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1、心肺交互作用首都醫(yī)科大學(xué)北京朝陽(yáng)醫(yī)院李文雄Basicphysiologyofheart–lunginteractionPumpfunction:PreloadatagivenHRPraorCVPAfterloadContractility.Returnfunction:Bloodvolume(vein)stressedandunstressedComplianceResistanceCOPreload—Transmuralpressure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(diǎn)）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
2、↑→RV前負(fù)荷↓自主呼吸或負(fù)壓呼吸時(shí)Ppl和血管內(nèi)主動(dòng)脈壓力均下降Ppl下降幅度大于主動(dòng)脈壓力下降幅度Ptm實(shí)際增加→LV后負(fù)荷↑、SV↓FourmechanismsparticipateinthecyclicchangesofSVobservedduringmechanicalventilation.First,duringinsufflation,venousreturndecreasesduetoanincreaseinpleuralpressure.ThisdecreaseinRVpreloadleadstoadecreaseinRVoutputthatsubsequentlyl
3、eadstoadecreaseinleftventricularoutput.Second,RVafterloadincreasesduringinspirationbecausetheincreaseinalveolarpressureisgreaterthantheincreaseinpleuralpressure.However,leftventricularpreloadin-creasesduringinsufflationbecausebloodisexpelledfromthecapillariestowardtheleftatrium.Finally,leftventri
4、cularafterloaddecreasesduringinspirationbecausepositivepleuralpressuredecreasestheintracardiacsystolicpressureandthetransmuralpressureoftheintrathoracicpartoftheaortaCCM.2009VentricularafterloadDefinition:theforceopposingejectionVentricularafterloadisrepresentedbytheleveloftransmuralpressure,inth
5、ecourseofsystole,withineithertheaorticroot(LVafterload)orthepulmonaryarterytrunk(RVafter-load)Thetransmuralratherthantheintraluminalpressuremustbeconsideredbecausethesegreatvesselsaswellastheventriclesareexposedtoanextramuralpressure(i.e.,ITP)whichisusuallynonatmospheric.Themechanismswherebyrespi
6、rationinteractswithLVandRVafterloadaredifferent.LVafterloadAttheonsetofspontaneousinspiration,theintraluminalpressureintheaorticrootdecreaseslessthandoesITP,duetotheconnectionofthisvesselwithextrathoracicarteries.Asaresult,aortictransmuralpressureincreases.Withspontaneousbreathingtherefore,LVafte
7、rloadisgreaterininspirationthaninexpiration.AsymmetricalchainofeventsleadstoareducedLVafterloadinthecourseofatransientincreaseinITP,suchaswithpositivepressureinflationofthelungs.SteadyincreasesinITP,aseffectedwithPEEP,
