BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A.

IMHOLTZ) HEART P1 OF 7

Theheartisresponsibleforgeneratingthepressurethatpropelsbloodthrubloodvessels.It
helpskeepoxygenatedanddeoxygenatedbloodseparateandalsoisinvolvedintheregulation
ofthebodysbloodsupply.

Theheartislocatedwithinthemediastinum,themedialcavityofthethorax.Itsapexrestson
thesuperiorsurfaceofthediaphragmandpointstowardthelefthip.Itsbasepointstowards
therightshoulder.Theheartismedialtothelungs,anteriortotheesophagusandvertebral
column,andposteriortothesternum.

Theheartisenclosedbythepericardiumadoublewalledsac.Themostsuperficiallayeristhe
fibrouspericardiumacollagenousstructurethatprotectsandanchorstheheartandprevents
itfromoverdistending.Deeperistheserouspericardium,a2layeredserousmembrane.The
parietalpericardiumistheouterofthe2andabutsthefibrouspericardium.Thevisceral
pericardiumistheinnerofthe2andistheexternalcoveringoftheheart.Itisa.k.a.the
epicardium.Theparietalandviscerallayersarecontinuouswithoneanotherwherethegreat
vesselsleavetheheart.Thepericardialcavityisthespacebtwntheparietalandviscerallayers.
Itcontainsserousfluid,whichreducesfriction.

Thewalloftheheartisdividedinto3layers.Theepicardiumisthemostsuperficialandisa.k.a.
visceralpericardium.Itiscomposedofsimplesquamousepitheliumoverlayingathinbitof
looseCT.Themyocardiumisthemiddlelayer.Itsprimarilycardiacmuscle,butalsocontains
bloodvessels,nerves,andconnectivetissue.TheCTofthemyocardiumformsadensenetwork
knownasthefibrousskeletonoftheheart.TheFSsupportstheheart(especiallythevalves),
actsasorigin/insertionforthecardiacmusclecellsandhelpsdirectthespreadofelectrical
activitywithintheheartalongdefinedpathways.Theinnerlayeristheendocardium.Itconsists
ofendothelium(simplesquamousepithelium)restingonalayerofthinconnectivetissue.It
linestheheartchambersanditsfoldscreatetheheartvalves.

Theheartisa4chamberedorganwith2superioratriaand2inferiorventricles.Thethin
interatrialseptumdividesthe2atria,whilethethickinterventricularseptumdividesthe2
ventricles.Theheartconsistsof2pumpsconnectedinseries.Eachpumpsendsbloodtoa
differentcircuit.Thepulmonarycircuitrunsbtwntheheartandthelungs.Thesystemiccircuit
runsbtwntheheartandtherestofthebodytissues.Therightsideoftheheartreceives
deoxygenatedbloodfromthesystemiccircuitandpumpsitthruthepulmonarycircuit.Theleft
sideoftheheartreceivesoxygenatedbloodfromthepulmonarycircuitandpumpsitthruthe
systemiccircuit.

Theatriaaretheheartsreceivingchambers.Theyaresmallandthinlymuscled.Largemuscle
massisnotnecessary,b/catrialmusclecontractionisonlyusedtopropelasmallamountof
bloodtotheventriclebelow.

Therightatriumreceivesbloodfromthesystemiccircuitvia3vessels:(1)Superiorvenacava
carrieslowO2/highCO2bloodfromarms,head,anduppertorso;(2)Inferiorvenacavacarries
lowO2/highCO2bloodfromthelegs,abdomen,andpelvis;(3)Coronarysinuscarrieslow
O2/highCO2bloodfromthecoronarycirculationwhichnourishestheheartwall.Theright
atriumpassesbloodtotherightventriclethruthetricuspidorifice,whichisassociatedwiththe
tricuspidvalve.

 BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A. IMHOLTZ) HEART P2 OF 7

LeftatriumreceiveshighO2/lowCO2bloodfromthepulmonarycircuitviathe4pulmonary
veins.Itpassesbloodtotheleftventricleviathemitral(orbicuspid)orifice,whichisassociated
withthemitral(orbicuspid)valve.

