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Flashcards in regulation of stroke volume and heart rate Deck (25)
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1
Q

what 2 things regulate heart rate

A

symp and parasymp NS

2
Q

how does the sympathetic NS regulate HR

A
symp nerves release NA
adrenal medulla releases adrenaline 
these act on beta 1 receptors on SAN 
increased slope of pacemaker potential 
increased HR
3
Q

how does the parasympathetic NS regulate HR

A

vagus nerve releases Ach which acts on muscarinic receptors on SAN
cells are hyperpolarised
decreased slope of pacemaker potential - cells start further from threshold and take longer to depolarise to threshold
HR decreases

4
Q

what nerve innervates SAN most heavily

A

vagus cranial nerve
at rest it is constantly working to slow down HR and keep it at 60-70bpm
HR is said to be under vagal restraint

5
Q

equation for CO

A

CO = HR X SV

6
Q

Effect of increasing HR with an electronic pacemaker

A

small increase in CO then SV decreases
shortened cardiac interval cuts into the rapid filling phase
reduced EDV, reduced preload, reduced SV

7
Q

physiological effects to offset reduced SV

A
  • HR increases via decreased vagal tone and increased symp tone
  • contractility increases via increased symp tone, alters inotropic state and shortens systole. Stronger but shorter contraction, increased SV
  • VR increases via venoconstriction and skeletal/resp pumps, maintaining preload
  • TPR falls (arteriolar dilation), reduced afterload
  • CO increases 4-6x
8
Q

physiological regulation of SV

A

preload
afterload
neural

9
Q

starling’s law

A

the energy of contraction is proportional to the initial length of the cardiac muscle fibre
stronger contraction in cardiac muscle = bigger SV

10
Q

define preload

A

Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.

11
Q

what is preload affected by

A

EDV
increased venous return = increased EDV and SV (vice versa)
this ensures self-regulation; matches SV of RV and LV so they work in series

12
Q

define afterload

A

the load against which the muscle tries to contract i.e. how easy it is to get the blood out through the arterioles - TPR

13
Q

define total peripheral resistance

A

TPR
how contracted/dilated all the arterioles are when added together
increased TPR = increased afterload, decreased SV

14
Q

what happens when TPR increases

A

aortic pressure will increase

ventricle has to work harder to push open the aortic valve and has less energy left to eject the blood

15
Q

what vessels set the preload

A

capacitance vessels set the preload

venoconstriction = increased preload, increased SV, helps the heart

16
Q

what vessels set the afterload

A

resistance vessels set the afterload
arteriolar constriction = harder for the blood to get out, increased pressure and afterload
heart has to work harder, reduced SV

17
Q

neural regulation of SV

A

symp and parasymp NS

18
Q

sympathetic NS and SV

A

symp nerves release NA
adrenal medulla releases adrenaline
these act on beta 1 receptors on myocytes
increased contractility - increased amount of calcium coming into the cell from outside, more released from internal stores
contraction is stronger but shorter as Ca is taken up quicker

19
Q

parasympathetic NS and SV

A

little effect on contraction
vagus nerve doesnt innervate ventricular muscle
muscarinic receptors present aren’t activated

20
Q

pathological regulation of SV

A

blood Ca levels
ischaemia
barbituates
Starling’s law

21
Q

hypercalcemia and SV

A

larger conc grad
more Ca enters when channels are open
stronger contraction
shifts Starling curve up and left

22
Q

hypocalcemia and SV

A

smaller conc grad
fewer X bridges form
less steep curve - shifts down and right

23
Q

ischaemia and SV

A
obstruction of blood supply to part of the heart 
can't contract properly 
smaller overall strength of contraction 
reduced SV 
curve shifts down and right
24
Q

barbiturates and SV

A

shifts curve down and right

reduced SV

25
Q

Starling’s law and the pumping ability of the heart

A

starling’s law lets the heart compensate for a reduced pumping ability by working around a larger EDV (less blood pumped out of the heart so EDV increases)
resting SV is achieved at a higher EDV
lower ejection fraction
reduced exercise capacity