5/ regulation of stroke volume and HR Flashcards

1
Q

where does HR regulation come from?

A

neural regulation

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2
Q

what governs regulation of stroke volume?

A

preload, afterload, neural, pathological regulation

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3
Q

what is the outcome of regulation of HR and stroke volume?

A

control of cardiac output

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4
Q

what do sympathetic nerves release?

A

noradrenaline

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5
Q

what other hormone is released by sympathetic system?

A

circulating adrenaline from adrenal medulla

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6
Q

where do noradrenaline and adrenaline act in HR regulation?

A

B1 receptor on sinoatrial node

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7
Q

what is the effect of the sympathetic system on the HR?

A

increases slope of the pacemaker potential (repolarisation of pacemaker cells becomes faster) -> increases HR, tachycardia if HR > 100

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8
Q

which nerve is by the parasympathetic system to influence the HR?

A

vagus nerve

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9
Q

what does this system release?

A

acetylcholine

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10
Q

what is the effect of the parasympathetic system on the HR?

A

hyperpolarises cells AND decreases slope of pacemaker potential, decreases heart rate (brachycardia, HR < 60)

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11
Q

what is the energy of contraction of a muscle fibre proportional to according to Starling’s law?

A

initial length of muscle fibre

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12
Q

what is preload affected by?

A

end diastolic volume

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13
Q

when increased venous return increases, how does EDV and stroke volume vary?

A

EDV increases, and so does stroke volume

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14
Q

what do these relations ensure?

A

ensures self-regulation: matching stroke volumes in left and right ventricle

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15
Q

what is afterload?

A

the load against which the muscle tries to contract (i.e: total peripheral resistance)

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16
Q

what is preload?

A

how much blood is pushed into the aorta (i.e: the cardiac output)

17
Q

What happens to aortic pressure if total periphery resistance (= afterload) increases?

A

it increases

18
Q

what happens to stroke volume if aortic pressure increases?

A

stroke volume will decrease as the ventricle will have to work harder to push open the aortic valve and will therefore have less energy left to do the useful bit of ejecting blood (= stroke volume) + (more energy is “wasted” building up sufficient pressure to open the aortic valve)

19
Q

what happens to stroke volume if TPR increase?

A

stroke volume decreases

20
Q

which vessels affect preload?

A

venules and veins (capacitance vessels)

21
Q

which vessels affect afterload?

A

arterioles (resistance vessels)

22
Q

what does the sympathetic system release to influence stroke volume?

A

noradrenaline + adrenaline from adrenal medulla

23
Q

what do noradrenaline and adrenaline act on for regulation of stroke volume?

A

B1 receptors on the myocytes

24
Q

what is the effect of the sympathetic system on the stroke volume?

A

increases contractility (an inotropic effect), giving stronger but shorter contraction

25
Q

what is the effect of the parasympathetic system on the stroke volume?

A

little effect

26
Q

what explains the parasympathetic system’s effect on stroke volume?

A

probably because the vagus does not innervate the ventricular muscle

27
Q

what are the effects of hypercalcemia on the stroke volume?

A

shifts curve up and left; higher stroke volume for same EDV

28
Q

what are the effects of hypocalcemia on the stroke volume?

A

shifts curve down and right; lower stroke volume for same EDV

29
Q

what are the effects of ischaemia on the stroke volume?

A

shifts curve down and right; lower stroke volume for same EDV

30
Q

what are the effects of barbiturates on the stroke volume?

A

shifts curve down and right; lower stroke volume for same EDV

31
Q

how do you calculate cardiac output from HR and stroke volume?

A

CO = HR x SV

32
Q

what will be the impact on CO and SV if HR is increased with an electronic pacemaker?

A

small increase in CO then SV decreases because the shortened cardiac interval cuts into the rapid filling phase and this reduces end diastolic volume (= reduces preload); reduces stroke volume by Starling’s law

33
Q

what happens neurally when HR increases physiologically?

A

HR increases:

  • via decreased vagal tone
  • & increased sympathetic tone
34
Q

how does the body offset these effects to cope with physiological increases in HR? (think integration and co-ordinated increase in CO)

A
contractility increases: 
- via increased sympathetic tone
- alters inotropic state &amp; shortens systole
venous return increases: 
- via venoconstriction 
- &amp; skeletal/ respiratory pumps 
- maintains preload
total periphery resistance falls
- due to arteriolar dilation in muscle, skin and heart
- reduces afterload
CO increase 4-6 times
35
Q
SUMMARY: 
HR
- sympathetic supply (?) HR? 
- parasympathetic supply (?) HR
SV
- preload (= EDV) (?) SV
- afterload (= TPR) (?) SV
- neural (= symp supply) (?) SV
A
HR
- sympathetic supply increases HR
- parasympathetic supply decreases HR
SV
- preload (= EDV) increases SV
- afterload (= TPR) decreases SV
- neural (= symp supply) increase SV