心肺交互作用simplifiedppt课件.pptVIP

心肺交互作用 1 Basicphysiologyofheart lunginteraction Pumpfunction PreloadatagivenHRPraorCVPAfterloadContractility Returnfunction Bloodvolume vein stressedandunstressedComplianceResistance CO 2 Preload Transmuralpressure 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 3 FourmechanismsparticipateinthecyclicchangesofSVobservedduringmechanicalventilation First duringinsufflation venousreturndecreasesduetoanincreaseinpleuralpressure ThisdecreaseinRVpreloadleadstoadecreaseinRVoutputthatsubsequentlyleadstoadecreaseinleftventricularoutput Second RVafterloadincreasesduringinspirationbecausetheincreaseinalveolarpressureisgreaterthantheincreaseinpleuralpressure However leftventricularpreloadin creasesduringinsufflationbecausebloodisexpelledfromthecapillariestowardtheleftatrium Finally leftventricularafterloaddecreasesduringinspirationbecausepositivepleuralpressuredecreasestheintracardiacsystolicpressureandthetransmuralpressureoftheintrathoracicpartoftheaorta CCM 2009 4 Ventricularafterload Definition theforceopposingejectionVentricularafterloadisrepresentedbytheleveloftransmuralpressure inthecourseofsystole withineithertheaorticroot LVafterload orthepulmonaryarterytrunk RVafter load Thetransmuralratherthantheintraluminalpressuremustbeconsideredbecausethesegreatvesselsaswellastheventriclesareexposedtoanextramuralpressure i e ITP whichisusuallynonatmospheric ThemechanismswherebyrespirationinteractswithLVandRVafterloadaredifferent 5 LVafterload Attheonsetofspontaneousinspiration theintraluminalpressureintheaorticrootdecreaseslessthandoesITP duetotheconnectionofthisvesselwithextrathoracicarteries Asaresult aortictransmuralpressureincreases Withspontaneousbreathingtherefore LVafterloadisgreaterininspirationthaninexpiration AsymmetricalchainofeventsleadstoareducedLVafterloadinthecourseofatransientincreaseinITP suchaswithpositivepressureinflationofthelungs SteadyincreasesinITP aseffectedwithPEEP similarlyunloadtheLVwithpotentiallybeneficialconsequencesinpresenceofleftheartfailure asdescribedingreaterdetailbelow Sect EffectsofPEEPoncardiacoutput inPartII Conversely patientswithobstructivesleepapneahaveboutsofgreatlynegativeITPwhichincreaseLVafter load thuscontributingtoLVhypertrophy 6 RVafterload AseminalpaperbyPermuttshowsthatRVafterloadishighlydependentonandincreaseswiththeproportionoflungtissueinWestzone1or2 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 7 Afterload 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Pv PA时影响很小 8 Zonesofthelung Zone1 PA Pa PvZone2 Pa PA PvZone3 Pa Pv PA Thezonesofthelungdividethelungintothreeverticalregions basedupontherelationshipbetweenthepressureinthealveoli PA inthearteries Pa andtheveins Pv 9 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PA WestJ DolleryC NaimarkA 1964 Distributionofbloodflowinisolatedlung relationtovascularandalveolarpressures JApplPhysiol19 713 24 10 Zonesofthelung 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 11 Zonesofthelung 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 12 Zonesofthelung 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 13 Zonesofthelung PA 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 14 Therelationbetweenlungvolumeandthepulmonaryvascularresistance Aslungvolumeincreasesfromresidualvolume RV tototallungcapacity TLC thealveolarvesselsbecomeincreasinglycompressedbythedistendingalveoli andsotheirresistanceincreases whereastheresistanceoftheextra alveolarvessels whichbecomelesstortuousaslungvolumeincreases falls Thecombinedeffectofincreasinglungvolumeonthepulmonaryvasculatureproducesthetypical Ushaped curveasshown withitsnadir oroptimum ataroundnormalfunctionalresidualcapacity FRC WhittenbergerJL etal JApplPhysiol1960 15 878 82 15 Frank Starlingrelationshipsbetweenventricularpreloadandstrokevolume Agivenchangeinpreloadinducesalargerchangeinstrokevolumewhentheventricleoperatesontheascendingportionoftherelationship A conditionofpreloaddependence thanwhenitoperatesontheflatportionofthecurve B conditionofpreloadindependence 16 Frank Starlingrelationshipsbetweenventricularpreloadandstrokevolume SchematicrepresentationofFrank Starlingrelationshipsbetweenventricularpreloadandstrokevolumeinanormalheart A andinafailingheart B Agivenvalueofpreloadcanbeassociatedwithpreloaddependenceinanormalheartorwithpreloadindependenceinafailingheart 17 Returnfunction Heart stressedvolume Unstressedvolume Height TotalBV EmptyingBV Resistance Compliance Surface Heightrelationship Returnfunction Bloodvolume veins venules stressedandunstressedComplianceResistance 18 Returnfunction 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 kg 19 Returnfunction Unstressedvolume Stressedvolume Stressedvolume Unstressedvolume Contractionofsmoothmuscleinvascularwalls Returntoheart 20 theinteractionofvenousreturncurve upperleft andcardiacfunctioncurve upperright definethe working cardiacoutput venousreturnandrightatrialpressure Pra values GuytonAC Determinationofcardiacoutputbyequatingvenousreturncurveswithcardiacresponsecurves PhysiolRev1955 35 123 129 21 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 22 Forexample 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 23 Modelofthecirculationshowingfactorsthatinfluencesystemicvenousdrainage 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 24 Effectsofincreaseinairwaypressureandvolume