MECHANICAL FUNCTION

OF THE HEART
IRAWAN YUSUF
DEPARTMENT OF PHYSIOLOGY

INTRODUCTION
Each potential action (electrical activity) in
heart muscle followed by contraction
(mechanical activity)
The purpose of contraction is to push out
blood in the ventricle
The amount of blood pumped by ventricle
during contraction is known as the stroke
volume

Excitation-Contraction Coupling
Excitation-contraction coupling (ECC) is the
process by which an action potential triggers a
myocyte to contract.
When a myocyte is depolarized by an action
potential, calcium ions enter the cell during
phase 2 of the action potential through L-type
calcium channels located on the sarcolemma.
This calcium triggers a subsequent release of
calcium
that
is
stored
in
the
sarcoplasmic reticulum (SR)

Excitation-Contraction Coupling
Calcium released by the SR increases the
intracellular calcium concentration from about
10-7 to 10-5 M.
The free calcium binds to troponin-C (TN-C) that
is part of the regulatory complex attached to the
thin filaments.
When calcium binds to the TN-C (up to 4 calcium
ions per TN-C), this induces a conformational
change in the regulatory complex such that
troponin-I (TN-I) exposes a site on the actin
molecule that is able to bind to the myosin ATPase
located on the myosin head.

Excitation-Contraction Coupling
This binding results in ATP hydrolysis that
supplies energy for a conformational change to
occur in the actin-myosin complex.
The result of these changes is a movement
("ratcheting") between the myosin heads and the
actin, such that the actin and myosin filaments
slide past each other thereby shortening the
sarcomere length(contraction).
At the end of the cycle, a new ATP binds to the
myosin head, displacing the ADP, and the initial
sarcomere length is restored.

Action potential in myocytes

Entry of small amount Ca2+
from ECF

Release large amount of

Ca2+ from SR

Cytosolic Ca2+
Troponin-tropomyosin
Complex in thin filament
pulled aside
Cross-bridge cycling
between
Thick and thin filaments
Thin filaments slide inward
Between thick filament
CONTRACTION

Epinephrine or Norepinephrine
bind to
1 receptor on myocyte
that activate
cAMP
phosphorylation
Voltage gate Ca channels
Open time increases
Ca2+ entry from ECF

Phospholamban
Ca2+-ATPase activity

Ca2+stores in SR

Faster Ca remove from

cytosol

Ca2+release from SR

Time of Ca-troponin
Binding shorter

Forceful contraction

Shorter duration of
contraction

CARDIAC OUTPUT
Cardiac output is defined as the amount of
blood pumped per ventricle per unit.
Cardiac output = heart rate x stroke volume

FACTORS THAT AFFECT

CARDIAC OUTPUT

Contractility
Heart rate
Preload
Afterload

FACTORS THAT AFFECT CARDIAC OUTPUT

CONTRACTILITY
PRELOAD

AFTERLOAD
STROKE VOLUME

Synergism of contraction
Ventricular integrity
Valve competent

HEART RATE

CARDIAC OUTPUT

The Effects of Contractility

Contractility depend on the rate of Ca2+ to enter
myocytes
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.

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 heart
rate. Heart rate more than 150 times/min
decreased cardiac output

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

Cardiac Muscle Length-Tension Curve

Cardiac muscle has similar
length-tension properties to
skeletal 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.

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.

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 between
afterload and cardiac output

The Arterial Pressure After-loads the Heart

Filling time

Distensibility

Filling pressure

Contractility

End distolic
volume

End systolic
volume

Heart
rate

Pheripheral
Resistant

Stroke
volume

Cardiac
output

Blood pressure

Afterload

The Effects of Heart Rate

Contractility depend on the rate of Ca 2+ to
enter myocytes
Contractility increase cardiac output
Changes in heart rate affect myocardial
contractility (heart rate more than 150
X/min reduced contractility).

Myocyte Changes by Mechanical Stress

Acute changes
Changes in cross-bridge number
Changes in contractility

Chronic changes
Signal transduction
Gene transcription

Stres mekanik
Sekresi Angiotensin II
(+/-)

Aktifasi second messenger

(-)

(+)
Induksi ekspresi proto-oncogenes
Induksi gen faktor pertumbuhan

R E S PO N H I PE R T R O PI J AN T U N G