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TheCirculatorySystem:Heart
Chapter19
ThePulmonaryandSystemicCircuits
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CO 2
O2
• Leftsideofheart
Pulmonarycircuit
O 2 -poor,
CO 2 -rich
blood
O 2 -rich,
CO 2 -poor
blood
– Fullyoxygenatedbloodarrives
fromlungsviapulmonaryveins
– Bloodsenttoallorgansofthe
bodyviaaorta
• Rightsideofheart
Systemiccircuit
CO 2
O2
Figure 19.1
– Oxygen-poorbloodarrivesfrom
inferiorandsuperiorvenacava
– Bloodsenttolungsvia
pulmonarytrunk
19-2
Position,Size,andShape
oftheHeart
• Heartlocatedinmediastinum,
betweenlungs
• Base—wide,superiorportion
ofheart,largevesselsattach
here
• Apex—taperedinferiorend,
tiltstotheleft
• Inadult:weighs10ounces,3.5
in.wideatbase,5in.frombase
toapex
• Atanyage,heartissizeoffist
19-3
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Aorta
Pulmonary
trunk
Superior
vena cava
Rightlung
Baseof
heart
Parietal
pleura (cut)
Pericardial
sac(cut)
Apex
ofheart
(c)
Diaphragm
Figure 19.2c
ThePericardium
• Pericardium—double-walledsacthatenclosestheheart
– Allowshearttobeatwithoutfriction,providesroomtoexpand,
yetresistsexcessiveexpansion
– Anchoredtodiaphragminferiorlyandsternumanteriorly
• Parietalpericardium—pericardialsac
– Superficialfibrouslayerofconnectivetissue
– Deep,thinserouslayer
• Visceralpericardium(epicardium)
– Serousmembranecoveringheart
• Pericardialcavity—spaceinsidethepericardialsacfilledwith5
to30mLofpericardialfluid
• Pericarditis—painfulinflammationofthemembranes
19-4
ThePericardium
19-5
Figure 19.3
TheHeartWall
• Heartwall hasthreelayers:epicardium,myocardiumandendocardium
• Epicardium (visceralpericardium)
– Serousmembranecoveringheart
– Coronarybloodvesselstravelthroughthislayer
• Endocardium
– Smoothinnerliningofheartandbloodvessels
– Coversthevalvesurfacesandiscontinuouswithendotheliumofbloodvessels
• Myocardium
– Layerofcardiacmuscleproportionaltoworkload
• Musclespiralsaroundheartwhichproduceswringingmotion
– Fibrousskeletonoftheheart:frameworkofcollagenous andelasticfibers
• Providesstructuralsupportandattachmentforcardiacmuscleandanchorforvalve
tissue
• Electricalinsulationbetweenatriaandventricles;importantintimingandcoordination
ofcontractileactivity
19-6
SpiralOrientationof
MyocardialMuscle
Figure 19.6
TheChambers
• Fourchambers
– Rightandleftatria
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forreproduction ordisplay.
• Twosuperiorchambers
Aorta
• Receivebloodreturningto Rightpulmonary
artery
Superior venacava
heart
Rightpulmonary
veins
• Auricles(seenonsurface) Interatrial
septum
Rightatrium
Fossaovalis
Pectinate muscles
enlargechamber
RightAV
– Rightandleftventricles
• Twoinferiorchambers
• Pumpbloodintoarteries
19-8
Leftpulmonaryarter
Pulmonarytrunk
Leftpulmonaryvein
Pulmonaryvalve
Leftatrium
Aortic valve
LeftAV(bicuspid)
valve
Leftventricle
(tricuspid) valve
Tendinous cords
Trabeculaecarneae
Rightventricle
Inferior venacava
Papillarymuscle
Interventricular sept
Endocardium
Myocardium
Epicardium
Figure
19.7
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requiredforreproduction ordisplay.
