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Cardiovascular System > Arrhythmias-Katz > Flashcards

Arrhythmias-Katz Flashcards

1
Q

Components of the cardiac conduction system

A

SA node-atrial pathways-AV node-AV junction-Bundle of His-Left and Right Bundle-Purkinje fibers

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2
Q

How do medications that affect Na or K affect atrial, ventricular and nodal cells?

A

Don’t affect nodal cells depolarization. They are affected by calcium.

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3
Q

Which cardiac layer has the longest action potential?

A

Myocardial region is longer than epi or endocardium.

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4
Q

How is transverse conduction different from longitudinal conductino?

A

Transverse is higher axial resistance, slower conduction velocity, higher safety factor, shorter action potential duration.

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5
Q

How is transverse conduction related to left bundle branch block?

A

QRS is wider because bundle is missing and conductance is transverse through the right ventricle, not through the normal path.

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6
Q

How does anti-arrhythmia medication affect the myocardial refractory period?

A

Prolongs the absolute refractory period or reduced.

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7
Q

Definition of automaticity

A

Ability to generate an action potential. Mostly the SA node.

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8
Q

What phase of the action potential does the ANS affect?

A

Phase 4 (refractory period)

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9
Q

What are the two mechanisms of arrhthmigenesis?

A
  1. Abnormal impulse generation, 2. Abnormal impulse conduction (reentry)
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10
Q

What are the forms of abnormal impulse generation?

A

Automaticity (enhanced or abnormal), triggered (EADs and DADs)

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11
Q

What are the forms of abnormal impulse conduction?

A

Reentry (anatomic, functional, anisotropy)

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12
Q

What kind of impulse formation is Possibly accelerated ventricular rhythms after MI?

A

Abnormal automaticity

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13
Q

What kind of impulse formation is idiopathic and acquired long QT syndromes?

A

Early after depolarizations (triggered activity) or can be acquired, caused by antihistamines together with arithromycin

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14
Q

What kind of impuse formation is digitalis-induced arrhythmia?

A

Delayed after depolarization/triggered activity

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15
Q

What is triggered activity impulse formation?

A

Rare generation of AP at times and at parts that usually don’t generate an AP.

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16
Q

What phase in the action potential has a problem in Delayed After Depolarization?

A

Phase 4 in not pacemaker cells. Na inside the cell generating an action potential.

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17
Q

What phase in the action potential has a problem in Early After Depolarization?

A

Phase 3 due to failure of potassium channels may lead to overactivation of sodium channels, accumulation of calcium. May lead to an inadequate but spreadable AP.

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18
Q

How does digoxin cause depolarization of the cell?

A

The overload of the sarcoplasmic reticulum may cause spontaneous Ca2+ release during repolarization, causing the released Ca2+ to exit the cell through the 3Na+/Ca2+-exchanger which results in a net depolarizing current.

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19
Q

What is Torsades de Pointes?

A

Twisting or changing of axis, can be a lethal arrhythmia, can generate into vfib, dangerous. Can be caused by EAD and long QT syndrome from depolarization during the relative refractory period.

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20
Q

What type of block are SA, AV, bundle branch, Purkinje-muscle?

A

Bidirection or unidirectional without reentry

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21
Q

What type of block are reciprocating tachycardia in WPW syndrome, AV nodal reentry, VT due to bundle branch reentry?

A

Unidirectinoal block with reentry

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22
Q

What is the most frequent type of arrhythmia?

A

Reentry

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23
Q

How do refractoriness and conduction relate to reentry disorder?

A

Increased refractoriness and decreased conduction in an adjacent electrical pathways.

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24
Q

What is the trigger needed for reentry?

A

Extrasystole, early beat enters junction of two pathways, if too early will get into fast pathway during refractory period and won’t pass but will trigger impulse in slow pathway.

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25
Q

How does the impulse reenter the fast pathway?

A

Passes through slow pathway and by the time it circles around to fast pathway it has repolarizaed and impulse can go backwards.

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26
Q

Which cardiac layer has the longest action potential?

A

Myocardial region is longer than epi or endocardium.

How well did you know this?
1
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2
3
4
5
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27
Q

How is transverse conduction different from longitudinal conductino?

A

Transverse is higher axial resistance, slower conduction velocity, higher safety factor, shorter action potential duration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is transverse conduction related to left bundle branch block?

A

QRS is wider because bundle is missing and conductance is transverse through the right ventricle, not through the normal path.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does anti-arrhythmia medication affect the myocardial refractory period?

