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Pharmacology > Antiarrythmics > Flashcards

Antiarrythmics Flashcards

1
Q

What types of people is arrhythmia a frequent problem in?

A

Patients treated with digitalis (heart failure), anesthetized patients and patients with MI

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2
Q

What is the sinoatrial (SA) node?

A

The main pacemaker and initiator of the heart, capable of spontaneous depolarization.
60-160 bpm (the rate can be changed by nerves innervating the heart)

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3
Q

What are the conduction fibres of the heart?

A

AV node, bundle of His and Purkinje fibres

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4
Q

What makes a healthy myocardium?

A

Atria, ventricles that are capable of robust excitation-contraction coupling.

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5
Q

What are required for normal cardiac excitation?

A

Pacemaker, conduction fibres and myocardium

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6
Q

What is an arrythmia?

A

Any rhythm that is not a normal sinus rhythm with normal AV conduction.
Can be irregular, too fast (tachycardia) or too slow (bradycardia).

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7
Q

What is the atrioventricular (AV) node?

A

The only electrical connection between the atria and ventricles. Delays conduction of action potential by 0.1 sec.
40-60 bpm
Rate can be changed by nerves innervating the heart.

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8
Q

Why is there a delay in action potential conduction?

A

Allows the atria to contract and ventricles to fill.

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9
Q

What do the conduction fibres do?

A

Excite the ventricular mass as near simultaneously as possible
Purkinje fibres act at 20-40 bpm (can be overridden)

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10
Q

What is the pathway for electrical impulses of the heart?

A

SA node impulse, conduction to atria, AV node, bundle of His-Purkinje fibres to ventricular myocardium to cause a contraction.

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11
Q

What are the different waves of an EKG and what are they from?

A

P wave for atrial depolarization.
QRS complex for ventricular depolarization.
T wave for ventricular repolarization.

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12
Q

What are the different intervals of an EKG and what are they from?

A

PR is the conduction time of atria and ventricles.
QRS is the time for all ventricular cells to be activated.
QT is the duration of ventricular action potential.

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13
Q

What are some class 1 antiarrhythmic drugs and what do they block?

A

Procainamide, lidocaine, flecanide

Block Na channels

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14
Q

What are some class 2 antiarrhythmic drugs and what do they block?

A

Propanolol, metoprolol, esmolol (very short duration of action)
Block beta-adrenergic receptors.

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15
Q

What are some class 3 antiarrhythmic drugs and what do they block?

A

Amiodarone, sotalol

Block K channels in phase 3, increasing QT interval (prolonging AP duration)

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16
Q

What are some class 4 antiarrhythmic drugs and what do they block?

A

Verapamil

Block Ca channels

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17
Q

What are some class 5 antiarrhythmic drugs and what do they do?

A

Magnesium, adenosine, digoxin

Use other mechanisms

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18
Q

What are the differences in ion concentrations like in a cell?

A

Na, Cl and Ca are higher extracellularly.
K is higher intracellularly (large movement out)
Negative intracellularly, positive extracellularly

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19
Q

What is the ion pump of the cell pumping?

A

2 K in and 3 Na out

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20
Q

What are the phases of the electrical potential of the non-pacemaker (fast) cells?

A 
Phase 0: Na inward
Phase 1: Cl inward
Phase 2: Ca inward (K outward) plateau
Phase 3: K outward (due to hERG protein)
Phase 4: Funny current-pacemaker (K outward) Slow depolarization
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21
Q

What is phase 0 for fast cells?

A

Depolarization (sharp spike)
Lots of voltage gated Na channels that are easily opened (“active”) due to low threshold potential.
The Na channels quickly become “inactive” ending depolarization.

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22
Q

What is phase 4 for fast cells?

A 
The diastolic (resting) potential
No time-dependent currents, this resting potential is much more negative (-80mV) than SA/AV nodes
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23
Q

What does it mean when resting membrane potential is depolarized?

A

There is a decreased number of available Na channels, which decreases the rate of depolarization and strength and speed of the impulse

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24
Q

What is phase 1 for fast cells?

A

Slight repolarization

Cl channels open briefly to let Cl in the cell

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25
Q

What is phase 2 for fast cells?

A

The plateau
Opening of voltage gated L-type Ca channels for Ca to enter the cell, causing further release of Ca from sarcoplasmic reticulum
Contraction is Ca dependent

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26
Q

What is phase 3 for fast cells?

A

Repolarization
K channels activate (open) and K moves out of the cell, returning to resting membrane potential
Ca is removed from the cytoplasm and the tissue relaxes

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27
Q

When is the absolute/refractory period for fast cells?

