者。AECOPD诊治中国专家共识（2014年修订版）.国际呼吸杂志,2014,34(1):1-11.GOLD2014692014GOLD加重期管理中关于糖皮质激素的更新推荐使用泼尼松30~40mg/d，10~14天改为推荐使用泼尼松40mg/d连续5天（B类证据），尽管没有充足的数据得出确切的结论关于最佳的激素治疗AECOPD持续时间。单独雾化布地奈德可替代口服激素。雾化镁剂（硫酸镁等）作为沙丁胺醇的辅助来治疗AECOPD对于FEV1改善是无效的。70目前不推荐应用抗病毒药物治疗AECOPD除扎那米韦和金刚烷胺能够有效地治疗流感之外,其他所有抗病毒药物均未证实有临床治疗效应。目前没有任何抗病毒药物批准用于治疗鼻病毒属感染,尤其是鼻病毒属感染诱发的AECOPD。抗病毒治疗仅适用于出现流感症状(发热、肌肉酸痛、全身乏力和呼吸道感染)时间小于2d、并且正处于流感爆发时期的高危患者。目前AECOPD患者发生呼吸衰竭时不推荐使用呼吸兴奋剂。只有在无条件使用或不建议使用无创通气时,可使用呼吸兴奋剂AECOPD治疗-抗病毒、呼吸兴奋剂AECOPD诊治中国专家共识（2014年修订版）.国际呼吸杂志,2014,34(1):1-11.71序贯通气的优势序贯通气显著降低：住院病死率VAP发生率住ICU时间总住院时间有创通气时间中机械通气时间722014GOLD对AECOPD并发症管理的更新住院的COPD急性加重患者会增加深静脉血栓和肺栓塞的风险，应加强预防血栓发生的措施。AECOPD患者并发肺栓塞的发病率高达24.7%。

未经治疗的肺栓塞,病死率几乎为30%。低血压和/或高流量吸氧后PaO2不能升至60mmHg以上常提示肺栓塞可能AECOPD并发肺栓塞的原因:(1)低氧血症导致继发性红细胞增多使血液黏稠度增加、血小板功能异常;(2)AECOPD患者并发肺源性心脏病时常伴有右室壁栓子形成(3)AECOPD患者的心肺储备功能差,体力活动受限,长期卧床,深静脉血栓发病率增加。73AECOPD并发肺栓塞AECOPD并发肺栓塞的预防:

对卧床、红细胞增多症或脱水的AECOPD患者,无论是否有血栓栓塞性疾病史,均需考虑使用肝素或低分子肝素抗凝治疗。AECOPD并发肺栓塞的治疗:参见肺血栓栓塞症诊断与治疗指南和急性肺血栓栓塞症诊断治疗中国专家共识。74Prognosis预后RelatetothevalueofFEV1FEV1<1.2Lsurvivefor10y，FEV1<1.0Lsurvivefor5y，FEV1<700mlsurvivefor2y

Decreasedcapillarybedandremodelingofbloodvessel血管床减少血管重构Vasospasmduetohypoxiaandhypercapnia血管痉挛Resistanceofbloodflowincreaseduetohighbloodvolumeandviscosity血粘度增高IncreasedResistanceofPAandpulmonaryHypertension肺动脉高压IncreasedRVcardiacloadandthickeningofRV右心负荷增加右室肥厚FailureofRVchronicpulmonaryheartdisease慢性肺心病Analterationinthestructureorfunctionoftherightventricle右室结构功能改变resultingfrom源自diseaseaffectingthestructureorfunctionofthelung影响肺结构和功能的疾病,exceptwhenthisalterationresultsfromdiseaseoftheleftheartorcongenitalheartdisease.chronicpulmonaryheartdisease

bronchial,lungorchestdisorder

resistance

increasepressureofPArisehypertrophyofRV

dilationofRV

failureofRVEtiology病因Diseaseaffectingairwayorlungparenchyma支气管肺疾病：COPD,asthma,TB,pulmonaryfibrosisDiseaseaffectingthethoraciccage胸腔疾病：kyphoscoliosis,thoracoplasty,neuromusculardiseasecausingmuscleweaknessDiseaseaffectingpulmonaryvasculature肺血管疾病：primarypulmonaryhypertension,polyarteritis,SLEHypoventilatorydisorders：sleepapneasyndrome睡眠呼吸暂停综合征Mechanismandpathophysiologicalfeatures导致肺血管阻力升高和肺动脉压力升高的因素

