Electrophysiology Flashcards

1
Q

Why does the CO starts falling, when we get above 150bpm?

A

Because the heart doesn’t have the time to fill up

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2
Q

What is the dominant pacemaker, initiating the first impulse?

A

The sinus (sinoatrial) node

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3
Q

Why does the AV node fires relatively slowly?

A

To prevent tachyarrhythmias

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4
Q

The AV node impulse goes to the ventricles via what?

A

The His-Purkinje system

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5
Q

What is the phase 0 of action potential of cells?

A

Phase 0 takes the cell from its negative polarization to its positive maximum

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6
Q

What are you doing when you’re hyperpolarizing the cell?

A

You make the cell more negative than it is at its resting phase

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7
Q

At resting phase, is there more K+ inside or outside the cell?

A

Inside the cell

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8
Q

At resting phase, is there more Na+ inside or outside the cell?

A

Outside

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9
Q

If cell was permeable to Na+, sodium would flow into the cell only to stop at which electrical charge?

A

+60mV

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10
Q

What happens at resting state phase of the cell membrane action potential?

A

Cell is only permeable to K+; K+ leaves the cell, leaving negative charge; electrical equilibrium potential balances at -85mV

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11
Q

What is phase 2 of the cell membrane action potential?

A

Calcium L-channels open; calcium enters and leaves positive charge, electrical equilibrium potential balances at +40mV

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12
Q

What is phase 0 of the cell action potential?

A

Sodium channels open; Na+ enters and leaves positive charge; electrical equilibrium potential balances at +60mV

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13
Q

What is phase 1 of the cell action potential?

A

Potassium continues to leave the cell, making the cell slightly more negative. Overall charge is still positive.

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14
Q

What is phase 3 of the cell action potential?

A

Delayed K+ channel: Potassium continues to leave the cell, making the cell more negative until it reaches resting phase.

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15
Q

Which phase of the cell action potential governs the action potential duration, or “refractoriness”?

A

Phase 3

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16
Q

What is special about the Phase 4 of the His-Purkinje cells?

A

The calcium channels are open, which creates a slight polarization until it reaches a threshold (at which point Phase 0 begins)

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17
Q

In fast channel action potential, refractoriness is determined by what?

A

APD (action potential duration)

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18
Q

In slow-channel action potential, refractoriness is determined by what?

A

Ca2+ channel recovery

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19
Q

Two examples of a slow channel cells?

A

SA & AV nodes

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20
Q

Example of a fast channel cell?

A

His-Purkinje cell

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21
Q

The ectopic beat characterized by no P-waves and a wide-shaped QRS complex is called what?

A

Premature ventricular contraction (PVC) also called Ventricular Tachycardia

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22
Q

What is called the ectopic beat with an early P wave?

A

Premature atrial contraction (PAC)

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23
Q

What are the two most common tachycardias (and give a clue to how to differentiate them)?

A

Atrial fibrillation

Paroxysmal atrial tachycardia (those start and stop abruptly)

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24
Q

Rate > 100 bpm
Arise elsewhere than in the sinus node
are signs of what?

A

Ectopic tachycardias

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25
Q

By what can a reduction of the slop of phase 4 during cell action potential duration be caused?

A

Reduction Na+ current in fast channel tissue

Reduction Ca2+ current in slow channel tissue

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26
Q

What is “early afterdepolarization” (EAD)?

A

When a cell becomes fully positive (depolarization) during Phase 2 or 3

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27
Q

What is “delayed afterdepolarization” (DAD)?

A

When a cell becomes fully positive (depolarization) during Phase 4, but before another action potential would normally occur via the normal conduction systems of the heart

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28
Q

EADs are caused (and favored) by what?

A

Excessive action potential prolongation allowing Ca2+ to depolarize the cell
Blocked K+ channels
Favored by slow heart rates

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29
Q

To which phase in the action potential does the T-wave corresponds?

A

Phase 3

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30
Q

In broad terms, how do you treat EAD?

A

You shorten action potential duration:
Stop any drugs blocking K+ channels
Normalize K+ concentration if low
Increase heart rate (temporary pacemaker)

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31
Q

Calcium released by the sarcoplasmic reticulum inside the cardiac cell cause what?

A

Contraction

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32
Q

The release of calcium by the sarcoplasmic reticulum is caused by what?

A

By the calcium entering the cell wall through Ca2+ channels

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33
Q

Reuptake of Ca2+ by the sarcoplasmic reticulum leads to what?

A

Relaxation

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34
Q

What is called the Ca2+ release channel on the sarcoplasmic reticulum?

A

Ryanodine receptor (RyR2)

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35
Q

What does DAD cause?

A

Reduce the sarcoplasmic reticulum Ca2+ loading

Blocks Na+ channels

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36
Q

PR interval goes from where to where on the ECG?

