循环系统生理

CardiovascularPhysiology

（心血管生理学）QiangXIA(夏强),PhDDepartmentofPhysiologyRoomC518,BlockC,ResearchBuilding,SchoolofMedicineTel:88208252Email:xiaqiang@第1页Componentsofthecardiovascularsystem:HeartVascularsystemBloodSystemOverview第2页Plasmaincludeswater,ions,proteins,nutrients,hormones,wastes,etc.Thehematocritisa

rapidassessment

ofbloodcomposition.

Itisthepercentofthe

bloodvolumethatis

composedofRBCs

(redbloodcells).第3页Theheartisthepumpthatpropelsthebloodthroughthesystemicandpulmonarycircuits.Redcolorindicatesbloodthatisfullyoxygenated.Bluecolorrepresentsbloodthatisonlypartiallyoxygenated.第4页Thedistributionofbloodinacomfortable,restingpersonisshownhere.Dynamicadjustmentsinblooddeliveryallowapersontorespondtowidelyvaryingcircumstances,includingemergencies.第5页第6页FunctionsoftheheartPumping（泵血）Endocrine（内分泌）Atrialnatriureticpeptide(ANP)Brainnatriureticpeptide(BNP)Otherbioactivators第7页Themajorexternalandinternalpartsoftheheartareshowninthisdiagram.Theblackarrowsindicatetheroutetakenbythebloodasitispumpedalong.TheHeart第8页Valvesoftheheart第9页第10页Thegeneralrouteofthebloodthroughthebodyisshown,includingpassagethroughtheheart(coloredbox).第11页Themajortypesofcardiacmuscle:AtrialmuscleVentricularmuscleSpecializedexcitatoryandconductivemuscleContractilecells（收缩细胞）Autorhythmiccells（自律细胞）第12页Conductingsystemoftheheart第13页Cardiacmuscle第14页Thesinoatrialnodeistheheart’spacemakerbecauseitinitiateseachwaveofexcitationwithatrialcontraction.TheBundleofHisandotherpartsoftheconductingsystemdelivertheexcitationtotheapexoftheheartsothatventricularcontractionoccursinanupwardsweep.Sequenceofcardiacexcitation第15页GeneralprocessofexcitationandcontractionofcardiacmuscleInitiationofactionpotentialsinsinoatrialnodeConductionofactionpotentialsalongspecializedconductivesystemExcitation-contractioncouplingMusclecontraction第16页ClickheretoplaytheConductingSystemoftheHeartFlashAnimation

第17页(250-300bpm)(350-600bpm)第18页第19页第20页Scalingfromtheleveloftheorganelletotheorgan第21页Transmembranepotentialsrecordedindifferentheartregions第22页Transmembranepotentialsinepicardiumandendocardium第23页TransmembranepotentialofventricularcellsanditsionicmechanismsRestingPotential:-90mVActionPotentialPhase0:DepolarizationPhase1:EarlyphaseofrapidrepolarizationPhase2:Plateau（平台期）Phase3:LatephaseofrapidrepolarizationPhase4:Restingphase第24页RestingpotentialK+equilibriumpotentialNa+-inwardbackgroundcurrentElectrogenicNa+-K+pumpIonicmechanisms第25页第26页Phase0Thresholdpotential(-70mV)OpeningoffastNa+channelRegenerativecycle（再生性循环）Theactionpotentialofamyocardialpumpingcell.第27页Phase1Transientoutwardcurrent,Ito K+currentactivatedat–20mVopeningfor5~10ms

第28页Phase2Inwardcurrent Outwardcurrent(Ca2+&Na+)(K+current)第29页TypesofCa2+channelsincardiaccells:

(1)L-type(long-lasting)(Nowycky,1985)(2)T-type(transient)(Nowycky,1985)第30页Ca2+channelsDurationofcurrent long-lasting transientActivationkinetics slower faster Inactivationkinetics slower fasterThreshold

high(-35mV) Low(-60mV)cAMP/cGMP-regulated Yes NoPhosphorylation-regulated Yes NoOpeners Bay-K-8644 -Blockers varapamil Tetramethrin nifedipine,diltiazem Ni2+