1、vasospasm血管痉挛：functional，mainlyduetohypoxia,hypercapniaandacidosis,ispartiallyreversible.2、bloodwallthickeningandlumendecreased血管壁厚:remodelingofvesselduetochronicarteritis.3、highalveolarpressurecausingcompressionofPulmonarycapillary肺泡压高致血管受压：byemphysema。4、destroyofpulmonarycapillarybed血管床破坏：byemphysemaorbleb.5、increasedbloodvolumeandviscosity血粘度高.StandardofPAHMeanPulmonaryarterypressureatrest≥20mmHg

overtPAH；PAPatrest＜20mmHg，onexertion>30mmHg

latentPAH。Clinicalpresentation表现Signandsymptomoftheunderlyingdisease基础疾病表现：Dyspnea呼吸困难isafrequentsymptomandisassociatedwithhypoxia低氧症andhypercapnia高二氧化碳症.Butinmanypatients,especialythosewithfibroticlungdiseaseorvasculaobstruction,dyspneaisnotnecessaryaccompaniedbyrestinghypoxemia.ClinicalpresentationManifestationofPAH肺动脉高压表现：

1、P2accentuationP2亢进:aloudpulmoniccomponentoftheS2.

2、auxiliaryexamination辅助检查如肺动脉段突出：seeninchestroentgenogram.ClinicalpresentationHypertrophyofRV右室肥厚表现：

1、palpitationonexertion活动后心悸2、anginalchestpain胸痛:insomeseverePHD,notusuallyresponsetonitrate

3、aloudheartbeatsoundunderxiphoid剑突下心音增强4、auxiliaryexamination:X-ray,ECGandUCG辅助检查ClinicalpresentationEnlargementandfailureofRV右室扩大衰竭：

1、systolicmurmuralongtheleftsternalborder胸骨左侧杂音:relativetricuspidinsufficiencyorregurgitation；

2、obstructionofsuperiorvenousreturn上腔静脉回流受阻：distensionofjugularvein（？）；

3、obstructionofinferiorvenousreturn下腔静脉回流受阻:enlargementofliver肝大（？）,edemaoflowerextremity水肿,ascites腹水ClinicalpresentationPresentationofrespiratoryfailure呼吸衰竭表现:Clinicalstage临床分期Compensationoflungandcardiacfunction肺心代偿期

mainlypresentationofunderlyingdiseaseandPAHandhypertrophyofRV。Decompensationoflungandcardiacfunction失代偿期

mainlyexhibitthemanifestationofrespiratoryfailureandfailureofRV。Examinationtools检查手段

Roentgenogram胸片,ECGandechocardiography超声心动图——assistingdiagnosis（helpfulforfindingPAH,hypertrophyofRV）Otherexamination：bloodgasanalysis血气（forrespiratoryfailure）、bloodroutine血常规（infection）、lungfunction肺功能、sputumculture痰培养（guidetheuseofantibiotics）。DistensionofrightdescendingPA,anditsdiameter≥15mm右下肺动脉宽；Theratioofdiameterofbloodtobronchi≥1.07；ProtrusionoflefthilarPA；EnlargementofRVRightaxisdeviation电轴右偏clockwiserotationoftheelectricaxis顺种转位(R/SamplitudeinV1>1,inV5<1)Rv1+Sv5≥1.05mVP-pulmonalepattern肺性P波(anincreaseinPwaveamplitudeinII,III,AVF)Echocardiography超声心动图1、innerdiameterofRVoutflow右室流出道(≥30mm)，2、RVinternaldimension右室内径(≥20mm)，3、RVanteriorwallthickening右室壁厚4、enlargementofrightatrium右房大Differentialdiagnosis

鉴别诊断Coronaryarterydisease冠心病：canexisttogether.Rheumaticheartdisease风心病:systolicmurmur.Primarycardiomyopathy心肌病：accompaniedwithdistensionofwholeheart.Complication合并症Pulmonaryencephalopathy肺脑：Acid-baseimbalanceandelectrolytedisturbance酸碱失衡：Arrhythmia心律失常：Shock休克：Alimentaryhemorrhage消化道出血：Disseminatedintravascularcoagulation（DIC）：Treatment

