mechanical function of the heart

7/28/2019 Mechanical Function of the Heart

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MECHANICAL FUNCTION

OF THE HEART

DEPARTMENT 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 Coupling

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

When a myocyte is depolarized by an actionpotential, calcium ions enter the cell duringphase2 of the action potential through L-type calciumchannels located on the sarcolemma.

This calcium triggers a subsequent release ofcalcium that is stored in the sarcoplasmicreticulum(SR)
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Calcium released by the SR increases theintracellular calcium concentration from about10-7 to 10-5 M.

The free calcium binds to troponin-C (TN-C) thatis part of the regulatory complex attached to thethin filaments.

When calcium binds to the TN-C (up to 4 calciumions per TN-C), this induces a conformationalchange in the regulatory complex such thattroponin-I (TN-I) exposes a site on the actinmolecule that is able to bind to the myosin ATPaselocated on themyosin head.
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This binding results in ATP hydrolysis thatsupplies energy for a conformational change tooccur in the actin-myosin complex.

The result of these changes is a movement("ratcheting") between the myosin heads and theactin, such that the actin and myosin filamentsslide past each other thereby shortening the

sarcomerelength(contraction). At the end of the cycle, a new ATP binds to the

myosin head, displacing the ADP, and the initialsarcomere length is restored.


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Action potential in myocytes

Entry of small amount Ca2+

from ECF

Cytosolic Ca2+Troponin-tropomyosin

Complex in thin filamentpulled aside

Release large amount of

Ca2+ from SR

Cross-bridge cycling

between

Thick and thin filaments

Thin filaments slide inward

Between thick filament

CONTRACTION


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Epinephrine or Norepinephrine

1 receptor on myocytecAMP

Voltage gate Ca channels

Open time increases

Ca2+ entry from ECF

Phospholamban

Ca2+-ATPase activity

Faster Ca remove fromcytosol

Time of Ca-troponin

Binding shorter

Shorter duration of

contractionForceful contraction

Ca2+stores in SRCa2+release from SR

bind to

that activate

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 x stroke volume


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FACTORS THAT AFFECT

CARDIAC OUTPUT

Contractility

Heart rate

Preload

Afterload


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FACTORS THAT AFFECT CARDIAC OUTPUT

CONTRACTILITY

STROKE VOLUME

CARDIAC OUTPUT

PRELOAD AFTERLOAD

HEART RATESynergism of contraction

Ventricular integrityValve competent


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The Effects of Contractility

Contractility depend on the rate of Ca2+ to entermyocytes

Contractility increase cardiac output Changes in heart rate affect myocardial

contractility

The ejection fraction is a good measure of

contractility. Contractility of the heart is the hearts performance

independent of loads.


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The Effects of Heart Rate

The relationship between heart rate and

cardiac output is complex Heart rate affected cardiac output by

changes ventricular filling

Cardiac output is varied depend on heartrate. Heart rate more than 150 times/min

decreased cardiac output


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The Effects of Preload

Preload is ventricular pressure at the end

of diastolic phase Preload depend on:

filling pressure,

filling time,

distensibility of ventricular wall


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Cardiac Muscle Length-Tension Curve

Cardiac muscle has similar

length-tension properties toskeletal muscle.

Cardiac muscle normally

operates well below optimum

length.

Increasing ventricular

volume stretches the

ventricular muscle towards

optimum length.

Stretching the ventricles

increases the pressure they

can generate.


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Cardiac Function Curve and Pre-load

Increasing venous return

increases the ventricular end

diastolic volume and

stretches the ventricles.

Venous return determines

the pre-load (cardiac end

diastolic pressure) on the

heart.

Normally increasing venous

return increases the force of

contraction.


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The Effects of Afterload

Afterload is the aortic pressure during

ejection phase The most realistic indicator for afterload is

arterial blood pressure

Complex relationship exist betweenafterload and cardiac output


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The Arterial Pressure After-loads the Heart


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Filling time Filling pressure Contractility

DistensibilityEnd distolic

volume

End systolic

volume

Heart

rate

Stroke

volume

PheripheralResistant

Cardiacoutput

Blood pressure Afterload


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The Effects of Heart Rate

Contractility depend on the rate of Ca2+ to

enter myocytes Contractility increase cardiac output

Changes in heart rate affect myocardial

contractility (heart rate more than 150X/min reduced contractility).


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Myocyte Changes by Mechanical Stress

Acute changes

Changes in cross-bridge number

Changes in contractility

Chronic changes

Signal transduction

Gene transcription


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Stres mekanik

Sekresi Angiotensin II

Aktifasi second messenger

Induksi ekspresi proto-oncogenes

Induksi gen faktor pertumbuhan

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

(-) (+)

(+/-)

mechanical function of the heart

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