Thereisashallowdepressioninbothsidesoftheadultatrialseptumknownasthefossaovalis.
Itsaremnantoftheforamenovale,aholeinthefetalatrialseptum.Fetalbloodflowed
throughtheholefromRAtoLAthusbypassingthepulmonarycircuit(sincethefetallungsare
neitherdevelopednoroxygenated).

Theventriclesarelarge,muscularchambers.Thickmusculatureisnecessarybecausetheyare
theactualpumps.Theventriclescontainmuscularridgesknownastrabeculaecarneaeaswell
asmuscularbulgesknownaspapillarymuscles.Therightventricledischargesbloodintothe
pulmonarytrunk,thefirstvesselofthepulmonarycircuit.Thepulmonarysemilunarvalve
separatestherightventricleandthepulmonarytrunk.Theleftventricledischargesbloodinto
theaorta,thefirstvesselofthesystemiccircuit.TheaorticsemilunarvalveseparatestheLV
andaortictrunk.Theleftventricleislarger(moremuscular)thantheright.Moremuscleis
necessarybecausetheleftventriclepumpsbloodafartherdistanceandagainstgreater
pressure(notetherightandleftventriclepumpthesamevolumeofbloodperbeat).

Systemiccircuit:

Lventricle
Aorta
Systemicarteries
Syst. capillaries
Syst. veins
Venaecavae

Pulmonarycircuit:

Rventricle
Pulmonarytrunk
Pulm.arteries
Pulm.capillaries
Pulm.veins

Ifwecombinethe2circuits,notethatwehave2pumpsinseries:

Latrium
Lventricle
SystemicBloodVessels

Ratrium
Pulmonarybloodvessels
Rightventricle

Thepulmonaryandsystemiccircuitsdifferinmanysignificantways.Thesystemiccircuitis
longeranditsbloodisunderfargreaterpressure.Theresistancetobloodmovementisalsofar
greaterinthesystemiccircuit.SystemicarteriesareO2richandCO2poor,whereaspulmonary
arteriesareO2poorandCO2rich.SystemicveinsareO2poorandCO2rich,whereaspulmonary
veinsareO2richandCO2poor.

Thehearthasitsownnetworkofbloodvessels(knownasthecoronarycircuit).Itsnecessary
b/ctheheartrequiresaprodigiousamountofoxygenandnutrients,andlittleoxygenand/or
nutrientsfrombloodwithinthechamberscandiffusethruthethickmyocardium.Thebasic
pathwayofbloodis:

Lventricle
Aorta
Coronaryarteries
Cor.capillaries
Cor.veins
Cor.sinus

Ratrium

Latrium

Ratrium

 BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A. IMHOLTZ) HEART P3 OF 7

Theleftandrightcoronaryarteriesbranchfromtheascendingaortaandbeginthecoronary
circuit.Theleftcoronaryarterydividesintotheanteriorinterventricularartery(whichsupplies
theinterventricularseptumandtheanteriorventricularwalls)andthecircumflexartery(which
suppliestheleftatriumandposteriorleftventricle).Therightcoronaryarterydividesintothe
rightmarginalartery(whichsuppliestherightsideoftheheart)andtheposterior
interventricularartery(whichsuppliestheposteriorventricularwalls).Coronarycapillariesinall
3layersreceivebloodfromthecoronaryarteries(w/themyocardiumreceivingthemost).
Coronarycapillariesemptyintosmallveinswhicheventuallyemptyintothe3primarycardiac
veins:thegreatcardiacvein(foundintheanteriorinterventricularsulcus),themiddlecardiac
vein(foundintheposteriorinterventricularsulcus),andthesmallcardiacvein(foundonthe
heartsrightinferiormargin).These3veinsemptyintoalargervessel,thecoronarysinus,
whichemptiesintotherightatrium.

Heartvalvesensure1wayflowwithintheheart.Thereare4valves:2atrioventricularvalves
separatingtheatriafromtheventricles;and2semilunarvalvesseparatingtheventriclesfrom
theirgreatvessels.