原发病Treatmentoftheunderlyingdisease:forexample,treatmentofinfectionandbronchodilationinCOPD.呼吸衰竭Treatmentofrespiratoryfailure:mostimportanttherapeuticmeasure.右心衰Treatmentofcardiacfailure:especiallywhenabovemeasurenoresponseorseriouscondition.TreatmentofRVfailureDiuretics利尿剂:excessivediuresiscanleadtohypokalamia低钾andmetabolicalkalosis代碱inducethedifficultyincoughingsputum痰不易咳出.Soalwaysbeusedinlowdosage小剂量andshortcourseoftherapy短疗程.TreatmentofRVfailureCardiacglycosides洋地黄类suitableforLVdysfunction适于左心衰ControversyinisolatedPHD右心衰有争论Poortoleranceduetohypoxemiaandhypokalamia,solowdosage(1/2–1/3routinedose),intravenousdrugberecommended.TreatmentofRVfailureVasodilatingagent血管扩张剂:betried试用于forintractableheartfailure.Treatmentofcomplication

并发症治疗alwaysrelatedtorespiratoryfailure.Pulmonaryencephalopathy肺脑Acid-baseimbalanceandelectrolytedisturbancearrhythmia心律失常shockalimentaryhemorrhage消化道出血DICTreatment

Nutritionalsupport营养支持治疗:Prognosis预后Unfavorableprognosis,mortality10％-15％.肺结核

PulmonaryTuberculosis甄国华同济医院呼吸内科概述Introduction

结核病是最古老的传染病之一，曾经是无药可治（卫生营养疗法）的瘟疫；

Tuberculosisisoneofthemostancientinfectiousdisease,anditstreatmentwasinefficientorlargelyempirical,suchasimprovednutrition,rest……从20世纪60年代起化学药物治疗是预防和治疗结核病最有效方法；Since1960,chemotherapyhasbeenthemosteffectivepreventionandtreatment

近二十余年来全球结核病的疫情明显回升：Theepidemicsituationoftuberculosisintheworldhasbeenincreasinginlast20years（1）客观因素：HIV感染的流行、多重耐药菌感染的增多、贫困、人口增长和移民等；

Objectivefactors:HIV,multi-drug-resistant(MDR)organism,poverty,populationpressureandimmigrant（2）主观因素：缺乏对结核病流行回升的警惕性和结核病控制复杂性的深刻认识、放松对结核病控制工作的管理、削弱对结核病控制工作的投入等。

Subjectivefactors:lackoftheguardagainsttheincreasingofthetuberculousincidence;lackoftherecognitionofthecomplexity,slackeningthemanagement,andreducingthefundingfortuberculosiscontrol.

对策——国家结核病防治规划Strategy------Nationaltuberculosiscontrolprogram核心内容：全程督导短程化学治疗Keypoint:directlyobservedtreatmentshort-course，DOTS流行病学

Epidemiology

1全球疫情

GlobalepidemicsituationTheWHOestimatesthatthereare7.9millionnewclinicalcaseseachyear,1.8milliondeathseachyearand1.8billionpersonsinfectedintheworld.

22个结核病高负担、高危险性国家，其中包括中国

22countriesofheavyburdenanddangeroftuberculosis,includingChina

2我国疫情

EpidemicsituationinChina

（1）高感染率

Highinfectionrate

（2）高患病率

Highmorbidityrate

（3）高耐药率

Highdrugresistancerate

（4）死亡人数多

Largenumberofdeaths

（5）递降率低

Lowdegradationrate

（6）中青年患病多

Largenumberofyoungandmiddle-agepatients

（7）地区患病率差异大

Bigdifferenceofmorbidityrateamongregions

（8）实施DOTS项目的地区患病率低

LowermorbidityrateintheregionpracticingDOTSprogram结核分枝杆菌TuberclebacilliMycobacteriumtuberculosisDiscoveredbyDr.Kochin1882Acid-fastAFB-Ziehl-Nielsonstain分类上属于放线菌目、分支杆菌科、分支杆菌属，包括人型、牛型、非洲型和鼠型4类。Categorization:Actinomycetales,Mycobacteriaceae,Mycobacterium,andnamedMycobacteriumtuberculosiscomplex,includingHuman,bovine,aficanum,andmurine

