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The Pressures of the Cardiac Cycle
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Frank Starling’s Law of the Heart
‘stroke volume will increase in response to an increase in the volume of
blood filling the heart when all other factors remain constant.’
Explanation: cardiac muscle not at
optimal stretch for force generation at
rest therefore increased filling
increases stretch and so increases
the force of contraction.
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The Length-Tension Relationship
• As preload increases there
is an increase in the active
tension that develops.
• This means there is a
greater velocity of
shortening
• So increasing preload
allows the muscle to
contract harder against a
given afterload.
• To increase Vmax you need
to increase the inotropy (the
force of the muscular
contractions)
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Preload
“The amount of filling of the ventricles before contraction, aka the end-diastolic
volume. Relates to the amount of stretch on the sarcomeres of the heart muscle
before contraction”
As a rule preload will be increased by anything
that increases the stretch of the cardiac muscle
and increases ventricular filling/venous return.
e.g. aortic stenosis, ventricular systolic failure
It will be decreased by anything that reduces
cardiac muscle stretch and reduces venous
return/ventricular filling.
e.g. mitral or tricuspid valve stenosis, atrial
fibrillation
The Peer Teaching Society is not liable for false or misleading information…
Afterload
“the work of the heart while ejecting the blood, depends on the ABP and
the thickness of the ventricles”
Increase in Afterload
DECREASES stroke volume, INCREASES
LVEDP
Reduces the fibre shortening velocity within the
finite time available, thus the contraction is not
as strong and more blood remains in the left
ventricle.
Decrease in Afterload
INCREASES stroke volume, DECREASES
LVEDP
Reduction in ABP leads to a reduction in
afterload so ventricles can eject more blood
and less remains.
The Peer Teaching Society is not liable for false or misleading information…
Afterload vs. Preload vs. Frank-Starling Law
• As afterload increases it causes an increase in left ventricular end-diastolic
pressure (LVEDP) (i.e., increases preload).
• This occurs because the increased end-systolic volume combines with the
venous return into the ventricle and this increases end-diastolic volume.
• This increase in preload activates the Frank-Starling mechanism to
partially compensate for the reduction in stroke volume caused by the
increase in afterload
• Consequently the heart muscle contracts more forcefully, therefore
increasing stroke volume again.
The Peer Teaching Society is not liable for false or misleading information…
Afterload vs. Preload vs. Frank-Starling Law
This principle is used in the treatment of heart failure…vasodilators reduce the ABP
therefore increases SV as ESV is reduced. EDV is subsequently reduced however SV
increases overall as the reduction in EDV is not as great as the reduction in ESV.
The Peer Teaching Society is not liable for false or misleading information…
Cardiac and Vascular Changes
Accompanying Heart Failure
Compensatory Mechanisms During
Heart Failure
Cardiac
Decreased stroke volume & cardiac
output
Increased end-diastolic pressure
Ventricular dilation or hypertrophy
Impaired filling (diastolic dysfunction)
Reduced ejection fraction (systolic
dysfunction)
Cardiac
Frank-Starling mechanism
Chronic ventricular dilation or hypertrophy
Tachycardia
Vascular
Increased systemic vascular resistance
Decreased arterial pressure
Impaired arterial pressure
Impaired organ perfusion
Decreased venous compliance
Increased venous pressure
Increased blood volume
Hormones
Renin-angiotensin-aldosterone system
Vasopressin (antidiuretic hormone)
Circulating catecholamines
Natriuretic peptides
Autonomic Nerves
Increased sympathetic adrenergic activity
Reduced vagal activity to heart
The Peer Teaching Society is not liable for false or misleading information…
Pressure-Volume Loops
Pressure and Volume Changes
During Two Cardiac Cycles
Image from https://www.emaze.com/@AOLIFFOZ/cvs.pptx
1. As mitral valve closes pressure in LV increases
2. Aortic valve opens and blood moves into the aorta
3. Ventricles ‘wring out’ all the blood into the aorta so pressure increases in both aorta and
ventricle
4. Pressure falls and the aortic valve closes. Here you see the ‘dicrotic notch’, a brief increase in
pressure as blood flows back towards heart but is blocked by the closed valves causing a
transient rise in aortic pressure.
5. Pressure falls until mitral valve opens and ventricles begin to fill again.
The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
The Normal ECG
Image from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ecg.html
The Normal ECG
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The Heart Sounds
Lub= S1, closing of
mitral and Tricuspid
valves
Dub= S2, closing of
aortic and pulmonary
valves
Summary
• Be able to define Frank-Starling, Preload, Afterload, SV,
CO, EDV and ESV
• Integrate them together and understand how changing
one affects others (as in heart failure)
• Learn the events of the cycle and how the pressure in the
heart and arteries changes throughout
• Be able to recognise the stages on the pressure volume
loops, cardiac cycle graphs and a normal ECG
The Peer Teaching Society is not liable for false or misleading information…
References
CV Physiology Concepts
http://www.cvphysiology.com/index.html
Vanders Human Physiology, 11th Ed.
http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ecg.html
The Peer Teaching Society is not liable for false or misleading information…