SUSUNAN PEREDARAN DARAH MANUSIA.ppt

7/25/2019 SUSUNAN PEREDARAN DARAH MANUSIA.ppt

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CARDIOVASCULARPHYSIOLOGY

Dr. Poland Room 3-007, Sanger Hall, Phone: 828-9557

E-mail: poland@h!."!#.ed#

Departemen Fisiologi

Fakultas Kedokteran

Universitas Sumatera Utara
http://www.harthosp.org/cardi/images/beat_heart.gifhttp://www.harthosp.org/cardi/images/beat_heart.gif


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Functions of the Cardio-Vascular System

Delivery of O2, Glucose and other

nutrients to active tissues.

Transport of metabolites and othersubstances to and from storagesites.

Transport of hormones, antibodiesand other substances to site ofaction.

Dr Peter K. cFa!n Department of Physiology "ueen#s University $otterell %all &thfloor

pkm'post.(ueensu.ca http)**meds.(ueensu.ca*physiol*underg.html

PrimaryF

unction

oftheCVSys

tem+

Transpor

t
mailto:[email protected]:[email protected]:[email protected]


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The Heart

Four Cham,ered rgan

Circulates $lood to ungs / Un-o0ygenated

Circulates $lood to the $ody /

0ygenated

Removal of CO2, Lactate

and other aste productsfrom active tissues.

Speciali1ed uscle 2ype / Cardiac Uni(ue Vascular System / Coronary

3rteries and Veins

Separate 4ervous System

$eats 5contracts6 appro0imately 78-98

times*minute

2he ungs :elationship to the

CV System

Pro"ide $or e%!hange o$

&%'gen and (ar)on

Dio%ide


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The Circulatory SystemThe Circulatory System

2 main divisions

Pulmonary circulation (heart lungs)

Pulmonary artery: deoxygenated blood from the heart to the lungs

Pulmonary vein: oxygenated blood from the lungs to the heart Systemic circulation: (Heart rest of the body)

Aorta: feeds oxygenated (arterial)blood to the body

Venae cavae: returns deoxygenated (venous)blood from the body


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Series andParallel Vascular

Beds.*The systemic and pulmonarycirculations are in Series with

each other.

*S'+emi! !apillar' )ed are in

parallel i+h ea!h o+her.*The kidney and hepatic/gut

capillary beds are an

exception. The portal vein and

kidney efferent arteriole linkcapillary systems in series.

PARALLEL SUBCIRCUITS

UNIDIRECTIONAL FLO


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PU43:;

C


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THE SYSTE!IC

CIRCULATION

C3P3C


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PACE!A,ER POTENTIALPACE!A,ER POTENTIAL

!!"astest# cells"astest# cells

located in $% nodelocated in $% node

&'(()minute*.&'(()minute*.

$% node sets$% node setspace.pace.

+undle of is can+undle of is can

provide ectopicprovide ectopic

pacema-er &2/pacema-er &2/

0()min*0()min*


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In-rinsic Cnduc-in)In-rinsic Cnduc-in)

S/s-e(S/s-e( $inoatrial node.$inoatrial node.

1 lectrical pace ma-er.lectrical pace ma-er.

%trioventricular node.%trioventricular node.

1 Receives impulsesReceives impulses

originating from $%originating from $%

node.node.

+undle of is+undle of is

1 lectrical lin- beteenlectrical lin- beteen

atria and ventricles.atria and ventricles.

3ur-in4e 5bres.3ur-in4e 5bres.

1 Distribute impulses toDistribute impulses to

ventricles.ventricles.


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3trio-ventricular 53V6 node

P3C=3K=:S

(in or!r o"#$!ir in$!r!n#

r$%#$m)

Sino-atrial 5S36 node

3trio-ventricular 53V6 node

$undle of %is

$undle ,ranches

Purkin?e fi,ers

lectrical vents !utorhythmicity"heart contracts

without help of hormonal or neuronal

stimulation.

The conduction or nodal system of the

heart consists of the !# and S! nodes$

the !# bundle and bundle branches

and %urkin&e fibers. This system coordinates the

depolari'ation and ensures the heart

beats as one.

The S! acts as the heart(s pacemaker

and sets the sinus rhythm.


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Properties of Cardiac Muscle

ELECTRICAL PROPERTIES

Resting Membrane & Action Potentials

The resting membrane potential of individualmammalian cardiac muscle cells is about -90 mV(interior negative to exterior).

