心肺交互作用

首都医科大学北京朝阳医院李文雄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.2009Definition:theforceopposingejectionVentricularafterloadisrepresentedbytheleveloftransmuralpressure,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,thuscontributingtoLVhypertrophyAseminalpaperbyPermuttshowsthatRVafterloadishighlydependentonandincreaseswiththeproportionoflungtissueinWestzone1or2,asopposedtozone3conditions.Zones1or2existwhenevertheextraluminalpressureofalveolarcapillaries(whichisclosetoalveolarpressure,PA)exceedstheintraluminalvalue,leadingtovesselcompression.Inzone3bycontrast,intraluminalcapillarypressureexceedsPAForhydrostaticreasons,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:PAPaPvZone2:PaPAPvZone3:PaPvPAThezonesofthelungdividethelungintothreeverticalregions,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.JApplPhysiol19:713–24.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=+15mmHgPAP=25/10mmHg（Mean=15mmHg）肺尖部mPAP=5mmHg肺底部mPAP=25mmHg正常人群全部肺区PaPAZone1正常情况下不存在正压通气时可以存在PAPa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＞zone3PAPv(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).Agivenvalueofpreloadcanbeassociatedwithpreloaddependenceinanorm