Download Cardiac Cycle

Cardiac Output
May 2, 2017
Cardiac Output
1
Cardiac output

volume of blood pumped



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


by each ventricle per minute
under resting conditions
BUT maximum may be as high as 25 35 liters per minute
May 2, 2017
Cardiac Output
2
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

May 2, 2017
dramatically during periods of
physical activity
Cardiac Output
3
Cardiac Index


Cardiac output in liters/min per square
meter of body surface area
CO varies widely

with level of body activity





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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
May 2, 2017
Cardiac Output
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Cardiac index L/min/M2
Cardiac Index Vs age
4 -
3-
2-
110
May 2, 2017
Age (years)
Cardiac Output
80
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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
May 2, 2017
Cardiac Output
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Regulation of Stroke volume

If the HR remain constant


Stroke volume is the result of the
balance

1.
between force of contraction and
afterload.
intrinsic control

2.
CO increases in proportion to SV
related to amount of venous return
extrinsic control

May 2, 2017
related to amount of ANS activity
Cardiac Output
7
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

May 2, 2017
is called the Frank-Starling law of
the heart:
Cardiac Output
8
Frank-Starling law of the
heart

Increased end-diastolic volume
 increases stretching of of
cardiac muscle
 increases strength of
contraction
 increases stroke volume
May 2, 2017
Cardiac Output
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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

May 2, 2017
the tension developed is maximal.
Cardiac Output
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Starling Law of the Heart
End diastolic fiber length
May 2, 2017
Cardiac Output
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Effects of Hypertrophy on SV

Myocardial hypertrophy

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Physical exercise & sustained elevation
of arterial pressure leads to repeated
bouts of increased CO


Increases the force of contraction
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.
May 2, 2017
Cardiac Output
12
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.
May 2, 2017
Cardiac Output
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Intrinsic control of stroke
volume

End diastolic volume


Depends on venous return
Venous return

May 2, 2017
is the amount of blood returning to
the heart through the veins
Cardiac Output
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Extrinsic control of stroke
volume

Increased sympathetic
stimulation


> increased strength of contraction
of cardiac muscle
Parasympathetic stimulation

May 2, 2017
has little effect in reducing the
strength of ventricular contraction
Cardiac Output
15
Increased sympathetic
stimulation
 release of norepinephrine

increased permeability of muscle
cell membranes to calcium

Activation of more cross-bridges

May 2, 2017
Giving stronger contraction
Cardiac Output
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Regulation of heart rate

Role of ANS

Changes in heart rate:

Parasympathetic stimulation
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Sympathetic stimulation
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May 2, 2017
reduces heart rate
increases heart rate
Cardiac Output
17
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
May 2, 2017
Cardiac Output
18
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
May 2, 2017
Cardiac Output
19
Sympathetic stimulation

Strong sympathetic stimulation


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increases HR up to 180 – 200 in
adult
and even 250 in young people
Sympathetic nerve fibers to the
heart


May 2, 2017
discharge continuously at slow rate
that maintains pumping at about
30% above that with no sympathetic
stimulation
Cardiac Output
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Effect of nervous stimulation to CO
Max. sympathetic stimulation
Normal sympathetic stimulation
Zero sympathetic stimulation
Parasympathetic stimulation
Rt atrial pressure (mmHg)
May 2, 2017
Cardiac Output
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Regulation of CO
May 2, 2017
Cardiac Output
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