內(nèi)科呼吸全冊(cè)配套完整課件3

內(nèi)科呼吸全冊(cè)配套完整課件3ChronicObstructivePulmonaryDisease(COPD)

慢性阻塞性肺疾病CharacterofCOPDChronicbronchitis

andemphysemaChronicObstructivePulmonaryDisease(chronic,cough,sputum,dyspnea)

CharacterofCOPDChronicbronchitis慢支+emphysema肺氣腫1.notfullyreversible

airflowlimitation不完全可逆氣道阻塞2.anabnormalinflammatoryresponse(Includerespiratoryandsystemic)異常炎癥反應(yīng)

RelationshipofCOPDandChronicbronchitis,AsthmaorEmphysemaNewDefinitionCOPDisapreventableandtreatablediseasestatecharacterizedbyairflowlimitationthatisnotfullyreversible氣流受限不完全可逆.Theairflowlimitationisusuallyprogressive進(jìn)行性andisassociatedwithanabnormalinflammatoryresponse異常炎癥反應(yīng)

ofthelungstonoxiousparticlesorgases,primarilycausedbycigarettesmoking.AlthoughCOPDaffectsthelungs,italsoproducessignificantsystemicconsequences全身并發(fā)癥.GOLD2006慢性阻塞性肺疾病是一種可預(yù)防、可治療的常見(jiàn)疾病特征為持續(xù)存在的氣流受限氣流受限呈進(jìn)行性發(fā)展，伴有氣道和肺對(duì)有害顆?；驓怏w所致慢性炎癥反應(yīng)的增加急性加重和合并癥影響患者整體疾病的嚴(yán)重程度GOLD2011

COPD的定義（GOLD2011)7肺充氣過(guò)度肺泡附著喪失氣道彈性回縮能力喪失支氣管平滑肌收縮力增加氣流受限COPD是一種以炎癥為核心的

多因素構(gòu)成的疾病杯狀細(xì)胞增生/化生粘液腺肥大支氣管平滑肌增多氣道纖維化肺泡破壞結(jié)構(gòu)改變炎癥細(xì)胞的數(shù)量/活性增加:

-CD8+T淋巴細(xì)胞

-中性粒細(xì)胞

-血液?jiǎn)魏思?xì)胞肺泡巨噬細(xì)胞

-肥大細(xì)胞炎癥介質(zhì)增多:

-IL-8

-TNF-

蛋白酶/抗蛋白酶失衡氣道炎癥營(yíng)養(yǎng)不良體重減輕骨骼肌受累骨質(zhì)疏松因心血管疾病死亡全身效應(yīng)粘液纖毛功能障礙氣道粘膜損傷粘液產(chǎn)生過(guò)多粘液清除減少肺部炎癥全身炎癥靶器官

肺部炎癥通過(guò)全身炎癥，

引起全身效應(yīng)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粘液分泌亢進(jìn)andcough咳嗽.ChronicBronchitis慢性支氣管炎Etiology病因

Exposure外因Tobaccosmoke吸煙Occupationaldustsandchemicals職業(yè)Infections感染Socio-economicstatus經(jīng)濟(jì)HostFactors內(nèi)因Genes基因Hyper-responsiveness高反應(yīng)性Lunggrowthanddefensemechanism肺發(fā)育smokerslung–NormalLungClinicalmanifestation

symptomsCharacter特征:chroniconset,recurrentattackandlongcourseofdiseaseMainsymptoms主要癥狀:

cough咳:chronic,longterm,repeated

expectoration痰:mucoidsputum,purulentsputumwheninfection

wheezing喘:seeninsomepatientsClinicalmanifestation

Sign體征:

1.noobvioussigninearlystage2.sometimesmoistrales濕羅音andrhonchi(sonorous)干羅音beheard,orwheezing哮鳴

Examination

Chestx-rayimagingExamination

Pulmonaryfunctiontest肺功能:maybenormalinearlystage.FEV75%decreasedwhensmallairwayobstruction.Graduallyobstructiveairwayfunctionappeared.Bloodroutine血常規(guī):elevatedneutrophiloreosinophilSputumexamination痰檢:bacterialcultureguideantibiotictreatmentDiagnosis診斷標(biāo)準(zhǔn)Persistenceofcoughandexcessivemucussecretionformostdaysoutof3monthsinatleast2successiveyears（≥3m/yⅹ2y）,excludingotherchroniclungdiseases(TB,Bronchiectasis)NotenoughcourseofdiseasebutdefinitechestimagingorlungfunctionType分型Typing:1、simple：cough,sputum2、wheezing：withwheezing(actuallyChronicbronchitisplusasthma)PartiallyobstructionofbronchiallumenEasilyinhaledduetoenlargementoflumenwheninspiredHardtoexhaleduetomorenarrowingoflumenwhenexspiredDilationofterminalairwayduetohigherPressureChronicbronchitisemphysemaContributingfactor

