Regulation of SV and HR Flashcards

(37 cards)

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?

24
Q

What vessels affect afterload?

25
What effect does the sympathetic system have on stroke volume?
Increases it
26
What receptors does the sympathetic system release noradrenaline into to increase SV?
- B1 receptors on myocytes
27
How does the sympathetic system effect contraction time?
Gives a shorter but stronger contraction (chronotropic effect)
28
How does the parasympathetic system effect stroke volume
- Doesn't really | - Vagus doesn't innervate ventricular muscle
29
What effect will hypercalcaemia have on SV?
- Shifts curve up and left (stronger shorter contraction)
30
What effect will hypocalcaemia have on SV?
- Shifts curve down and right (longer weaker contraction)
31
What effect will ischaemia have on SV?
- Shifts curve down and right (longer weaker contraction)
32
How does starling's law allow the heart to compensate for a reduced pumping ability?
- Allows the heart to work around a bigger EDV | - Results in a lower ejection fraction and reduced exercise capacity
33
What effect will barbiturates have on stroke volume?
Shifts curve down and right (longer weaker contraction)
34
In what ways can the cardiac output be controlled?
- HR Increase - Contractility increase - Venous return increase - TPR fall
35
How does an increase in contractility effect the CO?
Alters ionotropic state and shortens systole
36
How does a venous return increase affect CO?
- Venoconstriction | - Maintains preload
37
How does a fall in TPR control CO?
Reduces afterload