TheChambers
Ligamentum
arteriosum
Ascending
aorta
Aorticarch
• Atrioventricular
sulcus—separates
Leftpulmonary
atriaandventricles
Superior venacava
Branchesofthe
rightpulmonary
artery
Rightpulmonary
veins
artery
Pulmonarytrunk
Leftpulmonary
veins
• Interventricular
Leftauricle
sulcus—overliesthe
interventricular
septumthatdivides
therightventricle
Anterior
interventricular
fromtheleft
sulcus
Rightauricle
Rightatrium
Coronarysulcus
Rightventricle
Inferiorvenacava
Leftventricle
(a)Anteriorview
Figure 19.5a
Apexofheart
• Sulci contain
coronaryarteries
19-9
TheChambers
• Interatrialseptum
– Wallthatseparatesatria
• Pectinatemuscles
– Internalridgesofmyocardiuminrightatriumandboth
auricles
• Interventricularseptum
– Muscularwallthatseparatesventricles
• Trabeculaecarneae
– Internalridgesinbothventricles
– Maypreventventriclewallsfromstickingtogetherafter
contraction
19-10
TheChambers
19-11
Figure 19.7
TheValves
• Valvesensureone-wayflowofbloodthroughheart
• Atrioventricular(AV)valves—controlbloodflowbetweenatria
andventricles
– RightAVvalvehasthreecusps(tricuspidvalve)
– LeftAVvalvehastwocusps(mitralvalve,formerly‘bicuspid’)
– Chordaetendineae:cordsconnectAVvalvestopapillarymuscles
onfloorofventricles
• PreventAVvalvesfromflippingorbulgingintoatriawhenventricles
contract
• Eachpapillarymusclehas2-3attachmentstoheartfloor(likeEiffel
Tower)todistributephysicalstress,coordinatetimingofelectrical
conduction,andprovideredundancy
19-12
TheValves
• Semilunar valves—
controlflowinto
greatarteries;open
andclosebecauseof
bloodflowand
pressure
– Pulmonarysemilunar
valve:inopening
betweenright
ventricleand
pulmonarytrunk
– Aorticsemilunar
valve:inopening
betweenleftventricle
andaorta
19-13
BloodFlowThroughtheChambers
• Ventriclesrelax
– Pressure dropsinsidetheventricles
– Semilunar valvescloseasbloodattemptstobackupinto
theventriclesfromthevessels
– AVvalvesopen
– Bloodflowsfromatriatoventricles
• Ventriclescontract
– AVvalvescloseasbloodattemptstobackupintothe
atria
– Pressure risesinsideoftheventricles
– Semilunar valvesopenandbloodflowsintogreatvessels
19-14
BloodFlowThroughtheChambers
Figure 19.9
• Bloodpathwaytravelsfromtherightatriumthroughthepulmonarycircuit,then
systemiccircuit(throughthebody)andbacktothestartingpoint
19-15
TheCoronaryCirculation
• 5%ofbloodpumpedbyheartispumpedtotheheartitselfthrough
thecoronarycirculationtosustainitsstrenuousworkload
– 250mL ofbloodperminute
– NeedsabundantO2 andnutrients
19-16
Figure 19.10a,b
CoronaryArterialSupply
• Leftcoronaryartery(LCA)branchesofftheascendingaorta
– Anteriorinterventricular branch
• Suppliesbloodtobothventriclesandanteriortwo-thirdsofthe
interventricular septum
– Circumflexbranch
• Passesaroundleftsideofheartincoronarysulcus
• Givesoffleftmarginalbranchandthenendsontheposteriorsideof
theheart
• Suppliesleftatriumandposteriorwallofleftventricle
• Rightcoronaryartery(RCA)branchesofftheascendingaorta
– Suppliesrightatriumandsinoatrial node(pacemaker)
– Rightmarginalbranch
• Supplieslateralaspectofrightatriumandventricle
– Posteriorinterventricular branch
• Suppliesposteriorwallsofventricles
19-17
AnginaandHeartAttack
• Anginapectoris—chestpainfrompartialobstruction
ofcoronarybloodflow
– Paincausedbyischemiaofcardiacmuscle
– Obstructionpartiallyblocksbloodflow
– Myocardiumshiftstoanaerobicfermentation,producing
lacticacidandthusstimulatingpain
19-18
AnginaandHeartAttack
• Myocardialinfarction(MI)—suddendeathofapatchof
myocardiumresultingfromlong-termobstructionof
coronarycirculation
– Atheroma(bloodclotorfattydeposit)oftenobstructs
coronaryarteries
– Cardiacmuscledownstreamoftheblockagedies
– Heavypressureorsqueezingpainradiatingintotheleftarm
– Somepainlessheartattacksmaydisruptelectrical
conductionpathways,leadingtofibrillationandcardiac
arrest
• Silentheartattacksoccurindiabeticsandtheelderly
– MIresponsibleforabout27%ofalldeathsintheU.S.
19-19
CoronaryVenousDrainage
• 5%to10%ofcoronaryblooddrainsdirectlyintoheart
chambers(mostlyrightventricle)
• Mostcoronarybloodreturnstorightatriumbywayofthe
coronarysinuswhichhasthreemaininputs:greatcardiac,
posteriorinterventricular,andleftmarginalveins
– Greatcardiacvein
• Travelsalongsideanteriorinterventricular artery
• Collectsbloodfromanteriorportionofheart
• Emptiesintocoronarysinus
19-20
VenousDrainage
(Continued)
– Middlecardiacvein(posteriorinterventricular)
• Foundinposteriorsulcus
• Collectsbloodfromposteriorportionofheart
• Drainsintocoronarysinus
– Leftmarginalvein
• Emptiesintocoronarysinus
• Coronarysinus
– Largetransverseveinincoronarysulcusonposteriorsideof
heart
– Collectsbloodandemptiesintorightatrium
19-21
StructureofCardiacMuscle
• Cardiocytes—striated,short,thick,branchedcells,onecentral
nucleussurroundedbylight-stainingmassofglycogen
• Repairofdamageofcardiacmuscleisalmostentirelybyfibrosis
(scarring)
• Intercalateddiscs—joincardiocytes endtoendwiththreefeatures:
interdigitating folds,mechanicaljunctions,andelectricaljunctions
– Interdigitating folds:foldsinterlockwitheachother,andincreasesurface
areaofcontact
19-22
StructureofCardiacMuscle
Striatedmyofibril
(Continued)
Glycogen Nucleus MitochondriaIntercalateddiscs
– Mechanicaljunctionstightly
joincardiocytes
• Fasciaadherens—broadband
inwhichtheactin ofthethin
myofilamentsisanchoredto
theplasmamembrane
– Eachcellislinkedtothe