Inactivationby[Ca2+]i

Yes slightPatch-clamprecording run-down relativelystableL-type T-type第31页Outwardcurrent(K+current):

(1)inwardrectifierK+current(IK1)(2)delayedrectifierK+current(IK)第32页Phase3InactivationofCa2+channelOutwardK+currentdominates

IK:ProgressivelyincreasedIK1:RegenerativeK+OutwardCurrent第33页Phase4Na+-Ca2+exchangeSarcolemmalCa2+pumpSRCa2+pumpNa+-K+pump第34页第35页a,Thekeyionchannels(andanelectrogenictransporter)incardiaccells.K+channels(green)mediateK+effluxfromthecell;Na+channels(purple)andCa2+channels(yellow)mediateNa+andCa2+influx,respectively.TheNa+/Ca2+exchanger(red)iselectrogenic,asittransportsthreeNa+ionsforeachCa2+ionacrossthesurfacemembrane.b,Ioniccurrentsandgenesunderlyingthecardiacactionpotential.Top,depolarizingcurrentsasfunctionsoftime,andtheircorrespondinggenes;centre,aventricularactionpotential;bottom,repolarizingcurrentsandtheircorrespondinggenes.Fromthefollowingarticle:CardiacchannelopathiesEduardoMarbánNature415,213-218(10January2023)doi:10.1038/415213a第36页ClickheretoplaytheActionPotentialinCardiacMuscleCellFlashAnimation

第37页Transmembranepotentialsrecordedindifferentheartregions第38页Transmembranepotentialofautorhythmiccellsanditsionicmechanisms第39页Contractilecells

AutorhythmiccellsPhase4stablepotential

Phase4spontaneousdepolarization

（4期自动去极化）Restingpotential Maximalrepolarizationpotential

（最大复极电位）第40页Purkinjecells:Fastresponseautorhythmiccells4第41页IonicmechanismPhase0~3：similartoventricularcellsPhase4：(1)If–Funnycurrent,Pacemakercurrent（起搏电流）

(2)IkDecay（钾电流衰减）第42页第43页CharacteristicsofIfchannelNa+,K+Voltage-&time-dependentActivation──Repolarizedto-60mVFullactivation──Hyperpolarizedto-100mVInactivation──Depolarizedto-50mVBlockedbyCesium(Cs),notbyTTX第44页Sinoatrialcells第45页Maximalrepolarizationpotential-70mVThresholdpotential-40mVPhase0,3,4Sinoatrialcells:Slowresponseautorhythmiccells403第46页IonicmechanismPhase0:ICa(ICa,L)403第47页Phase3:InactivationofL-typeCa2+channelOutwardK+current(Ik)403第48页Phase4：IkdecayInactivatedwhenrepolarizedto-60mVICa,TActivatedwhendepolarizedto-50mVIf第49页Theactionpotentialofan

autorhythmiccardiaccell.第50页ClickheretoplaytheActionPotentialinSANodeFlashAnimation

第51页DuringwhichphaseoftheventricularactionpotentialisthemembranepotentialclosesttotheK+equilibriumpotential?(A)Phase0(B)Phase1(C)Phase2(D)Phase3(E)Phase4第52页DuringwhichphaseoftheventricularactionpotentialistheconductancetoCa2+highest?(A)Phase0(B)Phase1(C)Phase2(D)Phase3(E)Phase4第53页Whichphaseoftheventricularactionpotentialcoincideswithdiastole?(A)Phase0(B)Phase1(C)Phase2(D)Phase3(E)Phase4第54页Thelow-resistancepathwaysbetweenmyocardialcellsthatallowforthespreadofactionpotentialsarethe(A)gapjunctions(B)Ttubules(C)sarcoplasmicreticulum(SR)(D)intercalateddisks(E)mitochondria第55页Electrocardiogram(ECG)（心电图）Theelectrocardiogram(ECG)measureschangesinskinelectricalvoltage/potentialcausedbyelectricalcurrentsgeneratedbytheheart第56页Therelationshipbetweentheelectrocardiogram(ECG),recordedasthedifferencebetweencurrentsattheleftandrightwrists,

andanactionpotentialtypicalofventricularmyocardialcells.Electrocardiogram(ECG)第57页Thestandard12leadECG

