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Weightoftheheart300gWork:75/min,10000beats/day35millionbeats/year,2.5billionbeats/life70ml/beat,7200l/dayTheworkoftheheartinonelifeisequivalenttolifting30tonstotheMountEverestThebusyandhardworkingheart!IntercalateddiscsCardiacmuscletissueisstriatedwiththemyocytescontainingusuallyjustonecentralnucleusandbeingconnectedtoeachotherbyintercalateddiscsFunctionofintercalateddiscs:InterlockadjoiningcellsPreventadjoiningcellsfrompullingapartwhenheartcontracts—desmosomesIonflow—gapjunctions,toelectricallystimulateneighbors—actasunit心肌收縮的“全或無〞現(xiàn)象相鄰的心肌細(xì)胞是由閏盤連接,由于閏盤的特殊結(jié)構(gòu)和特性,興奮可以通過它由一個(gè)心肌細(xì)胞傳播到另一個(gè)心肌細(xì)胞。因此,整個(gè)心室〔或整個(gè)心房〕可以看成是一個(gè)功能上相互聯(lián)系的合胞體,產(chǎn)生于心室某一處的興奮可以在心肌細(xì)胞之間迅速傳遞,引起組成心室所有心肌細(xì)胞幾乎同步收縮。Ca2+releaseduringExcitation-ContractioncouplingRyanodyneRCa-releasech.ActionpotentialtravelsdownTtubulesVoltage-gatedCa2+channelsactivated,Ca2+flowsoutSRintocytoplasmCa2+channelsclosewhenactionpotentialends.ActivetransportpumpscontinuallyreturnCa2+toSRCaATPase(SERCA)Calciuminducedcalciumrelease,CICRSkeletalVs.CardiacMuscleContractionImpulsegeneration:Intrinsicincardiacmuscle,extrinsicinskeletalmusclePlateauphase:Presentincardiacmuscle,absentinskeletalmuscleRefractoryperiod:longincardiacmuscle,shorterinskeletalmuscleSummation:Impossibleincardiacmuscle,possibleinskeletalmuscleExtracellularcalcium-dependentincardiacmuscleContractilityNotetaniccontractionSimultaneouscontractionThecontractionisreliantonexogenousCa2+HeartValves1.Atrioventriculara.tricuspid--betweenRAandRV;threeleafletsb.Bicuspid--betweenLAandLV;twoleaflets2.Semilunara.pulmonic--threeleafletsb.aortic--threeleafletsPreventbackwardregurgitationProvidelowresistancetoforwardflowHeartValvesSystemicandPulmonaryCirculationHeartChambersCardiacCycleDiastoleSystoleI.TheCardiacCycleConcept:TheperiodfromtheendofoneheartcontractiontotheendofthenextProperties:1)Diastoleislongerthansystole2)Thesequenceofsystoleanddiastole2ThePhasesoftheCardiacCyclePeriodofisometric(isovolumetricorisovolumic)contractionEvents:ventricularcontraction
ventricularpressurerise
atrioventricularvalveclose
theventricularpressureincreasesharplyPeriod:0.05secImportance:enabletheventricularpressuretorisetothelevelofaorticpressure(after-load)(2)
PeriodofejectionEvents:ventricularcontractioncontinuouslytheventricularpressureriseabovethearterialpressuresemilumarvalvesopenbloodpoursoutoftheventriclesRapidejectionperiod(0.10s,70%ofthestrokevolume)Reducedejectionperiod(0.15s,30%ofthestrokevolume)(3)Periodofisometric(isovolumic)relaxationEvents:
ventricularmusclerelaxtheventricularpressurefalllowerthantheaorticpressureaorticvalveclosetheventricularpressurefallsharplyPeriod:0.06-0.08sImportance:Enabletheventricularpressurefalltothelevelneartheatrialpressure(4)PeriodoffillingoftheventriclesEvents:Ventricularmusclerelaxcontinuouslytheventricularpressureisequalorlowerthantheatrialpressureatrioventricularvalveopenbloodaccumulatedintheatriarushesintotheventricularchambersquicklyfromtheatriumtotheventricle.Periodofrapidfilling.(0.11s,amountoffilling,2/3)Periodofreducedfilling(0.22s,littlebloodfillsintotheventricle)(5)AtrialsystoleSignificance,30%ofthefillingDuringhighoutputstatesorinthefailingheart,theamountaddedbyatrialcontractionmaybeofmajorimportanceindeterminingthefinalcardiacoutput.CARDIACCYCLECARDIACCYCLEAtrialSystoleMitralClosesIsovolumiccontract.AorticopensS1RapidEjectionReducedEjectionIsovolumicRelax.AorticclosesRapidVentricularFillingMitralopensS2ReducedVentricularFillingAtrialSystolecwave,bulgingoftheA-Vvalveswhentheventriclesbegintocontract2〕Pressurechangesintheatria,thea,c,andvwaves.awave,theatrialcontractionvwave,attheendofventriclecontraction,causedbytheaccumulatedbloodintheatriawhiletheA-VvalvesareclosedThesoundsheardoverthecardiacregionproducedbythefunctioningoftheheart.HeartSoundsHeartSoundsS1-firstsoundAtrioventricularvalvesandsurroundingfluidvibrationsasvalvescloseatbeginningofventricularsystoleS2-secondsoundResultsfromclosureofaorticandpulmonarysemilunarvalvesatbeginningofventriculardiastoleS3-thirdsoundisproducedbyvibrationsoftheventricularwallswhensuddenlydistendedbytherushofbloodfromtheatriaIICardiacOutputStrokeVolume–Thevolumepumpedbytheheartwitheachbeat,=enddiastolevolume〔125ml〕–endsystolevolume〔55ml〕,about70ml2.EjectionFraction–Strokevolumeaccountsforthepercentageoftheenddiastolicvolume,=strokevolume/enddiastolevolumeX100%,normalrange,55-65%LeftVentricularVolumes-Definitions EndDiastolicVolume(EDV) Volumeattheendofdiastole (endofventricularfilling)EndSystolicVolume(ESV)Volumeattheendofsystole(endofventricularcontraction)StrokeVolume(SV)=EDV-ESVEjectionFraction(EF)=SV/EDV
