循環(huán)系統(tǒng)生理

CardiovascularPhysiology

（心血管生理學(xué)）QiangXIA(夏強),PhDDepartmentofPhysiologyRoomC518,BlockC,ResearchBuilding,SchoolofMedicineTel:88208252Componentsofthecardiovascularsystem:HeartVascularsystemBloodSystemOverviewPlasmaincludeswater,ions,proteins,nutrients,hormones,wastes,etc.Thehematocritisa

rapidassessment

ofbloodcomposition.

Itisthepercentofthe

bloodvolumethatis

composedofRBCs

(redbloodcells).Theheartisthepumpthatpropelsthebloodthroughthesystemicandpulmonarycircuits.Redcolorindicatesbloodthatisfullyoxygenated.Bluecolorrepresentsbloodthatisonlypartiallyoxygenated.Thedistributionofbloodinacomfortable,restingpersonisshownhere.Dynamicadjustmentsinblooddeliveryallowapersontorespondtowidelyvaryingcircumstances,includingemergencies.FunctionsoftheheartPumping（泵血）Endocrine（內(nèi)分泌）Atrialnatriureticpeptide(ANP)Brainnatriureticpeptide(BNP)OtherbioactivatorsThemajorexternalandinternalpartsoftheheartareshowninthisdiagram.Theblackarrowsindicatetheroutetakenbythebloodasitispumpedalong.TheHeartValvesoftheheartThegeneralrouteofthebloodthroughthebodyisshown,includingpassagethroughtheheart(coloredbox).Themajortypesofcardiacmuscle:AtrialmuscleVentricularmuscleSpecializedexcitatoryandconductivemuscleContractilecells（收縮細胞）Autorhythmiccells（自律細胞）ConductingsystemoftheheartCardiacmuscleThesinoatrialnodeistheheart’spacemakerbecauseitinitiateseachwaveofexcitationwithatrialcontraction.TheBundleofHisandotherpartsoftheconductingsystemdelivertheexcitationtotheapexoftheheartsothatventricularcontractionoccursinanupwardsweep.SequenceofcardiacexcitationGeneralprocessofexcitationandcontractionofcardiacmuscleInitiationofactionpotentialsinsinoatrialnodeConductionofactionpotentialsalongspecializedconductivesystemExcitation-contractioncouplingMusclecontractionClickheretoplaytheConductingSystemoftheHeartFlashAnimation

(250-300bpm)(350-600bpm)ScalingfromtheleveloftheorganelletotheorganTransmembranepotentialsrecordedindifferentheartregionsTransmembranepotentialsinepicardiumandendocardiumTransmembranepotentialofventricularcellsanditsionicmechanismsRestingPotential:-90mVActionPotentialPhase0:DepolarizationPhase1:EarlyphaseofrapidrepolarizationPhase2:Plateau（平臺期）Phase3:LatephaseofrapidrepolarizationPhase4:RestingphaseRestingpotentialK+equilibriumpotentialNa+-inwardbackgroundcurrentElectrogenicNa+-K+pumpIonicmechanismsPhase0Thresholdpotential(-70mV)OpeningoffastNa+channelRegenerativecycle（再生性循環(huán)）Theactionpotentialofamyocardialpumpingcell.Phase1Transientoutwardcurrent,Ito K+currentactivatedat–20mVopeningfor5~10ms

Phase2Inwardcurrent Outwardcurrent(Ca2+&Na+)(K+current)TypesofCa2+channelsincardiaccells:

(1)L-type(long-lasting)(Nowycky,1985)(2)T-type(transient)(Nowycky,1985)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-typeOutwardcurrent(K+current):

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

IK:ProgressivelyincreasedIK1:RegenerativeK+OutwardCurrentPhase4Na+-Ca2+exchangeSarcolemmalCa2+pumpSRCa2+pumpNa+-K+pumpa,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:10.1038/415213aClickheretoplaytheActionPotentialinCardiacMuscleCellFlashAnimation

TransmembranepotentialsrecordedindifferentheartregionsTransmembranepotentialofautorhythmiccellsanditsionicmechanismsContractilecells

AutorhythmiccellsPhase4stablepotential

Phase4spontaneousdepolarization

（4期自動去極化）Restingpotential Maximalrepolarizationpotential

（最大復(fù)極電位）Purkinjecells:Fastresponseautorhythmiccells4IonicmechanismPhase0~3：similartoventricularcellsPhase4：(1)If–Funnycurrent,Pacemakercurrent（起搏電流）