A

During phase 3, when repolarization recovers Na channels from inactive to resting.

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28
Q

What is the absolute refractory period for fast cells?

A

When the Na channels are in the inactive state so the myocyte cannot depolarize

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29
Q

What is the relative refractory period for fast cells?

A

When only a portion of the Na channels are in the active state so the myocytes may depolarize, but a lot less rapidly (fewer Na channels opened)

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30
Q

What occurs during phase 0 of the slow cells?

A

Ca influx into the cell through voltage gated L-type Ca channels when threshold is reached for rapid depolarization. Slow activation

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31
Q

What occurs during phase 3 of the slow cells?

A

K efflux out of the cell when voltage gated K channels open and the membrane repolarizes

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32
Q

What occurs during phase 4 of the slows cells?

A

Spontaneous depolarization
Increased Na influx (funny current)
Increased Ca influx
Decreased K efflux

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33
Q

What are the phases not present in slow cells?

A

Phase 1 or phase 2

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34
Q

How do the intrinsic firing rate of the cells of the heart compare?

A

SA>AV>Bundle of His>Purkinje fibres

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35
Q

Which cardiac cells have automaticity?

A

The pacemaking cells (AV, SA) and the Purkinje fibres have some.

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36
Q

What is a bradyarrhythmia?

A

Heart rate of less than 50-60 bpm due to sick sinus syndrome or an atrioventricular conduction block

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37
Q

What is a tachyarrythmia? What are the subsets?

A

Heart rate greater than 100 bpm

Supraventricular and ventricular

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38
Q

What are the supraventricular arrhythmias?

A 
Paroxysmal tachycardia (150-250 bpm, relatively benign)
Atrial Flutter (atria beat at 250-350 bpm, regular heart rhythm)
Atrial Fibrillation (atria beat up to 500 bpm, irregular rhythm, uncoordinated contraction)
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39
Q

What are the ventricular arrhythmias?

A 
Ventricular Tachycardia (>120 bpm, regular heart rhythm)
Ventricular Fibrillation (irregular rhythm with uncoordinated contraction, immediate cause of death)
Torsade de pointes (long QT syndrome)
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40
Q

What ions are most important in slow cells?

A

Ca and K

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41
Q

What ions are the most important in fast cells?

A

Na, Ca and K

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42
Q

What are arrhythmias caused by?

A

Insufficient oxygen to myocardial cells, acidosis (accumulation of waste products), electrolyte disturbances, structural damage to the conduction pathway and drugs
Abnormal impulse formation, abnormal conduction

43
Q

How does an abnormal automaticity occur?

A

Altered SA node firing rate through changes in autonomic activity or enhanced activity of spontaneous pacemackers (AV, Purkinje fibres) to ectopic pacemakers

44
Q

How does abnormal conduction occur?

A

Impaired AV node (heart block) leading to bradyarrhythmias

Re-entry (circus) conduction leading to tachyarrhythmias

45
Q

What are the 3 causes behind abnormal automaticity?

A

Decrease in phase 4 K conductance (hypokalemia) increases spontaneous depolarization
Inactivation of Na channels in depolarized cells (ischemia) converts fast cells into ectopic pacemakers
Localized supersensitivity to cathecholamines following ischemia

46
Q

How does a change in phase 4 slopes of fast cells affect heart rate?

A

Bigger slope, increased rate of depolarization, increased heart rate
Less slope, decreased rate of depolarization, decreased heart rate.

47
Q

How does a change in resting membrane potential affect heart rate?

A

Higher, more depolarized resting membrane potential, increased heart rate
Lower, more hyperpolarized resting membrane potential, decreased heart rate.

48
Q

How does a change in action potential threshold affect heart rate?

A

A lower, more negative threshold, increased heart rate

A higher, more positive threshold, decreased heart rate

49
Q

How does vagal tone affect heart rate? Who has better vagal tone?

A

Increased vagal tone decreases resting heart rate. Athletes and those who meditate have increased vagal tone.

50
Q

How does acetylcholine affect automaticity?

A

Slows the depolarization rate in phase 4. Decreases automaticity of the SA node, slows conduction of the AV node

51
Q

How does norepinephrine affect automaticity?

A

Increases the depolarization rate in phase 4 and reduces AP firing threshold. Increases automaticity of the SA node, increases conduction of the AV node.

52
Q

How does triggered activity of the cardiac cells occur?

A 
The cells depolarize before complete repolarization has occurred.
May be caused by prolonged duration of the action potential (QT interval) due to blockade of K channels by class 1 and 3 antiarrhythmics
The Ca channels can be ready before the Na channels.
53
Q

What can cause Torsade de pointes?