Theatrioventricularvalvesconsistofaflapofendotheliumwithacoreofconnectivetissue.The
tricuspidvalvepreventsbackflowofbloodfromtheRVtotheRA.Itscalledthetricuspid
becauseithas3flaps.ThemitralvalvepreventsbackflowfromtheLVtotheLA.Itcontains2
valveflapsandisa.k.a.thebicuspidvalve.Attachedtothevalveflapsarestringsofcollagen
calledchordaetendineae.Chordaetendineaeattachtopapillarymusclesintheventriclewall.

BloodenterstheventriclewhenatrialBPexceedsventricularBP.Bloodflowsdownitspressure
gradientandpushestheAVvalveopen.Atthistimethechordaetendineaeareslack,and
papillarymusclesarerelaxed.

WhentheventriclecontractsventricularBPwillexceedatrialBP.Bloodwillattempttoflow
downitspressuregradientbackintotheatria.However,bloodpushesthevalveflapstowards
theatria.Thisclosesthevalves.Thechordaetendineaetightenandthepapillarymuscles
contracttopreventthevalveflapsfromflippingupintotheatrium.

NotethatthechordaetendinaeandpapillarymusclesdoNOTclosetheAVvalvesthemselves.
Bloodsattempttoflowupwardiswhatpushesthevalvesshut.

Theaorticsemilunarvalvepreventsbackflowfromtheaortaintotheleftventricle.TheASVis
pushedopenwhenleftventricularBPexceedsaorticBP.ItsforcedshutwhenaorticBPexceeds
leftventricularBP.

Thepulmonarysemilunarvalvepreventsbackflowfromthepulmonarytrunkintotheright
ventricle.ThePSVispushedopenwhenrightventricularBPexceedspulmonarytrunkBP.Its
forcedshutwhenpulmonarytrunkBPexceedsrightventricularBP.

Notethatthesemilunarvalveshavenoassociatedchordaetendineaeorpapillarymuscles.

Thebulkoftheheartwalliscomposedofcardiacmuscle.Thereare2typesofcardiacmuscle
cells.Contractilecells(99%)generatetheforceinvolvedinpumping.Autorhythmiccells(1%)
spontaneouslydepolarizetosettherateofcontraction.Contractilecellsarestriated,short,and

 BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A. IMHOLTZ) HEART P4 OF 7

oftenbranching.Theyreinvoluntaryandarelinkedtooneanotherandtotheautorhythmic
cellsbyintercalateddiscs.Intercalateddiscscontain2separatestructures:gapjunctionsand
desmosomes.Gapjunctionsareproteinchannelsthatallowionstoflowbtwnadjacentcells.
Theycreateanelectricalconnectionbtwncardiacmusclecells.Theyallowthedepolarization
waveinitiatedbyautorhythmiccellstospreadthroughthecardiacmusculature.Thisallowsthe
hearttofunctionasasinglecoordinatedunit(functionalsyncytium),whichhelpsmaximizeits
efficiency.Desmosomesphysicallyconnectadjacentcardiacmusclecellsandpreventthem
fromseparatingduringcontraction.Electricalexcitationofcardiacmusclecellscausesan
increaseinintracellularCa2+levels.Calciumbindsw/troponintoproducecontractionviathe
familiarslidingfilamentmechanism.

Atrialcardiacmuscleisseparatedfromventricularcardiacmusclebythefibrousskeleton,which
consistsof4ringsofdenseconnectivetissuejoinedtogether.Eachringhasaheartvalve
attachedtoit.Theskeletonhelpsseparatetheatriafromtheventriclesbothphysicallyand
electricallyandprovidesanattachmentsiteforcardiacmusclecells.

Bothheartrate(measuredinbeats/minute)andtheforceofcontractionarecontrolled
intrinsically(byhearttissueitself)andextrinsically(vianervesignals,hormones,andother
bloodbornesubstances).

Intrinsiccontroloftheheartrateistheprovinceoftheautorhythmiccells(whichhavethe
abilitytospontaneouslyandrhythmicallydepolarize).Thereare5maingroupsofautorhythmic
cells:
1. SinoatrialnodegroupofautorhythmiccellsneartheopeningoftheSVC.
2. AtrioventricularnodegroupofACsintheinferiorIAseptumnearthetricuspidorifice.
3. AtrioventricularbundlegroupofACsinthesuperiorIVseptum.
4. RightandleftbundlebranchesgroupofACsinthemiddleandinferiorIVseptum.
5. Purkinjefibersseparateautorhythmiccellsthatwindtheirwaythroughtheventricles.

Theabovelistalsogivesthepathoftheelectricalconductionsystemwithintheheart.All
autorhythmiccellshavetheabilitytorhythmicallyandspontaneouslydepolarize.However,SA
nodecellshavethefastestrateofdepolarizationandthereforesetthepaceforother
autorhythmiccellsaswellastherestoftheheart.Forthisreason,theSAnodeisknownasthe
pacemakeroftheheart.Hereshowthespreadofdepolarizationtakesplace:

SAnodecellsdepolarize.

Depolarizationwavetravelstoatrial

contractilecells.

DepolarizationwavetravelstotheAVnode.Depolarizationwaveisbrieflydelayed,
whichallowstheatriatocompletecontractingbeforetheventriclesbegin.

Atrialcontractilecellscontract.

Notethattherightatriumbeginsto

DepolarizationwavetravelsdownAVbundleandbundlebranches.(Thefibrous
contractbeforetheleft.

skeletonpreventsthesignalfromtravelingdirectlyfromatriatoventricles)

DepolarizationwavetravelsthrutheventriclesviaPurkinjefibers.

 BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A. IMHOLTZ) HEART P5 OF 7

Ventricularcontractilecellsdepolarize.

Ventricularcontractilecellscontract.
Withoutanyinput(neuralorhormonal),theinherentrateofSAnodedepolarizationdetermines
theheartrate.Thenormaluninfluencedrateisroughly100depolarizationsperminute.

Thefibrousskeletonoftheheartelectricallyisolatestheatriaandtheventricles.TheAVbundle
istheonlyelectricalconnectionbtwnthem.

Notethatventriculardepolarizationandcontractionbeginattheapexoftheheartandproceed
upward.Thisallowsbloodtobepropelledupoutoftheventriclesintothegreatvessels.

Extrinsiccontroloftheheartratereferstofactorsoriginatingoutsideofcardiactissuethat
affectheartrate.Mostextrinsiccontrolisnervousorendocrineinnature.

Themedullaoblongatacontains2cardiaccentersthatcanaltertheheartsactivity.The
cardioacceleratorycenterprojectsviathecardiacsympatheticnervestotheSAnode,AVnode,
andtheventricularmyocardium.Theseneuronsreleasenorepinephrine,whichcausesan
increaseincontractionrateandforce.

Thecardioinhibitorycentercontainsparasympatheticneuronsthatproject(viathevagusnerve,
CNX)totheSAnodeandAVnodes.Theseneuronsreleaseacetylcholine,whichcausesa
decreaseinheartratebutnochangeintheheartscontractilestrength.

Atrest,bothparasympatheticandsympatheticneuronsarereleasingneurotransmittersonto
theheart,buttheparasympatheticbranchisdominant.Duringstress,exercise,andexcessive
heatthesympatheticinfluenceisdominant.

Hormonessuchasepinephrine(releasedbytheadrenalmedulla),thyroxine(releasedbythe
thyroidgland),andothersaffectheartrateaswell.

Thereare2heartsoundsassociatedwitheachheartbeat.The1stheartsoundistheLUBandis
causedbytheshuttingoftheatrioventricularvalvesthatoccursattheonsetofventricular
contraction.The2ndheartsoundistheDUPandiscausedbytheshuttingofthesemilunar
valvesthatoccursattheendofventricularcontraction.

Thecardiaccyclereferstoalltheeventsassociatedwithbloodflowthrutheheartduringone
completeheartbeat.Itincludesthecontraction(systole)andrelaxation(diastole)ofall4
chambers.Welldiscussthecardiaccycleintermsoftheleftsideoftheheart,butanalogous
eventsareoccurringontherightside.Thecardiaccycleisdividedinto4parts:ventricular
filling,isovolumetriccontraction,ventricularejection,andisovolumetricrelaxation.

