Heart as a Pump

Departemen Fisiologi
Fakultas Kedokteran
Universitas Sumatera Utara
Kondisi Jantung Normal

 Kontraksi reguler
dan sinkron
 Katup jantung
(normal)
 Kontraksi kuat
 Pengisian adequat
(diastole)
Cardiac Output (CO)

• Volume darah yang dipompakan

ventrikel dalam unit waktu
• CO = HR X SV
• Contoh :
HR (denyut jantung) = 70 X/1mnt
SV (stroke volume) = 70 ml/1 X
CO = 70 X 70 ml = 4.900 ml/1
menit

• CO laki-laki +/- 5,5 ltr/meni

wanita +/- 4,15ltr/menit
 CARDIAC OUTPUT
 Method of Measurement
direct Fick method and indicator
dilution method
 Ficks principle : Amount of a
substance taken up by an organ (whole
body) per unit time = arterial level of
the substance minus venous level (A –
V difference) times the blood flow.
 Cardiac index = cardiac output per square
meter of body surface , averages 3,2 L
 Indicator dilution technique
 Cardiac output = amount of indicator
injected divided by its average
concentration in arterial blood after a
single circulation through the heart.
 thermodilution, indicator used is cold
saline
 Distribusi Cardiac Output
Cardiac Output Konsumsi oksigen

Hati&GIT Ginjal Otak Jantung Hati&GIT Ginjal Otak Jantung

Skel. Mus. Kulit Lain2 Skel.mus. Kulit Lain2

10%
14%
25%
8%
2% 30%

20% 20%

20% 6%

4%
13% 10%
18%
• ejection fraction, percent of
end-diastolic ventricular
volume that is ejected with
each stroke, is about 65% (EF
= SV/ EDV)
NOTE: Resting Ejection
Fraction (EF) is the best
indicator of both heart
performance and heart
disease prognosis
 CARDIAC OUTPUT IN
VARIOUS CONDITIONS
 stroke volume is the amount of blood
pumped out of the heart per beat, is about
70 mL from each ventricle in a resting man
of average size in the supine position.
 cardiac output is the output of the heart
per unit of time.
 In a resting, supine man, it averages about
5.0 L/min (70 mL × 72 beats/min).
Factors Controlling Cardiac Output
• Cardiac accelerator action of catecholamines
liberated by sympathetic stimulation : chronotropic
action, whereas their action on the strength of
cardiac contraction : inotropic action.
• force of contraction of cardiac muscle is dependent
upon its preloading and its afterloading.
• preload is the degree to which the myocardium is
stretched before it contracts (= EDV)
• afterload is the resistance against which blood is
expelled (= Aortic Pressure & MAP)
 Relation of Tension to Length in Cardiac
Muscle
• when the muscle is stretched, the developed
tension increases to a maximum and then
declines as stretch becomes more extreme.
• Starling's law of the heart or Frank-Starling
law = "energy of contraction is proportional to
the initial length of cardiac muscle fiber."
= relation between ventricular stroke volume
and end-diastolic volume
= Length of muscle fiber = preload
 Relation of Tension to Length in Cardiac
Muscle

• The length-tension relationship in cardiac muscle is

similar to that in skeletal muscle as the muscle is
stretched, the developed tension increases to a maximum
and then declines as stretch becomes more extreme.
Kurva Frank Starling
Stimulasi
Adrenergik

Normal
Stroke volume

Fungsi jantung

Syok
Kardiogenik

End Diastolic Volume

 FACTORS AFFECTING END-DIASTOLIC
VOLUME
SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase

After-load

Isovolumetric
PRESSURE

Phase

Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume

 FACTORS AFFECTING END-DIASTOLIC
E D Y VOLUME
A S LI T
RE TI SYSTOLIC PRESSURE CURVE
C C
IN TRA
O N
C

Isotonic (Ejection) Phase

After-load

Isovolumetric
PRESSURE

Phase

Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume

 FACTORS AFFECTING END-DIASTOLIC
S ED TY VOLUME
E A I LI
C R CT SYSTOLIC PRESSURE CURVE
DE TRA
O N
C

Isotonic (Ejection) Phase

After-load

Isovolumetric
PRESSURE

Phase

Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume

 FACTORS AFFECTING END-DIASTOLIC
VOLUME

G D
IN E
LL AS
SYSTOLIC PRESSURE CURVE
FI RE
C
IN

Isotonic (Ejection) Phase

After-load

Isovolumetric
PRESSURE

Phase

Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume

 Physiological regulation of
contractile force

(1) length – tension relation

(2) chemically induced rises in the
calcium store leading to higher
sarcoplasmic Ca2+ concentration in
systole; sympathetic neurotransmitter
and cathecholamine.
Factors that normally increase or
decrease the length of ventricular
Myocardial Contractility
• Catecholamines exert their
inotropic eff ect via an
action on cardiac β 1
-adrenergic receptors and
Gs, with resultant
activation of adenylyl
cyclase and increased
intracellular cyclic
adenosine 3′,5′-
monophosphate (cAMP).
• Xanthines such as caffeine
and theophylline that
inhibit the breakdown of
cAMP are predictably
positively inotropic.
• The positively inotropic effect of digitalis
and related drugs, on the other hand, is due
to their inhibitory effect on the Na, K
ATPase in the myocardium, and a
subsequent decrease in calcium removal
from the cytosol by Na+ /Ca2+ exchange
• Hypercapnia, hypoxia, acidosis, and drugs
such as quinidine, procainamide, and
barbiturates depress myocardial
contractility.
 INTEGRATED CONTROL OF CARDIAC OUTPUT
• during muscular exercise, there
is increased sympathetic
discharge, so that myocardial
contractility is increased and
the heart rate rises.
• patients with transplanted
hearts are able to increase their
cardiac output during exercise
in the absence of cardiac
innervation through the
operation of the Frank–Starling
mechanism, circulating
catecholamines also contribute
• If venous return increases and there is no
change in sympathetic tone, venous pressure
rises, diastolic inflow is greater, ventricular
end-diastolic pressure increases, and the heart
muscle contracts more forcefully.
• During muscular exercise, venous return is
increased by the pumping action of the muscles
and the increase in respiration.
• because of vasodilation in the contracting
muscles, peripheral resistance and,
consequently, afterload are decreased.
• One of the differences between untrained
individuals and trained athletes is that the
athletes have lower heart rates, greater end-
systolic ventricular volumes, and greater stroke
volumes at rest.
• Therefore, they can potentially achieve a given
increase in cardiac output by further increases in
stroke volume without increasing their heart rate
to as great a degree as an untrained individual.
 OXYGEN CONSUMPTION
BY THE HEART
• Basal O2 consumption by the myocardium is about
2 mL/100 g/min.
• This value is considerably higher than that of
resting skeletal muscle. O2 consumption by the
beating heart is about 9 mL/100 g/min at rest.
• O2 consumption by the heart is determined
primarily by the intramyocardial tension, the
contractile state of the myocardium, and the heart
rate.
• The work is the product of stroke volume and mean
arterial pressure in the pulmonary artery or the aorta (for
the right and left ventricle, respectively).
 Referensi:
• Barret KE, Barman SM, Boitano S, Brooks HL,
Ganong’s Review of Medical Physiology, 24th
edition, McGraw Hill, Lange, 2012.
• Silverthorn DU, Human Physiology, an
Integrated approach, 6th edition, Pearson
education, 2013.
• Sherwood L, Fundamentals of Physiology, a
Human Perspective, 3rd edition, Thomson
Brooks/Cole, 2006
Let it
beat!