Leftventricularnorm:62%EjectionFractionisthebestindicatorofheartperformanceanddiseaseprognosis3.MinuteVolume,orCardiacOutput–thevolumeofthebloodpumpedbyoneventricle,=strokevolumeXheartrate.Itvarieswithsex,age,andexercise4.CardiacIndex,thecardiacoutputpersquaremeterofbodysurfacearea.thenormalizeddatafordifferentsizeindividuals,thenormalrangeisabout3.0–3.5L/min/m2HeartWorkStrokework〔kJ〕=strokevolume(L)(meanartrialpressure-meanpressureofleftatrium)DeterminantsofCardiacOutput(CO)PreloadHeartRate
AfterloadContractilityCardiacOutputStrokeVolumeDefinitionsPreloadamountofstretchontheventricularmyocardiumpriortocontractionAfterloadthearterialpressure(orsomeothermeasureoftheforce)thataventriclemustovercomewhileitcontractsduringejectionimpedancetoventricularejectionContractilitymyocardium’sintrinsicabilitytoefficientlycontractandemptytheventricle(independentofpreload&afterload)DefinitionsDeterminantsofCardiacOutput1.PreloadtheFrank-StarlingmechanismLeftventricle(LV)functioncurve,orFrank-Starlingcurve(1914):Optimalinitialpreload,12-20mmHg(Sarcomere,2.0–2.2μm)NormalrangeoftheLVEDP,5-6mmHgWhentheLVEDP>20mmHg,LVworkismaintainedatalmostthesamelevel,doesnotchangewiththeincreaseofLVEDPMechanismConceptofheterometricregulationStarlingsLawoftheHeartandContractilitySVleftventricularperformancepreload(venousreturn)↑
contractilitynormalcontractility↓contractility(heartfailure)Frank-StarlingSignificanceMostimportantfunctionistobalancetheoutputsofleftandrightventriclesIfoutputofrightventricleexceedsleft:PulmonaryvolumeincreasesIncreasedpressureinpulmonaryveinsLeftventricular(LV)fillingpressureincreasesLVbecomesmoredistended(stretched)IncreasedstrokevolumeWhycanthemyocardiumincreaseforceofcontractioninresponsetoincreasedfillingpressure?(1)Overlapofactinfilamentscausingmechanicalinterferenceatsarcomerelengthsbelow2M,soneedtostretchmoretocontractmusclemoresarcomere(2)Asmusclesstretched,sensitivitytocalciumincreases(thismayinvolvetroponin,theproteinthatregulatesaccesstobindingsitesonactin)Periodoftheventriclediastole(filling)–heartrateSpeedofthevenousreturn(differencebetweenthevenouspressureandatrialpressure)Factorsdeterminingthepreload(LVEDP)Periodoftheventriclediastole(filling)–heartrateSpeedofthevenousreturn(differencebetweenthevenouspressureandatrialpressure)ImportanceoftheheterometericregulationIngeneral,heterometricregulationplaysonlyashort-timerole,suchasduringthebodyposturechange,arterypressureincrease,andunbalanceofventricularoutputs.Inotherconditions,suchasexercise,cardiacoutputismainlyregulatedbyhomometricregulation.Factorsdeterminingthepreload(LVEDP)DeterminantsofCardiacOutput-AfterloadShorttimechangeofthearterialpressureTransientarterialpressureriseisovolumetriccontractionphasebecomelongerperiodofejectionshorterstrokevolumelessmorebloodleftintheleftventricle
LVEDPincreasethroughheterometericregulationstrokevolumereturntonormalinnextbeat.Longtimehigharterialpressure
throughneuralandhumoralregulation
thestrokevolumeismaintainedatnormallevel
pathogenesisofthecardiovascularsystemContractility(neuralandhumoralregulation)Sympatheticnerve(norepinephrine)ortheepinephrineandnorepinephrine(adrenalgland)enhancethestrengthandthevelocityofthecardiaccontraction.Thechangeofmyocardialpropertyisindependentofthepreload.Importance:exertalong–timeinfluenceonthecardiacoutput.DeterminantsofCardiacOutput-Contractility0120dP/dtdP/dtUsingVentricularPressureCurvesasIndicesofContractility&CardiacFunctionNormalHeartFailuredP/dt=changeinpressureperunitoftimeNoteelevationinenddiastolicpressureTIME↑Contractilityrelatedto:
beta-sympatheticadrenergicnerves catecholamines: epinephrine norepinephrine drugs: digitalis symp
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