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2. Cardiovascular System > 9. Regulation of Stroke Volume > Flashcards

9. Regulation of Stroke Volume Flashcards

1
Q

What nervous system is responsible for tachycardia?

A

Sympathetic nervous system

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2
Q

What hormone is responsible for tachycardia that is released from noradrenaline?

A

noradrenaline

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3
Q

Additionally to noradrenaline from sympathetic nerves, what else is released that causes tachycardia?

A

circulating adrenaline from adrenal medulla

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4
Q

What receptors does noradrenaline act on and where?

A

On beta 1 receptors on SA node

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5
Q

What effect does sympathetic system have on slope of pacemakers potential?

A

Increases slope of pacemaker potential ( becomes steeper)

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6
Q

What is the approximate treshold that needs to be reached to induce tachycardia in mV?

A

approx. 50mV

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7
Q

What happens when each cell depolarises to treshold?

A

It fires APs

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8
Q

What nervous system is responsible for bradycardia?

A

parasympathetic nervous system

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9
Q

What hormone is responsible for bradycardia and what releases it?

A

acetylcholine; released by vagus nerve

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10
Q

What receptor does acetylcholine act on and where are they found?

A

acts on muscarinic receptors on SA node

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11
Q

What effect does parasympathetic system have on slope of pacemaker potential?

A

decreases slope of pacemaker potential (becomes less steep)

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12
Q

What happens to cells that are in tachycardia?

A

they are depolarised

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13
Q

What happens to cells that are in bradycardia?

A

they are hyperpolarised and depolarisation takes longer

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14
Q

What does depolarisation in parasympathetic nerves take longer? (2)

A
  • It takes longer for cells to reach treshold

- Longer cardiac interval in cells

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15
Q

What doe Starling’s law state?

A

The energy of contraction is proportional to the initial length of the cardiac muscle fibre ( at optimal length, max. cross bridges formed therefore max tension produced and stronger the contraction)

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16
Q

What is meant by “prelaod”?

A

End distolic volume that stretches right or left ventricles to its greatest dimensions under physiological demand (stretching of ventricles before contraction)

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17
Q

In vivo, what is preload affected by?

A

The end diastolic volume (EDV)

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18
Q

What happens to preload during exercise?

A

It increases (and to bring it back down the body will try to decrease it)

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19
Q

What effect will increased venous return have on EDV and stroke volume? (e.g. during exercise)

A
  • increase in end diastolic volume

- increase in stroke volume

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20
Q

What effect will decreased venous return have on EDV and stroke volume?

A
  • decrease in end diastolic volume

- decrease in stroke volume

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21
Q

What regulation mechanism describes matching stroke volume of left and right ventricles?

A

self- regulation

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22
Q

What is meant by “afterload”?

A
  • It’s the load against which the muscle tries to contract blood ( eject blood)
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23
Q

What is a big factor which affects afterload?

A

aortic pressure

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24
Q

What 2 things affect aortic pressure?

A
  1. how much blood is pushed into the aorta (i.e.the cardiac output)
  2. how easy it is for that blood to get out of the aorta (i.e. the total peripheral resistance)
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25
Q

IF TPR increases, what is its effect on;

  • aortic pressure
  • stroke volume
  • afterload
A
  • aortic pressure will increase
  • stroke volume will decrease
  • afterload will increase
    (heart will have to work harder to push open aortic valve and will have less energy left to do useful bit of ejecting blood)
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26
Q

How does high pressure in aorta affect blood distribution?

A

High pressure will make it hard to push blood around the body whereas low pressure will make it easier

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27
Q

How does arteriole constriction affect afterload?

A
  • arterioles constricted
  • TPR resistance increased in peripharies
  • increase in afterload
    (harder to distribute blood)
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28
Q

How does arteriole dilation affect afterload?

A
  • arterioles dilate
  • TPR resistance decreased
  • decrease in afterload
    (easier to distribute blood)
29
Q

What is afterload set by/ influenced by?

A

arterial pressure against which the blood is expelled (which in the end depends upon TPR)

30
Q

What will happen to stroke volume if TPR increases?

A

Stroke volume will decrease (more energy is wasted building up sufficient pressure to open aortic valve so less blood ejected)

31
Q

What vessels affect preload?

