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PHSL 232 > lecture 5 module 1 > Flashcards

lecture 5 module 1 Flashcards

1
Q

Mean arterial pressure =

A

Cardiac output x total peripheral resistance

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2
Q

Why is it important that we maintain mean arterial blood pressure?

A

so that all the organs are perfused

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3
Q

Define total peripheral resistance

A

this is the resistance to blood flow through the blood vessels

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4
Q

Cardiac output =

A

heart rate x stroke volume

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5
Q

We control cardiac output by controlling what?

A

heart rate and stroke volume

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6
Q

We can control cardiac output by controlling heart rate and stroke volume from both intrinsic factors and from extrinsic factors. What are the extrinsic factors that control the heart rate and stroke volume?

A

hormones and nervous control

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7
Q

The whole control of MAP is a ________ loop. What does this mean?

A

closed

this means if you change anything in the cycle, it is going to have consequences for everything else

you never just switch on to increase your heart rate or switch on to decrease your heart rate, it is always a balance

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8
Q

Define stroke volume

A

the volume of blood ejected from either ventricle

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9
Q

What is the intrinsic control of the heart rate?

A

this is very limited

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10
Q

What is the extrinsic control of the heart rate?

A

parasympathetic and sympathetic control

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11
Q

Although we don’t change heart rate intrinsically, if we change heart rate, that has an intrinsic effect on stroke volume. True or false?

A

true

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12
Q

If we develop an action potential, it is going to generate some _______ and there will be a _________. If the action potentials are spaced out, they will generate the same amount of ________. If you increase the frequency of action potential, the force generation _________. What is this known as?

A

force

contraction

force

increases

this is known as the force/frequency relationship/ Treppe effect or Bowditch effect

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13
Q

What does the force/frequency relationship/ Treppe effect of Bowditch effect say?

A

that the myocardial contraction increases as frequency increases

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14
Q

Why does the myocardial contraction increase as frequency increases?

A

because there is an increase in the Ca2+ per unit time

with every action potential, not all Ca2+ will be cleared so the Ca2+ builds up over time so more force is generated

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15
Q

What is heart failure?

A

when the heart cannot generate enough cardiac output to perfuse your body sufficiently

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16
Q

What is the negative force-frequency relation and why is this a hallmark of heart failure? Why is this bad for the heart?

A

Normally, as the action potential increases, the force increases. If this is not the case then the heart is failing.

This is bad for the heart because if you are trying to increases cardiac output, you don’t want the stroke volume to go down so if heart rate goes up and stroke volume goes down cardiac output will not change

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17
Q

In a healthy heart, as heart rate goes up, when happens to stroke volume and cardiac output?

A

Due to the increase in heart rate, stroke volume increases and therefore cardiac output increases

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18
Q

How can stroke volume be controlled intrinsically?

A

By changing preload, afterload and contractility

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19
Q

What is afterload?

A

this is the load on the heart when it is trying to eject (how much resistance was there to blood output)

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20
Q

Define contractility

A

this is a measure of the quality of the pump

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21
Q

What is Pre-load also called?

A

the Frank-Starling mechanism

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22
Q

How does increases in preload affect the stroke volume?

A

increases in preload produces larger stroke volumes

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23
Q

How can you increase pre-load? Why is this?

A

by increasing venous return

Just prior to contraction (after atrial top-up), we have the largest volume of blood in the heart (the end-diastolic volume). If the ventricles are more filled with blood, they will be stretched. This means that each of the cardiac cells and sarcomere inside the muscle cell are stretched too. This increases contraction and therefore increases stroke volume

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24
Q

How does increasing pre-load increase stroke volume?

A

Just prior to contraction (after atrial top-up), we have the largest filling of blood in the heart (the end-diastolic volume). If the ventricles are more filled with blood, they will be stretched. This means that each of the cardiac cells and sarcomere inside the muscle cell are stretched too. This increases contraction and therefore increases stroke volume

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25
Q

What measurements need to be on each axis in order to show the Frank-Starling Mechanism (increasing preload increases stroke volume)?
What does this graph look like?

