Cardiac output refers to the volume of blood pumped by each ventricle per minute. It is calculated as stroke volume multiplied by heart rate. The average cardiac output is 5000 ml/minute. Cardiac output can vary based on activity level and is regulated by factors like heart rate, contractility, blood volume, and venous return. An increase in any of these factors can increase cardiac output, while a decrease can lower cardiac output. Pathologically, cardiac output can be too high due to conditions like beriberi that reduce peripheral resistance, or too low due to issues that decrease venous return or heart pumping effectiveness.

1. DR. ATHULYA
CARDIAC OUTPUT

2. CARDIAC OUTPUT
Cardiac output is defined as amount of
blood pumped out of each ventricle per
minute.
Cardiac output is expressed in two forms,
1)stroke volume
2) minute volume
Unit – liter (ml) / min

3. CO = SV x HR
cardiac output = stroke volume X heart rate
(ml/minute) (ml/beat) (beats/min)
a.Average heart rate = 70 bpm
b.Average stroke volume = 70−80 ml/beat
c.Average cardiac output = 5000 ml/minute
Cardiac output varies widely with the level
of activity of the body.
CO = SV x HR
cardiac output = stroke volume X heart
rate
(ml/minute) (ml/beat) (beats/min)

4. FACTORS EFFECTING CARDIAC
OUTPUT
 Heart rate
 When heart rate increases ,cardiac output also
increases. Any factor which changes heart rate
will also changes cardiac output.
 Force of contraction of heart
 When the force of contraction of the heart
increases, stroke volume will increase. Therefore
cardiac output will increase.
 Blood volume
 When blood volume increases cardiac output
increases.
 Venous return

6. STROKE VOLUME
Stroke volume ( SV ) is the volume
of blood pumped out of each ventricle per
beat or contraction .
 As the stroke volume increases the
cardiac output also increases.
 Stroke Volume depends upon
1. End diastolic Volume
2. Contractility
SV = EDV – ESV

7. The stroke volumes for each ventricle are
generally equal, both being approximately 70 ml
in a healthy 70 kg man.
Men, on average, have higher stroke volumes than
women due to the larger size of their hearts.

8. REGULATION OF STROKE VOLUME
 Regulated by three variables:
a.End diastolic volume (EDV): volume of
blood in the ventricles at the end of diastole.
1)Sometimes called preload
2)Stroke volume increases with
increased EDV.
b.Total peripheral resistance: Frictional
resistance in the arteries.
1)Inversely related to stroke volume
2)Called after load

9. c.Contractility: strength of ventricular
contraction
1)Stroke volume increases with contractility.
 Ejection fraction (EF) – percentage of the EDV
that is ejected per cardiac cycle.
Stroke volume = EDV – ESV
EF% = (SV / EDV) x 100
 Normal ejection fraction is about 50-65%.

10. VENOUS RETURN
 End diastolic volume is controlled by factors
that affect venous return:
a.Total blood volume
b.Venous pressure (driving force for blood
return)
 Veins have high compliance – stretch more at
a given pressure than arteries (veins have
thinner walls).
 Veins are capacitance vessels – 2/3 of the
total blood volume is in veins.
 They hold more blood than arteries but
maintain lower pressure.

11. FACTORS IN VENOUS RETURN
a.Pressure difference between arteries and
veins (about 10mm Hg)
b.Pressure difference in venous system -
highest pressure in venules vs. lowest
pressure in vena cava into the right atrium .
c.Sympathetic nerve activity to stimulate
smooth muscle contraction and lower
compliance
d. Pressure difference between abdominal and
thoracic cavities (respiration)
e. Blood volume

12. Physiological variations of cardiac
output
 Age:Cardiac output is more in adults than in
children because blood volume is more.
 Gender: cardiac output is more in male than
females.
 Altitude:cardiac output increases at high altitude
places.
 Pregnancy:cardiac output increases during
pregnancy
 Exercise:cardiac output increases during
exercise
 Emotion:cardiac output increases during
emotional expressions.

13. PATHOLOGICAL VARIATION OF
CARDIAC OUTPUT
Pathological increase:
 Hyperthyroidism
 Fever
Pathological decrease:
 Hypothyroidism
 Hypovolumia
 Haemorrhage
 Myocardial infarction

14. MEASURING CARDIAC OUTPUT
 1. The Fick principle
 2. Dilution methods
 3. Pulmonary artery thermo dilution (trans-
right-heart Thermo dilution)
 4. Doppler ultrasound method
 5. Impedance cardiography

15. RELATIONSHIP WITH BP
 As Cardiac output is made up of heart rate
and stroke volume - at rest these are relatively
constant.
 With exercise the heart beats faster - more
blood is pumped out with each beat
contributing to a rise in BP.
 Changes in the volume of blood within the
cardiovascular system will also affect Bp.

