Regulation of Stroke Volume and Heart Rate Flashcards

1
Q

Regulation of the heart rate is _______.

A

neural

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The sympathetic nervous system has what effect on regulation of heart?

A

Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the sympathetic nervous system release?

A

Noradrenaline released from sympathetic nerves and;

adrenaline released from the adrenal medulla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does noradrenaline and circulating adrenaline act on?B1 receptors on sinoatrial node

A

Beta-1 receptors on sinoatrial node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What impact does the sympathetic nervous system have on the SA node?

A

Increase slope of the pacemaker potential, pacemaker cells reach threshold quicker.

Increases heart rate (tachycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the parasympathetic system release?

A

Acetylcholine (ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What nerve from the parasympathetic system acts on the heart?

A

Vagus nerve (CN X)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does the parasympathetic system act on?

A

Muscurinic receptors on sinoatrial node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What effect does the parasympathetic system have on the sinoatrial node?

A

Hyperpolarises cells and decreases slope of pacemaker potential.

Decreases heart rate (bradycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 4 things that can alter the strength of contraction (stroke volume) of the heart?

A

Preload

Afterload

Neural

Pathological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does Starling’s Law state?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does tension of cardiac muscle fibres change with length (preload)?

A

Tension increases until it reaches a maximum then it decreases as the length increases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the relationship between tension and length (preload) due to?

A

Because the over lap of the actin and myosin filaments changes, therefore the number of potential cross bridges changes also.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the curve of tension against length (preload) essentially the same as?

A

End diastolic volume against stroke volume

EDV v SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In vivo, what affects preload?

A

EDV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What impact does increases venous return have on EDV and stroke volume?

A

EDV: increases
SV: increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What effect does decreasing venous return have on EDV and stroke volume?

A

EDV: decreases
SV: decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does the relationship between EDV and stroke volume ensure?

A

Self regulation so that the stroke volume of the left and right ventricles are the same.

Resting EDV is neither at the max or min SV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is afterload?

A

The load against which a muscle tries to contract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the aortic pressure impacted by?

A

Total peripheral resistance (TPR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens to the aortic pressure if total peripheral resistance increases?

A
  • aortic pressure increases
  • LV will have to use more work (energy) in opening the aortic valve
  • SV will decrease as there is less energy for the ejection phase of contraction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens to stroke volume if total peripheral resistance increases?

A

It decreases

23
Q

What affects the afterload of the heart?

A

The aortic pressure which in turn is determined by TPR.

24
Q

What kind of vessels affect preload?

A

capacitance (veins/venules)

25
Q

What kind of vessels affect afterload?

A

resistance (arterioles)

26
Q

How is the stroke volume regulated neurally?

A

By the sympathetic nervous system

27
Q

What does the sympathetic system act on to impact stroke volume?

A

Beta-1 receptors on the myocytes

28
Q

What does the sympathetic system acting on B1 receptors of myocytes cause?

A

Increases contractibility (inotropic effect)

Gives stronger, but shorter contractions.

29
Q

What impact does the parasympathetic system have on stroke volume?

Why?

A

Little effect

Due to vagus nerve not innervating the ventricular muscle.

30
Q

What is preload?

A

How full the ventricle is before it starts contracting (EDV).

31
Q

What is afterload?

What is it affected by?

A

How difficult it is for the heart to pump out the blood (i.e. the TPR).

Affected by the state of contraction of arterioles.

32
Q

What happens to stroke volume when veins/venules contract?

Why?

A

It increases

  • increased venous return to the heart
  • increases EDV
  • increases preload therefore increasing stroke volume.
33
Q

Does vasoconstriction affect stroke volume?

A

No, just arteriole constriction.

34
Q

Describe how arteriole constriction affects stroke volume?

A

SV decreases because:

  • TPR increases
  • aortic pressure increases
  • afterload increases
  • LV needs to work harder
35
Q

What is an inotropic effect?

A

A change in the force or speed of contraction of muscle.

36
Q

What are examples of pathological impacts on stroke volume?

4 points

A

Hypercalcemia
Hypocalcemia
Ischaemia
Barbiturates

37
Q

How does hypercalcemia impact the stroke volume/EDV curve?

Why?

A

Shifts it up and left

  • more Ca outside myocytes
  • more actin-myosin cross bridge formation
  • increased SV
38
Q

How does hypocalcemia impact the stroke volume/EDV curve?

A

Shifts it down and right

39
Q

How does ischaemia impact the stroke volume/EDV curve?

A

Shifts it down and right

40
Q

How does barbiturates impact the stroke volume/EDV curve?

A

Shifts it down and right, producing an anaesthetic effect.

41
Q

What is ischaemia?

A

Restriction in blood supply to tissues.

42
Q

Why does ischaemia cause the stroke volume vs EDV curve to shift down and to the right?

A

Down: stroke volume decreases as there are less living myocytes to contract.

Right: As the other side of the heart is still healthy and has a higher SV. This means the EDV in the ischaemic side of the heart increases and SV increases again by preload.

43
Q

What are barbiturates?

A

Drug that acts on the CNS as a depressant.

44
Q

Cardiac output = _____ + ______

A

SV + HR

45
Q

Increasing HR with an electronic pacemaker, causes a small increase in ____, but then _____ decreases.

Why?

A

CO
SV

  • Shortened cardiac interval cuts into the rapid filling phase.
  • Reduced EDV, reduces preload
  • SV decreases (Starlings)
46
Q

How does the heart compensate for a reduced pumping ability?

A

By working around a bigger EDV, resulting in a lower ejection fraction and reduced exercise capacity.

47
Q

Outline the things that accompany physiological increases in heart rate to offset the effect of decreased stroke volume? (4)

A
  • HR increases
  • Contractility increases
  • Venous return increases
  • TPR falls
48
Q

What causes the HR to increase? (2)

A
  • increased sympathetic tone

- decreased vagal tone

49
Q

What causes contractility to increase? (2)

A
  • increased sympathetic tone

- alters inotropic state & shortens systole (shorter but stronger contractions)

50
Q

What causes the venous return to increase? (3)

A
  • vasoconstriction
  • skeletal/resp. pumps
  • maintains preload
51
Q

What causes the TPR to fall? (2)

A
  • arteriole dilation

- reduces afterload

52
Q

How much can a pacemaker increase the CO by?

A

2x

53
Q

How much can the physiological mechanisms increase the CO by?

A

4-6x