基础医学各论Ⅰ：26-呼吸衰竭

RespiratoryFailure

OutlineReviewRespirationRespiratorysystemLungfunctionRespiratoryfailureDefinitionClassificationEtiologyMechanismChangesinthebodyPreventionandtherapy1.O2intake2.HbcarryingO23.O2transportincirculation4.O2utilizationinthetissueRespiration-aprocessofgasexchangeExternalrespirationRespiratorySystemConsistsofthreeparts:Pumpimgpart

respiratorymusclesrespiratorycontrolsystemConductivepartthecompletetracheasystemGasexchangepartAlveoliinthelung

GASEXCHANGEVENTILATIONLungfunctionVentilationO2inspiration&CO2expirationGasexchangeOxygenationofthebloodrespiratoryfunction6Non-respiratoryfunctionDefenseFiltrationMetabolismEndothelialcell

Pulmonarysurfactant(PS,肺泡表面活性物质)Metabolismofarachidonicacid---prostaglandinandleukotrienesAPUDcell(amineprecursoruptakeanddecarboxylationcell)---VIP血管活性肠肽,P,CCK胆囊收缩素, somatostatin生长抑素LungfunctionVentilationThedrivingforce(动力):contractionofrespiratorymusclesTheresistance:elasticandairwayresistanceVentilationAirwayresistanceVentilation顺应性=1/弹性阻力Pulmonarysurfactant(PS,肺泡表面活性物质)Elasticresistance9AirwayresistanceInfluencefactors:airwaydiameter,lengthandshape,rateofairflow气道内径，长度，形态，气流速度，形式等大气道阻力：直径>2mm，有软骨环支撑，不易塌陷，80%小气道阻力：直径<2mm，无软骨环支撑，易扭曲闭合，20%

R=8Lηπr4气道阻力与气道长度成正比，与气道半径的四次方成反比Gasexchange(oxygenation)Influencefactors:ThedifferenceofpartialpressurecrosstheaveolarmembraneMolecularweightandsolubilityofthegasThearea

andthickness

ofalveolarmembraneThecontacttimebetweenalveoliandblood.肺泡膜两侧的气体分压差气体的分子量与溶解度肺泡膜的面积与厚度血液与肺泡接触时间11 Concept ApathologicprocesscausedbysevereexternalrespiratorydysfunctionthatresultsindecreaseofPaO2withorwithoutretentionofCO2RespiratoryfailureDiagnosticcriteriaRespiratoryfailureisdefinedasPaO2<60mmHgwithorwithoutPaCO2>50mmHg.12ClassificationPaCO2MECHANISMPATHOGENICSITECOURSETypeIGas-exchangeCentralAcuteTypeIIVentilationPeripheralChronicClassificationPaO2↓IsPaCO2↑?noPaCO2↑--typeI(hypoxemic,低氧血症型)，failureofgasexhcangePaCO2↑--typeII(hypercapnic，高碳酸血症型),failureofventilationRespiratorySystemConsistsofthreeparts:Pump

respiratorymusclesrespiratorycontrolsystemConductivepartthecompletetracheasystemGasexchangepartAlveoliinthelung

GASEXCHANGEVENTILATIONRespiratoryfailureExternalrespirationdysfunctionVentilationfailure(通气障碍)Restrictivehypoventilation(限制性通气不足)Obstructivehypoventilation(阻塞通气不足)Gas-exchangefailure(换气障碍)Diffusiondisorder(弥散障碍)VA/Qmismatch(通气/血流比值失调)Increasedanatomicalshunt(解剖分流增加)EtiologyandPathophysiologyDysfunctionofexternalrespirationAirwayresistance↑VentilationElasticresistance↑VentilationfailureHypoventilation(通气不足)Drivingforce↓Resistance↑