nextviatransmembrane
proteins
• Desmosomes—mechanical
linkagesthatprevent
contractingcardiocytes from
beingpulled apartfromeach
other
(b)
Intercellularspace
Desmosomes
– Electricaljunctions(gap
junctions)allowionstoflow
betweencells;canstimulate
neighbors
Gapjunctions
• Entire myocardiumofeither
twoatriaortwoventricles
actslikesingle,unified cell
19-23
Figure 19.11a–c
(c)
(a):©EdReschke
MetabolismofCardiacMuscle
• Cardiacmuscledependsalmostexclusivelyonaerobic
respirationtomakeATP
– Richinmyoglobinandglycogen
– Hugemitochondria:fill25%ofcell
• Adaptabletodifferentorganicfuels
– Fattyacids(60%);glucose(35%);ketones,lacticacid,and
aminoacids(5%)
– Morevulnerabletooxygendeficiencythanlackofaspecific
fuel
• Fatigueresistantbecauseitmakeslittleuseofanaerobic
fermentationoroxygendebtmechanisms
– Doesnotfatigueforalifetime
19-24
TheConductionSystem
• Coordinatestheheartbeat
– Composedofaninternalpacemakerandnerve-like
conductionpathways throughmyocardium
• Generatesandconductsrhythmicelectricalsignalsin
thefollowingorder:
– Sinoatrial(SA)node:modifiedcardiocytes
• Pacemakerinitiateseachheartbeatanddeterminesheart
rate
• Pacemakerinrightatriumnearbaseofsuperiorvenacava
– Signalsspreadthroughoutatria
19-25
TheConductionSystem
(Continued)
– Atrioventricular(AV)node
• LocatedneartherightAVvalveatlowerendofinteratrialseptum
• Electricalgatewaytotheventricles
• Fibrousskeleton—insulatorpreventscurrentsfromgettingtoventricles
byanyotherroute
– Atrioventricular(AV)bundle(bundleofHis)
• Bundleforksintorightandleftbundlebranches
• Branchespassthroughinterventricularseptumtowardapex
– Purkinjefibers
• Nerve-likeprocessesspreadthroughoutventricularmyocardium
• Cardiocytesthenpasssignalfromcelltocellthroughgapjunctions
19-26
TheConductionSystem
19-27
Figure 19.12
NerveSupplytotheHeart
• Sympatheticnervesincreaseheartrateandcontraction
strength
– FibersterminateinSAandAVnodes,inatrialandventricular
myocardium(alsoaorta,pulmonarytrunk,andcoronary
arteries)
• Parasympatheticnervesslowheartrate
– Pathwaybeginswithnucleiofthevagus nervesinthe
medullaoblongata
– Fibersofrightvagus nerveleadtotheSAnode
– Fibersofleftvagus nerveleadtotheAVnode
– Littleornovagalstimulationofthemyocardium
19-28
ElectricalandContractile
ActivityoftheHeart
• Cycleofeventsinheart
– Systole: contraction
– Diastole: relaxation
• Although“systole”and“diastole”canreferto
contractionandrelaxationofeithertypeof
chamber,theyusuallyrefertotheactionofthe
ventricles
19-29
TheCardiacRhythm
• Sinusrhythm—normalheartbeattriggeredbythe
SAnode
– Adultatrestistypically70to80bpm(vagaltone)
• Ectopicfocus—aregionofspontaneousfiringother
thantheSAnode
– MaygovernheartrhythmifSAnodeisdamaged
– Nodalrhythm—ifSAnodeisdamaged,heartrateissetbyAV
node,40to50bpm
• Otherectopicfocalrhythmsare20to40bpmandtooslowto
sustainlife
19-30
PacemakerPhysiology
• SAnodedoesnothaveastablerestingmembrane
potential
– Startsat−60mVanddriftsupwardduetoslowNa+ inflow
• Gradualdepolarizationiscalledpacemakerpotential
– Whenitreachesthresholdof−40mV,voltage-gatedfast
Ca2+ and Na+ channelsopen
• Fasterdepolarization occurspeakingat0mV
– K+channelsthenopenandK+ leavesthecell
• Causingrepolarization
• OnceK+ channelsclose,pacemakerpotentialstartsover
• WhenSAnodefiresitsetsoffheartbeat
– Astheinternalpacemaker,ittypicallyfiresevery0.8
seconds,settingtherestingrateat75bpm
19-31
PacemakerPhysiology
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+10
Membranepotential(mV)
0
–10
–20
Action
potential
Threshold
–30
–40
Pacemaker
potential
–50
–60
SlowNa+
inflow
–70
0
19-32
FastK+
outflow
Fast
Ca2+–Na+
inflow
.4
.8
Time(sec)
Figure 19.13
1.2
1.6
ImpulseConductiontotheMyocardium
• SignalfromSAnodestimulatestwoatriatocontract
almostsimultaneously
– ReachesAVnodein50ms
• SignalslowsdownthroughAVnode
– Thincardiocyteswithfewergapjunctions
– Delayssignal100mswhichallowstheventriclestime
tofill
19-33
ImpulseConductiontotheMyocardium
• SignalstravelveryquicklythroughAVbundleand
Purkinjefibers
– Entireventricularmyocardiumdepolarizesandcontractsin
nearunison
• Signalsreachpapillarymusclesslightlylaterthanrestof
myocardium
• Ventricularsystoleprogressesupfromtheapexofthe
heart
– Spiralarrangementofmyocardiumtwistsventriclesslightly;
likesomeonewringingoutatowel
19-34
ElectricalBehavioroftheMyocardium
• Cardiocyteshaveastablerestingpotentialof−90mV,and
depolarizeonlywhenstimulated
• Threephasestocardiocyteactionpotential:depolarization,
plateau,repolarization
– Depolarizationphase(verybrief)
• Stimulusopensvoltage-regulatedNa+ gates(Na+ rushesin),membrane
depolarizesrapidly
• Actionpotentialpeaksat+30mV
• Na+ gatesclosequickly
– Plateauphaselasts200to250ms,sustainscontractionfor
expulsionofbloodfromheart
• Voltage-gatedslowCa2+ channelsopenadmittingCa2+ whichtriggers
openingofCa2+ channelsonsarcoplasmicreticulum(SR)
• Ca2+ (mostlyfromtheSR)bindstotroponintriggeringcontraction
19-35
ElectricalBehavioroftheMyocardium
• Cardiocyteactionpotential(Continued)
– Repolarizationphase:Ca2+ channelsclose,K+ channelsopen,
rapiddiffusionofK+ outofcellreturnsittorestingpotential
– Hasalongabsoluterefractoryperiodof250ms(compared
to1to2msinskeletalmuscle)
• Preventswavesummationandtetanuswhichwouldstopthe
pumpingactionoftheheart
19-36
ElectricalBehavioroftheMyocardium
Na+ gatesopen
2.