協(xié)同因素Poorlynutritionofalveoliorrespiratorybronchioleduetodecreasedbloodsupplybecauseofoppressionofhighairwaypressure血供減少Damagedbronchialcartilageandleadtothelossofsupportingfunction軟骨損傷Increasedproteinaseduetochronicairwayinflammationorsmoking炎癥蛋白酶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肺泡擴(kuò)大ruptureofalveoliandformationofbleb肺泡破裂融合PathologicalCategorize

病理類型PanlobularEmphysema全小葉型Centrilobularemphysema小葉中央型Inpanlobularemphysema,theenlargementanddestructionofairspaceinvolvetheacinusmoreorlessuniformly.Incentrilobularemphysema,respiratorybronchiolesareselectivelyanddominantlyinvolved.DefinitionofCOPDcharacterisedbyairflowlimitationthatisnotfullyreversible.TheairflowlimitationisusuallyprogressiveSomedefinitedisease(cysticfibrosisordiffusepanbronchiolitis)haveairflowlimitationbutisnotCOPDChronicsimplebronchitisorasthmaevensomeemphysemawithoutairflowlimitationisnotCOPDCOPDPathophysiology

病生機(jī)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進(jìn)行性加重的呼吸困難3.Chestpainortightness胸痛或緊縮感ClinicalmanifestationSign:1.notobviousinearlystage2.typicalsign:barrelchest桶狀胸,decreasedchestmovement胸廓運(yùn)動(dòng)下降,diminishedtactilefremitus觸覺(jué)語(yǔ)音下降,Hyperresonance過(guò)清音,decreasedvesicularbreathsound肺泡呼吸音下降andprolongexpiration呼氣延長(zhǎng)orwheeze哮鳴音examination

Spirometry肺量計(jì)DiagnosisAssessingseverityAssessingprognosisMonitoringprogressionFEV1/FVC,FEV1%predicted

toestimateobstructionandseverity。BronchodilatorReversibilityTesting:todetectthereversibility,afterbronchodilator,

FEV1/FVC<70%，F(xiàn)EV1%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肺功能分級(jí)

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評(píng)估方法的改變GOLD2006:COPD嚴(yán)重程度是根據(jù)肺功能來(lái)分級(jí)缺陷：肺功能級(jí)別不同的患者發(fā)生急性加重的頻率、住院率及病死率是不一樣的，但對(duì)于特定的個(gè)體，肺功能并不是衡量患者呼吸困難、運(yùn)動(dòng)耐力和健康狀態(tài)的可靠指標(biāo)。GOLD2011修訂版：使用分期（grade）保留COPD的肺功能分級(jí)系統(tǒng)，因?yàn)镕EV1仍是預(yù)測(cè)未來(lái)風(fēng)險(xiǎn)的重要因素。加入癥狀、風(fēng)險(xiǎn)等綜合評(píng)估。43癥狀（mMRCorCAT評(píng)分）如果mMRC0-1orCAT<10

較少癥狀(AorC)如果mMRC>2orCAT>10

較多癥狀(BorD)STEP1：評(píng)估癥狀(C)(D)(A)(B)mMRC0-1CAT<10mMRC>2CAT>

10GOLD201144CAT（COPD評(píng)估測(cè)試）我從不咳嗽○1○2○3○4○5我一直咳嗽我一點(diǎn)痰也沒(méi)有○1○2○3○4○5我有很多很多痰我一點(diǎn)也沒(méi)有胸悶的感覺(jué)○1○2○3○4○5我有很重的胸悶的感覺(jué)當(dāng)我爬坡或爬一層樓時(shí)，我并不感到喘不過(guò)氣來(lái)○1○2○3○4○5當(dāng)我爬坡或爬一層樓時(shí)，我感覺(jué)非常喘不過(guò)氣來(lái)我在家里的任何勞動(dòng)都不受慢阻肺的影響○1○2○3○4○5我在家里的任何活動(dòng)都很受慢阻肺的影響每當(dāng)我外出時(shí)就外出○1○2○3○4○5因?yàn)槲矣新璺?，我所以從?lái)沒(méi)有外出過(guò)我睡眠非常好○1○2○3○4○5因?yàn)槲矣新璺?，我的睡眠非常不好我精力旺盛?○2○3○4○5我一點(diǎn)精力都沒(méi)有評(píng)分＞3020＜評(píng)分≤3010＜評(píng)分≤20＜10分疾病狀態(tài)非常嚴(yán)重嚴(yán)重中等病情輕微45呼吸困難指數(shù)（mMRC）46Risk

