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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
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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
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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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Kurva Frank Starling
S
#ro)!2o*/m!
En &i'-#o*i3 4o*m!
;ormal
Stimulasi
!drenergik
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Kurva Frank Starling
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-