Rapiddepolarization
3.
4.
Na+
gatesclose
SlowCa2+
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display.
3
1 Voltage-gated Na+ channelsopen.
Plateau
+20
Membrane potential(mV)
1.
0
5.
channelsclose,K+
3 Na+ channelsclosewhenthecell
depolarizes,andthevoltage peaksat
nearly +30mV.
4 Ca2+ entering through slowCa2+
2
channelsprolongs depolarization of
membrane, creatingaplateau.Plateau
falls
slightlybecauseofsomeK+ leakage,but
most
5 +
K channelsremaincloseduntil endof
plateau.
Myocardial
contraction
Absolute
refractory
period
channelsopen
channelsopen
(repolarization)
19-37
Myocardial
relaxation
–60
–80
Ca2+
5
Action
potential
–20
–40
2 Na+ inflowdepolarizesthemembrane
andtriggers theopeningofstillmoreNa+
channels,creatinga positivefeedback
cycleandarapidly risingmembrane voltage.
4
1
0
.15
Time (sec)
.30
Figure19.14
Ca2+ channelscloseandCa2+ istransported
outofcell.K + channelsopen,andrapidK +
outflowreturnsmembrane toitsresting
potential.
TheElectrocardiogram
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0.8second
R
R
Millivolts
+1
PQ
segment
ST
segment
Twave
Pwave
0
PR
Q
interval
S
QT
interval
QRSinterval
–1
Atria
contract
Ventricles
contract
Atria
contract
Figure 19.15
19-38
Ventricles
contract
• Electrocardiogram
(ECGor EKG)
– Compositeofall
actionpotentialsof
nodalandmyocardial
cellsdetected,
amplifiedand
recordedby
electrodesonarms,
legs,andchest
TheElectrocardiogram
• Pwave
– SAnodefires,atriadepolarizeandcontract
– Atrialsystolebegins100msafterSAsignal
• QRScomplex
– Ventriculardepolarization
– Complexshapeofspikeduetodifferentthicknessand
shapeofthetwoventricles
• STsegment—ventricularsystole
– Correspondstoplateauinmyocardialactionpotential
• Twave
– Ventricularrepolarizationandrelaxation
19-39
TheElectrocardiogram
1.
2.
3.
4.
5.
6.
Atrialdepolarizationbegins
Atrialdepolarization
complete(atriacontracted)
Ventriclesbeginto
depolarizeatapex;atria
repolarize(atriarelaxed)
Ventriculardepolarization
complete(ventricles
contracted)
Ventriclesbeginto
repolarizeatapex
Ventricularrepolarization
complete(ventricles
relaxed)
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Key
Waveof
depolarization
Waveof
repolarization
R
P
P
Q
S
4 Ventricular depolarization complete.
1 Atria begin depolarizing.
R
Q
S
5 Ventricular repolarization begins atapex
and progresses superiorly.
2 Atrial depolarization complete.
R
R
T
P
P
Q
3 Ventricular depolarization begins atapex
and progresses superiorly as atria repolarize.
Q
S
6 Ventricular repolarization complete;heart
is readyfor thenext cycle.
Figure 19.16
19-40
T
P
P
ECGs:NormalandAbnormal
• DeviationsofECGfrom
normalcanindicate:
– Myocardialinfarction(MI)
– Abnormalitiesin
conductionpathways
– Heartenlargement
– Electrolyteandhormone
imbalances
Figure 19.17a,b
19-41
CardiacArrhythmias
• Ventricularfibrillation
– Seriousarrhythmia causedbyelectricalsignals
travelingrandomly
• Heartcannotpumpblood;nocoronaryperfusion
– Hallmarkofheartattack(MI)
– Killsquicklyifnotstopped
• Defibrillation—strongelectricalshockwithintentto
depolarizeentiremyocardiumandresethearttosinus
rhythm
– Notacureforarterydisease,butmayallowtimefor
othercorrectiveaction
19-42
TheCardiacRhythm
• Otherarrhythmias
– Heartblock—failureofconductionsystemtoconduct
– Prematureventricularcontraction—extrabeatsduetoa
ventricularectopicfocus
19-43
Figure 19.17d,e
BloodFlow,HeartSounds,
andtheCardiacCycle
• Cardiaccycle—onecompletecontractionand
relaxationofallfourchambersoftheheart
• Questionstoconsider:Howdoespressureaffectblood
flow?Howareheartsoundsproduced?