(GOLDClassificationofAirflowLimitation)Risk

(Exacerbationhistory)>21

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

Symptoms(mMRC，CAT)低風(fēng)險(xiǎn)（AorB）氣流受限1or20或1次急性加重/年高風(fēng)險(xiǎn)(CorD)氣流受限3or4≥2次急性加重/年只要出現(xiàn)一次由急性加重導(dǎo)致的住院即可被視為高風(fēng)險(xiǎn)STEP2：評(píng)估急性加重GOLD201347Stageofdisease分期AcuteExacerbations急性加重期Stable

stage穩(wěn)定期COPD急性加重（AECOPD)GOLD2011

AECOPD是一次急性事件，特征是COPD患者呼吸系統(tǒng)癥狀的惡化，而且是超出每日正常的變化，導(dǎo)致用藥方案的改變定義降低患者的生活質(zhì)量癥狀和肺功能的恢復(fù)延遲數(shù)周加劇了肺功能的下降速度與死亡增加有關(guān)，尤其是需要住院的患者加重社會(huì)經(jīng)濟(jì)負(fù)擔(dān)重要性4980%感染因素所致細(xì)菌感染40-60%病毒感染30%非典型病原體5-10%20%非感染因素所致環(huán)境因素服藥依從性差80%20%HoussetBetal.InterJAntimicrobialAgents.2007;29(suppl1):s11-s16.AECOPD的病因50致病菌平均值(%)范圍(%)流感嗜血桿菌352-69卡他莫拉菌162-33肺炎鏈球菌164-38銅綠假單胞菌92-35匯總結(jié)果來(lái)自54項(xiàng)使用抗菌藥物治療AECOPD的研究MartinezFJetal.ExpertRev.AntiInfect.Ther.2006;4:101–124流感嗜血桿菌是最常見(jiàn)的致病菌51組別病原微生物抗菌藥物I級(jí)及Ⅱ級(jí)COPD急性加重流感嗜血桿菌、肺炎鏈球菌、卡他莫拉菌青霉素、β-內(nèi)酰胺酶/酶抑制劑、大環(huán)內(nèi)酯類、第1/2代頭孢菌素、多西環(huán)素、左氧氟沙星等，一般可口服Ⅲ級(jí)及Ⅳ級(jí)COPD急性加重；無(wú)銅綠假單孢菌感染危險(xiǎn)因素流感嗜血桿菌、肺炎鏈球菌、卡他莫拉菌、肺炎克雷伯菌、大腸桿菌、腸桿菌屬

-內(nèi)酰胺類／酶抑制劑、第2/3代頭孢菌素、氟喹諾酮類(莫西沙星，左氧氟沙星及加替沙星)Ⅲ級(jí)及Ⅳ級(jí)COPD急性加重；有銅綠假單孢菌感染危險(xiǎn)因素以上細(xì)菌及銅綠假單胞菌第3代頭孢菌素、亞胺培南、美洛培南等，也可聯(lián)合用氨基糖苷類、氟喹諾酮類(環(huán)丙沙星)中華醫(yī)學(xué)會(huì)呼吸病學(xué)分會(huì)慢性阻塞性肺疾病學(xué)組.2007年(修訂版)中華醫(yī)學(xué)會(huì)呼吸病學(xué)會(huì)AECOPD推薦用藥52ComplicationsofCOPD

并發(fā)癥CorPulmonale

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

–hypoxia紅細(xì)胞增多癥Pneumothorax氣胸Differentialdiagnosis

鑒別診斷Bronchialasthma哮喘:reversibilityoftheairflowBronchiectasis支擴(kuò):especiallymildpatients,chroniccoughandmucussputumPulmonaryTB肺結(jié)核：positiveanti-fastsmearBronchogeniccarcinoma肺癌：Emphysemaduetoothercause其它肺氣腫:forcompensationorelder

ManagementofCOPDPreventdeclineinFEV1

延緩FEV1下降Reducemortality降低死亡率Improvequalityoflife改善生存質(zhì)量

symptoms

exercisetolerance

exacerbations Minimalside-effectsGoals治療目標(biāo)

緩解癥狀提高運(yùn)動(dòng)耐力

改善健康狀況

預(yù)防疾病進(jìn)展預(yù)防和治療急性加重降低死亡率GOLD

2013緩解癥狀降低風(fēng)險(xiǎn)GOLD提出穩(wěn)定期COPD的治療目標(biāo)原則：根據(jù)患者癥狀嚴(yán)重程度、急性加重風(fēng)險(xiǎn)、藥物可獲得性及患者對(duì)藥物療效反應(yīng)進(jìn)行個(gè)體化治療56Non-pharmacologicTherapies