Einthoven’sTriangleLimbleads(Bipolar)(I,II,III)Augmentedlimbleads(Unipolar)(aVR,aVL,aVF)Chestleads(Unipolar)(V1,V2,V3,V4,V5,V6)IIIIIIaVRaVLaVFV1V2V3V4V5V6WillemEinthoven:Dutchphysiologist.Hewona1924NobelPrizeforhiscontributionstoelectrocardiography.第58页第59页Placementofelectrodesinelectrocardiography第60页第61页NormalECG0.04secECGinterpretationMeasurementsRhythmanalysisConductionanalysisWaveformdescriptionComparisonwithpreviousECG(ifany)第62页AnimationofanormalECGwave第63页Pwave:thesequentialdepolarizationoftherightandleftatriaQRScomplex:rightandleftventriculardepolarizationST-Twave:ventricularrepolarizationUwave:originforthiswaveisnotclear-butprobablyrepresents"afterdepolarizations"intheventricles第64页PRinterval:timeintervalfromonsetofatrialdepolarization(Pwave)toonsetofventriculardepolarization(QRScomplex)QTinterval:durationofventriculardepolarizationandrepolarizationSTsegment:thetimeperiodbetweentheendoftheQRScomplexandthebeginningoftheTwave,

duringwhicheachmyocyteisintheplateauphase(phase2)oftheactionpotential

第65页第66页NormalPartialblockCompleteblock第67页ExcitabilityAutorhythmicityConductivityContractilityElectrophysiologicalproperties（电生理特性）Mechanicalproperty（机械特性）Physiologicalpropertiesofcardiaccells第68页FactorsaffectingexcitabilityRestingpotentialThresholdpotentialStatusofNa+orCa2+channelsExcitability（兴奋性）第69页Hyperkalemia（高钾血症）TheQRScomplexesmaywidensothattheymergewiththeTwaves,resultingina“sinewave”appearance.TheSTsegmentsdisappearwhentheserumpotassiumlevelreaches6mEq/LandtheTwavestypicallybecometallandpeakedatthissamerange.ThePwavesbegintoflattenoutandwidenwhenapatient‘sserumpotassiumlevelreachesabout6.5mEq/L;thiseffecttendstodisappearwhenlevelsreach7-9mEq/L.Sinusarrestmayoccurwhentheserumpotassiumlevelreachesabout7.5mEq/L,andcardiacstandstillorventricularfibrillationmayoccurwhenserumlevelsreach10to12mEq/L.第70页Periodicchangesinexcitability第71页第72页Postrepolarizationrefractorinessofslowresponsecells第73页ValuableprotectivemechanismThelongrefractoryperiodmeansthatcardiacmusclecannotberestimulateduntilcontractionisalmostover&thismakessummation&tetanusofcardiacmuscleimpossible第74页Prematuresystole&compensatorypause (extrasystole)第75页A39-year-oldladypresentingwithfrequentpalpitationslastingafewmonthsA39-year-oldladypresentstoyouwithfrequentpalpitationslastingafewmonths,whicharenotassociatedwithdizziness,syncopeorangina.Shehasenjoyedgoodhealthandisnotonanymedicationorherbalmedicine.Sheisanon-smokerandhasnoknowndiabetes,hypertensionorhypercholesterolaemia.Hermensesisregularandphysicalexaminationisunremarkableotherthanafewprematurebeats.ThisisherECG.Answers:Ventricularprematurebeatsarenoted.第76页PrematureventricularcontractionsunmaskthePwaves第77页HemodynamictracingstodemonstratetheincreasedvariabilityofsystolicBP(SBP),diastolicBP(DBP),andheartperiod(HP)inMIratwithfrequentVPB第78页Autorhythmicity（自律性）