Drivingforce↓VentilationfailureHypoventilation(通气不足)Drivingforce↓Resistance↑

Restrictivehypoventilation(限制性通气不足)Drivingforce↓orelasticresistance↑Limitedalveolardistension(肺泡扩张受限)Obstructivehypoventilation(阻塞通气不足)Airwayresistance↑duetoobstruction18Restrictivehypoventilation(限制性通气不足)Causedbydiseasesthataffecteitherthedistensibility(扩展性)

ofthelungsorchestwall.Inspiration-anactiveprocess—mostlyaffectedinrestrictivehypoventilationExpiration-anpassiveprocess19ParalysisofrespiratorymuscleDisordersofcentralorperipheralnerveInhibitionofrespiratorycenterIntrinsicdiseasesofrespiratorymuscleDecreasedcomplianceofchestwallSeverechestdeformityMultipleribfracturePleura(胸膜)

fibrosis;DecreasedcomplianceoflungDisordersoflung(diffusefibrosis,edema);Lackofalveolarsurfactant(asseeninARDS)Pneumothorax气胸orhydrothorax胸腔积水Restrictivehypoventilation(限制性通气不足)Obstructivehypoventilation(阻塞性通气不足)Airwayobstruction/narrowing→Airwayresistance↑→obstructivehypoventilationCentralairwayobstructionPeripheralairwayobstruction管壁收缩或增厚:支气管哮喘、慢支→支气管痉挛炎症→支气管粘膜下充血、水肿、纤维增生管腔阻塞：支气管哮喘、慢支→粘液↑纤毛损伤、肿瘤、异物管壁受压：肿瘤、肿大淋巴结肺组织对小气道管壁的牵拉作用减弱 outsidethethorax→inspiratorydyspnea吸气困难

阻塞位于胸外：声带麻痹、喉炎、喉头水肿，喉癌，白喉intheairwayinside→expiratorydyspnea呼气困难阻塞位于胸内：气管，大支气管的狭窄和阻塞如气管肿瘤，气管异物，气管外肿物压迫（甲状腺，纵隔肿瘤）Obstructivehypoventilation(阻塞性通气不足)Centralairwayobstruction-obstructionabovetheracheacrotch(气管分叉以上的阻塞)ExtrathoracicobstructionIntrathoracicobstructionExpiratorydyspneaInspiratorydyspneaCentralairwayobstruction23中央气道胸外段阻塞无呼气困难24中央气道胸外段阻塞吸气困难25中央气道胸内段阻塞呼气困难26中央气道胸内段阻塞无吸气困难ExtrathoracicobstructionIntrathoracicobstructionExpiratorydyspneaInspiratorydyspneaCentralairwayobstruction大气压(Patm)，气管内压(Ptr)，胸内压(PpI)三者之间的关系决定呼吸困难的形式28

Theperipheralairwayisusualreferredtoasthesmallerairways(diameter<2mm).

直径<2mm，无软骨环支撑，易扭曲闭合specificchemicalmediators

suchashistamine,prostaglandins,leukotrients,releasedduringinflammatoryandallergicresponsesAbnormalneuralregulationofairwaysmoothmuscletone

Edemaofmucosaandsecretionsinthelumenallcontributetothenarrowingofairway.

PeripheralairwayobstructionExpiratorydyspnea(呼气性呼吸困难)29+25+35IsobaricPoint等压点+20+20NormalEmphysemaExpiratorydyspnea(呼气性呼吸困难)COPDEmphysemaMechanism30

PAO2

,PACO2

PaO2

,PaCO2

TheratiobetweenthedecreasedPaO2andincreased

PaCO2isequaltotherespiratoryquotient(0.8)PA:pressureinthealveoli;Pa:pressureinthearterial

PAO2

=PiO2-PACO2/R

(PiO2=PO2ofinspiredgas)

PaCO2(PACO2)isoptimalparameterreflectingthetotalvolumeofalveolarventilation:

PaCO2

=

PACO2

=0.863×VCO2/VA

(VCO2=CO2production/mininvivo,VA=volumeofalveolarventilation/min)BloodgasmeasurementsuponventilationfailureHypoventilationPAO2↓PaO2↓PACO2↑PaCO2↑Hypoventilation→TypeIIrespiratoryfailureHypoventilation

dPaCO2↑dPaO2↓=RBloodgasmeasurementsuponventilationfailured:differencesVentilationfailure(通气障碍)Restrictivehypoventilation(限制性通气不足)Obstructivehypoventilation(阻塞通气不足)Gas-exchangefailure(换气障碍)Diffusiondisorder(弥散障碍)VA/Qmismatch(通气/血流比值失调)Increasedanatomicalshunt(解剖分流增加)EtiologyandPathophysiologyDysfunctionofexternalrespirationGas-exchangefailure(换气障碍) generallycharacterizedbythedisruptionintheexchangeofO2，CO2orbothacrossthealveolar-capillarymembrane.Diffusiondisorder(弥散障碍)