非藥物治療AdjustmentTherapy&Education教育AvoidanceofTobacco&Pollution戒煙Vaccination疫苗Nutrition營(yíng)養(yǎng)LungVolumeReductionorTransplantExercise&Rehabilitation康復(fù)COPDSmokingcessation戒煙Physicianinterventioncritical最關(guān)鍵干預(yù)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非藥物治療康復(fù)治療：改善活動(dòng)耐力，乏力和呼吸困難癥狀。長(zhǎng)期家庭氧療：流量1-2L/min,>15小時(shí)/天，適用于極重度伴有慢性呼衰的患者，能夠改善生存率。GOLD

201360COPD:Pharmacology

藥物治療Bronchodilators支氣管擴(kuò)張劑:

2-agonistbronchodilators激動(dòng)劑Theophylline茶堿Corticosteroids激素Longtermoxygentherapy長(zhǎng)期氧療ManagementofCOPDexacerbations急性發(fā)作期處理COPD:Pharmacology

2-agonistbronchodilators

激動(dòng)劑Rapid-acting2-agonists速效salbutamol,terbutalinesymptomaticrelief pre-exertional2puffs4-6x/dprn minimalriskLongacting

2-agonists長(zhǎng)效salmeterol,formoterolregulartherapy1-2puffsbid benefit:

activity/exertion,QOLCOPD:PharmacologyAnticholinergicbronchodilators抗膽堿類BenefitsvsRisksRegulartherapySymptomaticbenefit?

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

0CAT<10mMRC0-1

GOLD4

CAT>

10mMRC>

2GOLD3GOLD2GOLD1SAMAprnor

SABAprnLABAor

LAMAICS+LABAorLAMACOPD穩(wěn)定期藥物治療-首選ABDCICS+LABAand/or

LAMA?2014GlobalInitiativeforChronicObstructiveLungDisease2ormore

or

>1leadingtohospitaladmission1(notleadingtohospitaladmission)66COPD:ExacerbationsManagement急性加重處理Identifycause明確誘因Infection----最常見(jiàn)但不是唯一的誘因“Infectious”bronchitiscommoncauseMostcommonlyviralBacteria-S.pneumonia,H.influenzae,M. catarrhalisAntibioticsif2of3:

dyspnea,

sputum volume,or

purulenceAgents Clavulan,cefuroxime, macrolides,FQsAECOPD治療-氧療

氧療是AECOPD住院患者的基礎(chǔ)治療吸入氧濃度不宜過(guò)高,需注意可能發(fā)生潛在的CO2潴留及呼吸性酸中毒。氧療30min后應(yīng)復(fù)查動(dòng)脈血?dú)?，以確認(rèn)氧合滿意，且未引起CO2

