1. The Pressures of the Cardiac Cycle
Phase 1 CVR wrap up
The Pressures of the Cardiac Cycle
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2. 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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3. 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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4. 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
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5. 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.
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6. 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.
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7. 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.
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8. Cardiac and Vascular Changes Accompanying Heart Failure
Decreased stroke volume & cardiac output
Increased end-diastolic pressure
Ventricular dilation or hypertrophy
Impaired filling (diastolic dysfunction)
Reduced ejection fraction (systolic dysfunction)
Vascular
Increased systemic vascular resistance
Decreased arterial pressure
Impaired arterial pressure
Impaired organ perfusion
Decreased venous compliance
Increased venous pressure
Increased blood volume
Compensatory Mechanisms During
Heart Failure
Cardiac
Frank-Starling mechanism
Chronic ventricular dilation or hypertrophy
Tachycardia
Autonomic Nerves
Increased sympathetic adrenergic activity
Reduced vagal activity to heart
Hormones
Renin-angiotensin-aldosterone system
Vasopressin (antidiuretic hormone)
Circulating catecholamines
Natriuretic peptides
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9. Pressure-Volume Loops

10. Pressure and Volume Changes During Two Cardiac Cycles
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11. As mitral valve closes pressure in LV increases
Aortic valve opens and blood moves into the aorta
Ventricles ‘wring out’ all the blood into the aorta so pressure increases in both aorta and ventricle
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.
Pressure falls until mitral valve opens and ventricles begin to fill again.
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13. The Normal ECG
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14. The Normal ECG
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15. The Heart Sounds Lub= S1, closing of mitral and Tricuspid valves
Dub= S2, closing of aortic and pulmonary valves
S3 is usually a result of a pathological change in the over 40s although may be normal in the young or the very athletic. Most common cause is congestive heart failure. Gives a 'galloping rhythm' and is a result of the blood sloshing around the ventricles as it rushes in from the atria. Not heard immediately as not enough tension in the walls of the ventricles.

16. 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
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17. References CV Physiology Concepts
Vanders Human Physiology, 11th Ed.
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