regulation of stroke volume and heart rate

Question 1

what is the function of pacemaker cells?

Answer 1

responsible for the autorhythmicity of the heart

Question 2

what controls the sympathetic action of the heart?

Answer 2

noradrenaline released from sympathetic nerves and adrenaline released from the adrenal medulla

Question 3

what does noradrenaline act on in the heart?

Answer 3

Beta1 receptors

Question 4

where are the beta1 adrenergic receptors in the heart?

Answer 4

the sinoatrial node

Question 5

what is the action of NA and adrenaline on the sinoatrial node?

Answer 5

it increases the slope of the pacemaker potential so the pacemaker cells reach their threshold and depolarise more rapidly, this causes an increase in heart rate

Question 6

which nerve supplies the heart with parasympathetic supply?

Answer 6

the vagus nerve

Question 7

what neurotransmitter does the vagus nerve release and what receptors does it act on?

Answer 7

ACh, acting on muscarinic receptors in the sinoatrial node

Question 8

what does ACh from the vagus nerve acting on muscarinic receptors do to the pacemaker cells?

Answer 8

hyperpolarises them and decreases the slope of the pacemaker cells so the cells reach their threshold slower and heart rate decreases

Question 9

what are the 4 things that can alter the strength of contraction of the heart?

Answer 9

• preload
• afterload
• neural
• pathological

Question 10

what does Starling’s law state?

Answer 10

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

Question 11

how does the tension that a muscle can exert change with starting length of that muscle fibre?

Answer 11

tension increases steadily. the increase then slows until the peak tension is reached. After this the tension decreases

Question 12

why does the tension muscle can produce change when length is changed?

Answer 12

because the over lap of the actin and myosin filaments changes so the number of possibe cross bridges changes

Question 13

in vivo, what affects preload?

Answer 13

end diastolic volume

Question 14

how does an increased venous return affect stroke volume?

Answer 14

it causes an increase in end diastolic volume which causes an increased preload and so an increased stroke volume

Question 15

how does a decrease in venous return affect stroke volume?

Answer 15

it causes an increase in end diastolic volume which causes a decrease in preload and so stroke volume increases

Question 16

what does preload allow , in terms of cardiac output from left and right sides of the heart?

Answer 16

it ensures self-regulation as the resting EDV is not at the maximum for the max stroke volume, nor is at its minimum. this means stroke volume can vary to match the stroke volume on the other side of the heart

Question 17

what is afterload?

Answer 17

the load against which the muscle tries to contract

Question 18

what affects the afterload of the heart?

Answer 18

the aortic pressure which in turn is determined by the total peripheral resisitance

Question 19

what happens to stroke volume as total peripheral resistance increases?

Answer 19

it would decrease, as aortic pressure would increase so the pressure required in left ventricle to exceed this pressure would also increase. Afterload has increases so this means more energy would be used to create this pressure, and less on ejecting blood

Question 20

what happens to stroke volume when veins and venules contract? why?

Answer 20

it increases, as blood is forced from the capacitance vessels into the heart, increases EDV, so increasing preload and stroke volume

Question 21

does vasoconstriction affect stroke volume?

Answer 21

no, just arteriole constriction

Question 22

describe how arteriole constriction affects stroke volume?

Answer 22

it causes it to decrease, as total peripheral resistance increases and so aortic pressure increases and afterload increases

Question 23

how does noradrenaline and adrenaline affect the myocytes of the heart?

Answer 23

they bind to beta1 receptors on the myocytes which causes an inotropic effect that gives a stonger but shorter contraction

Question 24

what is an inotropic effect?

Answer 24

a change in the force or speed of contraction of muscle

Question 25

what is the parasympathetic effect on the myocytes of the heart?

Answer 25

little effect

Question 26

how does hypercalcaemia affect stroke volume? why?

Answer 26

it increases the stroke volume as there is more calcium outside the myocytes so more enters the cell, causing more myosin binding sites to be uncovered

Question 27

how does hypercalcaemia affect the stroke volume vs EDV curve?

Answer 27

shifts it up and to the left

Question 28

how does hypocalcaemia affect the stroke volume vs EDV curve?

Answer 28

shifts it down and to the right

Question 29

how does hypocalcaemia affect stroke volume? why?

Answer 29

causes a decrease in stroke volume, as less calcium enters the myocytes when calcium channels in their membranes open

Question 30

how does ischaemia shift the stroke volume vs EDV curve?

Answer 30

down and to the right

Question 31

why does ischaemia cause the stroke volume vs EDV curve to shift down and to the right?

Answer 31

down:
for the same EDV as before, stroke volume decreases as there are less living myocytes to contract
to the right:
as the other side of the heart is still healthy and has a higher stroke volume. this means the EDV in the ischaemic side of the heart increases and stroke volume increases again by preload.

Question 32

how do barbituates affect the stroke volume vs EDV curve?

Answer 32

causes it to shift down and to the right, producing an anaesthetic effect

Question 33

how can cardiac output be increased by 4-6 times physiologically but only by 2 times by a pacemaker?

Answer 33

a pacemaker can only increases the HR which can only increase cardiac output by 2 times until it cuts into the rapid filling time. Physiologically heart rate can be increases by:

• increasing heart rate
• increasing contractility
• increasing venous return
• decreasing total peripheral resistance