1多形性

Polymorphism2抗酸性抗酸染色阳性可作为镜检依据

Acidfastnessacid-faststainingpositive3生长缓慢培养时间长，增殖一代15-20小时，2～8周在培养基上形成菌落。

Slowgrowthcultureperoidislong,2-8weeks

4抵抗力强注意消毒灭菌方法

Strongpowerofresistance70%alcohol,ultraviolet

5菌体结构复杂

Complexstructureofcellwall结核病在人群中的传播Thetransmissionoftuberculosisamongpopulation1传染源

Infectionsources

2传播途径

Routeoftransmission

3易感人群

Susceptiblepopulation

4影响传染性的因素

Factorsaffectinginfection

5化学治疗对结核病传染性的影响

Affectingthetuberculousinfectionbychemotherapy结核病的发生与发展Pathogenesisoftuberculosis肺结核病自然过程示意图1原发性结核和继发性结核Primarytuberculosisandsecondarytuberculosis2结核病细胞免疫和迟发型变态反应

Cellmediatedimmunity(CMI)anddelayedtypehypersensitivity(DTH)

2至3天后局部红肿、深溃疡，播散至全身，死亡初次给予少量结核菌感染,4~6周后再给予同等量结核菌感染：++10至14天后局部红肿、浅溃疡，愈合Kochphenomenon初次即给予一定量结核菌感染病理学Pathology1基本病理变化1Basicpathologicalchange（1）渗出(1)Effusion（2）增生(2)HyperplasiaTuberculousGranulomas（3）干酪样坏死

Caseousnecrosis2病理变化转归

2Pathologicalchange渗出增生干酪样坏死抵抗力下降抵抗力增强变态反应强烈纤维化硬结钙化液化、形成空洞临床表现Clinicalmanifestation症状

SymptomsPulmonarysymptomsSystemicsymptoms（1）呼吸系统症状

Pulmonarysymptoms①咳嗽、咳痰Cough,sputumCoughisthecommonestrespiratorysymptom,usuallynonproductivebutpersistent,orsputumbeingmucoidorpurulentwithsomehaemoptysis.②咯血HaemoptysisThehaemoptysisisofteninsmallamountbutcanoccasionallybeinlargeamountifabronchialarteryerodesintoacavity.

③胸痛

ChestpainorpleuriticpainDullchestpaincanbeassociatedwithmediastinallymphadenopathy,orpleuriticpainmayaccompanypleuraldisease.

④呼吸困难DyspneaDyspneaisoftenalatesymptom,occurringonlyifsignificantlungdisease,orpleuraleffusion,hasdeveloped.

（2）全身症状

Systemicsymptoms发热、乏力、不适、盗汗、纳差、消瘦等Thegeneralsymptomsincludefever,fatigue,malaise,nightsweat,anorexia,weightloss,etal.Thefeverisusuallylow-grade,andcanbecomehectic,alongwithincreasingweightlossandnightsweats,asdiseaseprogresses.体征

Physicalsigns湿罗音，实变体征，局限性哮鸣音，气管移位Clinicalsignsfromthelungarefoundonlyinmoderate/extensivediseasewithupperzonecracklesorconsolidation.Alocalizedwheezeissometimesheardinendobronchialdisease.Trachealdeviationoccurs,towardsthesideofgreatestdamageinchronicdisease.

Signofpleuraleffusion.(1)临床分型

Clinicalclassification①原发型肺结核

Primarytuberculosis

原发综合征：病灶、引流淋巴管炎和肺门淋巴结肿大

Rankecomplex:focus(Ghonlesion),draininglymphangitisandhilaradenopathy②血行播散型肺结核

Hematogenousdisseminatedpulmonarytuberculosis

急性粟粒型肺结核

Acutemiliarytuberculosis

慢性粟粒型肺结核

CrypticmiliarytuberculosisMiliaryTBLungThetypicalchestradiographshowsadiffuse,buteven,distributionofuniform1-2mmnodulesthroughoutallthelungfields.Theearlychangesofmiliarydiseasearesubtleandmaybemissed,particularlyonanoverpenetratedfilm.Insuspectedcaseshigh-resolutionCTofthethoraxhasahighersensitivity.

双肺弥漫性粟粒样改变，呈毛玻璃样③继发型肺结核

Postprimarytuberculosis

Ⅰ

浸润性肺结核

ⅠInfiltrative