CardiovascularPhysiology

（心血管生理學）Themechanismthatcouplesexcitation–anactionpotentialintheplasmamembraneofthemusclecell–andcontractionofheartmuscleExcitation-ContractionCouplingInCardiacMusclePassageofanactionpotentialalongthetransversetubuleopensnearbyvoltage-gatedcalciumchannels,the“ryanodinereceptor,”locatedonthesarcoplasmic

reticulum,andcalciumionsreleasedintothecytosolbindtotroponin.

Thecalcium-troponincomplex“pulls”tropomyosinoffthemyosin-bindingsiteofactin,thusallowingthebindingofthecross-bridge,followedbyitsflexingto

slidetheactinfilament.Excitation-contractioncouplinginskeletalmuscleCalciumionsregulatethecontractionofcardiacmuscle: theentryofextracellularcalciumionscausesthereleaseofcalciumfromthesarcoplasmicreticulum(calcium-inducedcalciumrelease[鈣誘導的鈣釋放]),thesourceofabout95%ofthecalciuminthecytosol.

Excitation-contractioncouplingincardiacmuscleClickheretoplaytheCardiacECCouplingFlashAnimationCardiaccycle（心動周期）ThecardiaceventsthatoccurfrombeginningofoneheartbeattothebeginningofthenextarecalledthecardiaccyclePressureVolumeValvesBloodflowWhathappensintheheartduringeachcardiaccycle?Systole:ventriclescontracting Diastole: ventriclesrelaxedClickheretoplaytheMechanicalEventsoftheCardiacCycleFlashAnimationMechanicalEventsoftheCardiacCycleSummaryofeventsintheleftatrium,leftventricle,andaortaduringthecardiaccyclePressurechangesintherightheartduringacontractioncycle.Atria──primerpumpVentricles──majorsourceofpowerRoleofatriaandventriclesduringeachcardiaccycleHeartSounds1stsoundsoftlow-pitchedlubassociatedwithclosureoftheAVvalvesMarkstheonsetofsystole2ndsoundlouderdupassociatedwithclosureofthePAandaorticvalvesOccursattheonsetofdiastoleChestsurfaceareasforauscultationofnormalheartsoundsFourtraditionalvalueareas–Aorticspace:2RIS–Pulmonicvalve:2LIS–Tricuspidvalve:4ICSLLSB–Mitralvalve:ApexRIS--rightintercostalspaceLIS—leftintercostalspaceICS--intercostalspaceLLSB--leftlowersternalborderPhonocardiogram（心音圖）HeartvalvedefectscausingturbulentbloodflowandmurmursAcuterheumaticfever

Mitralstenosis--Accentuatedfirstsound

Mitralstenosis–Presystolicmurmur

Mitralregurgitation--systolicmurmurAorticinsufficiency--Loudsystolicejectionmurmur,thirdsound

EvaluationofHeartPumpingStrokevolume(SV)（搏出量）:volumeofbloodpumpedperbeat

SV=EDV–ESVEDV:end-diastolicvolume（舒張末期容積）ESV:end-systolicvolume（收縮末期容積） ~70ml(60~80ml)heartenlargementStrokevolumeforevaluatingdifferentpatients?2.Ejectionfraction(EF)（射血分數）EF=(SV/EDV)x100%55~65%3.Cardiacoutput(CO)（心輸出量）:thetotalvolumeofbloodpumpedbyeachventricleperminute CO=SVxheartrate(HR) 5L/min(4.5~6.0L/min)Whatparametersforcomparisonofpeopleindifferentsize?4.Cardiacindex(CI)（心指數）:cardiacoutputpersquaremeterofbodysurfacearea3.0~3.5L/min?m25.Cardiacreserve（心力儲備）:themaximumpercentagethatthecardiacoutputcanincreaseabovethenormallevelInthenormalyoungadultthecardiacreserveis300to400percentAchievedbyanincreaseineitherstrokevolume(SV)orheartrate(HR)orbothMeasurementofCardiacFunctionEchocardiographyCardiacangiographyCoronaryAngiographyfroma56-year-oldmanpresentedwithunstableanginaandacutepulmonaryedemaRerkpattanapipatP,etal.Circulation.1999;99:2965RegulationofheartpumpingRegulationofstrokevolume1.Preload–Frank-Starlingmechanism

