Control of Cardiac Output Flashcards

1
Q

Define preload, afterload and contracility, including the laws governing them.

A
  • PRELOAD:
    • The end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand.
    • It is governed by Starling’s Law.
  • AFTERLOAD:
    • The pressure against the walls of the ventricles during contraction / systole which the heart must work against to eject blood during systole.
    • It is governed by Laplace’s Law.
  • Contractility
    • Can be affected by neurotransmitters and sympathetic nervous innovation.
    • The heart contracts longer as it takes more calcium.
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2
Q

What does Starling’s Law state?

A
  • It states that the “energy of contraction of cardiac muscle is relative to the muscle fibre length at rest”.
  • This means that the greater the stretch of the ventricles in diastole (blood entering), the greater the energy of contraction and the greater the stroke volume achieved in systole.
  • So more blood in = more blood out.
  • This is not a control system, it is just an intrinsic property of the cardiac muscles.
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3
Q

Starling’s Law can be represented by a graph showing SV against CVP (central venous pressure). Describe what the graph presents, and what the last part of the graph means.

A
  • Throughout the graph, as the CVP increases, the SV increases.
  • However, at the end of the graph, with an increasing CVP, the SV starts falling.
  • This indicates the point at which the Laplace’s Law takes over, so the heart pumps less blood out.
  • This emphasises the importance of care with fluid replacement, as giving too much may have an opposing effect.
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4
Q

How did starling prove the law?

A
  • Starling gave a bolus of fluid into the vein (vena cava) that increaesd the end diastolic volume (causing the ventricles to fill up more) and this increase the strength of contraction. So more fluid is edjected from the heart (stroke volume).
  • If you remove some fluid (which will happen if you have a sudden haemorrage or an aneurysm) there is less blood filling the heart.
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5
Q

Why does Starling’s Law work (in the sense of contractile fibres)?

A
  • With an unstretched fibre, there is overlapping actin and myosin.
  • This means that there is mechanical interference, so there is less cross-bridge formation available for contraction.
  • With a stretched fibre, there is less overlapping actin and myosin.
  • This means that there is less mechanical interference, so there is potential for more cross-bridge formation.
  • There is also an increased sensitivity to Ca2+ ions.
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6
Q

List some roles of Starling’s Law in cardiac physiology.

A
  • It balances outputs of the right and left ventricle (which is important = isovolumetric).
  • It restores CO (cardiac output) in response to intravenous fluid transfusions.
  • It is responsible for the fall in CO during a drop in blood volume or vasodilation (eg. haemorrhage, sepsis).
  • It is also responsible for the fall in CO during orthostasis (standing for a long time), leading to postural hypotension and dizziness as blood pools in legs.
  • It contributes to increased SV (stroke volume) and CO during upright exercise.

Postural hypotension meaning - It occurs when a person’s blood pressure falls when suddenly standing up from a lying or sitting position.

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7
Q

What does Laplace’s law state?

A
  • Afterload opposes ejection from the blood from the heart and is determined by wall stress directed through the heart wall.
  • Stress through the wall of the heart prevents muscle contraction.
  • More energy of contraction is needed to overcome this wall stress to produce cell shortening and ejection.
  • Laplace’s law describes the parameters that determine afterload:
    • Wall tenstion (T), pressure (P), and radius (r) in a chamber (ventricle)
    • T = (P x r) / 2
    • Divided by 2 because a chamber has 2 directions of curvature.
  • Wall tension (T) is made up of wall stress (S) times wall thickness (w).
    • T = S x w
    • So..
    • S x w = (P x r) / 2
    • Or..
    • S = (P x r) / 2 x w
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8
Q

Why does the radius determine wall stress/afterload?

A
  • With a SMALLER ventricle RADIUS, there is greater wall curvature. This means that more wall stress is directed to the centre of the chamber. This, in turn, means that there is less afterload, so there is BETTER EJECTION.
  • With a LARGER ventricular RADIUS, there is less wall curvature. This means that more wall stress is directed to the heart wall. This, in turn, means that there is more afterload, so there is LESS EJECTION.
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9
Q

What is the importance of laplace’s law?

A
  • It opposes the starling’s law at rest
    • Increased preload gives increased stretch of chamber (starling’s law).
    • This increases chamber radius (decreases curvature) - increase afterload in a healthy heart.
    • Starlings law overcomes laplace’s law - so there is good ejection.
  • Facilitates ejection during contraction
    • Contraction reduces chamber radius so less afterload in ‘emptying’ chamber.
    • This aids expulsion and increases stroke volume.
  • Contributes to a failing heart at rest and during contraction.
    • In a failing heart the chambers are oftern dilated - so increased afterload opposing ejection.

Laplaces law is good ejection with a small radius, but bad with large radius.

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10
Q

How does afterload affect arterial blood pressure and stroke volume?

A

Laplace’s law states that increased blood pressure (P) will increase wall stress. This will increase afterload and reduce ejection.

  • Acute rise in blood pressure offset by..
    • For a short period of time the starlings law will overcome the increased BP as you are increasing the stretch on the heart muscles. This will result in increases contraction and increased SV.
    • The nervous system will increase your heart rate and contractility.
  • Chronic increase in arterial blood pressure
    • This causes a decrease in the cardiac output.
    • A lot of blood enters the heart and starlings law is not as efficient and the laplace’s law begins to dominate and the heart isn’t emptied properly.
    • There is an increased energy expenditure to maintain SV, & ultimately decrease in SV. The volume of blood left in systole is high.
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11
Q

Explain hypertrophy in heart failure.

A
  • Increased radius (r) - eg. Heart failure where heart does not contract properly (MI, cardiomyopathies, mitral valve re-gurgitation) causing blood to be left in ventricle leading to eventual volume overload. This causes the radius of the heart to increase in size.
  • Increased pressure (P) eg. Pressure-overload heart failure due to increased pressure/afterload in chamber (hypertension, aortic stenosis).
  • Increase in either radius or pressure will increase wall stress (afterload) which opposes ejection (cardiac output).
  • The heart compensates with ventricular hypertrophy (greater myocyte size and more sarcomeres), increasing wall thickness. This decreases wall stress per sarcomere and therefore afterload so maintains SV and CO.
  • But this requires more energy (more sarcomeres used) – greater oxygen requirement. The amount of energy required continues to increase so ultimately contractility will decrease and produce more heart failure…it is a vicious circle.
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12
Q

Starlings law and ventricular pressure - volume loop.

A
  • During exercise (running) the veins in the legs contract and send more blood back to the heart.
  • This causes increased preload (the left ventricular volume gets bigger).
  • This stretches the heart a bit and it begins to contract with more energy and reaches a pressure that is highter than the aorta more quickly.
  • So its used less energy in the isovolumetric contraction (isovolumetric contraction phase is also shorter) as its has had that stretch and is more eficient due to starlings law.
  • So it expels with greater force and you get a much bigger cardiac output.
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13
Q

Laplace’s law and ventricular pressure - volume loop.

A
  • For someone with chronic high blood pressure the afterload is high.
  • The aortic pressure is high and when the heart starts to squeeze it doesnt get extra stretch and the starlings law does not help.
  • When the heart starts to squeeze its less efficient and it takes longer to get to that pressure where it can release the blood.
  • So it uses soo much energy trying to overcome the pressure in the aorta that when it gets to the ejection phase there is hardly any energy left in it and it makes a very small output.
  • So there is a lot of blood left behind in the heart compared to normal.
  • The blood left behind will lead to volume overload or pressure overload.
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