Cardiac electrophysiology Flashcards

(52 cards)

1
Q

Can non-pacemaker myocardial cells turns into pacemaker cells?

A

Yes

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2
Q

what ion concentration influx dominates to generate action potentials in non-pacemaker myocardial cells?

A

Sodium influx

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3
Q

What type of cells is this actional potentials generated in?

How do you know?

A

non-pacemaker myocardiac cells

there is flat line of resting membrane potential after repolarization

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4
Q

What happen during phase 0 of action potentials?

A

the Na+ flows into the cell -> depolarization (cells become more positive inside) -> action potentials if pass threshold

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5
Q

How does the phase 4 - phase of achieving resting membrane potential different btw non-pacemaker & pacemaker cells?

A

the phase 4 of non-pacemaker cells has flat fline right of RMP after repolarization

the phase 4 of pacemaker cells has RMP shifting toward zero immediately after repolarizaton

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6
Q

How are the action potentials in pacemaker cells generated?

A

increase of Ca2+ & Na+ influx with increased membrane resistance to K+ permeability

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7
Q

How does the pacemaker cell transmit action potentials from one cell to another?

A

via intercalated disk

gap junction

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8
Q

What ion concetration influx dominate to generate action potentials of pacemaker cells?

A

the Ca2+ influx

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9
Q

Why does the pacemaker cell in SA node control the HR?

A

because it depolarize at faster rate (take less time to reach threshold)

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10
Q

What happen during phase 1 of action potentials?

A

the Na+ concentration is at the equilibrium -> Na+ channels inactivated

and the K+ channels start opening -> repolarization

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11
Q

intercalated disk

A

the joint at cells pack together and form low resitance bridge

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12
Q

gap junction

A

where the cell membrane fuse together and form the electrolytes channel

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13
Q

When does bradycardia happen?

What is the consequence?

What will happen to compensate this consequence?

A

when the SA node decreasing its fire rate

lower HR than normal

AV node will take over the control of ventricular beat

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14
Q

What happen during phase 2 of action potentials?

A

the plateau occur due to the activation of Ca2+ channels (Ca2+ influx) & the close of some K+ channels

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15
Q

inotropic factors

Two type of this factor

A

the chemical reagents that influence the force contraction of the heart

postive and negative

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16
Q

What happen during phase 3 of action potentials? and phase 4?

A

K+ channels open again while Ca2+ closes

the K+ concentration reach equilibrium -> achieve resting membrane potential

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17
Q

By what two systems that the heart rate is regulated?

A

autonomic system

endocrine system

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18
Q

What does the autonomic system consist of?

A

parasympathetic nervous system

sympathetic nervous system

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19
Q

What does the myocardial action potential conductivity velocities depend on?

A

length constant, which is the function of myocardial cell diameter

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20
Q

What nerve carry the electrical signals that decrease the HR?

What part of nervous system is it?

A

vagus nerve

parasympathetic NS

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21
Q

What chemical subtance that decrease the HR?

What is the mechanism of it?

A

Achetylcholine (Ach)

Ach increases the K+ conductance -> hyperpolarization longer

22
Q

What nerve is activated during exercise or emotional stress to increase HR?

A

cardiac plexus

23
Q

chronotropic factor

A

the chemical agents that influence the heart rate

24
Q

Does the parasympathetic NS & sympathetic NS work together at same time to influence HR?

25
What is the benefit of individual pacemaker myocardial cell stacked upon one another?
you can stimulate anywhere on the heart and the electrical impulse still distribute
26
During exercise, HR increases due to what?
decreases in vagus tone & increase in cardiac plexus
27
Catecholamine What is its efect on HR? Where is it released into?
group of hormones that released during physical or emotional sress increase the HR in blood circulation
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31
Effect of Norepinephrine on HR? When is it released?
increase the HR during exercise & emotional stress
32
What happen to the normal HR with an extended period of training? Why? Does the cardiac output decrease? Explain
normal HR decreases due to increased vagal tone the cardiac output is the same due to increase stroke volume
33
Where are the adrenal glands? What do they do?
on top of the kidney release catecholamines into blood stream in response to stress
34
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36
What chemical signals that control HR at rest? What is the nerve that signal this release?
Acetylcholine (Ach) vagus nerve
37
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39
positive chronotropic factor Examples?
the chemical agents that increase the HR Norepinephrine & epinephrine
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49
What type of family chemical are epinephrine & norepinephrine related to? What is the effect of this family chemical?
catecholamine increase HR
50
Effect of Acetylcholine (Ach) on HR? Is it positive or negative chronotropic What graph does Ach effect illustrate?
decrease HR negative chronotropic graph C
51
How does the SV and HR of athelete differ from normal person?
SV increase HR decrease
52
How does the norepinephrine & epinephrine increase the HR? Explain in term of generating action potentials Which graph represent these two chemical effects?
the local Ca2+ concentration increases -\> less time of depolarization -\> heart beat faster Graph A