潴留和(或)呼吸性酸中毒在有給氧設(shè)施情況下,吸入霧化液最好在氧流量6~8L/min的條件下給予霧化吸入AECOPD診治中國(guó)專家共識(shí)（2014年修訂版）.國(guó)際呼吸雜志,2014,34(1):1-11.GOLD201468AECOPD治療-支氣管擴(kuò)張劑首選短效支氣管擴(kuò)張劑為β2受體激動(dòng)劑,若效果不顯著,建議加用抗膽堿能藥物長(zhǎng)效支氣管擴(kuò)張劑合并/不合并吸入糖皮質(zhì)激素在急性加重時(shí)的治療效果不確定?；颊呓邮軝C(jī)械通氣治療時(shí),可通過(guò)特殊接合器進(jìn)行吸入治療。由于藥物顆?？沙恋碓诤粑鼨C(jī)管道內(nèi),因此所需藥量為正常的2~4倍。靜脈使用甲基黃嘌呤類藥物(茶堿或氨茶堿)為二線用藥,適用于對(duì)短效支氣管擴(kuò)張劑療效不佳以及某些較為嚴(yán)重的AECOPD患者。AECOPD診治中國(guó)專家共識(shí)（2014年修訂版）.國(guó)際呼吸雜志,2014,34(1):1-11.GOLD2014692014GOLD加重期管理中關(guān)于糖皮質(zhì)激素的更新推薦使用潑尼松30~40mg/d，10~14天改為推薦使用潑尼松40mg/d連續(xù)5天（B類證據(jù)），盡管沒(méi)有充足的數(shù)據(jù)得出確切的結(jié)論關(guān)于最佳的激素治療AECOPD持續(xù)時(shí)間。單獨(dú)霧化布地奈德可替代口服激素。霧化鎂劑（硫酸鎂等）作為沙丁胺醇的輔助來(lái)治療AECOPD對(duì)于FEV1改善是無(wú)效的。70目前不推薦應(yīng)用抗病毒藥物治療AECOPD除扎那米韋和金剛烷胺能夠有效地治療流感之外,其他所有抗病毒藥物均未證實(shí)有臨床治療效應(yīng)。目前沒(méi)有任何抗病毒藥物批準(zhǔn)用于治療鼻病毒屬感染,尤其是鼻病毒屬感染誘發(fā)的AECOPD。抗病毒治療僅適用于出現(xiàn)流感癥狀(發(fā)熱、肌肉酸痛、全身乏力和呼吸道感染)時(shí)間小于2d、并且正處于流感爆發(fā)時(shí)期的高?；颊摺Ｄ壳癆ECOPD患者發(fā)生呼吸衰竭時(shí)不推薦使用呼吸興奮劑。只有在無(wú)條件使用或不建議使用無(wú)創(chuàng)通氣時(shí),可使用呼吸興奮劑AECOPD治療-抗病毒、呼吸興奮劑AECOPD診治中國(guó)專家共識(shí)（2014年修訂版）.國(guó)際呼吸雜志,2014,34(1):1-11.71序貫通氣的優(yōu)勢(shì)序貫通氣顯著降低：住院病死率VAP發(fā)生率住ICU時(shí)間總住院時(shí)間有創(chuàng)通氣時(shí)間中機(jī)械通氣時(shí)間722014GOLD對(duì)AECOPD并發(fā)癥管理的更新住院的COPD急性加重患者會(huì)增加深靜脈血栓和肺栓塞的風(fēng)險(xiǎn)，應(yīng)加強(qiáng)預(yù)防血栓發(fā)生的措施。AECOPD患者并發(fā)肺栓塞的發(fā)病率高達(dá)24.7%。

未經(jīng)治療的肺栓塞,病死率幾乎為30%。低血壓和/或高流量吸氧后PaO2不能升至60mmHg以上常提示肺栓塞可能AECOPD并發(fā)肺栓塞的原因:(1)低氧血癥導(dǎo)致繼發(fā)性紅細(xì)胞增多使血液黏稠度增加、血小板功能異常;(2)AECOPD患者并發(fā)肺源性心臟病時(shí)常伴有右室壁栓子形成(3)AECOPD患者的心肺儲(chǔ)備功能差,體力活動(dòng)受限,長(zhǎng)期臥床,深靜脈血栓發(fā)病率增加。73AECOPD并發(fā)肺栓塞AECOPD并發(fā)肺栓塞的預(yù)防:

對(duì)臥床、紅細(xì)胞增多癥或脫水的AECOPD患者,無(wú)論是否有血栓栓塞性疾病史,均需考慮使用肝素或低分子肝素抗凝治療。AECOPD并發(fā)肺栓塞的治療:參見(jiàn)肺血栓栓塞癥診斷與治療指南和急性肺血栓栓塞癥診斷治療中國(guó)專家共識(shí)。74Prognosis預(yù)后RelatetothevalueofFEV1FEV1<1.2Lsurvivefor10y，F(xiàn)EV1<1.0Lsurvivefor5y，F(xiàn)EV1<700mlsurvivefor2y

Decreasedcapillarybedandremodelingofbloodvessel血管床減少血管重構(gòu)Vasospasmduetohypoxiaandhypercapnia血管痙攣Resistanceofbloodflowincreaseduetohighbloodvolumeandviscosity血粘度增高IncreasedResistanceofPAandpulmonaryHypertension肺動(dòng)脈高壓IncreasedRVcardiacloadandthickeningofRV右心負(fù)荷增加右室肥厚FailureofRVchronicpulmonaryheartdisease慢性肺心病Analterationinthestructureorfunctionoftherightventricle右室結(jié)構(gòu)功能改變r(jià)esultingfrom源自diseaseaffectingthestructureorfunctionofthelung影響肺結(jié)構(gòu)和功能的疾病,exceptwhenthisalterationresultsfromdiseaseoftheleftheartorcongenitalheartdisease.chronicpulmonaryheartdisease

bronchial,lungorchestdisorder

resistance

increasepressureofPArisehypertrophyofRV

dilationofRV

failureofRVEtiology病因Diseaseaffectingairwayorlungparenchyma支氣管肺疾病：COPD,asthma,TB,pulmonaryfibrosisDiseaseaffectingthethoraciccage胸腔疾?。簁yphoscoliosis,thoracoplasty,neuromusculardiseasecausingmuscleweaknessDiseaseaffectingpulmonaryvasculature肺血管疾病：primarypulmonaryhypertension,polyarteritis,SLEHypoventilatorydisorders：sleepapneasyndrome睡眠呼吸暫停綜合征Mechanismandpathophysiologicalfeatures導(dǎo)致肺血管阻力升高和肺動(dòng)脈壓力升高的因素