A

Blockage of hERG due to drugs or genetics channel which elongates QT

54
Q

What is Torsades de pointes?

A 
Characterized by twisting of isoelectric points on ECG and prolonged QT interval which can lead to ventricular fibrillation and sudden death
Responds to magnesium (class V antiarrhythmics)
55
Q

Which drugs can increase QT interval?

A 
Antiarrhythmics (class Ia and III)
Antihistamines
Antipsychotics
Antibiotics (erythromycin)
Need a hERG assay in drug development
56
Q

How does re-entry occur in the cardiac cells?

A

Local differences in conduction velocity and membrane characteristics lead to development of electrical circuits (circus conduction)
Normal electrical circuitry is rerouted, resulting in multiple beats before the next sinus beat is generated

57
Q

What can cause re-entry in cardiac cells?

A

Subendocardial ischemia caused by a coronary occlusion
Congenital
Hyperkalemia

58
Q

What is paroxysmal supraventricular tachycardia (PSVT)?

A

A special case of re-entry in the AV node whose cause is not clear and often short lasting.

59
Q

How is paroxysmal supraventricular tachycardia (PSVT) controlled?

A

By drugs that depress AV conduction, causing bidirectional block (Class IV, II and V)
An abnormal electrical pathway may be present (Wolff-Parkinson-White Syndrome)

60
Q

What is Wolff-Parkinson-White Syndrome?

A

An alternative conduction pathway from the ventricles back to the atria (bundle of Kent).

61
Q

How is Wolff-Parkinson-White Syndrome treated?

A

By catheter ablation of abnormal electrical pathway

Amiodaron is the 1st choice agent to stabilize heart rate

62
Q

What drugs should you avoid in an atrial fibrillation or flutter?

A

AV node blockers (beta blocker, Ca antagonist, adenosine or digoxin)

63
Q

How can antiarrhythmics reduce automaticity?

A

Increase membrane threshold protential for activation of Na or Ca channels
Hyperpolarizing resting membrane potential (more negative)
Blocking inactivated Na or Ca channels in depolarized tissues (prevent conversion to resting state)

64
Q

How can antiarrhythmics block re-entry mechanisms?

A

Convert unidirectional block to bidirectional block by slowing conduction
Prolong the effective refractory period (ERP) so conduction time

65
Q

How can antiarrhythmics normalize ventricular rate?

A

Slowing AV nodal conduction which reduces ventricular rate (increased time for ventricular filling) which improves stroke volume and CO.

66
Q

What do class IA Na channel blockers do?

A

Moderate phase 0 depression and slow conduction by blocking active (depolarized) Na channels. Prolonged repolarization (can cause arrhythmias) increased ERP to block reentry
Procainamide

67
Q

What do class IB Na channel blockers do?

A

Weak phase 0 depression and slow conduction by blocking activated and inactivated Na channels with fast kinetics (rapid association and dissociation). Block is increased in depolarized tissue (ischemic). Shortened repolarization (decreased ERP)
Lidocaine

68
Q

What do class IC Na channel blockers do?

A

Strong phase 0 depression and slow conduction, little effect on repolarization by powerful block of Na channels (slow dissociation/association)
Modest K channel block
Reduces propagation of action potential and automaticity of ecotopic
Flecainide

69
Q

What is Procainamide effective against?

A

Atrial flutter/fibrillation and ventricular tachycardia

70
Q

What are some problems with procainamide?

A

Depresses hemodynamics
Blockade of K channels (prolongation of QT interval that may cause Torsade)
May cause Lupus like syndrome (reversible)
Chronic treatment doesn’t reduce mortality rate

71
Q

What is lidocaine effective against?

A

Ventricular arrhythmias associated with MI

Given via IV

72
Q

What are some side effects of lidocaine?

A

Tremor, nausea, lightheadedness, convulsions

73
Q

When is flecainide contraindicated in?

A

In patients with previous MI (highly arrhythmogenic) due to increased re-entry

74
Q

What is the difference between propanolol and metoprolol and esmolol?

A

Propanolol is non-selective.

Metoprolol and esmolol are beta-1 selective

75
Q

How do beta blockers decrease heart rate?

A

Reduced phase 4 slope, reducing pacemaker current
Reduced AV conduction velocity by reducing voltage gated Ca current
Prolonged refractory period in nodal tissues

76
Q

What are beta-blockers used for?

A

To control ventricular in supraventricular tachycardias (atrial fibrillation or flutter)
Reduce short and long term mortality after MI

77
Q

When are beta blockers contraindicated?

