AL-Iraqia university/ College of Medicine Lect.

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Dr.Mahasen Mohammed CVS Physiology

Cardiac output
Objectives:
1. Define cardiac output and Ejection Fraction.
2. Describe how heart rate and stroke volume interact to control cardiac output.
3. State the influence of venous return on cardiac output.
4. Define the terms preload, and afterload then explain their effect on cardiac
output .

Ejection Fraction (EF%):

The proportion of the end-diastolic volume that is ejected against a given afterload
depends on the strength of ventricular contraction. Normally, contraction strength
is sufficient to eject 70 to 80 ml of blood out of a total end-diastolic volume of 110
to 120 ml (2/3 of blood is ejected). The ejection fraction is thus about 65%.
In other words, the ejection fraction is the ratio of stroke volume to end-diastolic
volume (EDV) and it reflects the ventricular contractility, expressed as percentage,
normally it averages at rest 65% (again, about 2/3 of the EDV is ejected).
Increased ventricular contractility causes an increase in ejection fraction.
In heart failure, the EF is reduced; < 50%.
EF can be measured by Echocardiogram (Echo) that can measure the EDV, ESV
and so the SV.
EF= ×100% = ×100%

Cardiac output is the amount of blood pumped by each ventricle per minute,
expressed in liters/minute. Normally, it is about 5 liters per minute.
The cardiac output (CO) is determined through multiplying the heart rate (HR) by
the stroke volume (SV).
CO = HR X SV
Heart rate = the number of heart beats/minute (average; 72 beat/minute).
Stroke volume = the volume of blood ejected by each ventricle with each beat.( 70
ml/beat)
If the HR = 72 beats/min., and the SV is of 70 ml;
Cardiac output = 72 X 70 = 5.04 L/min.
As the cardiovascular system is a closed system, cardiac output of the left ventricle
equals to the cardiac output of the right ventricle i.e., the two sides of the heart
have the same output per minute. It is also the volume of blood flowing through

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either the systemic or pulmonary circulation per minute. In other words, cardiac
output is the quantity of blood pumped into the aorta each minute by the heart.
This is also the quantity of blood that flows through the circulation.
Cardiac output= arterial blood flow = pulmonary blood flow.
Cardiac output varies widely with the level of activity of the body. Therefore, the
level of body metabolism, exercise, age and size of the body influence the cardiac
output. For young, healthy men, the resting cardiac output averages about 5.6
liter/min., for young women, this value is 10-20% less, but it is not constant. It
might be increased even up to 30 liters/min., depending on the activity of the body.
Therefore, cardiac output is a variable parameter usually it is not less than 5 liter /
min. at rest to supply the body with oxygen and to maintain normal BMR (basal
metabolic rate). The highest cardiac output recorded is 48 liters/min., in the
Roadrunners (Hyperdynamic circulation which mean the same blood volume; 5
liters circulating at a higher speed). Blood volume is about 5 - 6 liters. So the heart
pumps the whole blood in one minute.

Control of cardiac output:

The cardiac output is controlled (either increased or decreased or maintained) by
the following factors.
I. Venous return (preload).
II. Heart rate (HR)
III. Myocardial contractility.
IV. Cardiac compliance.
V. Afterload.
I- Venous return:
The venous return (VR) is the amount of the blood flowing from the tissues into
the veins and then into the right or left atrium each minute. So in steady state, they
are equal (CO = VR) because what is pumped out from the left ventricle equals to
what returned to the right side of the heart. In other words, It is the quantity of
blood flowing from the veins into the right atrium each minute. It represents the
preload. The venous return and CO must be equal to each other.

The CO is controlled by venous return through the following mechanisms:

 Frank-Starling law; the heart pumps automatically whatever amount of

blood flows into the right atrium from the veins. This law states that when
increased quantities of blood flow into the heart, this stretches the walls of
the heart chambers. As a result of the stretch, the cardiac muscle contracts
with increased force to empty the expanded chambers i.e. the extra blood

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 that flows into the heart (VR) is automatically pumped without delay into
the aorta and flows again through the circulation.

 The effect of the venous return on the heart rate by mean of stretching the
heart. Stretch of the SA node in the wall of the right atrium has a direct
effect on the rhythmicity of the SA node itself to increase heart rate 10 –
15% .

 Another factor, the stretched right atrim initiates a nervous reflex called the
Bainbridge reflex, passing first to the medullary vasomotor center and then
back to the heart by sympathetic nerves, to increase the heart rate. The
increase in the heart rate then helps to pump the extra blood.

Decrease in Cardiac Output Caused by Decreased Venous Return.

Anything that interferes with venous return also can lead to decreased cardiac
output. Some of these factors are the following:
1. Decreased blood volume. Ex, hemorrhage, Loss of blood decreases the filling
of the vascular system to such a low level that there is not enough blood in the
peripheral vessels to create peripheral vascular pressures high enough to push
the blood back to the heart.