19-44
PrinciplesofPressureandFlow
• Twomainvariablesgovernfluid
movement:pressure causesflow and
resistance opposesit
– Fluidwillonlyflowifthereisa
pressuregradient (pressure
difference)
• Fluidflowsfromhigh-pressurepoint
tolow-pressurepoint
• PressuremeasuredinmmHgwitha
manometer(sphygmomanometerfor
BP)
19-45
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1 Volume
increases
2 Pressure
decreases
3 Airflowsin
P1
P 2 >P 1
Pressuregradient
P2
(a)
1 Volume
decreases
2 Pressure
increases
3 Airflowsout
P1
P 2 <P 1
Pressuregradient
(b)
P2
Figure 19.18
PressureGradientsandFlow
• Eventsoccurringonleftsideofheart
– Whenventriclerelaxesandexpands,itsinternalpressure
falls
– Ifmitralvalveisopen,bloodflowsintoleftventricle
– Whenventriclecontracts,internalpressurerises
– AVvalvesclose,theaorticvalveispushedopenandblood
flowsintoaortafromleftventricle
• Openingandclosingofvalvesaregovernedbythese
pressurechanges
– AVvalveslimpwhenventriclesrelaxed
– Semilunarvalvesunderpressurefrombloodinvesselswhen
ventriclesrelaxed
19-46
OperationoftheHeartValves
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Atrium
Atrioventricular
valve
Ventricle
Atrioventricularvalvesopen
Atrioventricularvalvesclosed
(a)
Aorta
Pulmonary
artery
Semilunar
valve
19-47
Semilunarvalvesopen
(b)
Figure 19.19
Semilunarvalvesclosed
ValvularInsufficiencyDisorders
• Valvularinsufficiency(incompetence)—anyfailureofa
valvetopreventreflux(regurgitation),thebackward
flowofblood
– Valvularstenosis:cuspsarestiffenedandopeningis
constrictedbyscartissue
• Resultofrheumaticfever,autoimmuneattackonthemitraland
aorticvalves
• Heartoverworksandmaybecomeenlarged
• Heartmurmur—abnormalheartsoundproducedby
regurgitationofbloodthroughincompetentvalves
19-48
ValvularInsufficiencyDisorders
(Continued)
– Mitralvalveprolapse:insufficiencyinwhichoneor
bothmitralvalvecuspsbulgeintoatriaduring
ventricularcontraction
• Hereditaryin1outof40people
• Maycausechestpainandshortnessofbreath
19-49
HeartSounds
• Auscultation—listeningtosoundsmadebybody
• Firstheartsound(S1),louderandlonger“lubb,”
occurswithclosureofAVvalves,turbulenceinthe
bloodstream,andmovementsoftheheartwall
• Secondheartsound(S2),softerandsharper“dupp,”
occurswithclosureofsemilunar valves,turbulencein
thebloodstream,andmovementsoftheheartwall
19-50
PhasesoftheCardiacCycle
• Ventricularfilling(duringdiastole)
• Isovolumetriccontraction(duringsystole)
• Ventricularejection(duringsystole)
• Isovolumetricrelaxation(duringdiastole)
• Theentirecardiaccycle(allfourofthesephases)are
completedinlessthan1second
19-51
PhasesoftheCardiacCycle
• Ventricularfilling
– Ventriclesexpandandtheirpressuredropsbelowthatof
theatria
– AVvalvesopenandbloodflowsintotheventricles
– Filling occursinthreephases:
• Rapidventricularfilling:firstone-third
• Diastasis:secondone-third;slowerfilling
– Pwaveoccursattheendofdiastasis
• Atrialsystole:finalone-third;atriacontract
– End-diastolicvolume(EDV)achievedineachventricle(about
130mLofblood)
19-52
PhasesoftheCardiacCycle
• Isovolumetriccontraction
– Atriarepolarize,relaxandremainindiastoleforrestofcardiac
cycle
– Ventriclesdepolarize, causingQRScomplex,andbeginto
contract
– AVvalvescloseasventricularbloodsurgesbackagainstthe
cusps
– HeartsoundS1 occursatthebeginningofthisphase
– “Isovolumetric”becausealthoughventriclescontract,theydo
notejectblood
• Pressuresinaortaandpulmonarytrunkarestillgreaterthan
thoseintheventricles
– Cardiocytesexertforce,butwithallfourvalvesclosed,the
bloodcannotgoanywhere
19-53
PhasesoftheCardiacCycle
• Ventricularejection
– Beginswhenventricularpressureexceedsarterialpressureand
semilunarvalvesopen
– Pressurepeaksinleftventricleatabout120mmHgand25mm
Hgintheright
– First:rapidejection—blood spurtsoutofventriclesquickly
– Then:reducedejection—slowerflowwithlowerpressure
– Ejectionlastsabout200to250ms- correspondstoplateau
phaseofcardiacactionpotential
– TwaveofECGoccurslateinthisphase
– Strokevolume(SV)isabout70mL
• Ejectionfractionisabout54%ofEDV(130mL)
• 60mLremainingbloodisend-systolicvolume(ESV)=EDV- SV
19-54
PhasesoftheCardiacCycle
• Isovolumetricrelaxation
– Twaveendsandventriclesbegintoexpand
– Bloodfromaortaandpulmonarytrunkbrieflyflowsbackward
fillingcuspsandclosingsemilunarvalves
• Createspressurereboundthatappearsasdicroticnotch ingraph
ofarterypressure
• HeartsoundS2 occurs
– “Isovolumetric”becausesemilunarvalvesareclosedandAV
valveshavenotyetopened
• Ventriclesarethereforetakinginnoblood
• WhenAVvalvesopen,ventricularfillingbeginsagain
19-55
PhasesoftheCardiacCycle
• Inarestingperson
– Atrialsystolelastsabout0.1second
– Ventricularsystolelastsabout0.3second
– Quiescentperiod,whenallfourchambersareindiastole,
lastsabout0.4second
• Totaldurationofthecardiaccycleistherefore0.8
secondinaheartbeating75bpm
19-56
EventsoftheCardiacCycle
Copyright © TheMcGraw-Hill Companies, Inc.Permission required for reproduction ordisplay.