Stimulation produces a propagated action potentialthat is responsible for initiating contraction.


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Depolarization lasts about 2 ms, but plateau phase

and repolarization last 200 ms or more.

Repolarization is therefore not complete until the

contraction is half over.


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!utorhytmic cells begin depolari'ing due to a slow continuous

influx of sodium and reduced efflux of potassium


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hen threshold is reached$ the fast calcium channel open$

and calcium rushes in


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eversal of membrane potential triggers opening of potassiumchannels$ resulting in rapid efflux of potassium


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-iagram of the membrane potential of

pacemaker tissue.


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=C%34


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-uring its absoluterefractory period$ cardiac

muscle cannot be excitedagain

Therefore$ tetanus of thetype seen in skeletalmuscle cannot occur.

Crrela-in Be-0een !uscle Fi1er


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elation betweeninitial fiber lengthand total tension incardiac muscle is

similar to that inskeletal muscle2there is a restinglength at which thetension developedupon stimulation ismaximal.

Crrela-in Be-0een !uscle Fi1erLen)-2 3 Tensin


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3esanggupan intrinsik &antung untuk penyesuaian diri terhadap

beban yang berbeda

-alam batas fisiologis &antung akan memompakan semua darah

yang masuk kedalam &antung tanpa menimbulkan penumpukandarah berlebihan. +ni disebabkan oleh peregangan yang

ditimbulkan volume darah yang masuk menyebabkan kekuatan

kontraksi bertambah.

&!ng'n !r'#''n *'in+

,on#r'-i 'n#ng -!'# -i-#o*i- ''n

!r#'m'$ '# i*' !ngi-i'n 'r'$ *!i$ 'n%'

'' m'-' i'-#o*i.

Frank Starling#S 3>


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Kurva Frank Starling

S#ro)!2o*/m!

En &i'-#o*i3 4o*m!

%ada kurva dapat dilihat

4ila pengisian ventrikel bertambah $

darah yang dipompakan

5 -#ST63 #6789 :


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In the body, the initial length of the fibersis determined by the degree of diastolic

filling of the heart, and the pressuredeveloped in the ventricle is proportionateto the total tension developed (Starling'slaw of the heart).

Developed tension increases as thediastolic volume increases until it reachesa maximum (ascending limb of Starling

curve), then tends to decrease(descending limb of Starling curve).


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S

#ro)!2o*/m!

En &i'-#o*i3 4o*m!

;ormal

Stimulasi

!drenergik


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S#ro)!2o

*/m!

En &i'-#o*i3 4o*m!

STRETCHING O 67OCAR&

Total blood

volume

4ody

position

+ntrathoracic

pressure

!trial

contribution to

ventr.filling

%umping action of

skletal muscle#enous tone

+ntrapericardial

pressure


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he force of contraction of cardiac muscleis also increased by catecholamines, andthis increase occurs without a change inmuscle length.

he increase, which is called the positivelyinotropic effect of catecholamines, ismediated via innervated !"#adrenergic

receptors and cyclic $%&.


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When the cholinergic vagal fibers to nodaltissue are stimulated, the membranebecomes hyperpolarized and the slope of

the prepotentials is decreased becausethe acetylcholine released at the nerveendings increases the !conductance ofnodal tissue.


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Spread of Cardiac ExcitationDepolariation initiated in the S$ node

spreads radially through the atria, thenconverges on the $ node.$trial depolariation is complete in about

." s. *ecause conduction in the $ node is

slow, there is a delay of about ." s ($nodal delay) before excitation spreads to

the ventricles.his delay is shortened by stimulation of

the sympathetic nerves to the heart and

lengthened by stimulation of the vagi.


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+rom the top of the septum, the wave of

depolariation spreads in the rapidly

conducting &urin-e fibers to all parts of

the ventricles in the .#." s.In humans, depolariation of the

ventricular muscle starts at the left side ofthe interventricular septum and moves first

to the right across the midportion of the

septum.

he wave of depolariation then spreadsdown the septum to the apex of the heart.


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It returns along the ventricular walls to

the $ groove, proceeding from theendocardial to the epicardial surface.he last parts of the heart to be

depolaried are the posterobasal portion of

the left ventricle, the pulmonary conus,and the uppermost portion of the septum.


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;ormal spread of electrical activity in the heart.


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Le- i-

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