2. Acute venous dilation.

In case of sudden and acute vasodilatation especially the peripheral veins
involved. This results most often when the sympathetic nervous system suddenly
becomes inactive. For instance, fainting often results from sudden loss of
sympathetic nervous system activity, which causes the peripheral vessels,
(veins), to dilate markedly. This decreases the filling pressure of the vascular
system because the blood volume can no longer create adequate pressure in the
flaccid peripheral blood vessels. As a result, the blood “pools” in the vessels and
does not return to the heart.
3. Obstruction of the large veins so that the blood in the peripheral vessels cannot
flow back into the heart.
4. Decreased tissue mass, especially decreased skeletal muscle mass.
With normal aging or with prolonged periods of physical inactivity, there is
usually a reduction in the size of the skeletal muscles. This, in turn, decreases
the total oxygen consumption and blood flow needs of the muscles, resulting in
decreases in skeletal muscle blood flow and cardiac output.

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* Regardless of the cause of low cardiac output, if the cardiac output falls below
that level required for adequate nutrition of the tissues, the person is said to suffer
circulatory shock. This condition can be lethal within a few minutes to a few
hours.

II- Heart rate and cardiac output:

In resting state, (the venous return is constant), changes in heart rate between 100-
200 beats/min., not affect CO markedly. However, high heart rate (more than 200
beats/minute) in patient with ventricular tachycardia (VT) or supraventricular
tachycardia (SVT) may affect CO to be insufficient to maintain the nutritional
needs of the body because such increase in heart rate will reduces the duration of
ventricular diastole and so reduce the time available for ventricular filling that will
reduce the stroke volume. On the other hand, slow heart rate may also reduce CO,
as in complete heart block disease (HR < 40 beats/minute).

Exercise & CO
In exercise, cardiac output is increased to meet the body need by increasing in both
heart rate and stroke volume, the increase in heart rate is through sympathetic
stimulation as the exercise is a stressful situation, while the increase in stroke
volume is through the increase in venous return by the action of skeletal
muscles that squeezed and pumped the blood toward the heart, and through the
increased myocardial contractility.

III-Myocardial contractility:
Myocardial contractility exerts a major influence on stroke volume and in turn on
the cardiac output. It is reduced in heart failure.
It is measured by Ejection Fraction.
Myocardial contractility is affected by the following factors :
i. .Mechanical
 The preload (i.e., EDV): controls the power of cardiac contractility by
Frank-Starling's law.
 The afterload (i.e., aortic impedance)as in rise of the arterial blood
pressure, aortic stenosis or polycythaemia).
ii. .Cardiac :Ventricular hypertrophy; as in athletes 35 litres minute.
iii. . Extra cardiac :Sympathetic nerve supply.

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VI-Cardiac compliance:
It is the change in volume per unit change in pressure = ∆V/∆P, It is the
stretchability, elasticity, as decreased compliance in which there is a myocardial
stiffness, this is in disease condition which will affect cardiac output as in cases of
cadiomyopathies, and pericardial effusion.

V- Afterload:
It is the resistance that oppose cardiac output, e.g., increased arterial systolic
pressure (systolic hypertension), valve disease that obstruct the outflow of blood as
in case of aortic stenosis disease. So increased afterload will reduce cardiac output.
On the other hand, reduced total peripheral resistance (reduced afterload) causes
high cardiac output. Conditions that can decrease the total peripheral resistance and
at the same time increase the cardiac output to above normal include:

1. Beriberi. This disease is caused by insufficient quantity of the vitamin thiamine

(vitamin B1) in the diet cause marked compensatory peripheral vasodilation.
This greatly decreases the total peripheral resistance and, likewise, increases the
venous return and cardiac output.
2. Arteriovenous fistula (shunt, also called an AV shunt): occurs between a major
artery and a major vein, in which blood flow directly from the artery into the
vein. This greatly decreases the total peripheral resistance and, likewise,
increases the venous return and cardiac output.
3. Hyperthyroidism. In hyperthyroidism, the metabolism of most tissues of the
body becomes greatly increased. Oxygen usage increases, and vasodilator
products are released from the tissues. Therefore, the total peripheral resistance
decreases markedly because of the local tissue blood flow control reactions
throughout the body; consequently, the venous return and cardiac output often
increase to 40 to 80 percent above normal.
4. Anemia. In anemia, two peripheral effects greatly decrease the total peripheral
resistance, as a consequence, the cardiac output increases greatly. One of these is
reduced viscosity of the blood, resulting from the decreased concentration of red
blood cells. The other is diminished delivery of oxygen to the tissues, which
causes local vasodilation.
Low cardiac output: (Abnormalities)
 Fainting: low cardiac output leads to ischemia of the brain; causing fall
down (fainting). It is a protective mechanism to correct the brain ischemia
through increasing blood supply to the brain.
 Shock: also low cardiac output that may cause hypotension, again leading to
ischaemia to the brain.