Diastole
120
100
Pressure (mmHg)
Systole
Diastole
• Ventricularfilling
Aortic
pressure
Aortic
valve
opens
80
Left
ventricular
pressure
60
40
AV
valve
closes
Leftatrial
pressure
20
Aortic valve
closes
(dicroticnotch)
AV
valve
opens
• Isovolumetric
contraction
Ventricular
volume (mL)
0
End-diastolic
volume
120
90
60
End-systolic volume
R
R
T
P
P
• Ventricularejection
ECG
Q
Q
S
S
Heart
sounds
S2
S3
Phase of
cardiaccycle
S1
1a
1b
0
.2
1c
.4
Ventricular filling
1aRapid filling
1b Diastasis
19-57
1cAtrial systole
2
S2
3
.6
Time(sec)
S3
4
1a
.8
2
Isovolumetric
contraction
Figure 19.20
S1
1b
.2
3
Ventricular
ejection
1c
2
.4
4
Isovolumetric
relaxation
• Isovolumetric
relaxation
OverviewofVolumeChanges
End-systolicvolume(ESV)
Passivelyaddedtoventricle
duringatrialdiastole
Addedbyatrialsystole
Total:End-diastolicvolume(EDV)
Strokevolume(SV)ejected
byventricularsystole
Leaves:End-systolicvolume(ESV)
60mL
+30mL
+40mL
130mL
−70mL
60mL
Bothventriclesmustejectsameamountofblood
19-58
OverviewofVolumeChanges
• Normally,rightandleftsidesofheartejectthesame
volumeofbloodeventhoughtheyareunder
differentpressure
• Congestiveheartfailure(CHF)—resultsfromthe
failureofeitherventricletoejectbloodeffectively
– Usuallyduetoaheartweakenedbymyocardial
infarction,chronichypertension,valvularinsufficiency,
orcongenitaldefectsinheartstructure
19-59
OverviewofVolumeChanges
• Leftventricularfailure—bloodbacksupintothelungs
causingpulmonaryedema
– Shortnessofbreathorsenseofsuffocation
• Rightventricularfailure—bloodbacksupinthevena
cavacausingsystemicorgeneralizededema
– Enlargementoftheliver,ascites(poolingoffluidin
abdominalcavity),distensionofjugularveins,swellingof
thefingers,ankles,andfeet
• Eventuallyleadstototalheartfailure
19-60
OverviewofVolumeChanges
Copyright©TheMcGraw-HillCompanies,Inc.Permissionrequiredforreproductionordisplay.
1 Rightventricular
outputexceedsleft
Ventricularoutput.
2 Pressurebacksup.
3 Fluid accumulatesin
pulmonary tissue.
1
2
3
(a)Pulmonary edema
19-61
Figure 19.21a
• Iftheleftventricle
pumpslessblood
thantheright,the
bloodpressure
backsupintothe
lungsandcauses
pulmonaryedema
OverviewofVolumeChanges
Copyright©TheMcGraw-HillCompanies,Inc.Permissionrequiredforreproductionordisplay.
1 Leftventricular
outputexceedsright
ventricularoutput.
2 Pressurebacksup.
3 Fluid accumulatesin
systemictissue.
