How Preload and Afterload govern Cardiac Output Flashcards

1
Q

What is Cardiac Output?

A

CO = HR x SV

*Amount of blood ejected from the heart per minute

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2
Q

What controls stroke volume?

*Hint: 3 things

A

Stretching heart muscles at rest (preload).
Starlings law, the relationship between pressure, wall stress and radius.
La Place’s law and the strength of contraction at a given resting stretch (Contractility).

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3
Q

What is the equation for blood pressure?

A

BP = CO x TPO

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4
Q

Define preload.

A

Preload concerns the amount of blood in the ventricles that causes stretching of the heart muscle at rest, the more blood there is coming back to the heart, the more stretch. The EDV tells us how much stretch the cardiac myocytes are under. This is the preload and this is an important governing factor in how much we eject. This stretch is controlling the energy of contraction.

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5
Q

More preload = more or less ejection?

A

More volume so More stretch = more preload and so MORE EJECTION

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6
Q

Define afterload.

A

Afterload can be thought of as the “load” that the heart must eject blood against. In simple terms, the afterload is closely related to the aortic pressure (caused by resting blood in the arteries pushing back on the heart). To appreciate the afterload on individual muscle fibers, afterload is often expressed as ventricular wall stress.

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7
Q

What is energy of contraction?

A

The amount of work required to generate stroke volume, the amount of energy depends on Starlings law and contractility.

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8
Q

What are the 2 important actions in the cardiac cycle that stroke work is responsible for?

A

It increases the chamber pressure so it is greater than the aortic pressure i.e. isovolumetric contraction AND it causes ejection.

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9
Q

What does starlings law tell us?

A

“The energy of contraction of cardiac muscle is proportional to the muscle fibre length at rest”

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10
Q

Why does a large intravenous infusion lead to an increase in stroke volume?

A

There is more blood volume going back to the heart. The effect of this is that CVP goes up due to more blood going back to the heart. There is an increase in the EDV which makes sense because there is more solution to the blood, the ESV also goes up because there was more blood there to start with. Overall, we can see that the difference between the two has increased and this means stroke volume is larger.

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11
Q

In a starlings curve, if the CVP continues to increase then eventually the SV plateaus. Why does this happen?

A

The relationship begins to break down and it starts to plateau and if the pressure continues to go up it can actually begin to reduce stroke volume. Occurs because of overstretched muscles.

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12
Q

What is the difference between stretched and un-stretched muscle fibres?

A

In un-stretched fibres, there is limited movement. This is because of the mechanical interference between myosin and actin, leading to less cross-bridge formation available for contraction.
In stretched fibres, there is less overlapping between the actin and myosin, there is less mechanical interference.
potential for more cross-bridge formation leading to a greater contraction. This means, in a stretched fibre, there is much greater energy of contraction.
*If you stretch the fibre, there is increased sensitivity to calcium

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13
Q

What are some of the important roles of Starlings law?

A
  • Balances outputs of the RV and LV
  • Responsible for fall in CO during a drop in blood volume (e.g. haemorrhage, sepsis).
  • Restores CO in response to intravenous fluid transfusions
  • Responsible for fall in CO during orthostasis (standing) postural hypotension & dizziness - blood goes to the legs when we stand up, so less is returning to the heart, so CO is reduced.
  • Contributes to increased stroke volume during upright exercise
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14
Q

How does starlings law balance the outputs of the left and right ventricles?

A

If more blood is returning to the heart, the RV will be stretched more first, leading to greater energy of contraction so more blood volume will go to the lungs. Therefore, more blood volume will come back to the heart into the left atria which will push more blood into the ventricles which in turn will push more blood out to the systemic circulation.

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15
Q

What is the equation for La places law? Describe what it shows.

A

The law states how effectively wall tension is converted into pressure within the ventricles. We can add wall tension (which exerts a pressure) into La Place’ s law to give:
P = 2Sw/r
P = Pressure
S = Wall stress
w = Wall thickness
r = radius
*Value of 2 is because a chamber has 2 directions of curvature.

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16
Q

How is La Place’s law applied to the chambers of the heart?

A

If the chamber has a small radius and thus large curvature, then this causes more wall stress (one of the components of wall tension, as seen above in the equation) to be directed towards the centre of the chamber. Hence, there is going to be greater wall tension converted into pressure causing more ejection. Vice versa for chamber with large radius.

17
Q

In the ventricles, explain how Starlings law and La Places law oppose each other.

A

When the ventricles are full at EDV. Starlings law would mean there would be more stretch, more increased force of contraction and ejection but La Place’s law would mean there would be less pressure so decreased ejection.
*At rest these two forces are opposing and in a normal healthy heart, Starlings law “wins”.

18
Q

Write the rearranged La Places law equation for wall stress.

A

Wall Stress (S) or Afterload = P x r /2w (thickness)

19
Q

What causes an increase in afterload?

A

Pressure - Increased arterial pressure = More opposition to ejection.
Radius - Increased radius (e.g. due to illness), decreased curvature = Less stress towards chamber and more through walls opposing ejection.

20
Q

What causes wall stress to be reduced?

A

Increased wall thickness (As less wall stress is dissipated through wall).

21
Q

What are the consequences of a chronic increase in arterial BP?

A

Energy expenditure to maintain SV, ultimately  SV
Important reason why blood pressure needs to kept
fairly constant during exercise.

22
Q

What happens in volume overload heart failure?

A

Because the heart can’t contract properly it leads to blood volume being very high in the heart. This increased volume would naturally cause a larger radius (increase r), this would mean more wall stress dissipated through the walls and less in the centre so there will be less stroke volume.

23
Q

What happens in pressure overload heart failure?

A

There is more back pressure on the heart causing more wall stress through the walls, not the centre. This would also lead to less ejection and less stroke volume.

24
Q

How does the heart compensate for an increase in wall stress (over a prolonged period of time)?

A

The heart increases its wall thickness (w) - , this is ventricular hypertrophy. This decreases the afterload, because the radius of the chamber is being decreased, hence more wall stress is directed towards the centre (OR same wall stress over a greater area, this aids contractility, to overcome afterload and maintain SV as well as CO.

25
Q

How does ventricular hypertrophy lead to a decrease in contractility and heart failure?

A

Thicker wall requires more oxygen. If you’re unable to supply this increased level of O2, then ultimately there will be a decrease in contractility and heart failure will get worse.
*This is the vicious cycle of heart failure.

26
Q

What happens to the ventricular pressure volume loop when CVP increases?

A

We would get a much larger filling of the heart and a greater EDV (larger bottom of loop). Because of Starlings law we get much greater energy of contraction and hence greater ejection of blood from the heart so stroke volume is increased as well as the stroke work (but you get a good stroke volume for the stroke work you put in).

27
Q

What happens to the ventricular pressure volume loop when arterial BP increases?

A

This means that we may have the same return of blood to the ventricle (EDV same as normal) however as arterial BP is higher (in aorta and pulmonary artery), isovolumetric contraction needs to be greater to get over the threshold to open the valve.
So, we have used a lot of energy just to increase pressure of chamber to open the valve and now you have less energy of contraction, so you can’t eject as much. This means you end up with a greater end systolic volume, meaning your stroke volume (EDV - ESV) has gone down.
*You’ve put in more energy to eject less blood.