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Cardiopulmonary pathology > Cardiac electrophysiology > Flashcards

Cardiac electrophysiology Flashcards

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?

A

Yes, they do

25
Q

What is the benefit of individual pacemaker myocardial cell stacked upon one another?

A

you can stimulate anywhere on the heart and the electrical impulse still distribute

26
Q

During exercise, HR increases due to what?

A

decreases in vagus tone & increase in cardiac plexus

27
Q

Catecholamine

What is its efect on HR?

Where is it released into?

A

group of hormones that released during physical or emotional sress

increase the HR

in blood circulation

28
Q
A
29
Q
A
30
Q
A
31
Q

Effect of Norepinephrine on HR?

When is it released?

A

increase the HR

during exercise & emotional stress

32
Q

What happen to the normal HR with an extended period of training?

Why?

Does the cardiac output decrease? Explain

A

normal HR decreases due to increased vagal tone

the cardiac output is the same due to increase stroke volume

33
Q

Where are the adrenal glands?

What do they do?

A

on top of the kidney

release catecholamines into blood stream in response to stress

34
Q
A
35
Q
A
36
Q

What chemical signals that control HR at rest?

What is the nerve that signal this release?

A

Acetylcholine (Ach)

vagus nerve

37
Q
A
38
Q
A
39
Q

positive chronotropic factor

Examples?

A

the chemical agents that increase the HR

Norepinephrine & epinephrine

40
Q
A
41
Q
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Q
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44
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Q
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47
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48
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A
49
Q

What type of family chemical are epinephrine & norepinephrine related to?

What is the effect of this family chemical?

A

catecholamine

increase HR

50
Q

Effect of Acetylcholine (Ach) on HR?

Is it positive or negative chronotropic

What graph does Ach effect illustrate?

A

decrease HR

negative chronotropic

graph C

51
Q

How does the SV and HR of athelete differ from normal person?

A

SV increase

HR decrease

52
Q

How does the norepinephrine & epinephrine increase the HR?

Explain in term of generating action potentials

Which graph represent these two chemical effects?

A

the local Ca2+ concentration increases -> less time of depolarization -> heart beat faster

Graph A

Cardiopulmonary pathology (12 decks)

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