A

Prolongs the absolute refractory period or reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Definition of automaticity

A

Ability to generate an action potential. Mostly the SA node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What phase of the action potential does the ANS affect?

A

Phase 4 (refractory period)

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32
Q

What are the two mechanisms of arrhthmigenesis?

A
  1. Abnormal impulse generation, 2. Abnormal impulse conduction (reentry)
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33
Q

What are the forms of abnormal impulse generation?

A

Automaticity (enhanced or abnormal), triggered (EADs and DADs)

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34
Q

What are the forms of abnormal impulse conduction?

A

Reentry (anatomic, functional, anisotropy)

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35
Q

What kind of impulse formation is Possibly accelerated ventricular rhythms after MI?

A

Abnormal automaticity

How well did you know this?
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3
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5
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36
Q

What kind of impulse formation is idiopathic and acquired long QT syndromes?

A

Early after depolarizations (triggered activity) or can be acquired, caused by antihistamines together with arithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What kind of impuse formation is digitalis-induced arrhythmia?

A

Delayed after depolarization/triggered activity

How well did you know this?
1
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2
3
4
5
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38
Q

What is triggered activity impulse formation?

A

Rare generation of AP at times and at parts that usually don’t generate an AP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What phase in the action potential has a problem in Delayed After Depolarization?

A

Phase 4 in not pacemaker cells. Na inside the cell generating an action potential.

How well did you know this?
1
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2
3
4
5
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40
Q

What phase in the action potential has a problem in Early After Depolarization?

A

Phase 3 due to failure of potassium channels may lead to overactivation of sodium channels, accumulation of calcium. May lead to an inadequate but spreadable AP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does digoxin cause depolarization of the cell?

A

The overload of the sarcoplasmic reticulum may cause spontaneous Ca2+ release during repolarization, causing the released Ca2+ to exit the cell through the 3Na+/Ca2+-exchanger which results in a net depolarizing current.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which cardiac layer has the longest action potential?

A

Myocardial region is longer than epi or endocardium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is transverse conduction different from longitudinal conductino?

A

Transverse is higher axial resistance, slower conduction velocity, higher safety factor, shorter action potential duration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is transverse conduction related to left bundle branch block?

A

QRS is wider because bundle is missing and conductance is transverse through the right ventricle, not through the normal path.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does anti-arrhythmia medication affect the myocardial refractory period?

A

Prolongs the absolute refractory period or reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Definition of automaticity

A

Ability to generate an action potential. Mostly the SA node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What phase of the action potential does the ANS affect?

A

Phase 4 (refractory period)

How well did you know this?
1
Not at all
2
3
4
5
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48
Q

What are the two mechanisms of arrhthmigenesis?

A
  1. Abnormal impulse generation, 2. Abnormal impulse conduction (reentry)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the forms of abnormal impulse generation?

A

Automaticity (enhanced or abnormal), triggered (EADs and DADs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the forms of abnormal impulse conduction?

A

Reentry (anatomic, functional, anisotropy)

How well did you know this?
1
Not at all
2
3
4
5
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51
Q

What kind of impulse formation is Possibly accelerated ventricular rhythms after MI?

A

Abnormal automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What kind of impulse formation is idiopathic and acquired long QT syndromes?

A

Early after depolarizations (triggered activity) or can be acquired, caused by antihistamines together with arithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is Torsades de Pointes?

A

Twisting or changing of axis, can be a lethal arrhythmia, can generate into vfib, dangerous. Can be caused by EAD and long QT syndrome from depolarization during the relative refractory period.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What kind of impuse formation is digitalis-induced arrhythmia?

A

Delayed after depolarization/triggered activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What type of block are SA, AV, bundle branch, Purkinje-muscle?

A

Bidirection or unidirectional without reentry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is triggered activity impulse formation?

A

Rare generation of AP at times and at parts that usually don’t generate an AP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What type of block are reciprocating tachycardia in WPW syndrome, AV nodal reentry, VT due to bundle branch reentry?

A

Unidirectinoal block with reentry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What phase in the action potential has a problem in Delayed After Depolarization?

A

Phase 4 in not pacemaker cells. Na inside the cell generating an action potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the most frequent type of arrhythmia?

A

Reentry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What phase in the action potential has a problem in Early After Depolarization?

A

Phase 3 due to failure of potassium channels may lead to overactivation of sodium channels, accumulation of calcium. May lead to an inadequate but spreadable AP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How do refractoriness and conduction relate to reentry disorder?

