心肺交互作用

心肺交互作用Pumpfunction:PreloadatagivenHRPraorCVPAfterloadContractility.Returnfunction:Bloodvolume(vein)stressedandunstressedComplianceResistanceCO跨壁壓（Ptm）艙或血管內(nèi)外壓力差=血管內(nèi)收縮壓?Ppl非胸腔內(nèi)血管外壓=大氣壓（傳感器的零點）胸腔內(nèi)血管被胸膜腔內(nèi)壓包圍胸膜腔內(nèi)壓隨通氣周期變化Ppl↑→RV前負荷↓自主呼吸或負壓呼吸時Ppl和血管內(nèi)主動脈壓力均下降Ppl下降幅度大于主動脈壓力下降幅度Ptm實際增加→LV后負荷↑、SV↓FourmechanismsparticipateinthecyclicchangesofSVobservedduringmechanicalventilation.First,duringinsufflation,venousreturndecreasesduetoanincreaseinpleuralpressure.ThisdecreaseinRVpreloadleadstoadecreaseinRVoutputthatsubsequentlyleadstoadecreaseinleftventricularoutput.Second,RVafterloadincreasesduringinspirationbecausetheincreaseinalveolarpressureisgreaterthantheincreaseinpleuralpressure.However,leftventricularpreloadin-creasesduringinsufflationbecausebloodisexpelledfromthecapillariestowardtheleftatrium.Finally,leftventricularafterloaddecreasesduringinspirationbecausepositivepleuralpressuredecreasestheintracardiacsystolicpressureandthetransmuralpressureoftheintrathoracicpartoftheaortaCCM.2009Definition:theforceopposingejectionVentricularafterloadisrepresentedbytheleveloftransmuralpressure,inthecourseofsystole,withineithertheaorticroot(LVafterload)orthepulmonaryarterytrunk(RVafter-load)Thetransmuralratherthantheintraluminalpressuremustbeconsideredbecausethesegreatvesselsaswellastheventriclesareexposedtoanextramuralpressure(i.e.,ITP)whichisusuallynonatmospheric.ThemechanismswherebyrespirationinteractswithLVandRVafterloadaredifferent.Attheonsetofspontaneousinspiration,theintraluminalpressureintheaorticrootdecreaseslessthandoesITP,duetotheconnectionofthisvesselwithextrathoracicarteries.Asaresult,aortictransmuralpressureincreases.Withspontaneousbreathingtherefore,LVafterloadisgreaterininspirationthaninexpiration.AsymmetricalchainofeventsleadstoareducedLVafterloadinthecourseofatransientincreaseinITP,suchaswithpositivepressureinflationofthelungs.SteadyincreasesinITP,aseffectedwithPEEP,similarlyunloadtheLVwithpotentiallybeneficialconsequencesinpresenceofleftheartfailure,asdescribedingreaterdetailbelow(Sect.‘‘EffectsofPEEPoncardiacoutput’’inPartII).Conversely,patientswithobstructivesleepapneahaveboutsofgreatlynegativeITPwhichincreaseLVafter-load,thuscontributingtoLVhypertrophyAseminalpaperbyPermuttshowsthatRVafterloadishighlydependentonandincreaseswiththeproportionoflungtissueinWestzone1or2,asopposedtozone3conditions.Zones1or2existwhenevertheextraluminalpressureofalveolarcapillaries(whichisclosetoalveolarpressure,PA)exceedstheintraluminalvalue,leadingtovesselcompression.Inzone3bycontrast,intraluminalcapillarypressureexceedsPAForhydrostaticreasons,zones1and2aremorelikelytooccurinnondependentpartsofthelung.Furthermore,respiratorychangesintheintraluminalpressureofalveolarcapillariestendtotrackchangesinITPandthustodecreasemorethandoesPAduringaspontaneousinspirationandtoincreaselessthandoesPAoninflationofthelungwithpositivepressure.Thus,anyincreaseinlungvolume,whetherinthecontextofspontaneousormechanicallyassistedbreathing,hasthepotentialtopromotetheformationofzones1and2attheexpenseofzone3,andthustoincreaseRVafterload.Theseconsiderationsareofhighclinicalrelevance,notablyconcerningthepossibleinductionoraggravationofacutecorpulmonalebymechanicalventilation,asdescribedbelow(Sect.‘‘Mechanicalven-tilationandacutecorpulmonale’’inPartII).IntensiveCareMed(2009)35:45–54肺膨脹影響CO肺膨脹擠壓肺泡內(nèi)血管肺膨脹必須增加胸膜腔內(nèi)壓Pv＞PA時影響很小Zone1:PA>Pa>PvZone2:Pa>PA>PvZone3:Pa>Pv>PAThezonesofthelungdividethelungintothreeverticalregions,basedupontherelationshipbetweenthepressureinthealveoli(PA),inthearteries(Pa),andtheveins(Pv):肺動脈和靜脈壓力與肺部區(qū)域有關(guān)肺尖最低肺底最高直立位肺頂部Pa很可能低于PAWestJ,DolleryC,NaimarkA(1964)."Distributionofbloodflowinisolatedlung;relationtovascularandalveolarpressures".JApplPhysiol

19:713–24.全肺PA=0±2cmH2O直立位肺尖與肺底動脈壓差=20mmHg受重力影響全肺靜脈壓=5mmHg肺尖部靜脈壓=-5mmHg肺底部靜脈壓=+15mmHgPAP=25/10mmHg（Mean=15mmHg）肺尖部mPAP=5mmHg肺底部mPAP=25mmHg正常人群全部肺區(qū)Pa>PAZone1正常情況下不存在正壓通氣時可以存在PA>Pa受肺泡壓力影響區(qū)域血管徹底塌陷血流消失死腔通氣Zone2位于心臟上方3cm以上肺區(qū)區(qū)域血流呈搏動狀毛細血管床靜脈端阻塞→無血流動脈端壓力超過PA時產(chǎn)生血流如此反復循環(huán)正常肺大部分位于Zone3存在連續(xù)血流zone1通氣/血流比＞zone3PA>Pv(WestzoneII肺區(qū))右室后負荷隨肺膨脹增加隨肺泡壓1:1增加肺血管血流淤滯→肺水↑Aslungvolumeincreasesfromresidualvolume(RV)tototallungcapacity(TLC),thealveolarvesselsbecomeincreasinglycompressedbythedistendingalveoli,andsotheirresistanceincreases,whereastheresistanceoftheextra-alveolarvessels(whichbecomelesstortuousaslungvolumeincreases)falls.Thecombinedeffectofincreasinglungvolumeonthepulmonaryvasculatureproducesthetypical“Ushaped”curveasshown,withitsnadir,oroptimum,ataroundnormalfunctionalresidualcapacity(FRC).WhittenbergerJL,etal.JApplPhysiol1960;15:878–82.Agivenchangeinpreloadinducesalargerchangeinstrokevolumewhentheventricleoperatesontheascendingportionoftherelationship(A,conditionofpreloaddependence)thanwhenitoperatesontheflatportionofthecurve(B,conditionofpreloadindependence).SchematicrepresentationofFrank–Starlingrelationshipsbetweenventricularpreloadandstrokevolumeinanormalheart(A)andinafailingheart(B).Agivenvalueofpreloadcanbeassociatedwithpreloaddependenceinanormalheartorwithpreloadindependenceinafailingheart.HeartstressedvolumeUnstressedvolumeHeight:TotalBVEmptyingBVResistanceCompliance:Surface/HeightrelationshipReturnfunction:Bloodvolume(veins/venules)stressedandunstressedComplianceResistance正常靜脈回心反流梯度=4–8mmHgPpl小量增加可顯著改變靜脈回心反流梯度Ppl＞0時的兩種代償過程增加血容量補液一段時間后腎臟鹽潴留代償機制發(fā)揮作用靜脈容量血管收縮Unstressedstressedvolume→stressedvolume迅速增加stressedvolume10–15ml/kgUnstressedvolumeStressedvolumeStressedvolumeUnstressedvolumeContractionofsmoothmuscleinvascularwallsReturntoheart↑GuytonAC.Determinationofcardiacoutputbyequatingvenousreturncurveswithcardiacresponsecurves.PhysiolRev1955;35:123–129.患者：中度肺疾病，PEEP=20cmH2OPpl可能增加8cmH2O（約7mmHg）相對于大氣壓CVP=15mmHg室壁膨脹壓=8mmHg心臟水平外周毛細血管壓=15mmHg正常外周靜脈回心阻力=4–8mmHg外周靜脈靜水壓=19–23mmHg凈液體濾過到組織間隙背側(cè)毛細血管額外靜水壓平均值=7cm該部位外周靜脈靜水壓=26–30mmHg高的心臟充盈壓可能增加高PEEP患者CO代價：血管內(nèi)血漿液體滲出增加RH和胸腔內(nèi)大靜脈受Ppl影響，并隨呼吸周期變化吸氣時膈肌下降→IAP↑呼氣時IAP正常（接近大氣壓）外周靜脈壓不受呼吸周期影響全身性靜脈回流(brokenarrow)取決于驅(qū)動壓（胸腔外大靜脈[EGV]壓-RAP）自主吸氣時Ppl(RAP)↓，IAP(EGV)↑RightventricleDecreasedpreloadIncreasedafterloadReducedcontractilityCompressionofheartincardiacfossaLeftventricleDecreasedpreloadDecreasedcomplianceVariableeffectson(autonomousnervoussystemcontrolof)contractilityDecreasedafterloadCompressionofheartincardiacfossaMechanicalventilationaltersintrathoracicpressuresandtherebyaffectsthecardiovascularsystem,mainlytherightventricle氣道壓力和容量對心臟負荷和功能的影響很復雜對CO的影響取決于心臟和肺血管的基礎(chǔ)功能Paw↑對前負荷的影響通常占優(yōu)右室后負荷損害性增加難以預測血液動力學嚴重受損時應(yīng)考慮缺乏液體反應(yīng)時應(yīng)考慮Echocardiography可指導治療應(yīng)考慮心肺交互作用對臨床表現(xiàn)和治療的影響B(tài)P↓（隨呼吸機設(shè)置變化）意味著CO↓、組織氧合↓需要恢復先前通氣設(shè)置呼吸正壓↑而BP沒有下降并不意味著CO沒有下降CO↓時神經(jīng)-體液反射能迅速增加SRV以維持或增加BPBP↓檢測CO變化特異性高，敏感性低CVP不表示血容量CVP不能表示容量反應(yīng)性一個特定的CVP值不表明患者是否具有容量反應(yīng)性高CVP表明患者不太可能具有容量反應(yīng)性CVP＞10–12mmHg應(yīng)用CVP時首先要基于臨床和生化檢查來判斷患者是否需要優(yōu)化血液動力學其次是快速補液是否改善血液動力學最后是當CVP隨擴容增加時是否能增加COCVP應(yīng)在一定的安全范圍內(nèi)Forexample患者：中度肺疾病，PEEP=20cmH2OPpl可能增加8cmH2O（約7mmHg）相對于大氣壓CVP=15mmHg室壁膨脹壓=8mmHg心臟水平外周毛細血管壓=15mmHg外周靜脈回心阻力=4–8mmHg外周靜脈靜水壓=19–23mmHg凈液體濾過到組織間隙背側(cè)毛細血管額外靜水壓平均值=7cm該部位外周靜脈靜水壓=26–30mmHg高的心臟充盈壓可能增加高PEEP患者CO代價：血管內(nèi)血漿液體滲出增加存在較大肺分流時，低CO影響PaO2CO↓→SvO2↓→CaO2↓監(jiān)測SvO2orScvO2有用SvO2orScvO2很低表明增加CO將增加PaO2Interactionofvenousreturnandcardiacfunctioncurveswithrespiratoryvariation

