Regulation of stroke volume

Question 1

What set the HR and how?

Answer 1

Pacemaker cells in the sinoatrial node

SA reaches threshold first and evokes an AP and wave of depolarisation through the atria
The atria contracts and after a short delay so do the ventricles.

Question 2

What effect does sympathetic and parasymthapetic fibres do to heart rate?

Answer 2

Sympathetic = increases HR
Parasympathetic = decreases HR

Question 3

How does the sympathetic nervous system act?

Answer 3

Sympathetic fibres release noradrenaline and adrenaline.
These act on (adrenergic receptors) B1 receptors on SA node

Question 4

What is the effect of sympathetic nervous system on HR (detailed)?

Answer 4

Increases slope of pacemaker potential
- increase ion flow through funny Na and Ca channels causing pacemaker cells to depolarise to threshold sooner and evoke AP
- Decreases cardiac interval and increases HR

Question 5

What nerve supplies parasympathetic supply to the heart?

Answer 5

Vagus nerves

Question 6

What neurotransmitter is release by vagus nerve and what does it act on?

Answer 6

Acetylcholine
Acts on muscarinic receptors on SA node

Question 7

What is the response of the heart to parasympathetic activation?

Answer 7

Hyperpolarises cells and decreases slope of pacemaker potential
- Take longer to reach threshold and evoke AP
- Increase cardiac intervals and decrease HR

Question 8

What is the effect of sympathetic nervous system on myocytes and how does it do this?

Answer 8

Increases contractility
- More release of calcium
- More cross bridges between actin and myosin
- Shorter &stronger contractions
- Calcium taken up quicker

Question 9

What is the effect of parasympathetic nervous system on contractility and why?

Answer 9

Little effect on contractility
- Vagus nerve innervates the SA nod but not ventricular myocytes

Question 10

What is preload?

Answer 10

How full the ventricle is before it starts contracting (i.e. the EVD)

Question 11

What affects preload?

Answer 11

The state of contraction of the venules and veins

Question 12

What is contractility?

Answer 12

How strong a contraction is produced for any given preload or afterload

Question 13

What affects contractility?

Answer 13

Sympathetic system

Question 14

What is afterload?

Answer 14

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

Question 15

What is afterload affected by?

Answer 15

The state of contraction of the arterioles

Question 16

How can veins and venules increases EDV?

Answer 16

Veins and venules are squeezed which pushes more blood back to the heart

Question 17

Describe Starling’s curve?

Answer 17

Energy of contraction is proportional to the initial length of the cardiac muscle
Tension is proportional to preload (length)

Question 18

Starlings law: what happens at peak tension?

Answer 18

Optimal number cross bridges forming between actin and myosin
Gives really strong muscle contraction

Question 19

Starlings law: what happens at longest muscle

Answer 19

Muscle at larger length so fewer cross bridges can form
Weaker contraction

Question 20

Starlings law: At smallest and least tension

Answer 20

Too much overlap and actin and myosin filaments are interfering with each other
Less cross bridges
Insufficient contraction

Question 21

What happens to SV when there’s a small EDV?

Answer 21

Vessels not being stretched
Weak contraction
Small stroke volume

Question 22

What happens to SV when there’s a large EDV?

Answer 22

Stronger contraction
Bigger stroke volume

Question 23

What effect does increasing venous return have on SV?

Answer 23

Increases EDV and stretches cardiac muscle more.
Increasing stroke volume.

Question 24

What effect does decreasing venous return have on SV?

Answer 24

Decreases EDV
Decreasing stroke volume

Question 25

What determines afterload and what is it dependent on?

Answer 25

The arterial pressure against which the blood is ejected - this in turn depends on the total peripheral resistance (TPR)

Question 26

What effect does increasing TPR have on SV?

Answer 26

Stroke volume will decrease
(more energy is “wasted” building up enough pressure to open the aortic valve)

Question 27

What stops the muscles contracting during systole?

Answer 27

Mitral valve
- Ventricle has to build up pressure to push the mitral valve closed
Aortic valve
- Aortic pressure affected by how much blood your trying to pump out and how easy it is to get it into the arterioles

Question 28

What happens to TPR if arterioles are constricted?

Answer 28

Increases:
- Aortic pressure will increase
- Ventricle will have to work harder to push open aortic valve
- Has less energy to eject blood
- Stroke volume decreases

Question 29

What does cardiac output equal?

Answer 29

HR x stroke volume

Question 30

What does CO determine?

Answer 30

How much blood and thus O2 is getting to tissues

Question 31

What happens to CO and SV if you increase HR and why?

Answer 31

CO increases
SV decreases

Increased HR = shorter cardiac intervals
- Shorter rapid filling phase
- Decreased EDV and preload
- Cardiac muscle will stretch less
- Decreased strength of contraction
- Stroke volume will fall

Question 32

What 4 things happen during exercise?

Answer 32

Increased HR
Increased contractility
Increased venous return
Decrease in total peripheral resistance

Question 33

How does exercise increase HR?

Answer 33

Decreases vagal tone
Increased sympathetic tone

Question 34

How does exercise increase contractility?

Answer 34

Increased sympathetic tone
Alters inotropic state and shortens systole

Question 35

How does exercise increase venous return?

Answer 35

Skeletal muscle pump
- Squishes veins/venules which pushes more blood back to the heart increasing EDV

Question 36

How does exercise increase TPR?

Answer 36

Arteriolar dilation in muscles, skin and heart
- Makes it easier for the heart to pump blood
Reduces afterload

Question 37

By how much can exercise mechanisms increase CO?

Answer 37

4 fold