A

Increased refractoriness and decreased conduction in an adjacent electrical pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does digoxin cause depolarization of the cell?

A

The overload of the sarcoplasmic reticulum may cause spontaneous Ca2+ release during repolarization, causing the released Ca2+ to exit the cell through the 3Na+/Ca2+-exchanger which results in a net depolarizing current.

61
Q

What is the trigger needed for reentry?

A

Extrasystole, early beat enters junction of two pathways, if too early will get into fast pathway during refractory period and won’t pass but will trigger impulse in slow pathway.

61
Q

What is Torsades de Pointes?

A

Twisting or changing of axis, can be a lethal arrhythmia, can generate into vfib, dangerous. Can be caused by EAD and long QT syndrome from depolarization during the relative refractory period.

62
Q

How does the impulse reenter the fast pathway?

A

Passes through slow pathway and by the time it circles around to fast pathway it has repolarizaed and impulse can go backwards.

62
Q

What type of block are SA, AV, bundle branch, Purkinje-muscle?

A

Bidirection or unidirectional without reentry

63
Q

What type of block are reciprocating tachycardia in WPW syndrome, AV nodal reentry, VT due to bundle branch reentry?

A

Unidirectinoal block with reentry

64
Q

What is the most frequent type of arrhythmia?

A

Reentry

65
Q

How do refractoriness and conduction relate to reentry disorder?

A

Increased refractoriness and decreased conduction in an adjacent electrical pathways.

66
Q

What is the trigger needed for reentry?

A

Extrasystole, early beat enters junction of two pathways, if too early will get into fast pathway during refractory period and won’t pass but will trigger impulse in slow pathway.

67
Q

How does the impulse reenter the fast pathway?

A

Passes through slow pathway and by the time it circles around to fast pathway it has repolarizaed and impulse can go backwards.

68
Q

Which cardiac layer has the longest action potential?

A

Myocardial region is longer than epi or endocardium.

69
Q

How is transverse conduction different from longitudinal conductino?

A

Transverse is higher axial resistance, slower conduction velocity, higher safety factor, shorter action potential duration.

70
Q

How is transverse conduction related to left bundle branch block?

A

QRS is wider because bundle is missing and conductance is transverse through the right ventricle, not through the normal path.

71
Q

How does anti-arrhythmia medication affect the myocardial refractory period?

A

Prolongs the absolute refractory period or reduced.

72
Q

Definition of automaticity

A

Ability to generate an action potential. Mostly the SA node.

73
Q

What phase of the action potential does the ANS affect?

A

Phase 4 (refractory period)

74
Q

What are the two mechanisms of arrhthmigenesis?

A
  1. Abnormal impulse generation, 2. Abnormal impulse conduction (reentry)
75
Q

What are the forms of abnormal impulse generation?

A

Automaticity (enhanced or abnormal), triggered (EADs and DADs)

76
Q

What are the forms of abnormal impulse conduction?

A

Reentry (anatomic, functional, anisotropy)

77
Q

What kind of impulse formation is Possibly accelerated ventricular rhythms after MI?

A

Abnormal automaticity

78
Q

What kind of impulse formation is idiopathic and acquired long QT syndromes?

A

Early after depolarizations (triggered activity) or can be acquired, caused by antihistamines together with arithromycin

79
Q

What kind of impuse formation is digitalis-induced arrhythmia?

A

Delayed after depolarization/triggered activity

80
Q

What is triggered activity impulse formation?

A

Rare generation of AP at times and at parts that usually don’t generate an AP.

81
Q

What phase in the action potential has a problem in Delayed After Depolarization?

A

Phase 4 in not pacemaker cells. Na inside the cell generating an action potential.

82
Q

What phase in the action potential has a problem in Early After Depolarization?

A

Phase 3 due to failure of potassium channels may lead to overactivation of sodium channels, accumulation of calcium. May lead to an inadequate but spreadable AP.

83
Q

How does digoxin cause depolarization of the cell?

A

The overload of the sarcoplasmic reticulum may cause spontaneous Ca2+ release during repolarization, causing the released Ca2+ to exit the cell through the 3Na+/Ca2+-exchanger which results in a net depolarizing current.

84
Q

What is Torsades de Pointes?

A

Twisting or changing of axis, can be a lethal arrhythmia, can generate into vfib, dangerous. Can be caused by EAD and long QT syndrome from depolarization during the relative refractory period.