A

On the x axis there is ventricular end-diastolic volume (in mLs) and on the y axis, there is stroke volume (also in mLs). The graph shows that as you increase ventricular EDV, stroke volume also increases

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26
Q

Describe the pressure volume loop - what are the axis?

A

on the x axis there is volume of blood (mLs)

on the y axis, there is left ventricular pressure

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27
Q

Describe the pressure volume loop, starting at ventricular ejection until the filling phase

A

If we start at the end of ventricular ejection (circled in red on the diagram), there is closure of the aortic valve. Then there is isovolumetric relaxation. There is no change in volume but there is a big decrease in pressure so on the diagram there is a vertical line moving down the graph from 100mmHg to 15mmHg. At the end isovolumetric relaxation, the mitral valve opens and the ventricle fills with blood. Therefore the volume increases on the x axis.

28
Q

Describe the pressure volume loop, starting at the filling phase until the end of the ejection phase

A

Blood pressure is increasing only a small amount on the y axis.

Eventually the heart is filled with blood and we move into the phase of isovolumetric contraction. The heart contracts and the pressure in the ventricle increases, closing the AV valve. The heart is compressing so the pressure increases but the volume doesn’t change (as seen as a vertical line increasing from 15mmHg to 80mmHg).

We then get to the end of isovolumetric contraction, our aortic valve will open. We are going to start ejecting the blood which means the volume of blood decreases on the x axis, pressure still increases for the first part of the ejection phase because the ventricle is squeezing the blood really strongly into the aorta.

Eventually contraction of the heart slows down so there is a decreases in pressure on the y axis. It becomes low enough so the aortic valve closes and the cycle starts again

29
Q

Where can we find the end-diastolic volume of the pressure-volume relation?

A

at the point when the volume of blood is at its maximum after filling, so the pressure is at its lowest (bottom right point)

30
Q

Where can we find the end systolic volume on the pressure-volume relation?

A

At the end of the ejection phase when the volume is the lowest (top left point)

31
Q

If we increase pre-load, how does the pressure-volume relation change?

A

There is more filling which means that the EDV has shifted to the right (the loop has been stretched)
therefore the SV has also increased

32
Q

Does the end systolic volume change if preload has increased? Why?

A

no

because we may fill the blood more but we are squeezing it down to the same level

33
Q

Why does increases the pre-load not increase contractility?

A

because you end up with the same end systolic volume although you have pushed more blood out (increase in ejection fraction), the same amount of blood is left over and so the heart is not contracting any harder to squeeze the last bit out

34
Q

At what levels can you see the Frank-Starling mechanism?

A

at all levels (muscle, cells etc)

35
Q

Why does force increase with length?

A

Due to length-dependent activation:
If you increase the Ca2+ sensitivity of the myofilaments (regardless of the amount of Ca2+ there is) by stretching or shortening the muscle so for the same amount of Ca2+, you can produce more force.
It is also due to the overlap of actin and myosin to increase the number of cross-bridges

36
Q

Where is titin located?

A

it is running the entire length of the sarcomere

37
Q

What is the role of titin?

A

to keep actin and myosin somewhat close to each other

38
Q

What happens to titin as you stretch the sarcomere?

What effect does this have on the placement of actin and myosin?

A

If the sarcomere is short, titin will be floppy and so the myosin can just sit wherever whereas is the sarcomere is longer, titin will be more taut and so the actin and myosin are pulled together and so the head of myosin is closer to actin and so it is easier to interact and a cross-bridge to take place

39
Q

As well as increasing the sensitivity of the myofilaments and overlapping the actin and myosin, how does the length dependent relationship affects the actin-troponin-tropomyosin complex?

A

Ca2+ binds to TnC to allow cross-bridge formation. If you stretch your muscle, more Ca2+ binds to TnC at the same Ca2+ availability so more cross-bridges can form so there is increased contraction (the sensitivity to Ca2+ has increased).

40
Q

What is it called when more Ca2+ can bind to TnC at the same Ca2+ availability so there are more cross-bridges, when the sarcomere is stretched?

A

this is called cooperativity at the actin-troponin-tropomyosin (ATT) complex

41
Q

What is lattice spacing?