(2)IkDecay（鉀電流衰減）CharacteristicsofIfchannelNa+,K+Voltage-&time-dependentActivation──Repolarizedto-60mVFullactivation──Hyperpolarizedto-100mVInactivation──Depolarizedto-50mVBlockedbyCesium(Cs),notbyTTXSinoatrialcellsMaximalrepolarizationpotential-70mVThresholdpotential-40mVPhase0,3,4Sinoatrialcells:Slowresponseautorhythmiccells403IonicmechanismPhase0:ICa(ICa,L)403Phase3:InactivationofL-typeCa2+channelOutwardK+current(Ik)403Phase4：IkdecayInactivatedwhenrepolarizedto-60mVICa,TActivatedwhendepolarizedto-50mVIfTheactionpotentialofan

autorhythmiccardiaccell.ClickheretoplaytheActionPotentialinSANodeFlashAnimation

DuringwhichphaseoftheventricularactionpotentialisthemembranepotentialclosesttotheK+equilibriumpotential?(A)Phase0(B)Phase1(C)Phase2(D)Phase3(E)Phase4DuringwhichphaseoftheventricularactionpotentialistheconductancetoCa2+highest?(A)Phase0(B)Phase1(C)Phase2(D)Phase3(E)Phase4Whichphaseoftheventricularactionpotentialcoincideswithdiastole?(A)Phase0(B)Phase1(C)Phase2(D)Phase3(E)Phase4Thelow-resistancepathwaysbetweenmyocardialcellsthatallowforthespreadofactionpotentialsarethe(A)gapjunctions(B)Ttubules(C)sarcoplasmicreticulum(SR)(D)intercalateddisks(E)mitochondriaElectrocardiogram(ECG)（心電圖）Theelectrocardiogram(ECG)measureschangesinskinelectricalvoltage/potentialcausedbyelectricalcurrentsgeneratedbytheheartTherelationshipbetweentheelectrocardiogram(ECG),recordedasthedifferencebetweencurrentsattheleftandrightwrists,

andanactionpotentialtypicalofventricularmyocardialcells.Electrocardiogram(ECG)Thestandard12leadECG

Einthoven’sTriangleLimbleads(Bipolar)(I,II,III)Augmentedlimbleads(Unipolar)(aVR,aVL,aVF)Chestleads(Unipolar)(V1,V2,V3,V4,V5,V6)IIIIIIaVRaVLaVFV1V2V3V4V5V6WillemEinthoven:Dutchphysiologist.Hewona1924NobelPrizeforhiscontributionstoelectrocardiography.PlacementofelectrodesinelectrocardiographyNormalECG0.04secECGinterpretationMeasurementsRhythmanalysisConductionanalysisWaveformdescriptionComparisonwithpreviousECG(ifany)AnimationofanormalECGwavePwave:thesequentialdepolarizationoftherightandleftatriaQRScomplex:rightandleftventriculardepolarizationST-Twave:ventricularrepolarizationUwave:originforthiswaveisnotclear-butprobablyrepresents"afterdepolarizations"intheventriclesPRinterval:timeintervalfromonsetofatrialdepolarization(Pwave)toonsetofventriculardepolarization(QRScomplex)QTinterval:durationofventriculardepolarizationandrepolarizationSTsegment:thetimeperiodbetweentheendoftheQRScomplexandthebeginningoftheTwave,

duringwhicheachmyocyteisintheplateauphase(phase2)oftheactionpotential

NormalPartialblockCompleteblockExcitabilityAutorhythmicityConductivityContractilityElectrophysiologicalproperties（電生理特征）Mechanicalproperty（機械特征）PhysiologicalpropertiesofcardiaccellsFactorsaffectingexcitabilityRestingpotentialThresholdpotentialStatusofNa+orCa2+channelsExcitability（興奮性）Hyperkalemia（高鉀血癥）TheQRScomplexesmaywidensothattheymergewiththeTwaves,resultingina“sinewave”appearance.TheSTsegmentsdisappearwhentheserumpotassiumlevelreaches6mEq/LandtheTwavestypicallybecometallandpeakedatthissamerange.ThePwavesbegintoflattenoutandwidenwhenapatient‘sserumpotassiumlevelreachesabout6.5mEq/L;thiseffecttendstodisappearwhenlevelsreach7-9mEq/L.Sinusarrestmayoccurwhentheserumpotassiumlevelreachesabout7.5mEq/L,andcardiacstandstillorventricularfibrillationmayoccurwhenserumlevelsreach10to12mEq/L.PeriodicchangesinexcitabilityPostrepolarizationrefractorinessofslowresponsecellsValuableprotectivemechanismThelongrefractoryperiodmeansthatcardiacmusclecannotberestimulateduntilcontractionisalmostover&thismakessummation&tetanusofcardiacmuscleimpossiblePrematuresystole&compensatorypause (extrasystole)A39-year-oldladypresentingwithfrequentpalpitationslastingafewmonthsA39-year-oldladypresentstoyouwithfrequentpalpitationslastingafewmonths,whicharenotassociatedwithdizziness,syncopeorangina.Shehasenjoyedgoodhealthandisnotonanymedicationorherbalmedicine.Sheisanon-smokerandhasnoknowndiabetes,hypertensionorhypercholesterolaemia.Hermensesisregularandphysicalexaminationisunremarkableotherthanafewprematurebeats.ThisisherECG.Answers:Ventricularprematurebeatsarenoted.PrematureventricularcontractionsunmaskthePwavesHemodynamictracingstodemonstratetheincreasedvariabilityofsystolicBP(SBP),diastolicBP(DBP),andheartperiod(HP)inMIratwithfrequentVPBAutorhythmicity（自律性）