A

HA! It goes from P wave to Q!! NOT from P wave to R!

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37
Q

QT interval goes from where to where on the ECG?

A

From start of the QRS to end of T wave

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38
Q

Name two conditions that shortens the QT interval on the ECG

A

Hypercalcemia

Tachycardia

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39
Q

Name four conditions that lengthen the QT interval on the ECG

A

Hypocalcemia
Hypokalemia
Myocardial ischemia
Hypomagnesemia

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40
Q

Things that alter someone’s cardiac electrical axis?

A

Physical orientation of the heart
Ventricular hypertrophy
Infarction

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41
Q

What is the angle of right axis deviation?

A

90 to 180

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42
Q

What is the angle of left axis deviation?

A

-90 to -30

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43
Q

What is the angle of extreme axis deviation?

A

180 to -90

44
Q

What is the angle of normal axis?

A

-30 to 90

45
Q

What axis do you have if you have
Positive lead I
Positive lead 2

A

Normal axis

46
Q

What axis do you have if you have
Positive lead I
Negative lead 2
Negative aVF

A

Left axis deviation

47
Q

What axis do you have if you have
Negative lead I
Positive lead 2
Positive aVF

A

Right axis deviation

48
Q

What axis do you have if you have
Positive lead I
Negative aVF

A

Extreme axis deviation

49
Q

What does the P wave represent?

A

Depolarization of the right atrium followed by depolarization of the left atrium

50
Q

What are the ECG-lead and axis clues indicating a right ventricular hypertrophy?

A

Upward deflections of V1 and V2 leads

Right axis deviation

51
Q

What are the ECG-lead clues indicating a left ventricular hypertrophy?

A

R peak is higher than usual on aVL lead and lead I

52
Q

What may cause a bundle branch blocks (and what are those?)?

A

Right and left bundle branches are offshoots of the bundle of His on the interventricular septum, linking to the fibers of Purkinje.
Bundle branch blocks may be caused by ischemic or degenerative damage

53
Q

What is a sign of a right bundle branch block?

A

Bunny ears in the V1 to V3 leads in the QRS complex

54
Q

What is a sign of a left bundle branch block?

A

Abnormal QRS in leads I, aVL, V5 & V6

55
Q

Wide, deep and repeated pathological Q waves are signs of what?

A

Myocardial infarction

56
Q

Repeated wide, deep Q waves in lead V1 & V2 are signs of what?

A

(right) Anteroseptal infarct

57
Q

Repeated wide, deep Q waves in lead V2 & V4 are signs of what?

A

(apex) Anteroapical infarct

58
Q

Repeated wide, deep Q waves in lead V5, V6, aVL & lead I are signs of what?

A

(left) Anterolateral infarct

59
Q

Repeated wide, deep Q waves in lead I, II and aVF are signs of what?

A

Inferior infarct

60
Q

Tall R waves in leads V1 & V2 are signs of what?

A

Posterior infarct

61
Q

What is the coronary artery most often responsible for anteroseptal infarct?

A

Left anterior descending artery

also known as anterior interventricular branch of left coronary artery, or anterior descending branch

62
Q

What is the coronary artery most often responsible for anteroapical infarct?

A

Left anterior descending artery

also known as anterior interventricular branch of left coronary artery, or anterior descending branch

63
Q

What is the coronary artery most often responsible for anterolateral infarct?

A

Circumflex artery

64
Q

What is the coronary artery most often responsible for posterior infarct?

A

Right coronary artery

65
Q

What is the coronary artery most often responsible for inferior infarct?

A

Right coronary artery

66
Q

What is transient myocardial ischemia?

A

Momentarily lack of blood flow to the heart

67
Q

What are the ECG signs of transient myocardial ischemia?

A

T wave inversion

ST depression

68
Q

T wave inversion
ST depression
No Q waves
are signs of what?

A

Non-ST segment elevation myocardial ischemia

69
Q

What is non-ST segment elevation myocardial ischemia?

A

A clot is formed inside the heart, leading to an artery partial obstruction

70
Q

What is a ST segment elevation myocardial ischemia?

A

A clot is formed inside the heart, leading to an artery complete obstruction

71
Q

What is a syncope?

A

Fainting

72
Q

What is bradyarrhythmias?

A

<60bpm

73
Q

What is the most common form of bradyarrythmias?

A

Sick sinus syndrome

74
Q

Sinus node intermittently fails to fire
Usually cause syncope (not cardiac arrest)
Occurs generally in the elderly
what is the Dx?

A

Sick sinus syndrome

75
Q

What is first degree atrioventricular block?

A

A slowing in the atrioventricular conduction

76
Q

What is second-degree atrioventricular block of Mobitz Type 1 (also called Wenkebach block)?