A

how close actin and myosin are to one another

42
Q

Briefly describe the length dependent activation and explain why it happens

A

This is when the stroke volume increases when the length increases due to

  • increase in Ca2+ sensitivity
  • number and strength of cross-bridges because of actin and myosin overlap due to reduction of lattice spacing and cooperativty of the actin-troponin-tropomyosin complex
43
Q

The force production of cardiomyocyte increases at longer lengths due to:

i. increased concentrations of Ca2+
ii. increase in the number and strength of cross bridges
iii. increase in the Ca2+ sensitivity of the myofilaments

A

ii. and iii. are correct

44
Q

What is afterload an index for?

A

how much pressure has to be generated in order to start the blood ejection

45
Q

Afterload is a consequence of what? Why is this?

A

aortic pressure
if you have high blood pressure, you will have high aortic pressure and therefore your heart will have to squeeze harder to overcome the aortic pressure before the aortic pressure will be there

46
Q

How does afterload affect the ventricular volume?

A

The heart has to squeeze harder to generate enough pressure for the aortic valve to open. This means that there is less time for the blood to be ejected before the aortic valve closes again and therefore less blood is ejected from the heart

47
Q

How does afterload affect the pressure volume loop?

A

It will be taller and thinner because the pressure is greater in the y axis but the LV volume is smaller because the ejection time has decreased on the x axis and the stroke volume is less

48
Q

How does afterload affect stroke volume?

A

an increase in the afterload decreases stroke volume

49
Q

Increases the afterload causes what to increase and what to decrease?

A

the end systolic volume increases

the stroke volume decreases

the ejection fraction decreases

the end diastolic volume remains unchanged

50
Q

Define afterload?

A

the force the heart has the generate to eject the blood - the force the fibres have to work against in order to make the heart contract
the fibres are generating more and more force because the sarcomeres are trying to shorten more and more

51
Q

What equation do we use to look at afterload?

A

Law of LaPlace

52
Q

What is the law of laplace?

A

wall stress (σ) = Pressure (P) x radius (r)/2xwall thickness (h)

53
Q

If there is a spontaneous increase in afterload, how does the heart repsond?

A

if there is an increase in pressure, the wall stress will increase (the heart will just have to deal with it)

54
Q

If there is chronic pressure overload (chronic increase in afterload), what happens?

A

in order to keep wall stress the same for a long period of time, the heart will increase the thickness of the heart wall and the radius also gets smaller

55
Q

Afterload is caused by what?

A

an increase in aortic pressure

56
Q

What is afterload measured by?

A

wall stress

57
Q

What is the importance of afterload?

A

If we have increased our venous return (increased preload), this increases stroke volume and cardiac output. This increases venous return, so this just keep cycling round and round so there is a never-ending cycle trying to increase cardiac output. But, if we increase the cardiac output, we are also increasing the aortic pressure and therefore increasing the afterload. This is blunting the response because if we increase the cardiac output too much, our aortic pressure will get so high that our after load gets so high

58
Q

Define contractility?

A

this is the cardiac performance at a given preload and afterload (independent of both of these two)

59
Q

What will an increase in contractility do to stroke volume?

A

increase it

60
Q

What does afterload do to the Frank-Starling mechanism?

A

it shifts the curve down

61
Q

What does contractility do to the Frank-Starling mechanism?

A

it shifts the curve to the left

62
Q

Why does an increase in contractility lead to an increase in stroke volume?

A

because it decreases the end-systolic volume

63
Q

What is an increase in contractility called?

A

inotrophy

64
Q

What is the effect of preload on EDV, ESV, SV and EF?

A

EDV increases

ESV remains unchanged

SV increases

EF increases

65
Q

What effect does contractility have on EDV, ESV, SV and EF?

A

EDV remains unchanged

ESV decreases

SV increases

EF increases

66
Q

Contractility increases across the Starling curve (SV vs EDV) BECAUSE afterload is the tension developed in the left ventricle required to open the aortic valve?

A

Starling curve = preload

first statment is false and the second is true

67
Q

preload has an effect on…..

A

Starling curve

PHSL 232 (30 decks)

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