心肺交互作用

心肺交互作用Pumpfunction:PreloadatagivenHRPraorCVPAfterloadContractility.Returnfunction:Bloodvolume(vein)stressedandunstressedComplianceResistanceCO跨壁压（Ptm）舱或血管内外压力差=血管内收缩压−Ppl非胸腔内血管外压=大气压（传感器的零点）胸腔内血管被胸膜腔内压包围胸膜腔内压随通气周期变化Ppl↑→RV前负荷↓自主呼吸或负压呼吸时Ppl和血管内主动脉压力均下降Ppl下降幅度大于主动脉压力下降幅度Ptm实际增加→LV后负荷↑、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肺膨胀影响CO肺膨胀挤压肺泡内血管肺膨胀必须增加胸膜腔内压Pv＞PA时影响很小Zone1:PA>Pa>PvZone2:Pa>PA>PvZone3:Pa>Pv>PAThezonesofthelungdividethelungintothreeverticalregions,basedupontherelationshipbetweenthepressureinthealveoli(PA),inthearteries(Pa),andtheveins(Pv):肺动脉和静脉压力与肺部区域有关肺尖最低肺底最高直立位肺顶部Pa很可能低于PAWestJ,DolleryC,NaimarkA(1964)."Distributionofbloodflowinisolatedlung;relationtovascularandalveolarpressures".JApplPhysiol

19:713–24.全肺PA=0±2cmH2O直立位肺尖与肺底动脉压差=20mmHg受重力影响全肺静脉压=5mmHg肺尖部静脉压=-5mmHg肺底部静脉压=+15mmHgPAP=25/10mmHg（Mean=15mmHg）肺尖部mPAP=5mmHg肺底部mPAP=25mmHg正常人群全部肺区Pa>PAZone1正常情况下不存在正压通气时可以存在PA>Pa受肺泡压力影响区域血管彻底塌陷血流消失死腔通气Zone2位于心脏上方3cm以上肺区区域血流呈搏动状毛细血管床静脉端阻塞→无血流动脉端压力超过PA时产生血流如此反复循环正常肺大部分位于Zone3存在连续血流zone1通气/血流比＞zone3PA>Pv(WestzoneII肺区)右室后负荷随肺膨胀增加随肺泡压1:1增加肺血管血流淤滞→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正常静脉回心反流梯度=4–8mmHgPpl小量增加可显著改变静脉回心反流梯度Ppl＞0时的两种代偿过程增加血容量补液一段时间后肾脏盐潴留代偿机制发挥作用静脉容量血管收缩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（约7mmHg）相对于大气压CVP=15mmHg室壁膨胀压=8mmHg心脏水平外周毛细血管压=15mmHg正常外周静脉回心阻力=4–8mmHg外周静脉静水压=19–23mmHg净液体滤过到组织间隙背侧毛细血管额外静水压平均值=7cm该部位外周静脉静水压=26–30mmHg高的心脏充盈压可能增加高PEEP患者CO代价：血管内血浆液体渗出增加RH和胸腔内大静脉受Ppl影响，并随呼吸周期变化吸气时膈肌下降→IAP↑呼气时IAP正常（接近大气压）外周静脉压不受呼吸周期影响全身性静脉回流(brokenarrow)取决于驱动压（胸腔外大静脉[EGV]压-RAP）自主吸气时Ppl(RAP)↓，IAP(EGV)↑RightventricleDecreasedpreloadIncreasedafterloadReducedcontractilityCompressionofheartincardiacfossaLeftventricleDecreasedpreloadDecreasedcomplianceVariableeffectson(autonomousnervoussystemcontrolof)contractilityDecreasedafterloadCompressionofheartincardiacfossaMechanicalventilationaltersintrathoracicpressuresandtherebyaffectsthecardiovascularsystem,mainlytherightventricle气道压力和容量对心脏负荷和功能的影响很复杂对CO的影响取决于心脏和肺血管的基础功能Paw↑对前负荷的影响通常占优右室后负荷损害性增加难以预测血液动力学严重受损时应考虑缺乏液体反应时应考虑Echocardiography可指导治疗应考虑心肺交互作用对临床表现和治疗的影响BP↓（随呼吸机设置变化）意味着CO↓、组织氧合↓需要恢复先前通气设置呼吸正压↑而BP没有下降并不意味着CO没有下降CO↓时神经-体液反射能迅速增加SRV以维持或增加BPBP↓检测CO变化特异性高，敏感性低CVP不表示血容量CVP不能表示容量反应性一个特定的CVP值不表明患者是否具有容量反应性高CVP表明患者不太可能具有容量反应性CVP＞10–12mmHg应用CVP时首先要基于临床和生化检查来判断患者是否需要优化血液动力学其次是快速补液是否改善血液动力学最后是当CVP随扩容增加时是否能增加COCVP应在一定的安全范围内Forexample患者：中度肺疾病，PEEP=20cmH2OPpl可能增加8cmH2O（约7mmHg）相对于大气压CVP=15mmHg室壁膨胀压=8mmHg心脏水平外周毛细血管压=15mmHg外周静脉回心阻力=4–8mmHg外周静脉静水压=19–23mmHg净液体滤过到组织间隙背侧毛细血管额外静水压平均值=7cm该部位外周静脉静水压=26–30mmHg高的心脏充盈压可能增加高PEEP患者CO代价：血管内血浆液体渗出增加存在较大肺分流时，低CO影响PaO2CO↓→SvO2↓→CaO2↓监测SvO2orScvO2有用SvO2orScvO2很低表明增加CO将增加PaO2Interactionofvenousreturnandcardiacfunctioncurveswithrespiratoryvariation

CVP与PAOP可用来评价通气功能PAOP通气变异度可表明Ppl的变化[27].自主负压吸气时，PAOP下降轻度低估了Ppl的下降大多数病人肺充气时左室充盈增加正压呼吸时，PAOP增加轻度高估了Ppl的增加CVP的变化基本不反应Ppl的变化右心容量来源于胸腔外基本不随Ppl而变化吸气触发时CVPorPAOP出现大的负向变化trigger设置不当Raw↑肺顺应性↓吸气驱动增强需调整通气设置或增强镇静CVP随MV显著增加表明Ppl显著增加胸壁顺应性↓胸壁水肿胸腔积液量大IAP增加用力呼气使CVP增高需观察多个呼吸周期取呼气末获得值（最长和最低值）(Fig.3b)呼气阶段患者增加收缩呼气肌时，整个呼气阶段心脏充盈压增加(Fig.3c)这些患者CVP呼气末值误导前负荷的估价取呼气开始时的CVP值可能更有效患者试图谈话时消失气管插管降低呼气肌收缩后消失对于简单的MV患者间断观察BP和SpO2足够了通气管理很困难时监测血液动力学试图增加PaO2时需评价CO以保证MV不降低DO2从CVP和BP波形可获得很多信息指导治疗控制通气吸气段Ppl↑→静脉回心梯度↓→RV充盈和CO↓BP↑肺充气→肺静脉排空→LV充盈增加→LVCO↑Ppl↑→LV后负荷↓控制通气呼气段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谢谢Anaesthesiology1997,86:308-315RHandintrathoracicgreatveinsaresubjectedtopleuralpressure(PPl),whichvariesthroughouttherespiratorycycle.IAPincreaseswithinspiratorydiaphragmaticdescent,andnormalisestoatmospheric(Patmos)withexpiration.Peripheralvenouspressureisunaffectedbyrespirationandsoremainsatatmosphericpressurethroughouttherespiratorycycle.Systemicvenousdrainage(brokenarrow)dependsonadrivingpressuregradientbetweenext