充血性心力衰竭患者陈施氏呼吸发生机制.ppt

CSR-CSA,王菡侨河北医科大学第三附属医院呼吸睡眠科,DefinitionofCSA,Centralsleepapneas,Centralsleepapneasandhypopneasarisefromcompleteorpartialreductionsincentralneuraloutflowtotherespiratorymusclesduringsleepthatleadtocompleteorpartialcessationofairflowforatleast10seconds,respectively,CSA与OSA,whenstudyingpatientswithcardiovasculardiseases,especiallythosewithHFandstroke,whereCSAismuchcommonerthaninthegeneralpopulation,distinguishingcentralfromobstructiveeventsassumesgreaterimportance,DiagnosisofCSA,InpatientswithHF,adiagnosisofCSAcanbeestablishedonovernightpolysomnography,usingeitherRIPornasalpressurecannulaforrespiratorymonitoring,whenthereisanAHIofatleast5to15,andwhenatleast50%ofapneasandhypopneasarecentral.,Cheyne-Stokesrespiration(CSR),Cheyne-Stokesrespiration(CSR)isaformofperiodicbreathingTheventilatoryperiodischaracterizedbyaprolongedwaxingwaningpatternoftidalvolumefollowedbycentralapneaorhypopnea.ItisnoteworthythatthepatientinwhomCheynefirstdescribedthisbreathingdisordersufferedfromHF,atrialfibrillation,andastroke,andundoubtedlyhadalowcardiacoutputandprolongedcirculationtime.,CSRcanbeobservedbothduringsleepandwakefulness,althoughitappearstobefarmorecommonduringsleepWhenitoccursduringsleep,itissimplyaformofCSAwithaprolongedhyperpnea.WhenspecifyingtheoccurrenceofCSRduringsleep,wehaveusedthetermCheyne-Stokesrespirationwithcentralsleepapnea(CSR-CSA).,Thepresenceofaprolongedhyperpneawithawaxing-waningpatternoftidalvolume,andprolongedcycleduration,thatdistinguishesCSRfromotherformsofperiodicbreathingasidiopathicCSAorhigh-altitudeperiodicbreathingwithoutHF,AB（apnealength）=18s，21sC=nadirofSaO2BC（lung-tocarotidbodycirculationtime）=8s，26sBD(hyperpnealength)=7s，46sAD(cyclelength)=25s,65sHallMJ,AmJRespirCritCareMed1996;154:376381,Pathophysiolory,hyperventilation,RespiratorycontrolsysteminstabilityVentilationisdependentmainlyonthemetabolicratherthanthebehavioralrespiratorycontrolsystemduringsleep,andtheprimarystimulationforventilationwhileasleepisPaCO2CentralapneaduringsleepoccurswhenPaCO2fallsbelowtheapneathreshold.CSR-CSAispresentwhencentralapneaoccurscyclically,InpatientswithHFwithCSR-CSA,PaCO2tendsnottoincreasemuchmorefromwakefulnesstosleepcomparedtotheapneicthresholddoes.LoopgainXieAetal,AmJRespirCritCareMed2002;165:12451250.FerrierKetal,Chest2005;128:21162122.,Thischronichyperventilationoccursbecauseofpulmonaryvagalirritantreceptorstimulationbypulmonarycongestionandincreasesincentralandperipheralchemosensitivity.LoweringwedgepressurewithdrugsorCPAPisassociatedwithariseinPaCO2andalleviationofCSRCSA.SolinPetalCirculation1999;99:15741579.JavaheriS.NEnglJMed1999;341:949954.SolinPetal,AmJRespirCritCareMed2000;162:21942200.,arousals,inOSAarousalsactasadefensemechanismtoterminateapneas,andactivatepharyngealmusclesthatallowresumptionofairflow,inCSAtheyappeartoinstigatecentral，apneasbyprovokingventilatoryovershoot.,CSA与OSA,Increasesinventilationinresponsetoarousalsoccurduetobothnonchemicalhandchemicalfactors.TheabruptchangeinstateNREMWakewakingneurogenicdrivetobreathelowerPaCO2setpointventilatoryovershootWakeNREMPaCO