85
Q

What type of block are SA, AV, bundle branch, Purkinje-muscle?

A

Bidirection or unidirectional without reentry

86
Q

What type of block are reciprocating tachycardia in WPW syndrome, AV nodal reentry, VT due to bundle branch reentry?

A

Unidirectinoal block with reentry

87
Q

What is the most frequent type of arrhythmia?

A

Reentry

88
Q

How do refractoriness and conduction relate to reentry disorder?

A

Increased refractoriness and decreased conduction in an adjacent electrical pathways.

89
Q

What is the trigger needed for reentry?

A

Extrasystole, early beat enters junction of two pathways, if too early will get into fast pathway during refractory period and won’t pass but will trigger impulse in slow pathway.

90
Q

How does the impulse reenter the fast pathway?

A

Passes through slow pathway and by the time it circles around to fast pathway it has repolarizaed and impulse can go backwards.

91
Q

Which cardiac layer has the longest action potential?

A

Myocardial region is longer than epi or endocardium.

92
Q

How is transverse conduction different from longitudinal conductino?

A

Transverse is higher axial resistance, slower conduction velocity, higher safety factor, shorter action potential duration.

93
Q

How is transverse conduction related to left bundle branch block?

A

QRS is wider because bundle is missing and conductance is transverse through the right ventricle, not through the normal path.

94
Q

How does anti-arrhythmia medication affect the myocardial refractory period?

A

Prolongs the absolute refractory period or reduced.

95
Q

Definition of automaticity

A

Ability to generate an action potential. Mostly the SA node.

96
Q

What phase of the action potential does the ANS affect?

A

Phase 4 (refractory period)

97
Q

What are the two mechanisms of arrhthmigenesis?

A
  1. Abnormal impulse generation, 2. Abnormal impulse conduction (reentry)
98
Q

What are the forms of abnormal impulse generation?

A

Automaticity (enhanced or abnormal), triggered (EADs and DADs)

99
Q

What are the forms of abnormal impulse conduction?

A

Reentry (anatomic, functional, anisotropy)

100
Q

What kind of impulse formation is Possibly accelerated ventricular rhythms after MI?

A

Abnormal automaticity

101
Q

What kind of impulse formation is idiopathic and acquired long QT syndromes?

A

Early after depolarizations (triggered activity) or can be acquired, caused by antihistamines together with arithromycin

102
Q

What kind of impuse formation is digitalis-induced arrhythmia?

A

Delayed after depolarization/triggered activity

103
Q

What is triggered activity impulse formation?

A

Rare generation of AP at times and at parts that usually don’t generate an AP.

104
Q

What phase in the action potential has a problem in Delayed After Depolarization?

A

Phase 4 in not pacemaker cells. Na inside the cell generating an action potential.

105
Q

What phase in the action potential has a problem in Early After Depolarization?

A

Phase 3 due to failure of potassium channels may lead to overactivation of sodium channels, accumulation of calcium. May lead to an inadequate but spreadable AP.

106
Q

How does digoxin cause depolarization of the cell?

A

The overload of the sarcoplasmic reticulum may cause spontaneous Ca2+ release during repolarization, causing the released Ca2+ to exit the cell through the 3Na+/Ca2+-exchanger which results in a net depolarizing current.

107
Q

What is Torsades de Pointes?

A

Twisting or changing of axis, can be a lethal arrhythmia, can generate into vfib, dangerous. Can be caused by EAD and long QT syndrome from depolarization during the relative refractory period.

108
Q

What type of block are SA, AV, bundle branch, Purkinje-muscle?

A

Bidirection or unidirectional without reentry

109
Q

What type of block are reciprocating tachycardia in WPW syndrome, AV nodal reentry, VT due to bundle branch reentry?

A

Unidirectinoal block with reentry

110
Q

What is the most frequent type of arrhythmia?

A

Reentry

111
Q

How do refractoriness and conduction relate to reentry disorder?

A

Increased refractoriness and decreased conduction in an adjacent electrical pathways.

112
Q

What is the trigger needed for reentry?

A

Extrasystole, early beat enters junction of two pathways, if too early will get into fast pathway during refractory period and won’t pass but will trigger impulse in slow pathway.

113
Q

How does the impulse reenter the fast pathway?

A

Passes through slow pathway and by the time it circles around to fast pathway it has repolarizaed and impulse can go backwards.

114
Q

How does AV nodal reentry affect arrhythmia?