1、vasospasm血管痙攣：functional，mainlyduetohypoxia,hypercapniaandacidosis,ispartiallyreversible.2、bloodwallthickeningandlumendecreased血管壁厚:remodelingofvesselduetochronicarteritis.3、highalveolarpressurecausingcompressionofPulmonarycapillary肺泡壓高致血管受壓：byemphysema。4、destroyofpulmonarycapillarybed血管床破壞：byemphysemaorbleb.5、increasedbloodvolumeandviscosity血粘度高.StandardofPAHMeanPulmonaryarterypressureatrest≥20mmHg

overtPAH；PAPatrest＜20mmHg，onexertion>30mmHg

latentPAH。Clinicalpresentation表現(xiàn)Signandsymptomoftheunderlyingdisease基礎(chǔ)疾病表現(xiàn)：Dyspnea呼吸困難isafrequentsymptomandisassociatedwithhypoxia低氧癥andhypercapnia高二氧化碳癥.Butinmanypatients,especialythosewithfibroticlungdiseaseorvasculaobstruction,dyspneaisnotnecessaryaccompaniedbyrestinghypoxemia.ClinicalpresentationManifestationofPAH肺動(dòng)脈高壓表現(xiàn)：

1、P2accentuationP2亢進(jìn):aloudpulmoniccomponentoftheS2.

2、auxiliaryexamination輔助檢查如肺動(dòng)脈段突出：seeninchestroentgenogram.ClinicalpresentationHypertrophyofRV右室肥厚表現(xiàn)：

1、palpitationonexertion活動(dòng)后心悸2、anginalchestpain胸痛:insomeseverePHD,notusuallyresponsetonitrate

3、aloudheartbeatsoundunderxiphoid劍突下心音增強(qiáng)4、auxiliaryexamination:X-ray,ECGandUCG輔助檢查ClinicalpresentationEnlargementandfailureofRV右室擴(kuò)大衰竭：

1、systolicmurmuralongtheleftsternalborder胸骨左側(cè)雜音:relativetricuspidinsufficiencyorregurgitation；

2、obstructionofsuperiorvenousreturn上腔靜脈回流受阻：distensionofjugularvein（？）；

3、obstructionofinferiorvenousreturn下腔靜脈回流受阻:enlargementofliver肝大（？）,edemaoflowerextremity水腫,ascites腹水ClinicalpresentationPresentationofrespiratoryfailure呼吸衰竭表現(xiàn):Clinicalstage臨床分期Compensationoflungandcardiacfunction肺心代償期

mainlypresentationofunderlyingdiseaseandPAHandhypertrophyofRV。Decompensationoflungandcardiacfunction失代償期

mainlyexhibitthemanifestationofrespiratoryfailureandfailureofRV。Examinationtools檢查手段

Roentgenogram胸片,ECGandechocardiography超聲心動(dòng)圖——assistingdiagnosis（helpfulforfindingPAH,hypertrophyofRV）Otherexamination：bloodgasanalysis血?dú)猓╢orrespiratoryfailure）、bloodroutine血常規(guī)（infection）、lungfunction肺功能、sputumculture痰培養(yǎng)（guidetheuseofantibiotics）。DistensionofrightdescendingPA,anditsdiameter≥15mm右下肺動(dòng)脈寬；Theratioofdiameterofbloodtobronchi≥1.07；ProtrusionoflefthilarPA；EnlargementofRVRightaxisdeviation電軸右偏clockwiserotationoftheelectricaxis順?lè)N轉(zhuǎn)位(R/SamplitudeinV1>1,inV5<1)Rv1+Sv5≥1.05mVP-pulmonalepattern肺性P波(anincreaseinPwaveamplitudeinII,III,AVF)Echocardiography超聲心動(dòng)圖1、innerdiameterofRVoutflow右室流出道(≥30mm)，2、RVinternaldimension右室內(nèi)徑(≥20mm)，3、RVanteriorwallthickening右室壁厚4、enlargementofrightatrium右房大Differentialdiagnosis

鑒別診斷Coronaryarterydisease冠心病：canexisttogether.Rheumaticheartdisease風(fēng)心病:systolicmurmur.Primarycardiomyopathy心肌?。篴ccompaniedwithdistensionofwholeheart.Complication合并癥Pulmonaryencephalopathy肺腦：Acid-baseimbalanceandelectrolytedisturbance酸堿失衡：Arrhythmia心律失常：Shock休克：Alimentaryhemorrhage消化道出血：Disseminatedintravascularcoagulation（DIC）：Treatment