CVP與PAOP可用來評價通氣功能PAOP通氣變異度可表明Ppl的變化[27].自主負壓吸氣時，PAOP下降輕度低估了Ppl的下降大多數(shù)病人肺充氣時左室充盈增加正壓呼吸時，PAOP增加輕度高估了Ppl的增加CVP的變化基本不反應(yīng)Ppl的變化右心容量來源于胸腔外基本不隨Ppl而變化吸氣觸發(fā)時CVPorPAOP出現(xiàn)大的負向變化trigger設(shè)置不當Raw↑肺順應(yīng)性↓吸氣驅(qū)動增強需調(diào)整通氣設(shè)置或增強鎮(zhèn)靜CVP隨MV顯著增加表明Ppl顯著增加胸壁順應(yīng)性↓胸壁水腫胸腔積液量大IAP增加用力呼氣使CVP增高需觀察多個呼吸周期取呼氣末獲得值（最長和最低值）(Fig.3b)呼氣階段患者增加收縮呼氣肌時，整個呼氣階段心臟充盈壓增加(Fig.3c)這些患者CVP呼氣末值誤導前負荷的估價取呼氣開始時的CVP值可能更有效患者試圖談話時消失氣管插管降低呼氣肌收縮后消失對于簡單的MV患者間斷觀察BP和SpO2足夠了通氣管理很困難時監(jiān)測血液動力學試圖增加PaO2時需評價CO以保證MV不降低DO2從CVP和BP波形可獲得很多信息指導治療控制通氣吸氣段Ppl↑→靜脈回心梯度↓→RV充盈和CO↓BP↑肺充氣→肺靜脈排空→LV充盈增加→LVCO↑Ppl↑→LV后負荷↓控制通氣呼氣段BP↓SV↓Thepulsepressure(systolicminusdiastolicpressure)ismaximal(PPmax)attheendoftheinspiratoryperiodandminimal(PPmin)threeheartbeatslater(ieduringtheexpiratoryperiod).SVRI=CI/(MAP-CVP)MAP=CI/SVRI+CVPRelationshipbetweentherespiratorychangesinpulsepressurebeforevolumeexpansion(Baseline；△PP)andthevolumeexpansion-inducedchangesincardiacindex(y-axis)in40septicpatientswithacutecirculatoryfailure.Thehigher△PPisbeforevolumeexpansion,themoremarkedtheincreaseincardiacindexinducedbyvolumeexpansion.MichardF.AmJRespirCritCareMed2000,162:134–138RelationshipbetweentherespiratorychangesinpulsepressureonZEEP(y-axis)andthePEEP-inducedchangesincardiacindex(x-axis)in14ventilatedpatientswithacutelunginjury.Thehigher△PPisonZEEP,themoremarkedthedecreaseincardiacindexinducedbyPEEP.MichardF.AmJRespirCritCareMed1999,159:935–939.MichardF.AmJRespairCritCareMed1999;159:935–939.Ventilatoryvariationsinarterialpressureorstrokevolumehavealsobeenshownnottobepredictiveinpatientswithsmallertidalvolumes,increasedWestzoneIIconditionsandinpatientswithpulmonaryhypertension[24,25,26]Patternsofcardiacfunctionandplasmacatecholaminelevelsdifferedbetweenpatientswhodidordidnotachievespontaneousventilationwithatrialofcontinuouspositiveairwaypressure.Cardiacfunctionmustbesystematicallyconsideredbeforeandduringthereturntospontaneousventilationtooptimizethelikelihoodofsuccess.SusanKF.AmericanJournalofCriticalCare.2006;15:580-594EffectsofincreaseinairwaypressureandvolumeonrightandleftventricleHeart-lunginteractionsmayplayaroleinthemanifestationsandtreatmentofavarietyofdisordersUsingheart–lunginteractions(PPV)canassessfluidresponsivenessduringmechanicalventilationCardiacfunctionmustbesystematicallyconsideredbeforeandduringthereturntospontaneousventilationtooptimizethelikelihoodofsuccess謝謝Anaesthesiology1997,86:308-315RHandintrathoracicgreatveinsaresubjectedtopleuralpressure(PPl),whichvariesthroughouttherespiratorycycle.IAPincreaseswithinspiratorydiaphragmaticdescent,andnormalisestoatmospheric(Patmos)withexpiration.Peripheralvenouspressureisunaffectedbyrespirationandsoremainsatatmosphericpressurethroughouttherespiratorycycle.Systemicvenousdrainage(brokenarrow)dependsonadrivingpressuregradientbetweenext