DuringventricularfillingleftatrialBPislowerthantheBPofthepulmonaryvasculature,so
bloodenterstheleftatrium.LABPisgreaterthanLVBP,sobloodenterstheLV.B/cLABPis
greaterthanLVBP,theAVvalvesarepushedopen.NotethatLVBPislessthanaorticBP.Asa
result,bloodtriestobackflowfromtheaortaintotheLVandthisforcesthesemilunarvalves

 BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A. IMHOLTZ) HEART P6 OF 7

closed.Neithertheatrialorventricularmuscleiscontractingduringthisphase.Atthispoint
boththeLAandtheLVareindiastole.About80%oftheultimateventricularvolumewillenter
inthispassivemanner.However,attheendofventricularfilling,whiletheLVisstillrelaxing,
theLAdepolarizesandcontracts.Thispushesroughlythefinal20%ofbloodintotheLV.TheLV
nowhasthemaximumvolumeitwillcontainduringthisparticularcycle.Thisisknownasthe
enddiastolicvolume(EDV).AtypicalvalueforEDVis130mL.Notethatfortherestofthecycle,
theLAwillbeindiastole.

DuringisovolumetriccontractiontheLVdepolarizesandbeginstocontract.Asitcontracts,LV
BPrisesquickly.LVBPalmostimmediatelyexceedsLABPandbloodispushedupwardforcing
themitralvalveshutcreatingthe1stheartsound(LUB).However,theopeningoftheaortic
semilunarvalverequiresmuchmorepressurethanwasnecessarytoclosethemitralvalve.So
afterthemitralvalveisshut,theLVcontinuestocontractanditsBPrises,butuntilLVBP
exceedsaorticBP,theaorticsemilunarvalveremainsshut.Thus,duringthisperiod,theAVand
semilunarvalvesareshutandthevolumewithintheLVisnotchanging.Hencethisphaseis
knownasisovolumetriccontraction.

DuringventricularejectiontheLVBPexceedsaorticBP(typicallyabout80mmHg),thesemilunar
valveisforcedopen,andbloodisejectedfromtheLVintotheascendingaorta.Notallofthe
bloodintheLVisejected.Theamountremainingafterventricularcontractionisknownasthe
endsystolicvolume(ESV).Atypicalvalueis70mL.Thisgivesareserveamountofbloodthat
couldalsobeejectedifnecessary(e.g.,duringexercise).Theamountofbloodejectedduring
thisphaseisknownasthestrokevolume.Mathematicallythestrokevolumecanbeexpressed
asthedifferencebtwntheenddiastolicandendsystolicvolumes:SV=EDVESV.Amore
vigorouscontractionwillresultinadecreasedESVandanincreasedSV.

Thefinalphaseisisovolumetricrelaxation.OncetheLVhascompletedcontracting,itsBP
beginstofall.ItquicklybecomeslessthanaorticBPandbloodtriestobackflow,whichcauses
thesemilunarvalvetosnapshutcreatingthe2ndheartsound(DUP).However,ittakesabit
longerfortheLVBPtodropbelowtheLABPandcausethemitralvalvetoopen.Duringthis
time,asLVBPisfalling,theAVandsemilunarvalvesareshutandLVvolumeisnotchanging.
OnceLVBPfallsbelowLABP(whichisrisingasbloodreturnstotheheart),themitralvalvewill
openandthecyclewillbeginanewwithanotherroundofventricularfilling.

Notethattheeventsontheleftsideoftheheartduringanormalcardiaccyclearemirroredby
theeventsontherightsideoftheheart.Boththerightandtheleftsideoftheheartcontractat
thesamerate.Theyhaveidenticalstrokevolumes.Theonlydifferenceisthepressureinvolved.
TheLVmustcontracthardertoopenitssemilunarvalve.Thisisbecausethesystemiccircuitis
underamuchhigherpressurethanthepulmonarycircuit.Theleftandrightventriclemusthave
identicalstrokevolumes.IfLVSV>RVSV,thenbloodwouldbackupinthesystemiccircuit.If
LVSV<RVSV,thenbloodwouldbackupinthepulmonarycircuit.