原發(fā)病Treatmentoftheunderlyingdisease:forexample,treatmentofinfectionandbronchodilationinCOPD.呼吸衰竭Treatmentofrespiratoryfailure:mostimportanttherapeuticmeasure.右心衰Treatmentofcardiacfailure:especiallywhenabovemeasurenoresponseorseriouscondition.TreatmentofRVfailureDiuretics利尿劑:excessivediuresiscanleadtohypokalamia低鉀andmetabolicalkalosis代堿inducethedifficultyincoughingsputum痰不易咳出.Soalwaysbeusedinlowdosage小劑量andshortcourseoftherapy短療程.TreatmentofRVfailureCardiacglycosides洋地黃類suitableforLVdysfunction適于左心衰ControversyinisolatedPHD右心衰有爭(zhēng)論P(yáng)oortoleranceduetohypoxemiaandhypokalamia,solowdosage(1/2–1/3routinedose),intravenousdrugberecommended.TreatmentofRVfailureVasodilatingagent血管擴(kuò)張劑:betried試用于forintractableheartfailure.Treatmentofcomplication

并發(fā)癥治療alwaysrelatedtorespiratoryfailure.Pulmonaryencephalopathy肺腦Acid-baseimbalanceandelectrolytedisturbancearrhythmia心律失常shockalimentaryhemorrhage消化道出血DICTreatment

Nutritionalsupport營(yíng)養(yǎng)支持治療:Prognosis預(yù)后Unfavorableprognosis,mortality10％-15％.肺結(jié)核

PulmonaryTuberculosis甄國(guó)華同濟(jì)醫(yī)院呼吸內(nèi)科概述Introduction

結(jié)核病是最古老的傳染病之一，曾經(jīng)是無(wú)藥可治（衛(wèi)生營(yíng)養(yǎng)療法）的瘟疫；

Tuberculosisisoneofthemostancientinfectiousdisease,anditstreatmentwasinefficientorlargelyempirical,suchasimprovednutrition,rest……從20世紀(jì)60年代起化學(xué)藥物治療是預(yù)防和治療結(jié)核病最有效方法；Since1960,chemotherapyhasbeenthemosteffectivepreventionandtreatment

近二十余年來(lái)全球結(jié)核病的疫情明顯回升：Theepidemicsituationoftuberculosisintheworldhasbeenincreasinginlast20years（1）客觀因素：HIV感染的流行、多重耐藥菌感染的增多、貧困、人口增長(zhǎng)和移民等；

Objectivefactors:HIV,multi-drug-resistant(MDR)organism,poverty,populationpressureandimmigrant（2）主觀因素：缺乏對(duì)結(jié)核病流行回升的警惕性和結(jié)核病控制復(fù)雜性的深刻認(rèn)識(shí)、放松對(duì)結(jié)核病控制工作的管理、削弱對(duì)結(jié)核病控制工作的投入等。

Subjectivefactors:lackoftheguardagainsttheincreasingofthetuberculousincidence;lackoftherecognitionofthecomplexity,slackeningthemanagement,andreducingthefundingfortuberculosiscontrol.

對(duì)策——國(guó)家結(jié)核病防治規(guī)劃Strategy------Nationaltuberculosiscontrolprogram核心內(nèi)容：全程督導(dǎo)短程化學(xué)治療Keypoint:directlyobservedtreatmentshort-course，DOTS流行病學(xué)

Epidemiology

1全球疫情

GlobalepidemicsituationTheWHOestimatesthatthereare7.9millionnewclinicalcaseseachyear,1.8milliondeathseachyearand1.8billionpersonsinfectedintheworld.

22個(gè)結(jié)核病高負(fù)擔(dān)、高危險(xiǎn)性國(guó)家，其中包括中國(guó)

22countriesofheavyburdenanddangeroftuberculosis,includingChina

2我國(guó)疫情

EpidemicsituationinChina

（1）高感染率

Highinfectionrate

（2）高患病率

Highmorbidityrate

（3）高耐藥率

Highdrugresistancerate

（4）死亡人數(shù)多

Largenumberofdeaths

（5）遞降率低

Lowdegradationrate

（6）中青年患病多

Largenumberofyoungandmiddle-agepatients

（7）地區(qū)患病率差異大

Bigdifferenceofmorbidityrateamongregions

（8）實(shí)施DOTS項(xiàng)目的地區(qū)患病率低

LowermorbidityrateintheregionpracticingDOTSprogram結(jié)核分枝桿菌TuberclebacilliMycobacteriumtuberculosisDiscoveredbyDr.Kochin1882Acid-fastAFB-Ziehl-Nielsonstain分類上屬于放線菌目、分支桿菌科、分支桿菌屬，包括人型、牛型、非洲型和鼠型4類。Categorization:Actinomycetales,Mycobacteriaceae,Mycobacterium,andnamedMycobacteriumtuberculosiscomplex,includingHuman,bovine,aficanum,andmurine

