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

(31 cards)

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
how does sympathetic stimulation increase contraction force?- 5 steps
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
why does epinephrine have a similar effect to norepinephrine
both bind to B1 receptors
27
PKA phosphorylates:
L type calcium channel Ryanodine receptor Phopsholamban troponin
28
how does parasympathetic stimulation decrease contraction force?
Ach binds to muscarinic M2 receptors activates Gi protein inhib effecgt on adenylate cyclase opposes effects of symp stim
29
effects on symp NS stim
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
effect of parasymp NS stim
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
If
funny current helps innitiate and regulate heart's rythmic contractions