A

capacitance vessels

32
Q

What are capacitance vessels?

A

venules/ veins

33
Q

What vessels affect afterload?

A

resitance vessels

34
Q

What are resistance vessels?

A

arterioles

35
Q

What neural systems regulates stroke volume?

A

sympathetic nervous system

36
Q

What affect does sympathetic nervous system have on contractions?

A

Gives stronger but shorter contraction (more Ca released from cells and taken up quicker)

37
Q

What is the name of the effect that increases contractility?

A

inotropic effect

38
Q

What is the effect of parasympathetic nervous system on stroke volume specifically?

A

little effect

39
Q

Why does parasympathetic system have little effect on stroke volume?

A

probably because the vagus nerve doesn’t innervate the ventricular muscle

40
Q

What is the term that describes factors that affect heart RATE?

A

chronotropic effect

41
Q

What is the term that describes the factors affecting heart STRENGTH of contraction?

A

inotropic effect

42
Q

What 3 factors affect stroke volume? (pathological causes)

A
  1. hypercalcemia
  2. hypocalcemia
  3. ischaemia
43
Q

What effect does hypercalcemia have on curve?

A

Shifts curve up and left (more steep), since contractions stronger and more cross bridges formed

44
Q

What effect does hypocalcemia have on curve?

A

Shift curve down and right (less steep), since contraction is weaker and less cross bridges formed

45
Q

What effect does ischaemia have on the curve?

A

Shifts curve down and right

46
Q

State the effect of Starling’s wall when the heart needs to compensate for a reduced pumping ability.

A
  • I.e. the heart will compensate for a reduced pumping ability by working around a bigger EDV. This results in lower ejection faction and reduced exercise capacity.
  • resting cardiac input is same but higher EDV
47
Q

What effect do barbiturates have on pathological curve?

A

shifts curve down and right

48
Q

What effect do barbiturates have? (drugs)

A
  • from mild sedation to anesthesia

- lower heart rate

49
Q

What is the equation for calculating cardiac output?

A

cardiac output= heart rate x stroke volume

50
Q

What is the average cardiac output in a body?

A

~5L/min

51
Q

Increasing heart rate with an electronic pacemaker causes a small increase in cardiac output but stroke volume decreases. Why?

A
  • shortened cardiac interval cuts into RAPID FILLING phase which means less blood is ejected because of this overlap of blood coming in and out of ventricles (during tachycardia)
  • reduced end diastolic volume reduces preload
  • By Starling’s law, it reduces stroke volume
52
Q

What happens to blood during systole?

A

it’s ejected from ventricles

53
Q

What happens to blood during diastole?

A

it fills up the ventricles

54
Q

What two effects do the 2 nervous systems have on increasing heart rate?

A
  1. decreased vagal tone

2. increase sympathetic tone

55
Q

What happens to contractility in tachycardia?

A

Increases

56
Q

What increases contractility during tachycardia? How does it occur?

A

Via increased sympathetic systole; alters inotropic state (strength increases) and shortens systole

57
Q

What happens to venous return during tachycardia?

A

Increases (therefore preload increases)

58
Q

What mechanism increases venous return during preload?

A

venoconstriction (skeletal and respiratory pumps action) maintain increased preload

59
Q

What happens to TPR during tachycardia?

A

It decreases/ falls

60
Q

What mechanism causes a decrease in TPR during tachycardia?

A

arteriolar dilation in muscle, skin and heart

61
Q

What does a decrease in TPR correspond to directly?

A

decrease in afterload

62
Q

What effect does tachycardia have on cardiac output?

A

Increases it 4-6 times (but not stroke volume due to cutting into rapid filling phase)

63
Q

What effect on heart rate does sympathetic system have?

A

increases heart rate

64
Q

What effect on heart rate does parasympathetic system have?

A

decreases heart rate

65
Q

What 4 factors influence stroke volume?

A
  1. preload (=EDV)
  2. afterload (=TPR)
  3. neural =(sympathetic supply)
  4. pathological effects
66
Q

What does preload directly correspond to?

A

end diastolic volume (EDV)

67
Q

What effect on stroke volume does (increasing) preload have?

A

increases stroke volume

68
Q

What effect on stroke volume does (increasing) aferload have?

A

decreases stroke volume

2. Cardiovascular System (42 decks)

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