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Systems 2: Cardiovascular > Regulation of SV and HR > Flashcards

Regulation of SV and HR Flashcards

1
Q

What regulates HR?

A

Neural

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2
Q

What regulates stroke volume?

A
  • Preload
  • Afterload
  • Neural
  • Pathological
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3
Q

What part of the nervous system controls HR?

A

Autonomic

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4
Q

What neurotransmitter is released by the sympathetic system to increase HR?

A

Noradrenaline

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5
Q

Where else can the noradrenaline come from that increases HR?

A

Adrenal medulla

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6
Q

What receptors does the noradrenaline act on?

A

B1 receptors

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7
Q

Where are the B1 receptors that the noradrenaline acts on?

A

Sinoatrial node

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8
Q

What effect does the sympathetic this have on the pacemaker potential?

A

Increases slope

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9
Q

What neurotransmitter is released by the parasympathetic system?

A

ACh

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10
Q

What cranial nerve slows HR?

A

Vagus

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11
Q

What receptors are acted on by the ACh released by the parasympathetic system?

A

Muscarinic receptors in the SA node

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12
Q

What effect does the ACh have on pacemaker cells?

A

Hyperpolarises them

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13
Q

What effect does ACh have on the slope of the pacemaker potential?

A

Decreases slope

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14
Q

What does starlings law state?

A

The energy of contraction is proportional to the initial length of the cardiac muscle fibre

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15
Q

What is the length of the cardiac muscle fibre known as?

A

Preload

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16
Q

What is preload affected by?

A

End diastolic volume

17
Q

What effect would an increased/decreased venous load have on EDV?

A

Increased load = higher EDV

Decreased load = lower EDV

18
Q

What happens to stroke volume as EDV increases/decreases?

A
  • Stroke volume increases as EDV increases

- Stroke volume decreases as EDV decreases

19
Q

How does the directly proportional relationship of EDV and SV ensure self regulation?

A

Means the SV of the left and right ventricles is equal

20
Q

What is afterload?

A

The load against which the muscle fibre contracts

21
Q

In what two ways is aortic pressure affected?

A
  • How much blood is pushed into the aorta (CA)

- How easy it is for the blood to get out of the aorta (TPR)

22
Q

If TPR increases what will happen to the ventricle and stroke volume?

A
  • Ventricle will have to work harder to open the aortic valve
  • Less energy will remain to actually inject the blood so STROKE VOLUME decreases
23
Q

What vessels affect preload?

A

Capacitance

24
Q

What vessels affect afterload?

A

Resistance

25
Q

What effect does the sympathetic system have on stroke volume?

A

Increases it

26
Q

What receptors does the sympathetic system release noradrenaline into to increase SV?

A
  • B1 receptors on myocytes
27
Q

How does the sympathetic system effect contraction time?

A

Gives a shorter but stronger contraction (chronotropic effect)

28
Q

How does the parasympathetic system effect stroke volume

A
  • Doesn’t really

- Vagus doesn’t innervate ventricular muscle

29
Q

What effect will hypercalcaemia have on SV?

A
  • Shifts curve up and left (stronger shorter contraction)
30
Q

What effect will hypocalcaemia have on SV?

A
  • Shifts curve down and right (longer weaker contraction)
31
Q

What effect will ischaemia have on SV?

A
  • Shifts curve down and right (longer weaker contraction)
32
Q

How does starling’s law allow the heart to compensate for a reduced pumping ability?

A
  • Allows the heart to work around a bigger EDV

- Results in a lower ejection fraction and reduced exercise capacity

33
Q

What effect will barbiturates have on stroke volume?

A

Shifts curve down and right (longer weaker contraction)

34
Q

In what ways can the cardiac output be controlled?

A
  • HR Increase
  • Contractility increase
  • Venous return increase
  • TPR fall
35
Q

How does an increase in contractility effect the CO?

A

Alters ionotropic state and shortens systole

36
Q

How does a venous return increase affect CO?

A
  • Venoconstriction

- Maintains preload

37
Q

How does a fall in TPR control CO?

A

Reduces afterload

Systems 2: Cardiovascular (19 decks)

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