第79页AutorhythmicitySAnode 100times/minAVnode 50times/minBundleofHis 40times/minPurkinjefibers 25times/min第80页Normalpacemaker（正常起搏点）SAnodeLatentpacemaker（潜在起搏点）(Ectopicpacemaker[异位起搏点]underpathophysiologicalconditions) AVnode BundleofHis Purkinjefibers第81页ThemechanismsofSAnodetocontrollatentpacemakersCapture（夺获）Overdrivesuppression（超速克制）第82页FactorsAffectingAutorhythmicityMaximalrepolarizationpotentialThresholdpotentialTherateofphase4spontaneousdepolarization第83页SinusBradycardia（窦性心动过缓）

第84页Pacemaker第85页第86页Conductivity（传导性）第87页Gapjunction第88页SAnode Atria A-Vnode

0.05m/s 0.4m/s 0.02~0.05m/sHisbundle Purkinjefiber Ventricle1.2~2.0m/s 2.0~4.0m/s

1.0m/s

ConductingvelocityAtrioventriculardelay（房室延搁）:Asynchronizationofatrialandventriculardepolarizationtoprovideadequatecardiacoutput第89页FactorsAffectingConductivityStructuralfactorsDiameterofcardiaccellsGapjunctionsatIntercalateddiskPhysiologicalfactorsThevelocityandamplitudeofphase0depolarizationExcitabilityofadjacentregion第90页FirstDegreeAVBlockDefinition:1AVBisarhythminwhichtheelectricalimpulsewhichleavestheSAnodeandtravelsthroughtheatria,AVnode,BundleofHistopurkininjiefibersissloweddownandtakeslongerthannormaltoarriveatitsdestination.ThenormalPRintervalis0.12-0.20seconds.A1AVBTisgreaterthan0.20seconds.Thecauserangesfromcoronaryheartdisease,inferiorwallMI's,hyperkalemia,congenitalabnormalities,andmedicationssuchasquinidine,digitalis,betablockers,andcalciumchannelblockers.第91页SeconddegreeAVBlocktype1(Mobitz)Definition:SeconddegreeAVblockisalsoknownasSecondDegreeTypeI,MobitzI,orWenckelbach.ThisarrhythmiaischaracterizedbyaprogressivedelayoftheconductionattheAVnode,untiltheconductioniscompletelyblocked.Thisoccursbecausetheimpulsearrivesduringtheabsoluterefractoryperiod,resultinginanabsenceofconduction,andnoQRS.ThenextPwaveoccursandthecyclebeginsagain.Possiblecausesareacuteinferiorwallmyocardialinfraction,digitalis,betablockers,calciumchannelblockers,rheumaticfever,myocarditis,orexcessivevagaltone.第92页MobitzIIischaracterizedby2-4PwavesbeforeeachQRS.ThePRoftheconductedPwavewillbeconstantforeachQRS.Itisusuallyassociatedwithacuteanteriororanteroseptalmyocardialinfarction.Othercausesarecardiomyopathy,rheumaticheartdisease,coronaryarterydisease,digitalis,betablockers,andcalciumchannelblockers.MobitzIIhasthepotentialofprogressingintoathirddegreeheartblockorventricularstandstill.SeconddegreeAVBlockTypeII第93页Athirddegreeatrialventricularblockisalsoknowasacompleteheartblockartrioventricularblockof3degreeAVblock.Itisaproblemwithelectricalconduction.AllelectricalconductionfromtheatriaareblockedattheAVjunction,therefore,theatriaandtheventriclesbeatindependentlyfromeachother.Thisarrhythmiaisdangerousbecauseitsignificantlydecreasescardiacoutput,andcouldleadtoasystole.Possiblecauses:acuteinferiorandanteriormyocardicinfraction,coronaryheartdisease,excessivevagaltone,myocarditis,endocarditis,age,edema