Preload（前負荷）ofventricles:end-diastolicvolume(EDV)end-diastolicpressure(EDP)Frank-Starlingmechanism(Intrinsicregulationorheterometricregulation)（內在調節，或，異長調節）ThefundamentalprincipleofcardiacbehaviorwhichstatesthattheforceofcontractionofthecardiacmuscleisproportionaltoitsinitiallengthSignificance:PreciseregulationofSVToincreasetheheart’sstrokevolume: fillitmorefullywithblood.Theincreasedstretchoftheventriclewillalignitsactinandmyosininamoreoptimalpatternofoverlap.ControlofstrokevolumeFrank-StarlingmechanismVentricularfunctioncurve(Frank-Starlingcurve)Ventricularfunctioncurve(Frank-Starlingcurve)Factorsaffectingpreload(EDV)(1)VenousreturnFillingtimeVenousreturnrateCompliance(2)Residualbloodinventriclesafterejection2.Afterload（后負荷）(Usuallymeasuredasarterialpressure)AfterloadhasverylittleeffectonthenormalventricleHowever,assystolicfailuredevelopsevensmallincreasesinafterloadhavesignificanteffectsoncompromisedventricularsystolicfunctionConversely,smallreductionsinafterloadinafailingventriclecanhavesignificantbeneficialeffectsonimpairedcontractility

Congestiveheartfailure(CHF)

3.Myocardialcontractility(Inotropicstate)（心肌收縮性[變力狀態]）Homometricregulation（等長調節）Tofurtherincreasethestrokevolume:

fillitmorefullywithblood AND deliversympatheticsignals(norepinephrineandepinephrine); itwillalsorelaxmorerapidly,allowingmoretimetorefill.Sympatheticsignals(norepinephrineandepinephrine)causeastrongerandmorerapidcontractionandamorerapidrelaxation.FactorsregulatingcontractilityHRCO(CO=SVxHR)HRContractility(Treppeeffect)HR

diastolicfillingtime

Regulationofheartrate40~180/min，HRCO>180/min，or<40/min，CO

ControlofheartrateTospeeduptheheartrate:deliverthesympathetichormone,epinephrine,and/orreleasemoresympatheticneurotransmitter(norepinephrine),and/orreducereleaseofparasympatheticneurotransmitter(acetylcholine).T,ions,metabolites,otherhormonesStaircasephenomenon(Treppeeffect,Force-frequencyrelationship)Increaseinrateofcontraction(heartrate)causesincreaseincontractilityToincreaseSV,increase:

end-diastolicvolume,

norepinephrinedeliveryfrom

sympatheticneurons,andepinephrinedeliveryfromtheadrenalmedulla.ToincreaseHR,increase:norepinephrinedeliveryfromsympatheticneurons,andepinephrinedeliveryfromadrenalmedulla(reduceparasympathetic).Itisnotpossible,undernormalcircumstances,toincreaseonebutnottheotherofthesedeterminantsofcardiacoutput.CaseA70-year-oldmanwasadmittedtothehospitalwithshortnessofbreath,severefatigueandweakness,abdominaldistension,andswellingofankles.Atnightherequiresfourpillowsandoftenwakesupbecauseofacuteairhunger.Hishistoryrevealedepisodesofanginapectorisandaprogressiveshortnessofbreathwithexertionforseveralyears.Onexaminationthechiefabnormalitieswereslightcyanosis(bluishcasttotheskin),distensionoftheneckveins,rapidrespirations(20/min),rales(cracklingsounds)atthelungbasesbilaterally,anenlargedheartwithslighttachycardia(110beats/min)andadiastolicgalloprhythm(soundslikegalloping