A

Progressive PR interval lengthening until blocked by P-wave

Rarely progress in 3rd degree

77
Q
Blocked P-wave without lengthening of PR interval
Disease in the His-Purkinje system
QRS complex is long
Indication for a pacemaker
What is the Dx?
A

Second-degree atrioventricular block of Mobitz Type 2

78
Q

What is 3rd degree atrioventricular block and is a good predictor that it will occur?

A

No sinus impulse gets to the ventricles
Requires a pacemakers
Second-degree atrioventricular block of Mobitz Type 2 is a good predictor

79
Q

When an atrioventricular block occcurs, the His-Pirkunje system will rely on Escape Rhythms. What is the bpm of His-Purkinje escape rhythm?

A

30bpm

80
Q

When sinoatrial node fails, the atrioventricular system will rely on Escape Rhythms. What is the bpm of atrioventricular escape rhythm?

A

50bpm

81
Q

What is the treatment for acute bradyarrythmias?

A

Atropine to remove cholinergic tone slowing the sinoatrial and atrioventricular nodes
Isoproternol to stimulate Beta-adrenergic receptors and accelerate pacemakers

82
Q

What are the supraventricular pacemakers?

A

Sinoatrial node

Atrioventricular node

83
Q

What is the treatment for chronic bradyarrythmias?

A

Permanent pacemaker

84
Q

Substained reentry requires what?

A

It requires the circuit time to be greater than the longest refractory period

85
Q

Atrioventricular node reentry
Common among healthy people
What is the Dx?

A

Paroxysmal supraventricular tachycardias

86
Q

How do you stop atrioventricular reentry?

A

Block Ca2+ channel mediating atrioventricular conduction or
Intravenous adenosine or enhancing vagal tone by vasalva or carotid mssage.
This will hyperpolarize atrioventricular node by enhancing K+ current and the action potential will be further from threshold (Ca2+ current is unsufficient on its own to allow continued firing)

87
Q

What are the best methods to prevent atrioventricular node reentry?

A

Eliminate anatomical by remove AV nodal pathway

Block Ca2+ channels mediating AV node conduction

88
Q

Name a not-so effective treatment to prevent atrioventricular reentry

A

Beta-blockers suppressing adrenergic enhancement of Ca2+ current

89
Q

What is the atria firing for atrial fibrillation?

A

400-600bpm

90
Q

What is the most common cause of stroke in the elderly and why?

A

Atrial fibrillation: static blood pool in fibrillating left atrium will embolize

91
Q

What is the therapy for atrial fibrillation?

A

Reduce ventricular response rate
Restore sinus rhythm with drugs that slowly increase atrial refractory period or an electric shock that terminates reentry by depolarizing tissue

92
Q

Explain the risk prediction scheme

A
CHADS:
Congestive heart failure
Hypertension
Age > 65y
Diabetes
Prior stroke/transient ischemic attack/thromboembolism (2 points)
93
Q

What is the atria firing for atrial flutter?

A

240-300bpm

94
Q

What is the atrial flutter ECG pattern?

A

Dents-de-scie

95
Q

What is the most effective treatment for atrial flutter?

A

Ablation: it’s simpler because there’s only one macroreentrant circuit
This and oral anticoagulants

96
Q

What is the typical rate of ventricular tachycardia rhythm?

A

150-180bpm

97
Q

By what can ventricular tachycardia be caused?

A

Enhanced automaticity
Delayed afterdepolarization
Early afterdepolarization
Reentry

98
Q

What is the most usual region of the heart where we see ventricular tachycardia?

A

Ventricular region, of course, but the correct answer is the His-Purkinje system

99
Q

The patient suffered a mycardial infarction and has now an enhanced automaticity that caused ventricular tachycardia. What is the best treatment?

A

Drugs of class 1 (they block Na+ channels responsible for phase 0 activation in fast channel tissue)

100
Q

Ca2+ loading
Abnormal ryanodine receptor function (mutation)
are common in what?

A

Cardiac hypertrophy

101
Q

The patient suffers cardiac hypertrophy and has now a DAD that caused ventricular tachycardia. What is the best treatment?

A

Drugs of class 1 (they block Na+ channels responsible for phase 0 activation in fast channel tissue)

102
Q

The patient suffers from ventricular tachycardia and Long QT syndrome. What is the best treatment?

A

Long QT syndrome is associated with EAD, which is caused impaired K+ channel function.
Treatment for those are correcting K+ serum and increasing heart rate

103
Q

The patient has ventricular tachycardia and a myocardial scar. What is the cause of ventricular tachycardia and the treatment?

A

Cause is reentry

Treatment is drugs increasing refractory period

104
Q

What is the treatment for ventricular fibrillation (and prevention)?

A

(implanted) Electrical defibrillator

105
Q

Typical rate of ventricular fibrillation?

A

350-500bpm

106
Q

Is there pumping via the escape rhythms during ventricular fibrillation?

A

No. Ventricular fibrillation is lethal within minutes.