CARDIOVASCULAR PHYSIOLOGY: THE HEARTfaculty.mtsac.edu/mpresch/36_lecture_files_unit_3/18 The Heart S17.pdf · Cardiac Muscle •Characteristics –Some cells in the atria secrete

CARDIOVASCULARPHYSIOLOGY:THEHEART

PhysiologyUnit3

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CardiovascularSystemOverview• Cardiovascularsystemcomponents

– Heart– Bloodvessels– Blood

• Cardiovascularsystemfunctions– Transportationofsubstances

• Respiration• Nutrition• Excretion• Hormones

– Regulation– Protection

CardiacMuscle• Characteristics

– Somecellsintheatriasecreteapeptidehormonecalledatrialnatriureticfactor(ANF)

• Causesnatriuresis• Vasodilation

• Conductingsystem– 1%ofcells– Initiatesheartbeatandspreadstheimpulsethroughouttheheart

• Innervation• Bloodsupply

– Coronarycirculation

HeartbeatCoordination• SAnodeisthepacemakerof

theheart– Initializesdepolarization– Determinesheartrate

• Pathway– SAnode– Acrossatria,thendown– AVnode– BundleofHis

• R/Lbundlebranches

– Purkinjefibers

Sinus Rhythm: Heartbeat Dance

SequenceofCardiacExcitation

MyocardialActionPotential

• vgNa+ channelsopen(depolarization)

• L-typeCa2+channelsopen• Membraneremainsdepolarized– Ca2+influxsustainsdepolarization

– K+ channelsremainclosed

• vgK+ channelsopen(repolarization)

RMP = -90 mVThreshold = -60 mV

NodalCellActionPotential• Pacemakerpotential

– Slowdepolarization– Automaticity(spontaneous,

rhythmical)

• Voltage-gatedK+ channelsclose

• F-typeNa+ channelsopenwhenthemembranepotentialisatnegativevalues

• T-typeCa2+channelsopenbriefly– InwardCa2+current– Finaldepolarizingboostto

thresholdNodal Cell threshold -40mmHg

ElectricalEventsoftheHeart• Electrocardiogram(ECG)

– MeasuresthecurrentsgeneratedintheECFbythechangesinmanycardiaccells

• Pwave– Atrialdepolarization

• QRScomplex– Ventriculardepolarization– Atrialrepolarization

• Twave– Ventricularrepolarization

Excitation-ContractionCoupling• Ca2+enteringthrough

L-typeCa2+channelstriggersthereleaseofmoreCa2+fromtheryanodinereceptorsintheSR– Calciuminducedcalcium

release

• Cross-bridgecyclingoccurs• ContractionendswhenCa2+

ispumpedbackintotheSRbyCa2+/ATPasepumpsandNa+/Ca2+ counter-transporters

RefractoryPeriodoftheHeart

• Longabsoluterefractoryperiodpreventstetany– Musclecannotbestimulatedintimetoproducesummation

• Absoluterefractoryperiodforcardiacmuscleis20-200ms– Skeletalmuscle1-2ms

MechanicalEventsoftheHeart• Cardiaccycle

– Pressureandvolumechangesthatoccurduringthecardiaccycle– Averageheartrate72bpm– Eachcardiaccyclelasts0.8s

• 0.3sinsystole• O.5sindiastole

• 2alternatingphases– Systole

• Ventricularcontractionandbloodejection– Diastole

• Ventricularrelaxationandbloodfilling

CardiacCycle

CardiacCycleSystole

• IsovolumetricVentricularContraction–Ventriclecontracting

• Musclefibersdevelopingtension• Musclefibersdonotshorten• Increasingpressureinsidetheventricles

–Allvalvesclosed–Nobloodejection–Ventricularvolumeremainsthesame

CardiacCycleSystole

• VentricularEjection– Pressureintheventriclesexceedpressureinaorta/pulmonarytrunk

– Semilunarvalvesopen– Bloodforcedintoaorta/pulmonarytrunk– Musclefibersshorten– Strokevolume(SV)

