9. Regulation of Stroke Volume Flashcards Preview

Systems: Cardio. WK > 9. Regulation of Stroke Volume > Flashcards

Flashcards in 9. Regulation of Stroke Volume Deck (68)
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1
Q

What nervous system is responsible for tachycardia?

A

Sympathetic nervous system

2
Q

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

A

noradrenaline

3
Q

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

A

circulating adrenaline from adrenal medulla

4
Q

What receptors does noradrenaline act on and where?

A

On beta 1 receptors on SA node

5
Q

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

A

Increases slope of pacemaker potential ( becomes steeper)

6
Q

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

A

approx. 50mV

7
Q

What happens when each cell depolarises to treshold?

A

It fires APs

8
Q

What nervous system is responsible for bradycardia?

A

parasympathetic nervous system

9
Q

What hormone is responsible for bradycardia and what releases it?

A

acetylcholine; released by vagus nerve

10
Q

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

A

acts on muscarinic receptors on SA node

11
Q

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

A

decreases slope of pacemaker potential (becomes less steep)

12
Q

What happens to cells that are in tachycardia?

A

they are depolarised

13
Q

What happens to cells that are in bradycardia?

A

they are hyperpolarised and depolarisation takes longer

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

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)

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)

17
Q

In vivo, what is preload affected by?

A

The end diastolic volume (EDV)

18
Q

What happens to preload during exercise?

A

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

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

20
Q

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

A
  • decrease in end diastolic volume

- decrease in stroke volume

21
Q

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

A

self- regulation

22
Q

What is meant by “afterload”?

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

What is a big factor which affects afterload?

A

aortic pressure

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)
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)
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

27
Q

How does arteriole constriction affect afterload?

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

Decks in Systems: Cardio. WK Class (42):