1
2
(b)Systemicedema
3
19-62
Figure 19.21b
• Iftherightventricle
pumpslessbloodthan
theleft,pressure
backsupinthe
systemiccirculation
andcausessystemic
edema
CardiacOutput
• Cardiacoutput(CO)—amountejectedbyeachventricle
in1minute
• Cardiacoutput=heartratexstrokevolume
– About4to6L/minatrest
– ARBCleavingtheleftventriclewillarrivebackattheleft
ventricleinabout1minute
– VigorousexerciseincreasesCOto21L/minforafitpersonand
upto35L/minforaworld-classathlete
• Cardiacreserve—thedifferencebetweenaperson’s
maximumandrestingCO
– Increases withfitness,decreases withdisease
19-63
HeartRate
• Pulse—surgeofpressureproducedbyheartbeatthat
canbefeltbypalpatingasuperficialartery
–
–
–
–
19-64
InfantshaveHRof120bpmormore
Youngadultfemalesaverage72to80bpm
Youngadultmalesaverage64to72bpm
Heartraterisesagainintheelderly
HeartRate
• Tachycardia—restingadultheartrateabove100
bpm
– Stress,anxiety,drugs,heartdisease,orfever
– Lossofbloodordamagetomyocardium
• Bradycardia—restingadultheartrateoflessthan60
bpm
– Insleep,lowbodytemperature,andendurance-trained
athletes
• Positivechronotropicagents—factorsthatraisethe
heartrate
• Negativechronotropicagents—factorsthatlower
theheartrate
19-65
ChronotropicEffectsofthe
AutonomicNervousSystem
• Autonomicnervoussystemdoesnotinitiatethe
heartbeat,itmodulatesrhythmandforce
• Cardiaccentersinthereticularformationofthe
medullaoblongata initiateautonomicoutputtothe
heart
• Cardiostimulatoryeffect—someneuronsofthecardiac
centertransmitsignalstotheheartbywayof
sympathetic pathways
• Cardioinhibitoryeffect—otherstransmit
parasympathetic signalsbywayofthevagusnerve
19-66
ChronotropicEffectsofthe
AutonomicNervousSystem
• Sympathetic postganglionicfibersareadrenergic
– Theyrelease norepinephrine
– Bindtoβ-adrenergicfibersintheheart
– ActivatecAMP second-messengersystemincardiocytes andnodal
cells
– LeadtoopeningofCa2+channelsinplasmamembrane
– IncreasedCa2+inflowacceleratesdepolarizationofSAnode
– cAMP acceleratesuptakeofCa2+bysarcoplasmic reticulumallowing
cardiocytes torelaxmorequickly
– Byacceleratingbothcontractionandrelaxation,norepinephrine
(throughcAMP)increasesheartrateashighas230bpm
– Butatexcessivelyhighheartrates(>180bpm)diastolebecomestoo
briefforadequatefilling
• Bothstrokevolumeandcardiacoutputarereduced
19-67
ChronotropicEffectsofthe
AutonomicNervousSystem
• Parasympatheticvagusnerveshavecholinergic,
inhibitoryeffectsonSAandAVnodes
– Acetylcholine(ACh)bindstomuscarinicreceptors
– OpensK+gatesinthenodalcells
– AsK+ leavesthecells,theybecomehyperpolarized andfire
lessfrequently
– Heartslowsdown
19-68
ChronotropicEffectsofthe
AutonomicNervousSystem
• Withoutinfluencefromcardiaccenters,thehearthas
an intrinsicfiringrateof100bpm
• Vagaltone—holdsdowntheheartrateto70to80
bpmatrest
– Steadybackgroundfiringrateofthevagusnerves
19-69
ChronotropicEffectsofthe
AutonomicNervousSystem
• Inputstocardiaccentersinmedullaarediverse
– Sourcesincludehigherbraincenterssuchascerebralcortex,limbic
system,hypothalamus
• Sensoryoremotionalstimuli
– Medullaalsoreceivesinputfrommuscles,joints,arteries,and
brainstem
• Proprioceptors inmusclesandjoints informcardiaccentersabout
changesinactivity,soHRincreases beforemetabolicdemandson
musclearise
– Baroreceptors signalcardiaccenter
• Pressuresensorsinaortaandinternalcarotidarteries
• Bloodpressuredecreases,signalratedrops,cardiaccenterincreases
heartrate
• Ifbloodpressureincreases,signalraterises,cardiaccenterdecreases
heartrate
19-70
ChronotropicEffectsofthe
AutonomicNervousSystem
• Inputstocardiaccenters(Continued)
– Chemoreceptors
• Inaorticarch,carotidarteries,andmedullaoblongata
• SensitivetobloodpH,CO2 andO2 levels
• Moreimportantinrespiratorycontrolthancardiaccontrol,butwill
triggeranincreaseinheartratewhenhighCO2levels(hypercapnia)
leadtoacidosis
• Alsorespondtohypoxemia(oxygendeficiencyinblood)usuallyby
slowingdowntheheart
– Baroreflexes and chemoreflexes—responsestofluctuationinblood
pressureandchemistry—arebothnegativefeedbackloops
19-71
ChronotropicEffectsofChemicals
• Severalchemicalsaffectheartrate
– Autonomicneurotransmitters(NEandAch)
– Blood-borneadrenalcatecholamines(NEandepinephrine)
arepotentcardiacstimulants
• Nicotine stimulatescatecholaminesecretion
• Thyroidhormoneincreasesnumberofadrenergicreceptors
onheartsoitismoreresponsivetoadrenergicstimulation
• Caffeine inhibitscAMPbreakdown,prolongingadrenergic
effect
19-72
ChronotropicEffectsofChemicals
• Electrolytes
– K+ hasgreatestchronotropiceffect
• Hyperkalemia—excessK+ diffusesintocardiocytes
– Myocardiumlessexcitable,heartrateslowsand
becomesirregular
• Hypokalemia—deficiencyinK+