2isbelowthehigherapneathresholdCSACHFhighsensitivitytoPaCO2CSR-CSA,Severaladditionalfactors,suchasmetabolicalkalosis,lowfunctionalresidualcapacity,upperairwayinstability,prolongationofcirculationtimeandhypoxia,mayfurthercontributetorespiratoryinstabilityandCSRCSA.,Prevalence,Sinetal450patients:33%withCSAvs37%withOSABecausethiswasasleepclinicpopulation,theprevalenceofCSR-CSAmaynothavebeenrepresentativeofitsprevalenceinthegeneralpopulationwithHF.JavaheriS49%ofmalepatientswithsystolicHFsufferfromSACSAoccursinabout37%,andOSAin12%,Wangandcolleaguesperformedsleepstudieson218consecutivepatientswithHF(168menand50womenwithLVEF45%)enrolledfromasingleHFclinicbetween1997and2004withoutregardtosuspicionofsleepapnea.TheprevalenceofCSR-CSA,definedasanAHIgreaterthanorequalto15ofwhichmorethan50%werecentral,was21%.HuKeetal41.7%hadperiodicbreathingwithAHI15WangH,etalJAmCollCardiol2007;49:16251631胡克,等.中华老年医学杂志,2002,21(1):15-18.,patientswithHF,OSAandCSAcanbepartofaspectrumofperiodicbreathingwhosepredominanttypecantransformovertimeinresponsetoalterationsincardiacfunction.WangH,etal.JSleepRes2006;15:321328.,RiskfactorsforCSAinCHF,IndependentoddsratiosforCSAinCHFMaleAwakePCO238mmHgAge60yearsAtrialfibrillationHigherpulmonarycapillarywedgepressure,andLVend-diastolicvolume,SinDD,etalAmJRespirCritCareMed1999;160:11011106.,TkacovaR,etalAmJRespirCritCareMed1997;156:15491555.,CardiovascularEffectsofCSR-CSA,OnceCSR-CSAinitiated，itmayparticipateinapathophysiologicviciouscyclethatcontributestodeteriorationincardiovascularfunction,CSR-CSAcontributestosympatheticactivation：,CSAcausecyclicalsurgesinsympatheticnervoussystemactivity(SNA)insynchronywiththeventilatoryoscillationsofCSR-CSAbloodpressureandheartrateoscillateinconcertwithCheyne-Stokescycles,verymuchastheydoduringOSAThesympatheticstimulatoryeffectsofCSR-CSAarenotisolatedtosleep,butalsocarryoverintowakefulness.NaughtonMT,etal.AmJRespirCritCareMed,1995;152:473479.,Increasepreloadandafterloadand,thus,workforthedamagedmyocardiumDecreasemyocardialcontractilityVentriculararrhythmiasMyocytehypertrophyandadverseremodelingLanfranchiPA,etal.Circulation2003;107:727732.,ThemainclinicalsignificanceofCSR-CSAinHFisitspotentialtoadverselyinfluencesurvival.SeveralstudiesshowedthatCSR-CSAisasignificantindependentpredictorofmortalityinpatientswithHFAHIgreaterthan30wasanindependentpredictorofmortalitySinDD,etal.Circulation2000;102:6166.CorraU,etal.Circulation2006;113:4450.JavaheriS,etal.JAmCollCardiol2007;49:20282034.,DaiYuminoetalProcAmThoracSocVol5.pp226236,2008,1WangHanqiaoetal.JACCEpub2007Apr22HanlyPJ,etalAmJRespirCritCareMed,1996,153(1):272-6,SDBsignificantlyreducesurvivalwithoutcardiactransplantation(transplant-freesurvival),Summary,InpatientswithHF,CSR-CSAiscommonandisduetorespiratorycontrolsysteminstabilitysecondarytotheeffectsofelevatedLVfillingpressures,pulmonarycongestion,increasedcentralandperipheralchemoreceptorsensitivity,reducedcerebrovascularbloodflow,andpossiblyotherfactors.CentralapneaoccurswhenPaCO2fallsbelowthethresholdforapneaduringsleep.Althoughlowcardiacoutputandincreasedlungtochemore