A

Bradycardia and heart block
Patients with pulmonary problems (selective with caution)
Decompensated congestive heart failure
Diabetics (may mask symptoms of hypoglycemia)
Wolff-Parkinson-White Syndrome (may increase reentry)

78
Q

What does amiodarone do?

A

Block K channels, inactivated Na ion channels and modest beta block
Becoming 1st line agent

79
Q

What does sotalol do?

A

Block K channels, beta blocker

80
Q

What is the risk of class III agents?

A

By prolonging AP duration, you prolong QT interval which may predispose to torsade de pointes

81
Q

What is amiodarone effective in treating?

A 
Both supraventricular (maintains sinus rhythm in those with recurrent paroxysmal atrial fibrillation) and ventricular tachycardia (effective with less risk of proarrhythmic effect)
In cardiac surgery (decreases incidence of atrial fibrillation and ventricular tachycardia)
82
Q

What is amiodarone being replaced by?

A

Implanted cardioinverters

May add amiodarone to decrease defibrillator discharges

83
Q

What are some side effects of amiodarone?

A

Prolongs QT interval (Torsade), sinus bradycardia (requiring a permanent pacemaker), photosensitivity (grey/blue discolouration), hypothyroidism

84
Q

What is the duration of amiodarone action?

A

Very long half-life, plateau in 5-7 weeks, effects for 1-3 months after discontinuing therapy

85
Q

What does verapamil do?

A

Blocks L-type Ca channels (active and inactive) to slow conduction of AV node

86
Q

What is verapramil used to treat?

A

To reduce ventricular rate in supraventricular tachycardias (atrial fibrillation and flutter)
Acute paroxysmal supraventricular tachycardia

87
Q

What is verapramil contraindicated in?

A

Wolff-Parkinson-White Syndrome

88
Q

What is the possible mechanism of Mg?

A

May involve regulating Ca accumulation by reducing Na and Ca currents, reducing Ca release from the sarcoplasmic reticulum and is a cofactor of the Na/K ATPase pump

89
Q

What is Mg used for?

A

Torsade de Pointes (1st line agent)

In ventricular arrhythmias in ischemic cells associated with loss of cellular Mg

90
Q

How does adenosine work?

A

From the breakdown of ATP, acts on purine receptors of the SA and AV nodes to increase K conductance (hyperpolarization), depress slow inward Ca current and low phase 4

91
Q

What does adenosine do and what is it used for?

A

Slows sinus rate and decreases AV node conduction

Used for supraventricular tachycardia

92
Q

What does adenosine interact with?

A

Methylxanthines (caffeine/theophylline) block adenosine receptors

93
Q

How does digoxin work?

A

Decreases AV node conduction by stimulating the vagus nerve, releasing Ach and inhibits Ca currents and activating K currents

94
Q

When is digoxin used?

A

In atrial fibrillation, atrial flutter and supraventricular tachycardia with a rapid ventricular response

95
Q

What does digoxin action result in?

A

Reducing ventricular rate to increase stroke volume and CO

Does not always stop arrhythmias and can lead to late delayed afterdepolarizations

96
Q

When is digoxin contraindicated?

A

Wolff-Parkinson-White Syndrome

97
Q

What can bradycardia be treated with?

A

A pacemaker

98
Q

What can tachycardia be treated with?

A

Short runs or isolated, if asymptomatic: No treatment

Symptomatic/severe: Immediate cardioversion (electrical/pharmacological) with beta-blocker

99
Q

How can supraventricular tachycardia be treated?

A

Vagal maneuvers (valsalva, carotid massage)
Adenosine, verapamil, beta-blocker
If site responsible can be identified: Radiofrequency ablation

100
Q

How can atrial fibrillation be treated?

A

Anticoagulation
Control of ventricular rate (verapamil, beta-blocker, digoxin)
If highly symptomatic: Amiodarone to maintain sinus rhythm

101
Q

How can ventricular fibrillation be treated?

A

Transthoracic defibrillation with amiodarone possibly used as an adjunct

102
Q

How can ventricular tachycardia be treated?

A 
Cardioversion in those unconscious and hypotensive
Lidocaine, flecainide or amiodarone in stable hemodynamics
IV drugs (amiodaron, procainamide) in incessant episodes
103
Q

How is chronic tachycardia treated?

A

Implantable cardioverter defibrillators (ICD) with possible adjunct amiodarone to reduce risks of shocks

104
Q

What are the side effects of implantable cardioverter defibrillators?

A

Anxiety, depression, PTSD

Pharmacology (11 decks)

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