A

Doesn’t really cause arrhythmia because both the slow and the fast conduction are close to each other and don’t cause that much problem.

115
Q

What is Wolff-Parkinson-White syndrome?

A

Congenital Reentry. Accessory pathway on the anterior wall-Bundle of Kent. Normal conduction acts as the slow pathway and accessory pathway acts as the fast pathway (because there is no AV delay) that gets reentered. Delta waves.

116
Q

What is the most common type of arrhythmia?

A

Atrial fibrillation

117
Q

How can ventricular tachycardia be caused by reentry?

A

In scarring, normal tissue acts as fast pathway and scar tissue is the slow pathway.

118
Q

What is Brugada syndrome?

A

Genetic disease caused by defective cardiac sodium channels causing abnormal EKG and increased risk of sudden death. ST elevation in V1, V2 and sometimes V3. Can be caused by reentry between LV and RV.

119
Q

What is the definition of cardiac arrest?

A

No electrical signal. Can be sinus, ventricular or both. Total arrest is a straight line.

120
Q

What is the rate of flutter?

A

250-350

121
Q

What is the rate of paroxysmal tachycardia?

A

150-250

122
Q

What is the rate of fibrillation?

A

350-450

123
Q

What are the types of arrhythmias in WPW?

A

Orthodromic (premature beat through normal and returns through accessory pathway), antidromic (down through AP and up through AV node), AFib

124
Q

What is the biggest sign of non-sinus tachycardia origin?

A

Inverted or absent P wave

125
Q

What leads are the best to show a P wave?

A

II, III, AVF and V1

126
Q

What is the carotid massage used to determine?

A

Atrial or ventricular (will stop) origin of arrhythmia by vagal tonal control.

127
Q

What are the AV node dependent arrhythmias?

A

AV node reentry, SVT

128
Q

What are the AV node independent arrhythmias?

A

Atrial tachycardia, atrial flutter, atrial fibrillation

129
Q

What medications are used to treat the AV node?

A

Calcium channel blocker, adenosine, digoxin, beta blockers, amiodarone

130
Q

Definition of nonsustained ventricular tachycardia/arrhythmia

A

Ventricular origin, over 120bpm, more than 3 in a row, lasting less that 30 seconds, without hemodynamic collapse.

131
Q

What is a normal length for the QT interval?

A

0.4s

132
Q

What can long QT interval indicate?

A

Early after depolarization,

133
Q

At what time of day are cardiac incidents more common?

A

In the morning because of a surge of catecholamines and cortisol.

134
Q

What is the normal length of a QRS interval?

A

0.06-0.1s

135
Q

What are the possible pathologies involving a wide QRS?

A

PVC or VTach, RBBB, LBBB, left fascicular hemiblock, hyperkalemia

136
Q

What are the possible pathologies involving a narrow QRS?

A

SVT, idiojunctional rhythm, premature junctional complex

137
Q

Pharmacologic treatment of bradyarrhythmias

A

Dopamine, atropine, isoproternol, adrenaline

138
Q

What is the best predictor pathologically of sudden cardiac arrest?

A

Depression of left ventricular ejection fraction (

139
Q

What is the biggest cause of fatal arrhythmias?

A

Coronary artery disease

140
Q

What is the most common cause of sudden cardiac death within cardiac pathology?

A

Arrhythmias. Otherwise, pulmonary emboli.

141
Q

What’s the most common arrhythmia in sudden cardiac arrest?

A

Ventricular tachycardia

142
Q

What is the only condition which improves survivability during VFib?

A

Previous resuscitation from VFib during the acute phase of STeMI (during the first 24-48h). Sometimes don’t need defibrillation, only cath lab.

143
Q

What treatment is given if the ICD gives shocks often?

A

Amiodarone, otherwise Maze

144
Q

What is the treatment for SVT in young patient?

A

Maze ablation

145
Q

What is the acute treatment for SVT?

A

Carotid massage (vagal maneuver), adenosine, verapamil,

146
Q

What is the treatment for symptomatic bradycardia, third degree or second degree block?

A

Pacemaker

147
Q

What is the appearance of the QRS on the EKG in RV pacemaker?

A

Looks wide, if at apex, looks like LBBB

148
Q

What is the effect of biventricular pacing?

A

Narrow QRS, better patient well-being. Need anticoagulation for LV unless epicardium.

149
Q

What is rate responsive pacing?

A

Senses resistance through the lungs to get oxygen demand and when higher paces faster to provide more CO.

Cardiovascular System (28 decks)

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