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7/26/2019 05 Cardiovascular System Physiology
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Cardiovascular PhysiologyGian Carlo Delante, PhB PTRP RPT
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Anatomy Review: The Heart
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The Intrinsic ConductionSystem
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Important things toremember
The intrinsic conduction system ofthe heart initiates depolariationimpulses
Action potentials spread throughoutthe heart! causing a coordinatedheart contraction
An "C# wave tracing records theelectrical activity of the heart
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$yocardial Cells
Contractile cells Have features similar to s%eletal
muscles
&odal'Conducting cells Have features similar to nerves
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Contractile Cells
Considered to be the realmuscle cells of theheart
Contain the same contractile proteins actin(myosin
arranged in bundles ofmyofbrils
surrounded by a SR
)i*erence: only one nucleus ( far moremitochondria
"+tremely e,cient at e+tracting -. from blood/about .+ more than other cells0
1ranched and 2oined together by intercalateddiscs
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Tight 3unctions ( #ap3unctions
Intercalated )iscs contain tightjunctions and gap junctions
TI#HT 34&CTI-&S: bind cells together
#AP 34&CTI-&S: allow for themovement of ions and ion currentsbetween myocardial cells5 allows theconduction of action potentials fromcell to cell withoutthe need fornerves
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&odal'Conducting Cells
Special cells able to spontaneously generateaction potentials without the help of nervoussystem input
Properties: Sel-!citability! Con"ucting
Rhythmicity 6 chronotropy
"+citability 6 bathmotropy
Contractility 6 inotropy
Conductivity 7 dromotropy
Rela+ation 6 lusitropy
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-rigin of Self6"+citability
#eneral site of origin: SI&-ATRIA8&-)" or SA &-)"
The 9rst area to spontaneouslydepolarie hence thepacema#er othe heart
Spontaneous depolariation of the SAnode: Pacema#er potential
8ocation: upper posterior wall of theright atrium
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The Cardiac Cycle
Two primary phases Systole
)iastole
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ive Steps of the CardiacCycle
Step ;
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Step .< Isovolumetric ventricularcontraction (also called earlyventricular systole).This begins with
the ventricles depolariing /&RScomple!0 then contracting=>entricular pressure increases rapidly
/above atrial but below aorticpressures0= The mitral valve closes=No change in ventricular volume=
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Step < Ventricular systole (alsocalled ejection period)= Theventricles are still contracting! but
now ventricular pressure is aboveaortic= The aortic valve opens= 1lood?ows into the aorta! and ventricular
volume decreases=
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Step B< Early ventricular diastole(also called isovolumetricrelaxation phase)= >entricular
pressure falls below aortic pressure!and the aortic valve closes= Someblood remains in the ventricles /end
systolic volume0= >entricular pressurecontinues to fall= No change inventricular volume=
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Step < Late ventricular diastole=>entricular pressure drops belowatrial pressure= The mitral valve
opens! and blood ?ows into theventricle= >entricular volumeincreases= P wave begins! and the
cycle repeats=
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Period of "2ection
or blood to be e2ected from theheart: >entricular pressure D ' E ' F aortic
pressureG
Aortic pressure F mmHg
>entricular pressure: reaches up to JJ
mmHg
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Heart Sounds
-pening of heart valves Slowly developing process
Produces no sound
Closing of heart valvesThere are sudden pressure di*erences
Produces sound that resonate around the chest
'(B/9rst heart sound0 Closure of A> valves
8ow pitched and of relatively longer duration
D(P/second heart sound0 Closure of semilunar valves
High pitched and of relatively shorter duration
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Cardiac -utput
>olume of blood that the heart canpump out in one minute
At rest F liters
)uring vigorous e+ercise &ormal individual F . liters
Trained athlete F up to B liters
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Cardiac -utput
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Control of Heart Rate
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Control of Heart Rate
Kithout A&S in?uence over theheart! it will beat at an intrinsic rateof ;bpm via the autorhythmic SA
node Constant in?uence by the P&S at rest
e+plains why normal HR is usually
around Lbpm AMA: %agal tone
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A&S and &eurotransmitters
P&S: Acetylcholine
S&S: "pinephrine and &orepinephrine
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Stro%e >olume
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actors A*ecting Stro%e>olume
Input from the A&S 7 either P&S orS&S
")> andpreload
"S>
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Control of Stro%e >olume throughA&S Input
How will the A&S control S> /or")>'"S>0
Calciumion in?u+ control Acetylcholine
S&S or P&SG Increase or decrease Ca in?u+
"pinephrine'&orepinephrine
S&S or P&SG Increase or decrease Ca in?u+
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Control of Stro%e >olume throughChanging ")> and Preload
Preload is directly related to enddiastolic volume /")>0
#reater ")> means also a greaterPreload
So how can SV be afected by EVDand preload?
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ran%6Starling 8aw
A muscle! including heart muscle!responds to increased stretching atrest by an increased force of
contraction when stimulated In other words! an increase in end
diastolic volume /")>0 will result to
an increase in stro%e volume /S>0
So how then can we increase
EDVpreload?
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Increasing ")>'Preload
S&S Constriction of veins
"+ercise $uscle pump