Download 18 The Heart new

Physiology
Unit3
CARDIOVASCULARPHYSIOLOGY:
THEHEART
InPhysiologyToday
CardiovascularSystemOverview
• Cardiovascularsystemcomponents
– Heart
– Bloodvessels
– Blood
• Cardiovascularsystemfunctions
– Transportationofsubstances
•
•
•
•
Respiration
Nutrition
Excretion
Hormones
– Regulation
– Protection
CardiacMuscle
• Characteristics
– Somecellsintheatriasecreteapeptidehormonecalled
atrialnatriureticfactor(ANF)
• Causesnatriuresis
• Vasodilation
• Conductingsystem
– 1%ofcells
– Initiatesheartbeatandspreadstheimpulsethroughout
theheart
• 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
• Membraneremains
depolarized
– Ca2+influxsustains
depolarization
– K+ channelsremainclosed
• vgK+ channelsopen
(repolarization)
RMP = -90 mV
Threshold = -60 mV
NodalCellActionPotential
• Pacemakerpotential
– Slowdepolarization
– Automaticity(spontaneous,
rhythmical)
• Voltage-gatedK+ channels
close
• F-typeNa+ channelsopen
whenthemembrane
potentialisatnegativevalues
• T-typeCa2+channelsopen
briefly
Nodal Cell threshold -40mmHg
– InwardCa2+current
– Finaldepolarizingboostto
threshold
ElectricalEventsoftheHeart
• Electrocardiogram(ECG)
– Measuresthecurrents
generatedintheECFbythe
changesinmanycardiaccells
• Pwave
– Atrialdepolarization
• QRScomplex
– Ventriculardepolarization
– Atrialrepolarization
• Twave
– Ventricularrepolarization
Excitation-ContractionCoupling
• Ca2+enteringthrough
L-typeCa2+channelstriggers
thereleaseofmoreCa2+
fromtheryanodine
receptorsintheSR
– Calciuminducedcalcium
release
• Cross-bridgecyclingoccurs
• ContractionendswhenCa2+
ispumpedbackintotheSR
byCa2+/ATPasepumpsand
Na+/Ca2+ countertransporters
RefractoryPeriodoftheHeart
• Longabsolute
refractoryperiod
preventstetany
– Musclecannotbe
stimulatedintimeto
producesummation
• Absoluterefractory
periodforcardiac
muscleis20-200ms
– Skeletalmuscle1-2ms
MechanicalEventsoftheHeart
• Cardiaccycle
– Pressureandvolumechangesthatoccurduringthecardiaccycle
– Averageheartrate72bpm
– Eachcardiaccyclelasts0.8s
• 0.3sinsystole
• O.5sindiastole
• 2alternatingphases
– Systole
• Ventricularcontractionandbloodejection
– Diastole
• Ventricularrelaxationandbloodfilling
CardiacCycle
CardiacCycle
Systole
• IsovolumetricVentricularContraction
– Ventriclecontracting
• Musclefibersdevelopingtension
• Musclefibersdonotshorten
• Increasingpressureinsidetheventricles
– Allvalvesclosed
– Nobloodejection
– Ventricularvolumeremainsthesame
CardiacCycle
Systole
• VentricularEjection
– Pressureintheventriclesexceedpressurein
aorta/pulmonarytrunk
– Semilunarvalvesopen
– Bloodforcedintoaorta/pulmonarytrunk
– Musclefibersshorten
– Strokevolume(SV)
• Volumeofbloodejectedduringsystole
• SV=135mL(EDV)– 65mL(ESV)
• AverageSVis70mL/beat(0.07L/beat)
CardiacCycle
Diastole
• IsovolumetricVentricularRelaxation
– Ventriclesbegintorelax
– Semilunarvalvesclose
– AVvalvesclosed
– Nobloodenteringorleavingtheventricles
– Ventricularvolumeremainsthesame
CardiacCycle
Diastole
• VentricularFilling
– AVvalvesopen
– Bloodflowsfromatriatoventricles
– 80%ofventricularfillingispassive
– Atrialcontractionoccursattheendof
diastole
• Atrialkickmovestheremaining20%ofbloodin
atriaintoventricles
CardiacCycle
Volumes
• End-diastolicvolume
– EDV
– Volumeintheventriclesattheendofdiastole
• End-systolicvolume
– ESV
– Volumeintheventriclesattheendofsystole
PressureChanges
VolumeChanges
ECG
HeartSounds
• Lub
– Softsound
– ClosingoftheAVvalves
– Onsetofsystole
• Dup
– Loudersound
– Closingofthesemilunar
valves
– Onsetofdiastole
CardiacOutput(CO)
• Volumeofbloodpumpedoutoftheventricles
expressedasL/min
– Volumeofbloodflowingthrougheitherthe
pulmonaryorsystemiccircuitperminute
•
•
•
•
CO=HRxSV
CO=72beats/minx0.07L/beat
CO=5.0L/min
Totalbloodvolumeispumpedaroundthecircuit
onceeachminute
– 1,440perday!
ControlofHeartRate
HRisavariablethatdeterminesCO
• 100BPMwithoutnerveor
hormoneinfluenceonthe
SAnode
• However,SAnodeisunder
constantinfluenceofnerves
andhormones
– Activityofthe
parasympatheticnerves
causesadecreaseinheart
rate
– Activityofsympatheticnerves
causesanincreaseinheart
rate
ControlofHeartRate
HRisavariablethatdeterminesCO
• Sympatheticstimulation
– Increasesslope
– IncreasesF-typeNa+ channel
permeability
– Fasterdepolarization
• Parasympatheticstimulation
– Slopedecreases
– Hyperpolarizesplasma
membraneofSAnode
– IncreasesK+ permeability
ControlofHeartRate
HRisavariablethatdeterminesCO
• Epinephrine
– IncreasesHR
– Bindstobeta-adrenergic
receptorsintheSAnode
• Heartrateisalso
sensitivetochangesin:
– BodyTemperature
– Plasmaelectrolyte
concentrations
• K+
• Ca2+
ControlofStrokeVolume
SVisavariablethatdeterminesCO
• Ventriclesdonotcompletelyemptyduring
contraction
• Moreforcefulcontractioncanproducean
increaseinSV bycausinggreateremptying
• 3mainfactors
1. ChangesinEDV (preload)
2. Changesincontractility
3. Changesinafterload
• arterialpressuresagainstwhichtheventriclespump
• Increaseintotalperipheralresistance(TPR)
Starling’sLawoftheHeart
RelationshipbetweenEDVandSV
• Ventriclescontractmore
forcefullyduringsystole
whenithasbeenfilledtoa
greaterdegreeduring
diastole
• SVincreasesasEDV
increases
• SVisDependentofEDV
• Increaseinvenousreturn
forcesanincreaseinCOby
increasingEDVwhich
increasesSV
SympatheticRegulation
• Sympatheticnerves
innervatetheentire
myocardium
• NEandEpibindtobetaadrenergicreceptorsto
increasecontractility
– Increasesstrengthof
contractionatanygiven
EDV
– SVisIndependentof
EDV
– Leadstoanincreasein
ejectionfraction
EjectionFraction(EF)
• EFquantifiescontractility
• EF=SV/EDV
• Underrestingconditions,averageisbetween
50–75%
• IncreasedcontractilitycausesincreasedEF
SympatheticRegulation
• Increasedsympathetic
activity
– IncreasesHRwithout
decreasingCO
– Increasescontractility
– Ventriclescontractmore
forcefullytocompensate
fortheincreaseinHR
SympatheticRegulationofMyocardial
Contractility
ControlofCardiacOutputSummary