Regulation of Stroke Volume and Heart Rate

Question 1

How does the sympathetic system affect heart rate?

Answer 1

Releases noradrenaline
Plus circulating adrenaline from adrenal medulla
Both act on β1-receptors on sinoatrial node
Increases slope of the pacemaker potential
Increases heart rate, tachycardia

Question 2

How does the parasympathetic system affect heart rate?

Answer 2

Vagus releases ACh
Acts on muscarinic receptors on sinoatrial node
Hyperpolarises cells and decreases slope of pacemaker potential
Decreases heart rate, bradycardia

Question 3

How does the sympathetic system affect stroke volume?

Answer 3

Release of noradrenaline and circulating adrenaline from adrenal medulla
Both act on β1-receptors on the myocytes
Increases contractility: inotropic effect
Gives stronger but shorter contraction

Question 4

How does the parasympathetic system affect stroke volume?

Answer 4

Little effect

Probably because the vagus does not innervate the ventricular muscle

Question 5

What are some examples of pathological regulation of stroke volume?

Answer 5

Hypercalcaemia
Hypocalcaemia
Ischaemia
Barbiturates

Question 6

How does hypercalcaemia affect the stroke volume/end diastolic volume curve?

Answer 6

Shifts curve up and left

Question 7

How does hypocalcaemia affect the stroke volume/end diastolic volume curve?

Answer 7

Shifts curve down and right

Question 8

How does ischaemia affect the stroke volume/end diastolic volume curve?

Answer 8

Shifts curve down and right

Question 9

How do barbiturates affect the stroke volume/diastolic volume curve?

Answer 9

Shifts curve down and right

Question 10

How does the heart compensate for a reduced pumping ability?

Answer 10

Starling’s law
Heart will compensate for a reduced pumping ability by working around a bigger EDV
Results in lower ejection fraction and reduced exercise capacity

Question 11

What is Starling’s Law?

Answer 11

Energy of contraction is proportional to the initial length of the cardiac muscle fibre

Question 12

What is preload? What is it affected by in vivo?

Answer 12

It is the length of the cardiac muscle fibre

End diastolic volume

Question 13

What happens to EDV and stroke volume when venous return increases?

Answer 13

EDV increases, stroke volume increases

Question 14

What happens to EDV and stroke volume when venous return decreases?

Answer 14

EDV decreases, stroke volume decreases

Question 15

What does a Starling’s Law ensure?

Answer 15

Self regulation

SV of left and right ventricles match

Question 16

What is afterload?

Answer 16

Load against which the muscle tries to contract

Question 17

What is afterload affected by?

Answer 17

Cardiac output: how much blood is pushed into the aorta

Total peripheral resistance: how easy it is for that blood to get out of the aorta

Question 18

In practical terms, how does an increase in total peripheral resistance affect stroke volume?

Answer 18

TPR increases -> aortic pressure increases -> ventricle has to work harder to push open the aortic valve and it will have less energy left to do the useful bit of ejecting blood -> stroke volume will decrease

Question 19

How are cardiac output, HR and SV related?

Answer 19

Cardiac output = HR x SV

Question 20

How does increasing the HR with an electronic pacemaker affect CO and SV? Why?

Answer 20

• Small increase in CO but then SV decreases
• Shortened cardiac interval cuts into rapid filling phase
• Reduces end diastolic volume, reduces preload
• So by Starling’s Law reduces stroke volume

Question 21

When the heart rate is increased physiologically, why doesn’t it have the same effect as increasing the HR with an electronic pacemaker?

Answer 21

HR increases: via decreased vagal tone and increased sympathetic tone
Contractility increases: via sympathetic tone, alters inotropic state and shortens systole
Venous return increases: via venoconstriction, skeletal/respiratory pumps, maintains preload
TPR falls: arteriolar dilatation in muscle, skin and heart, reduces afterload
CO increases 4-6 times