Regulation of stroke rate

Question 1

What regulates stroke rate?

Answer 1

Sympathetic & parasympathetic nervous systems

Question 2

What causes an increase in stroke rate?

Answer 2

Stimulation of the sympathetic nervous system

Question 3

What causes an decrease in stroke rate?

Answer 3

Stimulation of parasympathetic nervous system

Question 4

Describe how stroke rate is increased

Answer 4

• Sympathetic nervous system stimulated*
  1) Sympathetic nerves release NA & Adrenal medulla releases Adrenaline into the blood
  2) NA & A act on ß1-receptors on sinoatrial node
  3) This increases the slope of the Pacemaker potential meaning a higher frequency
  4) Higher frequency = higher rate

Question 5

Describe how stroke rate is decreased

Answer 5

• Para-s nervous system stimulated*
  1) Vagus nerve releases ACh
  2) Acts on muscarinic receptors on sinoatrial node
  3) Hyperpolarises cells and decreases slope of pacemaker potential meaning a lower frequency
  4) Lower frequency = lower rate

Question 6

What is the importance of ‘Pre-load’ of cardiac muscle fibres?

Answer 6

Starling’s law states that the energy of contraction of these cardiac muscle fibres is proportional to the initial length of the muscle fibres

Question 7

What is the effect of venous return on cardiac output?

Answer 7

In vivo, preload is affected by the End Diastolic Volume

Increased venous return = higher end diastolic volume & thus an increase in stroke volume

Decreased venous return thus causes a decrease in stroke volume

Question 8

How does regulating stroke volume, based on end diastolic volume benefit the CVS?

Answer 8

Ensures self-regulation – matches SV of left & right ventricles

Question 9

Afterload is another factor affecting the stroke volume

What is afterload?

Answer 9

Afterload is the load against which the muscle tries to contract

Question 10

What might cause an increase in afterload?

How would this affect Stroke volume?

Answer 10

Afterload is controlled by TPR

If TPR increases (due to stenosis or something) then the pressure holding the aortic valve closed would increase (kind of)

This means the cardiac muscle will need to use more energy to open the aortic valve and thus less energy is used ejecting blood

This would cause the Stroke volume to decrease

Question 11

So, in general, what vessels determine preload and what vessels determine afterload?

Answer 11

Preload - venules and veins (capacitance vessels)

Afterload - arterioles (resistance vessels)

Question 12

How does the sympathetic nervous system affect Stroke VOLUME and how?

Answer 12

1) Sympathetic nerves release NA & Adrenal medulla release adrenaline into the blood
2) These act on B1 receptors on Myocytes
3) This causes an increase in contractility (inotropic effect)
4) This causes a stronger, shorter contraction (overall giving a higher SV)

Question 13

How does the parasympathetic NS affect Stroke VOLUME?

Answer 13

V little effect

Vagus nerve is the parasymp nerve that is associated with the heart, however it DOES NOT innervate the ventricular MUSCLE thus does not affect it’s contractility

Question 14

Summarise how stroke volume is controlled (in a healthy person)…

Answer 14

Preload:

• How stretched/full the heart when it starts contracting
• Affected by EDV which is to do with how much blood the veins/venules return

Afterload:

• How much energy is needed to open the aortic valve and push blood out
• Affected by TPR which is basically controlled by arteriolar resistance

Contractility:

• The strength of contraction at any given pre/afterload
• Affected by sympathetic NS

Question 15

What pathology affects stroke volume and how?

in vivo

Answer 15

Hypercalcemia:

• shifts curve up and left
• Increased SV

Hypocalcemia:

• shifts curve down and right
• Decreased SV

Ischaemia:

• shifts curve down and right
• Decreased SV

Question 16

How does the heart compensate for reduced pumping ability?

Answer 16

Hypocalcemia and Ischaemia, in vivo, would cause a decreased SV as the curve shifts down

However, the heart in real life, just starts working at a higher End diastolic volume (it fills up more before contracting) - to a level such that SV is the same

This results in a lower ejection fraction and reduced exercise capability

Question 17

What do barbiturates do?

Answer 17

Shift curve down and right

in vivo they would cause a decreased SV

Question 18

What is the general rule with anything affecting heart rate or Stroke volume?

Answer 18

Cardiac output = heart rate x stroke volume

BODY WANTS TO MAINTAIN CO (or increase/decrease it in accordance with exercise and all that stuff)

So the body will change one factor, in order to balance out a change in the other

Question 19

Increasing the heart rate with a pacemaker will cause an initial increase in CO

What happens next and why?

Answer 19

After a while, Stroke volume decreases

Increased HR = Reduced interval between pumps

Reduced interval cuts into rapid filling phase ∴ Reduced EDV

Reduced EDV ∴ reduced stretch of muscle ∴ reduced preload

Reduced preload ∴ reduced stroke volume by Starling’s law

Question 20

Summarise what causes an increase in HR

Answer 20

Sympathetic stimulation - increased sympathetic tone

Reduced parasympathetic stimulation - decreased vagus nerve tone

Question 21

Summarise what causes an increase in contractility

Answer 21

via increased sympathetic tone/stimulation

alters inotropic state & shortens systole

Question 22

What causes higher venous return?

Answer 22

Venoconstriction

Skeletal/respiratory pumps & lying down etc

Maintains preload

Question 23

What will cause a fall in total peripheral resistance?

Answer 23

Arteriolar dilation in skin/muscles/heart

Reduces afterload