1. Cardiac Output
April 28, 2017
Cardiac Output

2. Cardiac output volume of blood pumped
by each ventricle per minute
C.O = HEART RATE x SROKE VOLUME (H.R X S.V)
typically about 5,500 ml (or 5.5 liters) per minute
which is about equal to total blood volume;
so, each ventricle pumps the equivalent of total blood volume each minute
under resting conditions
BUT maximum may be as high as liters per minute
April 28, 2017
Cardiac Output

3. Cardiac reserve the difference between
cardiac output at rest &
the maximum volume of blood
the heart is capable of pumping per minute
permits cardiac output to increase
dramatically during periods of physical activity
April 28, 2017
Cardiac Output

4. Cardiac Index
Cardiac output in liters/min per square meter of body surface area
CO varies widely
with level of body activity
level of body metabolism,
whether a person is exercising
age,
size of the body
Increases approximately in proportional to the surface area of the body
CO is 20 – 30% less in female
April 28, 2017
Cardiac Output

5. Cardiac Index Vs age 4 - 3 - Cardiac index L/min/M2 2 - 1- 80 10
4 -
3 -
2 - 1-
Cardiac index L/min/M2 80 10
April 28, 2017
Cardiac Output
Age (years)

6. Regulation of cardiac output
At rest heart pumps 4 – 6 liters per minute.
Volume pumped by the heart is regulated by:
Intrinsic cardiac regulation
in response to change in volume of blood flowing into the heart.
Autonomic nervous system
Frank – Starling law of the heart
Explains the intrinsic ability of the heart to adapt to changing volume of inflowing blood
CO = stroke vol. X HR
April 28, 2017
Cardiac Output

7. Regulation of Stroke volume
If the HR remain constant
CO increases in proportion to SV
Stroke volume is the result of the balance
between force of contraction and afterload.
intrinsic control
related to amount of venous return
extrinsic control
related to amount of ANS activity
April 28, 2017
Cardiac Output

8. Intrinsic control of stroke volume
Increased end-diastolic volume
increased strength of cardiac contraction
increased stroke volume
The increase in strength of contraction due to an increase in end-diastolic volume
is called the Frank-Starling law of the heart:
April 28, 2017
Cardiac Output

9. Frank-Starling law of the heart
Increased end-diastolic volume
increases stretching of of cardiac muscle
increases strength of contraction
increases stroke volume
April 28, 2017
Cardiac Output

10. Frank-Starling law of the heart
There is a relation between initial length and total tension in cardiac muscle
similar to that in skeletal muscles.
There is optimal length at which
the tension developed is maximal.
April 28, 2017
Cardiac Output

11. Starling Law of the Heart
Stroke Volume
End diastolic fiber length
April 28, 2017
Cardiac Output

12. Effects of Hypertrophy on SV
Myocardial hypertrophy
Increases the force of contraction
Physical exercise & sustained elevation of arterial pressure leads to repeated bouts of increased CO
As a result in increased synthesis of contractile proteins and enlargement of cardiac myocytes
As each cell enlarges the ventricular wall thickens and is capable of greater force development.
April 28, 2017
Cardiac Output

13. Effects of Afterload on SV
The force against which the ventricular muscle fibers must shorten.
In normal circumstances, after load can be equated to the aortic pressure during systole.
If the arterial pressure is suddenly increased
a ventricular contraction.(at a given level of contractility and EDFL)
Produce a lower stroke volume.
April 28, 2017
Cardiac Output

14. Intrinsic control of stroke volume
End diastolic volume
Depends on venous return
Venous return
is the amount of blood returning to the heart through the veins
April 28, 2017
Cardiac Output

15. Extrinsic control of stroke volume
Increased sympathetic stimulation
> increased strength of contraction of cardiac muscle
Parasympathetic stimulation
has little effect in reducing the strength of ventricular contraction
April 28, 2017
Cardiac Output

16. Increased sympathetic stimulation
release of norepinephrine
increased permeability of muscle cell membranes to calcium
Activation of more cross-bridges
Giving stronger contraction
April 28, 2017
Cardiac Output

17. Regulation of heart rate
Role of ANS
Changes in heart rate:
Parasympathetic stimulation
reduces heart rate
Sympathetic stimulation
increases heart rate
April 28, 2017
Cardiac Output

18. Parasympathetic stimulation
Increased parasympathetic stimulation
release of acetylcholine at the SA node
increased permeability of SA node cell membranes to potassium
'hyperpolarized' membrane
fewer action potentials
and, therefore, fewer contractions) per minute
April 28, 2017
Cardiac Output

19. Sympathetic stimulation
Increased sympathetic stimulation
release of norepinephrine at SA node
decreased permeability of SA node cell membranes to potassium
membrane potential becomes less negative (closer to threshold)
more action potentials (and more contractions) per minute
April 28, 2017
Cardiac Output

20. Sympathetic stimulation
Strong sympathetic stimulation
increases HR up to 180 – 200 in adult
and even 250 in young people
Sympathetic nerve fibers to the heart
discharge continuously at slow rate
that maintains pumping at about 30% above that with no sympathetic stimulation
April 28, 2017
Cardiac Output

21. Effect of nervous stimulation to CO
Max. sympathetic stimulation
Normal sympathetic stimulation
CO L/min
Zero sympathetic stimulation
Parasympathetic stimulation
Rt atrial pressure (mmHg)
April 28, 2017
Cardiac Output

22. Regulation of CO
April 28, 2017
Cardiac Output