• Volumeofbloodejectedduringsystole• SV=135mL(EDV)– 65mL(ESV)• AverageSVis70mL/beat(0.07L/beat)

CardiacCycleDiastole

• IsovolumetricVentricularRelaxation–Ventriclesbegintorelax– Semilunarvalvesclose–AVvalvesclosed–Nobloodenteringorleavingtheventricles–Ventricularvolumeremainsthesame

CardiacCycleDiastole

• VentricularFilling–AVvalvesopen–Bloodflowsfromatriatoventricles–80%ofventricularfillingispassive–Atrialcontractionoccursattheendofdiastole• Atrialkickmovestheremaining20%ofbloodinatriaintoventricles

CardiacCycleVolumes

• End-diastolicvolume– EDV– Volumeintheventriclesattheendofdiastole

• End-systolicvolume– ESV– Volumeintheventriclesattheendofsystole

PressureChanges

VolumeChanges

ECG

HeartSounds

• Lub– Softsound– ClosingoftheAVvalves– Onsetofsystole

• Dup– Loudersound– Closingofthesemilunarvalves

– Onsetofdiastole

CardiacOutput(CO)

• VolumeofbloodpumpedoutoftheventriclesexpressedasL/min– Volumeofbloodflowingthrougheitherthepulmonaryorsystemiccircuitperminute

• CO=HRxSV• CO=72beats/minx0.07L/beat• CO=5.0L/min• Totalbloodvolumeispumpedaroundthecircuitonceeachminute– 1,440perday!

ControlofHeartRateHRisavariablethatdeterminesCO

• 100BPMwithoutnerveorhormoneinfluenceontheSAnode

• However,SAnodeisunderconstantinfluenceofnervesandhormones– Activityofthe

parasympatheticnervescausesadecreaseinheartrate

– Activityofsympatheticnervescausesanincreaseinheartrate

ControlofHeartRateHRisavariablethatdeterminesCO

• Sympatheticstimulation– Increasesslope– IncreasesF-typeNa+ channelpermeability

– Fasterdepolarization

• Parasympatheticstimulation– Slopedecreases– HyperpolarizesplasmamembraneofSAnode

– IncreasesK+ permeability

ControlofHeartRateHRisavariablethatdeterminesCO

• Epinephrine– IncreasesHR– Bindstobeta-adrenergicreceptorsintheSAnode

• Heartrateisalsosensitivetochangesin:– BodyTemperature– Plasmaelectrolyteconcentrations

• K+

• Ca2+

ControlofStrokeVolumeSVisavariablethatdeterminesCO

• Ventriclesdonotcompletelyemptyduringcontraction

• MoreforcefulcontractioncanproduceanincreaseinSV bycausinggreateremptying

• 3mainfactors1. ChangesinEDV (preload)2. Changesincontractility3. Changesinafterload

• arterialpressuresagainstwhichtheventriclespump• Increaseintotalperipheralresistance(TPR)

Starling’sLawoftheHeartRelationshipbetweenEDVandSV

• Ventriclescontractmoreforcefullyduringsystolewhenithasbeenfilledtoagreaterdegreeduringdiastole

• SVincreasesasEDVincreases

• SVisDependentofEDV• Increaseinvenousreturn

forcesanincreaseinCObyincreasingEDVwhichincreasesSV

SympatheticRegulation

• Sympatheticnervesinnervatetheentiremyocardium

• NEandEpibindtobeta-adrenergicreceptorstoincreasecontractility– IncreasesstrengthofcontractionatanygivenEDV

– SVisIndependentofEDV

– Leadstoanincreaseinejectionfraction

EjectionFraction(EF)

• EFquantifiescontractility• EF=SV/EDV• Underrestingconditions,averageisbetween50–75%

• IncreasedcontractilitycausesincreasedEF

SympatheticRegulation

• Increasedsympatheticactivity– IncreasesHRwithoutdecreasingCO

– Increasescontractility– VentriclescontractmoreforcefullytocompensatefortheincreaseinHR

SympatheticRegulationofMyocardialContractility

ControlofCardiacOutputSummary