stroke volume and heart rate regulation

Question 1

explain the effects of the sympathetic nervous system in increasing heart rate:

Answer 1

• SNS activate the release of noradrenaline and adrenaline from the adrenal medulla
• Act on ß1 receptors (adrenergic) on the SA node
• Increase the slope of the pacemaker potential so it reaches the threshold quicker

-> tachycardia (depolarisation)
-> Increase heart rate

Question 2

explain the effects of the parasympathetic nervous system in decreasing heart rate:

Answer 2

• Vagus nerves release acetylcholine
• Act on muscarinic receptors on the SA node
• Decreases slope of the pacemaker potential so it reaches threshold slower

-> bradycardia (hyperpolarisation)
-> Decreases heart rate

Question 3

what is the law that relates to the preload of stroke volume?

Answer 3

Starling’s law: the energy of contraction (of cardiac muscle fibres) is proportional to the initial length of the cardiac muscle fibres

length-tension relationship -> higher preload
= bigger strength of contraction

Question 4

what is preload?

Answer 4

the initial stretching of the cardiac myocytes before contraction

affected by EDV (how full the ventricle is before it starts contracting)

Question 5

what effect does increased venous return have on stroke volume?

Answer 5

• Increased venous return, increased end-diastolic volume, & therefore increased stroke volume

stretches sarcomeres -> increases preload

Question 6

what effect does decreased venous return have on stroke volume?

Answer 6

• Decreased venous return, decreased EDV, & therefore decreased stroke volume

shortens sarcomeres -> decreasing preload

Question 7

what is afterload?

Answer 7

the load against which the muscle tries to contract.

How difficult it is for the heart to pump out the blood.

Question 8

what is afterload set by?

Answer 8

by the arterial pressure against which the blood is expelled (this in turn depends on the Total Peripheral Resistance).

Question 9

explain why if TPR increases, stroke volume will go down:

Answer 9

aortic pressure will increase, the ventricles will have to work harder to push open the aortic valve, and it will have less energy to eject blood i.e. SV will decrease (more energy is being wasted building up sufficient pressure to open the aortic valve)

Question 10

define the total peripheral resistance (TPR)?

Answer 10

how easy it is for blood to get through the arterioles.

Depends on the length of the arterioles, the viscosity of the fluid and the radius of the arterioles.

Question 11

what happens to the stroke volume when you constrict the arterioles?

Answer 11

If you constrict arterioles, you affect the afterload, the afterload goes up making it more difficult for the heart to pump the blood out and SV goes down.

Question 12

what happens to the stroke volume when you constrict the venules and veins?

Answer 12

If you constrict the venules and veins, blood will be squeezed towards the heart and increases the venous return (which increases EDV and in turn preload, and that increases SV).

Question 13

roles of venules/veins and arterioles:

Answer 13

Venules/veins - (venous return) are capacitance vessels that affect preload

Arterioles are resistance (TPR) vessels that affect afterload

Question 14

explain the effects of parasympathetic system on stroke volume

Answer 14

little effect

because the vagus does not innervate the ventricular muscle (only the top and the nodes)

Question 15

explain the effects of sympathetic system on stroke volume

Answer 15

• sympathetic nerves releasing noradrenaline
• plus, circulating adrenaline from adrenal medulla
• both act on ß1-receptors on the myocytes
• increases contractility (an inotropic effect) – Inos[strength] tronos[time] ie positive inotropic agents increase force of contraction
• gives stronger (because more Ca2+ is released), but shorter contraction

Question 16

define inotropic and chronotropic:

Answer 16

Inotropic → increase contractility

Chronotropic → increase heart rate

Question 17

what effect does hypercalcemia have on the curve?

Answer 17

shifts curve up and left, has the same effect as sympathetic stimulation

Question 18

what effect does hypocalcaemia have on the curve?

Answer 18

shifts curve down and right

Question 19

what effect does ischaemia have on the curve?

Answer 19

(that side of the heart will pump less strongly) – shifts curve down and right

Question 20

what effect does barbiturates (or other drugs) have on the curve?

Answer 20

shifts curve down and right. (if used too much)

Question 21

why do you have a low stroke volume if you had a myocardial infarction?

Answer 21

the curve will be shift down and you will end up with a smaller SV for any given EDV

Question 22

what is the equation for cardiac output?

Answer 22

CO = HR x SV

Question 23

what effect does heart rate have on stroke volume and cardiac output?

Answer 23

increasing HR higher and higher, decreases SV lower and lower = CO stays the same.

Question 24

Increasing heart rate above 140/150 causes a small increase in cardiac output, but then stroke volume starts decreasing. Why?

Answer 24

[1] The shortened cardiac interval cuts into the rapid filling phase

[2] The reduced end-diastolic volume reduces preload

[3] So according to Starling’s law, stroke volume is reduced.

Question 25

Control of cardiac output (4-6 time increase during exercise.. how?)

Answer 25

[1] HR goes up due to decreased vagal tone and increased sympathetic tone.

[2] Contractility goes up due to increased sympathetic tone which then alters the inotropic state and shortens systole

[3] Venous return increases go up due to vasoconstriction and skeletal/respiratory pumps, which maintain the preload.

[4] Total Peripheral Resistance (TPR) falls due to arteriolar dilation in muscle, skin & heart, which reduces the afterload, making it easier for the heart to pump blood.