S1W2 L2- Circulatory Physiology- Regulation of Cardiac Function-Ruth Norman Flashcards

1
Q

cardiac output=

A

heart rate x stroke vol

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2
Q

stroke volume=

A

end diastolic vol- end systolic vol

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3
Q

end diastolic volume:

A

volume of blood in ventricle before contraction

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4
Q

end systolic vol:

A

vol of blood in ventricle after contraction

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5
Q

ejection fraction:

A

SV/EDV

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6
Q

what is a normal ejection fraction?

A

55-75%

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7
Q

what can the ejection fraction reach during exercise

A

90%

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8
Q

4 factors that effect HR

A

autonomic innervation
hormones
fitness levels
age

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9
Q

7 factors affecting SV

A

heart size
gender
fitness
contractility
contraction duration
preload (EDV)
afterload (resistance)

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10
Q

what is preload

A

degree of filling of a ventricle and how much ventricular muscle is being stretched by during filling

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11
Q

what is afterload

A

pressure ventricles need to overcome in arteries to eject blood during systole

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12
Q

contractility

A

how well the ventricles contract

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13
Q

what does EDV determine

A

preload (preload directly affects amount of stretch experienced by ventricular muscle fibres at the end of diastole)

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14
Q

what is EDV determined by

A

filling pressure (from venous return)
filling time

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15
Q

relationship between filling pressure and edv

A

higher filling pressure (due to high venous return and atrial pressure) = higher edv

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16
Q

relationship between filling time and HR

A

filling time: time ventricles are in systole and are filling with blood
HR increases, filling time decreases
can lead to lower edv if heart doesnt compensate by increasing

17
Q

what is the effect on SV and CO when preload increases

A

both increase

18
Q

what is the frank starling law

A

as degree of stretch increases, force of contraction increases

19
Q

why does the frank starling mechanism help the heart

A

maintains efficient circulation levels by helping heart adjust its output to accommodate varying levels of blood return

20
Q

what is the afterload on the left ventricle

A

diastolic aortic pressure

21
Q

4 consequences of afterload increasing

A

less blood ejected from ventircle,
increased ESV,
SV and CO decrease,
heart muscle hypertrophies (left v wall)

22
Q

what is a positive ionotropic influence

A

factor which increases contractility of heart muscle therefore enhances strength and force of contraction
leads to increased SV

23
Q

how are sympathetic fibres an example of an extrinsic factor regulating CO

A

terminate throughout the heart, outside of the heard muscle

24
Q

what do sympathetic fibres release

A

noradrenaline

25
Q

how does sympathetic stimulation increase contraction force?- 5 steps

A

1.) norepinepherine binds to B1 receptoes in membrane
2.) alpha subunit of Gs protein activates adenylate cyclase
3.) increases cAMP production from ATP
4.) cAMP activates PKA
5.) PKA phosphorylates protein targets to affect functions

26
Q

why does epinephrine have a similar effect to norepinephrine

A

both bind to B1 receptors

27
Q

PKA phosphorylates:

A

L type calcium channel
Ryanodine receptor
Phopsholamban
troponin

28
Q

how does parasympathetic stimulation decrease contraction force?

A

Ach binds to muscarinic M2 receptors
activates Gi protein
inhib effecgt on adenylate cyclase
opposes effects of symp stim

29
Q

effects on symp NS stim

A

rise in cAMP
increases If, pacemaker potential rate accelerated
threshold reached faster
reduction to k permeability
max diastolic potnetial becomes more +
threshold easier to reach
increased L-type Ca 2+ current
upstroke faster
more APs per unit time
increased speed of contraction

30
Q

effect of parasymp NS stim

A

Ach decreases If by reducing cAMP
threshold potential takes longer to reach
increase K permeability of SA node cells, hyperpolarises MDP
fewer APs per unit time

31
Q

If

A

funny current
helps innitiate and regulate heart’s rythmic contractions