05 cardiovascular system physiology

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

05 cardiovascular system physiology

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