Cardiacoutputistheamountofbloodpumpedbyeachventricleinoneminute.Cardiacoutput
canbeexpressedmathematicallyastheproductofheartrateandstrokevolume:CO(mL/min)=
HR(beats/min)xSV(mL/beat).RecallthatSVisthedifferencebtwnEDVandESV.Changesin
eitherstrokevolumeorheartratecanaltercardiacoutput.Duringexercise,cardiacoutputcan
increasedramatically.

 BIOLOGY 2060 LECTURE NOTES ANATOMY & PHYSIOLOGY II (A. IMHOLTZ) HEART P7 OF 7

Thenervoussystemplaysalargeroleintheregulationofheartrate.Recallthatthecardiac
centersinthemedullaoblongataexertinfluenceontherateofSAnodedepolarization,i.e.,
heartrate.Increasesinheartrateareachievedby:
1. Increaseincardioacceleratorycenteractivity.Thisresultsinanincreaseinsympathetic
nerveactivityandanincreaseinnorepinephrinereleaseontheheart.
2. Decreaseincardioinhibitorycenteractivity.Thisresultsinadecreasein
parasympatheticnerveactivityandadecreaseinacetylcholinereleaseontheheart.
Decreasesinheartrateareachievedby:
1. Decreaseincardioacceleratorycenteractivity.Thisresultsinadecreaseinsympathetic
nerveactivityandadecreaseinnorepinephrinereleaseontheheart.
2. Increaseincardioinhibitorycenteractivity.Thisresultsinanincreasein
parasympatheticnerveactivity,anincreaseinvagusnerveactivity(a.k.a.vagaltone),
andanincreaseinacetylcholinereleaseontheheart.

Notethatifheartratechangeswithoutachangeincontractility(thestrengthofthe
contraction),strokevolumewillchangealso.Thisisbecausechangingtheheartratealtersthe
fillingtime(i.e.,thetimebtwnbeatsduringwhichtheheartfillsupwithblood).

Therearealsohormonalinfluencesonheartrate.Epinephrine,releasedbytheadrenalmedulla
(anendocrineorganfoundatopthekidney),causesanincreaseinheartrate.Thyroxine,
releasedbythethyroidgland(locatedintheanteriorneck),alsoactstoincreaseheartrate.

Strokevolumedependson3mainvariables:preload,contractility,andafterload.

Preloadreferstothedegreeofventricularstretchduringfilling.Themoreheartmuscleis
stretched(uptoapoint),themoreforcefulitscontraction.Theincreaseinstretchcausesmore
optimumcrossbridgeformationbtwnactinandmyosinandastrongercontraction,thus
ejectingalargervolume.TheFrankStarlinglawnicelysumsitup:Whatreturnstotheheart
willgetpumpedoutoftheheart.Inotherwords,asvenousreturn(thevolumeofblood
returningtotheheartperminute)increases,EDVincreases,andstrokevolumeincreases.An
decreaseinheartratewillincreasethefillingtimeandthusincreaseEDV(andpreload).An
increaseinvenouspressurewillalsoincreaseEDV(andpreload).Thestrokevolumeisgreatly
influencedbychangesinpreload.

Contractilityisthestrengthoftheheartscontractionindependentofitsdegreeofstretch.
Thinkofitashowhardtheheartcontractsnomatterhowmuchbloodiswithinit.Anincrease
incontractilitywillresultinanincreaseinstrokevolumeandadecreaseinendsystolicvolume.
Factorsthatincreasecontractilityinclude:increasedcardioacceleratoryactivity;andhormones
suchasepinephrineandthyroxine.

Afterloadreferstothepressurethatmustbeovercometoopenthesemilunarvalveandeject
blood.Afterloadisequivalenttoarterialbloodpressure.AnincreaseinarterialBPwillincrease
afterload.Thismakestheheartexpendmoretime/energyonopeningthesemilunarvalveand
lessonejectingblood.Thus,anincreaseinafterloadwillcausestrokevolumetodecreaseand
endsystolicvolumetoincrease.However,ittakesasignificantincreaseinafterloadbeforethe
pumpingoutputoftheheartishampered.