心肺交互作用simplified优质PPT.ppt

心肺交互作用simplified优质PPT.ppt

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心心肺交互作用肺交互作用首都医科大学北京朝阳医院李文雄BasicphysiologyofheartlunginteractionPumpfunction:

@#@PreloadatagivenHRPraorCVPAfterloadContractility.Returnfunction:

@#@Bloodvolume（vein）stressedandunstressedComplianceResistanceCOPreloadTransmuralpressure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PplRV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、SVFourmechanismsparticipateinthecyclicchangesofSVobservedduringmechanicalventilation.First,duringinsufflation,venousreturndecreasesduetoanincreaseinpleuralpressure.ThisdecreaseinRVpreloadleadstoadecreaseinRVoutputthatsubsequentlyleadstoadecreaseinleftventricularoutput.Second,RVafterloadincreasesduringinspirationbecausetheincreaseinalveolarpressureisgreaterthantheincreaseinpleuralpressure.However,leftventricularpreloadin-creasesduringinsufflationbecausebloodisexpelledfromthecapillariestowardtheleftatrium.Finally,leftventricularafterloaddecreasesduringinspirationbecausepositivepleuralpressuredecreasestheintracardiacsystolicpressureandthetransmuralpressureoftheintrathoracicpartoftheaortaCCM.2009VentricularafterloadDefinition:

@#@theforceopposingejectionVentricularafterloadisrepresentedbytheleveloftransmuralpressure,inthecourseofsystole,withineithertheaorticroot（LVafterload）orthepulmonaryarterytrunk（RVafter-load）Thetransmuralratherthantheintraluminalpressuremustbeconsideredbecausethesegreatvesselsaswellastheventriclesareexposedtoanextramuralpressure（i.e.,ITP）whichisusuallynonatmospheric.ThemechanismswherebyrespirationinteractswithLVandRVafterloadaredifferent.LVafterloadAttheonsetofspontaneousinspiration,theintraluminalpressureintheaorticrootdecreaseslessthandoesITP,duetotheconnectionofthisvesselwithextrathoracicarteries.Asaresult,aortictransmuralpressureincreases.Withspontaneousbreathingtherefore,LVafterloadisgreaterininspirationthaninexpiration.AsymmetricalchainofeventsleadstoareducedLVafterloadinthecourseofatransientincreaseinITP,suchaswithpositivepressureinflationofthelungs.SteadyincreasesinITP,aseffectedwithPEEP,similarlyunloadtheLVwithpotentiallybeneficialconsequencesinpresenceofleftheartfailure,asdescribedingreaterdetailbelow（Sect.EffectsofPEEPoncardiacoutputinPartII）.Conversely,patientswithobstructivesleepapneahaveboutsofgreatlynegativeITPwhichincreaseLVafter-load,thuscontributingtoLVhypertrophyRVafterloadAseminalpaperbyPermuttshowsthatRVafterloadishighlydependentonandincreaseswiththeproportionoflungtissueinWestzone1or2,asopposedtozone3conditions.Zones1or2existwhenevertheextraluminalpressureofalveolarcapillaries（whichisclosetoalveolarpressure,PA）exceedstheintraluminalvalue,leadingtovesselcompression.Inzone3bycontrast,intraluminalcapillarypressureexceedsPAForhydrostaticreasons,zones1and2aremorelikelytooccurinnondependentpartsofthelung.Furthermore,respiratorychangesintheintraluminalpressureofalveolarcapillariestendtotrackchangesinITPandthustodecreasemorethandoesPAduringaspontaneousinspirationandtoincreaselessthandoesPAoninflationofthelungwithpositivepressure.Thus,anyincreaseinlungvolume,whetherinthecontextofspontaneousormechanicallyassistedbreathing,hasthepotentialtopromotetheformationofzones1and2attheexpenseofzone3,andthustoincreaseRVafterload.Theseconsiderationsareofhighclinicalrelevance,notablyconcerningthepossibleinductionoraggravationofacutecorpulmonalebymechanicalventilation,asdescribedbelow（Sect.Mechanicalven-tilationandacutecorpulmonaleinPartII）.IntensiveCareMed（2009）35:

@#@4554Afterload：

@#@effectoflunginflation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PvPA时影响很小ZonesofthelungZone1:

@#@PAPaPvZone2:

@#@PaPAPvZone3:

@#@PaPvPAThezonesofthelungdividethelungintothreeverticalregions,basedupontherelationshipbetweenthepressureinthealveoli（PA）,inthearteries（Pa）,andtheveins（Pv）:

@#@Zonesofthelung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:

@#@71324.Zonesofthelung全肺PA=02cmH2O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=25mmHgZonesofthelung正常人群全部肺区PaPAZone1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ZonesofthelungZone2位于心脏上方位于心脏上方3cm以上肺区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正常肺大部分位于Zone3存在连续血流zone1通气/血流比zone3ZonesofthelungPAPv（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TherelationbetweenlungvolumeandthepulmonaryvascularresistanceAslungvolumeincreasesfromresidualvolume（RV）tototallungcapacity（TLC）,thealveo