1多形性

Polymorphism2抗酸性抗酸染色陽(yáng)性可作為鏡檢依據(jù)

Acidfastnessacid-faststainingpositive3生長(zhǎng)緩慢培養(yǎng)時(shí)間長(zhǎng)，增殖一代15-20小時(shí)，2～8周在培養(yǎng)基上形成菌落。

Slowgrowthcultureperoidislong,2-8weeks

4抵抗力強(qiáng)注意消毒滅菌方法

Strongpowerofresistance70%alcohol,ultraviolet

5菌體結(jié)構(gòu)復(fù)雜

Complexstructureofcellwall結(jié)核病在人群中的傳播Thetransmissionoftuberculosisamongpopulation1傳染源

Infectionsources

2傳播途徑

Routeoftransmission

3易感人群

Susceptiblepopulation

4影響傳染性的因素

Factorsaffectinginfection

5化學(xué)治療對(duì)結(jié)核病傳染性的影響

Affectingthetuberculousinfectionbychemotherapy結(jié)核病的發(fā)生與發(fā)展Pathogenesisoftuberculosis肺結(jié)核病自然過(guò)程示意圖1原發(fā)性結(jié)核和繼發(fā)性結(jié)核Primarytuberculosisandsecondarytuberculosis2結(jié)核病細(xì)胞免疫和遲發(fā)型變態(tài)反應(yīng)

Cellmediatedimmunity(CMI)anddelayedtypehypersensitivity(DTH)

2至3天后局部紅腫、深潰瘍，播散至全身，死亡初次給予少量結(jié)核菌感染,4~6周后再給予同等量結(jié)核菌感染：++10至14天后局部紅腫、淺潰瘍，愈合Kochphenomenon初次即給予一定量結(jié)核菌感染病理學(xué)Pathology1基本病理變化1Basicpathologicalchange（1）滲出(1)Effusion（2）增生(2)HyperplasiaTuberculousGranulomas（3）干酪樣壞死

Caseousnecrosis2病理變化轉(zhuǎn)歸

2Pathologicalchange滲出增生干酪樣壞死抵抗力下降抵抗力增強(qiáng)變態(tài)反應(yīng)強(qiáng)烈纖維化硬結(jié)鈣化液化、形成空洞臨床表現(xiàn)Clinicalmanifestation癥狀

SymptomsPulmonarysymptomsSystemicsymptoms（1）呼吸系統(tǒng)癥狀

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

③胸痛

ChestpainorpleuriticpainDullchestpaincanbeassociatedwithmediastinallymphadenopathy,orpleuriticpainmayaccompanypleuraldisease.

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

（2）全身癥狀

Systemicsymptoms發(fā)熱、乏力、不適、盜汗、納差、消瘦等Thegeneralsymptomsincludefever,fatigue,malaise,nightsweat,anorexia,weightloss,etal.Thefeverisusuallylow-grade,andcanbecomehectic,alongwithincreasingweightlossandnightsweats,asdiseaseprogresses.體征

Physicalsigns濕羅音，實(shí)變體征，局限性哮鳴音，氣管移位Clinicalsignsfromthelungarefoundonlyinmoderate/extensivediseasewithupperzonecracklesorconsolidation.Alocalizedwheezeissometimesheardinendobronchialdisease.Trachealdeviationoccurs,towardsthesideofgreatestdamageinchronicdisease.

Signofpleuraleffusion.(1)臨床分型

Clinicalclassification①原發(fā)型肺結(jié)核

Primarytuberculosis

原發(fā)綜合征：病灶、引流淋巴管炎和肺門(mén)淋巴結(jié)腫大

Rankecomplex:focus(Ghonlesion),draininglymphangitisandhilaradenopathy②血行播散型肺結(jié)核

Hematogenousdisseminatedpulmonarytuberculosis

急性粟粒型肺結(jié)核

Acutemiliarytuberculosis

慢性粟粒型肺結(jié)核

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

雙肺彌漫性粟粒樣改變，呈毛玻璃樣③繼發(fā)型肺結(jié)核

Postprimarytuberculosis

Ⅰ

浸潤(rùn)性肺結(jié)核

ⅠInfiltrative