RightventricleDecreasedpreloadIncreasedafterloadReducedcontractilityCompressionofheartincardiacfossa LeftventricleDecreasedpreloadDecreasedcomplianceVariableeffectson autonomousnervoussystemcontrolof contractilityDecreasedafterloadCompressionofheartincardiacfossa Mechanicalventilationaltersintrathoracicpressuresandtherebyaffectsthecardiovascularsystem mainlytherightventricle 25 CardiovasculareffectsofmechanicalventilationandapplicationofPEEP 26 Effectsofincreaseinairwaypressureandvolume 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 27 Hemodynamicmonitoring Bloodpressure 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 28 Hemodynamicmonitoring CVP 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 29 Hemodynamicmonitoring CVP 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 30 Hemodynamicmonitoring CVP 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 31 Hemodynamicmonitoring CVP 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 32 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PaO2 33 Diagnosticusesofventilatoryvariationinvascularpressurewaves Respiratoryvariationsincentralvenouspressure Interactionofvenousreturnandcardiacfunctioncurveswithrespiratoryvariation 34 Interactionofvenousreturnandcardiacfunctioncurveswithrespiratoryvariations 35 Evaluationofrespiratoryfunction 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 36 Evaluationofrespiratoryfunction 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 37 Evaluationofrespiratoryfunction 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 38 Evaluationofrespiratoryfunction 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 39 Exampleofpulmonaryarteryocclusionpressure Ppao areflectionofleftatrialpressure andCVPinapatientonapressuresupportof6cmH2O 40 Conclusion 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 41 Usingheart lunginteractionstoassessfluidresponsivenessduringmechanicalventilation 42 Respiratoryvariationsinarterialpressureandstrokevolume 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 43 Respiratorychangesinairwayandarterialpressuresinamechanicallyventilatedpatient Thepulsepressure systolicminusdiastolicpressure ismaximal PPmax attheendoftheinspiratoryperiodandminimal PPmin threeheartbeatslater ieduringtheexpiratoryperiod SVRI CI MAP CVP MAP CI SVRI CVP 44 Usingheart lunginteractionstoassessfluidresponsivenessduringmechanicalventilation Relationshipbetweentherespiratorychangesinpulsepressurebeforevolumeexpansion Baseline PP andthevolumeexpansion inducedchangesincardiacindex y axis in40septicpatientswithacutecirculatoryfailure Thehigher PPisbeforevolumeexpansion themoremarkedtheincreaseincardiacindexinducedbyvolumeexpansion MichardF AmJRespirCritCareMed2000 162 134 138 45 Usingheart lunginteractionstoassessfluidresponsivenessduringmechanicalventilation RelationshipbetweentherespiratorychangesinpulsepressureonZEEP y axis andthePEEP inducedchangesincardiacindex x axis in14ventilatedpatientswithacutelunginjury Thehigher PPisonZEEP themoremarkedthedecreaseincardiacindexinducedbyPEEP MichardF AmJRespirCritCareMed1999 159 935 939 46 47 Usingheart lunginteractionstoassessfluidresponsivenessduringmechanicalventilation 48 Usingheart lunginteractionstoassessfluidresponsivenessduringmechanicalventilation 49 50 Usingheart lunginteractionstoassessfluidresponsivenessduringmechanicalventilation MichardF AmJRespairCritCareMed1999 159 935 939 51 Determinantsofpulsevariation 52 Ventilatoryvariationsinarterialpressureorstrokevolumehavealsobeenshownnottobepredictiveinpatientswithsmallertidalvolumes increasedWestzoneIIconditionsandinpatientswithpulmonaryhypertension 24 25 26 53 Hemodynamicchangesduringdiscontinuationofmachanicalventilationinmedicalintensivecareunitpatients 54 Hemodynamicchangesduringdiscontinuationofmachanicalventilationinmedicalintensivecareunitpatients 55 Hemodynamicchangesduringdiscontinuationofmachanicalventilationinmedicalintensivecareunitpatients 56 Hemodynamicchangesduringdiscontinuationofmachanicalventilationinmedicalintensivecareunitpatients 57 Patternsofcardiacfunctionandplasmacatecholaminelevelsdifferedbetweenpatientswhodidordidnotachievespontaneousventilationwithatrialofcontinuouspositiveairwaypressure Cardiacfunctionmustbesystematicallyconsideredbeforeandduringthereturntospontaneousventilationtooptimizethelikelihoodofsuccess SusanKF AmericanJournalofCriticalCare 2006 15 580 594 58 summary EffectsofincreaseinairwaypressureandvolumeonrightandleftventricleHeart lunginteractionsmayplayaroleinthemanifestationsandtreatmentofavarietyofdisordersUsingheart lunginteractions PPV canassessfluidresponsivenessduringmechanicalventilationCardiacfunctionmustbesystematicallyconsideredbeforeandduringthereturntospontaneousventilationtooptimizethelikelihoodofsuccess 59 谢谢 60 Hypoxicpulmonaryvasoconstrictioninhumanlungs Anaesthesiology1997 86 308 315 61 Hypoxicpulmonaryvasoconstrictioninhumanlungs 62 Modelofthecirculationshowingfactorsthatinfluencesystemicvenousdrainage RHandintrathoracicgreatveinsaresubjectedtopleuralpressure PPl whichvariesthroughouttherespiratorycycle IAPincreaseswithinspiratorydiaphragmaticdescent andnormalisestoatmospheric Patmos withexpiration Peripheralvenouspressureisunaffectedbyrespirationandsoremainsatatmosphericpressurethroughouttherespiratorycycle Systemicvenousdrainage brokenarrow dependsonadrivi