Influencefactors:ThedifferenceofpartialpressurecrosstheaveolarmembraneMolecularweightandsolubilityofthegasThearea

andthickness

ofalveolarmembraneThecontacttimebetweenalveoliandblood34Reductionofthealveolarmembranesurfacearea(normal:80m2

，only35-40m2isinvolvedatrest)Atelectasis(肺不张),emphysema(肺气肿),

pneumonectomy（肺叶切除）Increasedthicknessofalveolarmembrane(normal:1~5µm)Pulmonaryedema,fibrosis,hyalinemembrane(透明膜形成）formation,pulmonarycapillaryextensionShorteneddiffusiontime(normal0.75s)Usuallyonlyneed0.25s,thePaO2canincreasetoPAO2Increasedcardiacoutput

increases，faster

bloodflowCausesofdiffusiondisorderAtrestBloodgasnormalInlaborPaO2

,PaCO2normal

Bloodgasmeasurementsindiffusiondisorder

PvO2PaO2

PaCO2

PvCO24640PO2

PCO2(mmHg)100

80

60

402000.250.500.75sVentilationfailure(通气障碍)Restrictivehypoventilation(限制性通气不足)Obstructivehypoventilation(阻塞通气不足)Gas-exchangefailure(换气障碍)Diffusiondisorder(弥散障碍)VA/Qmismatch(通气/血流比值失调)Increasedanatomicalshunt(解剖分流增加)EtiologyandPathophysiologyDysfunctionofexternalrespiration37

==正常VAQ4L5L

0.8VA/Qmismatch(通气/血流比值失调)themostcommonmechanismofrespiratoryfailurecausedbypulmonarydiseases.

differencesranged3.0~0.6fromthetoptothebottomofthelungHypoventilationinsomealveoli→VA/Q↓Whileinchronicbronchitisandobstructiveemphysema,itismarkedlyincreasedupto30-50%.SimilartoA-Vshunt(functionalshunt)

Functionalshunt(venousadmixture)(功能性分流)Normally,onlyaccountfor~3%oftotalpulmonarybloodflowReducedventilationwithnormalbloodflowVA/Qmismatch(通气/血流比值失调)Chronicbronchitis,asthma,COPDDIC,pulmonaryarteritis,

pulmonaryarteryembolization,pulmonaryvasoconstriction,maybeincreasedupto60-70%.Reducedbloodflowinsomealveoli→VA/Q

Similartodeadspaceventilation

deadspace-likeventilation(死腔样通气)Normally,thephysiologicaldeadspaceaccountforabout30%oftidalvolume.ReducedbloodflowwithnormalventilationVA/Qmismatch(通气/血流比值失调)40BloodgasmeasurementsinVA/QmismatchFunctionalShuntVA/Q↓DeadSpace-likeVentilationVA/Q↑PaO2

PaCO2N(,)

COPDEmphysemaDIC,pulmonaryarteritis41DiseasedNormalTotalV/Q<0.8>0.8≈0.8PaO2

CaO2

PaCO2

N

CaCO2

N

FunctionalShuntBloodgasmeasurementsinQA/Vmismatch42DeadSpace-likeVentilationDiseasedNormalTotalV/Q>0.8<0.8≈0.8PaO2

CaO2

PaCO2

N

CaCO2

N

BloodgasmeasurementsinQA/VmismatchVentilationfailure(通气障碍)Restrictivehypoventilation(限制性通气不足)Obstructivehypoventilation(阻塞通气不足)Gas-exchangefailure(换气障碍)Diffusiondisorder(弥散障碍)VA/Qmismatch(通气/血流比值失调)Increasedanatomicalshunt(解剖分流增加)EtiologyandPathophysiologyDysfunctionofexternalrespiration44IncreasedanatomicalshuntsTrueshunt-abnormalanatomicpathwayInnormalpersons:2-3%ofthecardiacoutput.Bronchiectasis(支气管扩张)bronchogeniccarcinomapulmonaryarterio-venousfistulas(瘘管) Inmostpulmonaryedema,atelectasis(肺不张)

andpneumonia,thealveoliarefilledbyfluidorclosed.Thereisperfusionbutnoventilationatall.