AutorhythmicitySAnode 100times/minAVnode 50times/minBundleofHis 40times/minPurkinjefibers 25times/minNormalpacemaker（正常起搏點）SAnodeLatentpacemaker（潛在起搏點）(Ectopicpacemaker[異位起搏點]underpathophysiologicalconditions) AVnode BundleofHis PurkinjefibersThemechanismsofSAnodetocontrollatentpacemakersCapture（奪獲）Overdrivesuppression（超速克制）FactorsAffectingAutorhythmicityMaximalrepolarizationpotentialThresholdpotentialTherateofphase4spontaneousdepolarizationSinusBradycardia（竇性心動過緩）

PacemakerConductivity（傳導(dǎo)性）GapjunctionSAnode 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（房室延擱）:AsynchronizationofatrialandventriculardepolarizationtoprovideadequatecardiacoutputFactorsAffectingConductivityStructuralfactorsDiameterofcardiaccellsGapjunctionsatIntercalateddiskPhysiologicalfactorsThevelocityandamplitudeofphase0depolarizationExcitabilityofadjacentregionFirstDegreeAVBlockDefinition:1AVBisarhythminwhichtheelectricalimpulsewhichleavestheSAnodeandtravelsthroughtheatria,AVnode,BundleofHistopurkininjiefibersissloweddownandtakeslongerthannormaltoarriveatitsdestination.ThenormalPRintervalis0.12-0.20seconds.A1AVBTisgreaterthan0.20seconds.Thecauserangesfromcoronaryheartdisease,inferiorwallMI's,hyperkalemia,congenitalabnormalities,andmedicationssuchasquinidine,digitalis,betablockers,andcalciumchannelblockers.SeconddegreeAVBlocktype1(Mobitz)Definition:SeconddegreeAVblockisalsoknownasSecondDegreeTypeI,MobitzI,orWenckelbach.ThisarrhythmiaischaracterizedbyaprogressivedelayoftheconductionattheAVnode,untiltheconductioniscompletelyblocked.Thisoccursbecausetheimpulsearrivesduringtheabsoluterefractoryperiod,resultinginanabsenceofconduction,andnoQRS.ThenextPwaveoccursandthecyclebeginsagain.Possiblecausesareacuteinferiorwallmyocardialinfraction,digitalis,betablockers,calciumchannelblockers,rheumaticfever,myocarditis,orexcessivevagaltone.MobitzIIischaracterizedby2-4PwavesbeforeeachQRS.ThePRoftheconductedPwavewillbeconstantforeachQRS.Itisusuallyassociatedwithacuteanteriororanteroseptalmyocardialinfarction.Othercausesarecardiomyopathy,rheumaticheartdisease,coronaryarterydisease,digitalis,betablockers,andcalciumchannelblockers.MobitzIIhasthepotentialofprogressingintoathirddegreeheartblockorventricularstandstill.SeconddegreeAVBlockTypeIIAthirddegreeatrialventricularblockisalsoknowasacompleteheartblockartrioventricularblockof3degreeAVblock.Itisaproblemwithelectricalconduction.AllelectricalconductionfromtheatriaareblockedattheAVjunction,therefore,theatriaandtheventriclesbeatindependentlyfromeachother.Thisarrhythmiaisdangerousbecauseitsignificantlydecreasescardiacoutput,andcouldleadtoasystole.Possiblecauses:acuteinferiorandanteriormyocardicinfraction,coronaryheartdisease,excessivevagaltone,myocarditis,endocarditis,age,edemafromheartsurg