Regulation of stroke volume & heart rate Flashcards

1
Q

How does the sympathetic nervous system regulate heart rate?

A
  • Sympathetic nerves release noradrenaline
  • plus circulating adrenaline from adrenal medulla
  • Both act on B1-receptors on the surface of sinoatrial node
  • Increases heart rate = tachycardia
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2
Q

What is Tachycardia?

A
  • Heart rate that exceeds the normal resting rate.

- In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults.

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3
Q

How does the parasympathetic nervous system regulate heart rate?

A
  • Vagus releases ACh
  • acts on muscarinic receptors in sinoatrial node
  • Hyperpolarises cells
  • Decreases heart rate = bradycardia
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4
Q

What is Bradycardia?

A

It is a slower than normal heart rate

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5
Q

What is normal stroke volume?

A

60-120 ml/beat

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6
Q

What 3 things affect stroke volume?

A
  • Contractility
  • Preload
  • Afterload
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7
Q

What does Starling’s law state?

A

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

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8
Q

What is Preload?

A

Preload is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand.
- It is how much volume is in the ventricles at the end of diastole : EDV.

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9
Q

What volume is preload affected by, in vivo?

A

End diastolic volume

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10
Q

What are factors determining cardiac Preload? (to increase it)

A
  • Increased EDV
  • Increased atrial contractility
  • Increased aortic pressure
  • Increased atrial contractility
  • Decreased heart rate
  • Increased central venous pressure
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11
Q

Which valve closes after diastole?

A

The mitral valve

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12
Q

What is Afterload?

A

It is the pressure required to open the aortic valve.

- It is the load against which the muscle tries to contract

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13
Q

What is total (systemic) peripheral resistance?

A

The total resistance to flow of blood in the systemic circuit

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14
Q

What occurs to Aortic pressure, if total peripheral resistance increases?

A

If TPR increases, aortic pressure will increase, the ventricle will have to work harder to push open the aortic valve..
- Stroke volume will decrease.

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15
Q

What is required for the aortic valve to open?

A

The pressure in the ventricle needs to be greater than the pressure distal to the aortic valve.

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16
Q

In vivo, how is afterload set?

A
  • Afterload is set by the arterial pressure against which the blood is expelled - this in turn depends on the Total Peripheral Resistance.
17
Q

Which vessels affect preload?

A

Capacitance vessels

e.g. venules/veins

18
Q

Which vessels affect afterload?

A

Resistance vessels

e.g. Arterioles

19
Q

What is contractility?

A

The inherent vigor of contraction of the heart muscles during systole.

20
Q

How does the sympathetic system affect the regulation of stroke volume?

A
  • Sympathetic nerves releasing noradrenaline
  • plus circulating adrenaline from adrenal medulla
  • Both act on ß1-receptors on the myocytes
  • Increases contractility (an inotropic effect)
    gives stronger, but shorter contraction
21
Q

Does the parasympathetic nervous system affect regulation of stroke volume?

A
  • Little effect

- Probably because the vagus does not innervate the ventricular muscle.

22
Q

How does Hypercalcemia affect the stroke volume-EDV curve?

A

Shifts curve up and left

23
Q

How does Hypocalcemia affect the stroke volume-EDV curve?

A

Shifts curve down and right

24
Q

How does Ischaemia affect the stroke volume-EDV curve?

A

Shifts curve down and right

Ischaemia - loss of blood supply to the cardiac muscle.

25
Q

How will the heart compensate for a reduced pumping ability?

A

By working around a bigger EDV.

- Results in lower ejection fraction, and reduced exercise capacity.

26
Q

How do Barbiturates affect the stroke volume-EDV curve?

A

Shifts curve down and right

  • A barbiturate is a drug that acts as a central nervous system depressant.
27
Q

Equation to calculate cardiac output

A

Cardiac output = Heart rate x Stroke volume

28
Q

Increasing heart rate with an electronic pacemaker, causes a small increase in CO, but then SV(stroke volume) decreases, Why?

A
  • Shortened cardiac interval cuts into the rapid filling phase.
  • Reduced end diastolic volume reduces preload
  • So by Sterling’s law, reduces stroke volume.
29
Q

Mechanisms that cause heart rate to decrease for control of cardiac output

A
  • via decreased vagal tone

- & increased sympathetic tone

30
Q

How does contractility increase for control of cardiac output?

A
  • via increased sympathetic tone

- alters inotropic state & shortens systole

31
Q

How does venous return increase for control of cardiac output?

A
  • Via venoconstriction (via a1 receptors)
  • & skeletal/respiratory pumps
  • maintains preload
32
Q

How does total peripheral resistance fall (TPR) to control cardiac output?

A
  • Due to arteriolar dilation in muscle, skin & heart (via b2 receptors)
  • reduces afterload
33
Q

How much does Cardiac output increase during exercise?

A

4-6 times