16.  A person was severely dehydrated or lost
a large quantity of blood through a wound,
there would be less blood for the heart to
pump, thereby reducing cardiac output
and BP.
 For a typical, fit young person, the cardiac
output might go up to about 20 litres/min at
the peak of exercise.
 For a world-class athlete in an endurance
sport, the maximum cardiac output might
be around 35 litres/min.

17. REGULATION OF CARDIAC OUTPUT
 It means maintaining a constant cardiac
output around 5 litres/min under normal
conditions and adjusting the cardiac output as
per the physiological demands.
 It has to be regulated to have an optimum
cardiovascular efficiency.

18. MECHANISM OF REGULATION
1)By venous return:
Force of contraction of a muscle fibre is
proportional to its initial length .It is known as
Starling’s law of muscle contraction.

19. Role Of Frank-Starling Mechanism
 Frank-Starling Law:
It states that “ Within
physiologic limits, the
heart pumps all the
blood that returns to it
by the way of veins.”
 Increased Venous Return
 Cardiac muscles stretches
to greater length
 Ventricular muscle
contracts with greater force
 Increased Cardiac Output

20. 2)By nervous system:
 Autonomic nervous system takes a major
role in the regulation of cardiac output.
 Whenever sympathetic nervous activity
increases e.g. ; during emotions, exercise
etc,it will stimulate both SA node as well as
ventricular myocardium.
 This will increase both heart rate as well as
force of contraction of muscles or stroke
volume .This will inturn increase cardiac
output.
 If parasympathetic activity increases as during
sleep, it will inhibit SA node, it will decrease
heart rate, this will inturn decrease cardiac
output.

21. 3)Hormonal regulation of cardiac output:
 Whenever adrenaline level in the
blood increases it will stimulate SA node and
ventricular myocardium. This will increase
both heart rate and stroke volume.
 This will inturn increase cardiac output.

22. LIMITATIONS FOR THE CARDIAC
OUTPUT
 There are definite limits to the amount
of blood that the heart can pump,
which is expressed quantitatively in the
form of cardiac output curves.
Normal:
The plateau level of this normal cardiac
output curve is about 13 L/min.
Hypo effective:
The lowermost curves are for hypo
effective
hearts that are pumping at levels below
normal.Hypoeffective heart plateau – 5
L/min
Hyper effective:
 The uppermost curves are for Hyper
effective hearts that are pumping better
than normal. Hyper effective heart plateau
– 20 L/min

23. HYPO EFFECTIVE HEART
 In this the heart is pumping at a
very slow rate and the cardiac
output decreases.
Factors that can cause hypo -
effectivity are following:
 1. Increased Arterial Pressure
 2. Inhibition of Nervous excitation
 3. Abnormal Heart Rhythm
 4. Coronary Artery Blockage
 5. Valvular Heart Disease
 6. Congenital Heart Disease
 7. Myocarditis
 8. Cardiac Hypoxia

24. HYPEREFFECTIVE HEART
 In this the heart is pumping at a
high rate and the cardiac output
increases.
Two type of factors can
make the heart a better pump than
normal:
1. Nervous Stimulation:
 It involves Sympathetic stimulation
and Parasympathetic Inhibition.
2. Hypertrophy of The Heart
Muscles:
 It involves the increased mass and
contractile strength due to
exercise and causing hypertrophy
which allows increased cardiac

25. PATHOLOGICALLY HIGH OR LOW
CADIAC OUTPUT
In healthy humans, the average
Cardiac Outputs are surprisingly constant
from one person to another. However multiple
clinical abnormalities can cause either high or
low cardiac outputs.

26. HIGH CARDIAC OUTPUT
 High cardiac output is
mostly caused by reduced
total peripheral Resistance.
Following are some of
the conditions that can
decrease the Peripheral
Resistance and at the same
time increase the Cardiac
Output to above the normal.
 1. Beriberi
 2. Arteriovenous Fistula
 3.Hyperthyroidism
 4. Anaemia

27. LOW CARDIAC OUTPUT
 There are two
factors that cause
Low Cardiac
Output:
 A. Abnormalities
that cause the
Venous Return to
fall too low
 B. Abnormalities
that cause pumping
effectiveness of
the Heart to fall too

28. Reference
 Text book of physiology-Dr AP Krishna
 Essentials of medical physiology,2nd edition
by K. Sembulingam and Prema Sembulingam

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