– Cellshyperpolarized,requireincreasedstimulation
– Calcium
• Hypercalcemia—excessofCa2+
– Decreasesheartrateandcontractionstrength
• Hypocalcemia—deficiencyofCa2+
– Increasesheartrateandcontractionstrength
19-73
StrokeVolume
• Theotherfactorincardiacoutput,besidesheartrate,
isstrokevolume(SV)
• Threevariablesgovernstrokevolume
– Preload
– Contractility
– Afterload
• Examples
– Increasedpreloadorcontractilityincreasesstroke
volume
– Increasedafterloaddecreasesstrokevolume
19-74
Preload
• Preload—theamountoftensioninventricular
myocardiumimmediatelybeforeitbeginstocontract
– Increasedpreloadcausesincreasedforceof
contraction
– Exerciseincreasesvenousreturnandstretches
myocardium
– Cardiocytesgeneratemoretensionduringcontraction
– Increasedcardiacoutputmatchesincreasedvenous
return
19-75
Preload
• Frank–Starlinglawoftheheart:SVµEDV
– Strokevolumeisproportionaltotheenddiastolic
volume
– Ventriclesejectalmostasmuchbloodastheyreceive
– Themoretheyarestretched,thehardertheycontract
– Relatestothelength-tensionrelationshipofstriated
muscle
19-76
Contractility
• Contractility referstohowhardthemyocardium
contractsforagivenpreload
• Positiveinotropicagentsincreasecontractility
– Hypercalcemia cancausestrong,prolongedcontractions
andevencardiacarrestinsystole
– Catecholamines increasecalciumlevels
– Glucagon stimulatescAMPproduction
– Digitalisraisesintracellularcalciumlevelsand
contractionstrength
19-77
Contractility
• Negativeinotropicagents reducecontractility
– Hypocalcemia cancauseweak,irregularheartbeatand
cardiacarrestindiastole
– Hyperkalemia reducesstrengthofmyocardialaction
potentialsandthereleaseofCa2+intothesarcoplasm
– Vagusnerveshaveeffectonatria,buttoofewnervesto
ventriclesforasignificanteffect
19-78
Afterload
• Afterload—sumofallforcesopposingejectionofblood
fromventricle
• Largestpartofafterloadisbloodpressureinaortaand
pulmonarytrunk
– Opposestheopeningofsemilunarvalves
– Limitsstrokevolume
• Hypertension increasesafterloadandopposes
ventricularejection
19-79
Afterload
• Anythingthatimpedesarterialcirculationcanalso
increaseafterload
– Lungdiseasesthatrestrictpulmonarycirculation
– Corpulmonale:rightventricularfailureduetoobstructed
pulmonarycirculation
• Inemphysema,chronicbronchitis,andblacklungdisease
19-80
ExerciseandCardiacOutput
• Exercisemakestheheartworkharderandincreases
cardiacoutput
• Proprioceptorssignalcardiaccenter
– Atbeginningofexercise,signalsfromjointsandmuscles
reachthecardiaccenterofbrain
– Sympatheticoutputfromcardiaccenterincreasescardiac
output
• Increasedmuscularactivityincreasesvenousreturn
– Increasespreloadandultimatelycardiacoutput
19-81
ExerciseandCardiacOutput
• Increasesinheartrateandstrokevolumecausean
increaseincardiacoutput
• Exerciseproducesventricularhypertrophy
– Increasedstrokevolumeallowshearttobeatmoreslowly
atrest
– Athleteswithincreasedcardiacreservecantoleratemore
exertionthanasedentaryperson
19-82
CoronaryArteryDisease
• Coronaryarterydisease(CAD)—aconstrictionofthe
coronaryarteries
– Usuallytheresultofatherosclerosis:anaccumulationof
lipiddepositsthatdegradethearterialwallandobstruct
thelumen
– Beginswhenendotheliumdamagedbyhypertension,
diabetes,orothercauses
19-83
CoronaryArteryDisease
(Continued)
– Monocytespenetratewallsofdamagedvesselsandtransform
intomacrophages
• Absorbcholesterolandfatstobecalledfoamcells
– Cangrowintoatheroscleroticplaques(atheromas)
– Plateletsadheretodamagedareasandsecreteplateletderivedgrowthfactor
• Attractingimmunecellsandpromotingmitosisofmuscleand
fibroblasts,andthedepositionofcollagen
• Bulging massgrowstoobstructarteriallumen
19-84
CoronaryArteryDisease
• Causesanginapectoris, intermittentchestpain,by
obstructing75%ormoreofthebloodflow
• Immunecellsofatheromastimulateinflammation
– Mayrupture,resultingintravelingclotsorfattyemboli
• Causecoronaryarteryspasmsduetolackofsecretion
ofnitricoxide(vasodilator)
• Inflammationtransformsatheromaintoahardened
complicatedplaque
– Onecauseofarteriosclerosis
19-85
CoronaryArteryDisease
• MajorriskfactorforCADisexcessoflow-density
lipoprotein(LDL)inthebloodcombinedwithdefective
LDLreceptorsinarterialwalls
– LDLs—protein-coateddropletsofcholesterol,neutralfats,
freefattyacids,andphospholipids
– Dysfunctionalreceptorsinarterialcellscausethemto
accumulateexcesscholesterol
19-86
CoronaryArteryDisease
• Unavoidableriskfactors:heredity,aging,beingmale
• Preventableriskfactors:obesity,smoking,lackof
exercise,anxiouspersonality,stress,aggression,and
diet
• Treatment
– Coronarybypasssurgery
• Usesgreatsaphenousveinfromlegorsmallthoracicarteries
– Balloonorlaserangioplasty
– Insertionofastenttopreventrestenosis
19-87