Blooddisturbances:PaO2

,PaCO2N(

,

)45Functionalshuntsv.s.Trueshunts功能性分流与真性分流的鉴别诊断PureO2intakefor30mincancorrectfunctionalbutnotrealshunts.DifferentialdiagnosisGasexchangedisorderCompensatoryhyperventilationPaO2↑PaCO2NTypeI

respiratoryfailure46致病因子激活中性粒细胞/单核巨噬细胞/血小板/内皮细胞释放体液介质肺泡-毛细血管膜损伤和通透性增高微血栓形成ARDS病理改变：肺出血、水肿、肺不张、微血栓、肺泡透明膜形成AcuteRespiratoryDistressSyndrome（ARDS)

急性呼吸窘迫综合征47ARDS引起呼衰的机制肺水肿透明膜形成肺不张支气管阻塞支气管痉挛微血栓形成肺血管收缩弥散障碍功能性分流死腔样通气

PaO2↓PaCO2N或↓Ⅰ型呼衰VA/Qmismatch48Chronicobstructivepulmonarydisease(COPD)

Chronicobstructivepulmonarydisease(COPD)ischronicairwayobstructioncausedbychronicbronchitisandemphysema.49????COPDPathogenesis:VentilatoryinadequacyVentilation-perfusionmismatchingDiffusiondisorderVentilatoryinadequacyObstructiveRestrictiveCongestion,swelling,spasm,blockageofbronchiwallUpwardshiftofIsobaricpointDecreasedalveolarsurfactantRespiratorymusclefailureDecreasedalveolarsurfacearea

LowventilationinpartofalveoliLowbloodflowinpartofalveoli50ChangesinthebodyAlterationofbloodgasAcid-baseandelectrolytedisturbancesDisordersofvitalorgansystems51Disordersofacid-basebalanceandelectrolytemetabolism(l)RFtypeII→H2CO3↑→H+—

K+

exchange

(cells)Cl–—HCO3–exchange(RBC)excreted(NH4Cl,NaCl)bykidney(2)Hypoxia→acidproduct↑

Renalinsufficiency(excretingacid/reservingbase↓)aniongapnormal,Cl－↑

(3)RFtypeI→hyperventilation→pCO2↓K+↑Cl–N→Respiratoryalkalosis→K↓,Cl－↑MetabolicacidosisRespiratoryacidosisK+↑Cl－↓52AlterationsinrespiratorysystemAlterationscausedbyhypoxiaandhypercapniaPCRRCTotaleffectPaO<60<30PaCO>50,<80>80(PCR:peripheralchemicalreceptor;RC:respiratorycenter)

－－＋＋＋＋<－－－＋>－＋O2therapyforchronicTypeIIRF:lowconcentration,lowflowrate,continuousO2supply,maintainPaO2~60mmHg53Alterationsincirculatorysystem(1)MildPaO2

,PaCO2

excitation(reflex):CardiacOutput

Bloodredistribution(peripheralconstriction,coronary&cerebralarterydilation)

(2)SeverePaO2

,PaCO2

inhibition(direct):BP

Cardiaccontractility

,arrhythmia(3)Chroniclungdisease

right-heartfailure

PulmonaryHeartDisease(PHD)54Hypoxia,Hypercapnia,OverloadDisorderofelectrolytemetabolismMyocardialinjuryResistance↑PaO2

,PaCO2→constrictionofpulmonaryarteriolePrimarydisease→thickeningandsclerosisofvesselwall,Narrowingofvessellumen

Persistenthypoxia→RBC↑,bloodvolume↑,viscosity↑PHD→Pulmonaryarteryhypertension55Alterationsincentralnervoussystem

Respiratoryfailure

dysfunctionofbrainPulmonaryencephalopathy肺性脑病56Dilation,permeability↑→vasogenicbrainedemaATP

→Na-K-ATPase

→cytoxicbrainedemaCerebralbloodvesselsCerebralcellsGlutamatedecarboxylase↑→GABA↑→CNSinhibitionPhospholipase↑→releaselisozyme→injuryofbraincellsIntracranialPressure↑HypoxiaAcidosisPulmonaryencephalopathyRespiratoryfailure

Pulmonaryencephalopathy57Hypoxiaandacidosis→sympatheticstimulation→renalvasoconstriction→decreasedrenalbloodflow→functionalrenalfailureAlterationsinkidney58AlterationsingastrointestineSeverehypoxia→vasoconstrictioninstomachwall→mucosadamage→lossofbarrierfunctionmucosaulcerbleedingandnec