MECHANICAL FUNCTION OF THE HEART.ppt

8/18/2019 MECHANICAL FUNCTION OF THE HEART.ppt

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MECHANICAL FUNCTION

OF THE HEART

IRAWAN YUSUFDEPARTMENT OF PHYSIOLOGY


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INTRODUCTION

• Each potential action (electrical activity) inheart muscle followed by contraction

(mechanical activity)• The purpose of contraction is to push out

blood in the ventricle

• The amount of blood pumped by ventricleduring contraction is known as the strokevolume


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Excitation-Contraction Coupin!

• Excitation-contraction coupling (ECC) is the process by which an action potential triggers amyocyte to contract.

• When a myocyte is depolarized by an action potential, calcium ions enter the cell during phase 2 o the action potential through !-typecalcium channels located on the sarcolemma.

• "his calcium triggers a subse#uent release ocalcium that is stored in thesarcoplasmic reticulum ($%)

http://www.cvphysiology.com/Arrhythmias/A006.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Arrhythmias/A006.htm


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• Calcium released by the $% increases theintracellular calcium concentration rom about&'-( to &'-) *.

• "he ree calcium binds to troponin-C ("+-C) thatis part o the regulatory complex attached to thethin ilaments.

• When calcium binds to the "+-C (up to calcium

ions per "+-C), this induces a conormationalchange in the regulatory complex such thattroponin- ("+-) exposes a site on the actinmolecule that is able to bind to the myosin "/aselocated on the myosin head.

http://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF020.htm


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• "his binding results in "/ hydrolysis that

supplies energy or a conormational change to

occur in the actin-myosin complex.

• "he result o these changes is a mo0ement(1ratcheting1) between the myosin heads and the

actin, such that the actin and myosin ilaments

slide past each other thereby shortening the

sarcomere length(contraction).

• t the end o the cycle, a new "/ binds to the

myosin head, displacing the /, and the initial

sarcomere length is restored.


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Action pot"ntia in #$oc$t"%

Entr$ o& %#a a#ount Ca'(

&ro# ECF

C$to%oic Ca'(

Troponin-tropo#$o%in

Co#p"x in t)in &ia#"ntpu"* a%i*"

R""a%" ar!" a#ount o&

Ca'( &ro# SR

Cro%%-+ri*!" c$cin!

+"t,""n

T)ic an* t)in &ia#"nt%

T)in &ia#"nt% %i*" in,ar*

."t,""n t)ic &ia#"nt

CONTRACTION


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Epin"p)rin" or Nor"pin"p)rin"

/ r"c"ptor on #$oc$t"

cAMP

0ota!" !at" Ca c)ann"%

Op"n ti#" incr"a%"%

Ca'( "ntr$ &ro# ECF

P)o%p)oa#+an

Ca'(-ATPa%" acti1it$

Fa%t"r Ca r"#o1" &ro#c$to%o

Ti#" o& Ca-troponin

.in*in! %)ort"r

S)ort"r *uration o&

contractionForc"&u contraction

Ca'(%tor"% in SR

Ca'(r""a%" &ro# SR

bind to

that acti0ate

phosphorylation


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CARDIAC OUTPUT

• Cardiac output is defined as the amount of

blood pumped per ventricle per unit.

Cardiac output = heart rate stroke volume


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FACTORS THAT AFFECT

CARDIAC OUTPUT

• Contractility

• !eart rate

• "reload

• #fterload


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FACTORS THAT AFFECT CARDIAC OUTPUT

CONTRACTILITY

STRO2E 0OLUME

CARDIAC OUTPUT

/%E!3 4"E%!3

HEART RATE•$ynergism of contraction

•%entricular integrity•%alve competent


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T)" E&&"ct% o& Contractiit$

• Contractility depend on the rate of Ca&' to entermyocytes

• Contractility increase cardiac output• Changes in heart rate affect myocardial

contractility

• The eection fraction is a good measure of

contractility.• Contractility of the heart is the hearts performance

independent of loads.


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T)" E&&"ct% o& H"art Rat"

• The relationship between heart rate and

cardiac output is comple• !eart rate affected cardiac output by

changes ventricular filling

• Cardiac output is varied depend on heartrate. !eart rate more than *+ times,min

decreased cardiac output


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T)" E&&"ct% o& Pr"oa*

• Pr"oa* i% 1"ntricuar pr"%%ur" at t)" "n*

o& *ia%toic p)a%"• Pr"oa* *"p"n* on3

- &iin! pr"%%ur"4

- &iin! ti#"4 - *i%t"n%i+iit$ o& 1"ntricuar ,a


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Car*iac Mu%c" L"n!t)-T"n%ion Cur1"

Cardiac muscle has similar

lengthtension properties toskeletal muscle.

Cardiac muscle normally

operates well below optimum

length.

/ncreasing ventricular

volume stretches the

ventricular muscle towards

optimum length.

$tretching the ventricles

increases the pressure they

can generate.


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Car*iac Function Cur1" an* Pr"-oa*

/ncreasing venous return

increases the ventricular end

diastolic volume and

stretches the ventricles.

%enous return determines

the preload (cardiac end

diastolic pressure) on the

heart.

0ormally increasing venous

return increases the force of

contraction.


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T)" E&&"ct% o& A&t"roa*

• #fterload is the aortic pressure during

eection phase• The most realistic indicator for afterload is

arterial blood pressure

• Comple relationship eist betweenafterload and cardiac output


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T)" Art"ria Pr"%%ur" A&t"r-oa*% t)" H"art


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Fiin! ti#" Fiin! pr"%%ur" Contractiit$

Di%t"n%i+iit$En* *i%toic

1ou#"

En* %$%toic

1ou#"

H"art

rat"

Stro"

1ou#"

P)"rip)"raR"%i%tant

Car*iacoutput

.oo* pr"%%ur" A&t"roa*


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T)" E&&"ct% o& H"art Rat"

• Contractility depend on the rate of Ca&' to

enter myocytes• Contractility increase cardiac output

• Changes in heart rate affect myocardial

contractility (heart rate more than *+1,min reduced contractility).


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M$oc$t" C)an!"% +$ M"c)anica Str"%%

• #cute changes

- Changes in crossbridge number - Changes in contractility

• Chronic changes

- $ignal transduction - 2ene transcription


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Str"% #"ani

S"r"%i An!iot"n%in II

Ati&a%i second messenger

In*u%i "%pr"%i proto-oncogenes

In*u%i !"n &ator p"rtu#+u)an

R E S P O N H I P E R T R O P I 5 A N T U N G

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MECHANICAL FUNCTION OF THE HEART.ppt

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