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Pharmacology - Winter > 6 - Antiarrhythmic Drugs > Flashcards

6 - Antiarrhythmic Drugs Flashcards

1
Q

What are predisposing factors for arrhythmias?

A
  • Px treated w/ digitalis for heart failure
  • Anesthetized px
  • Px w/ myocardial infarction
  • Anti-arrhythmic drugs
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2
Q

What is normally the pacemaker of the heart?

A

SA node

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3
Q

Where are conduction fibres?

A

AV node

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4
Q

What is an arrhythmia?

A

Any rhythm that is not a normal sinus rhythm w/ normal AV conduction

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5
Q

The SA node spontaneously discharges ______ beats per minute

A

60-100

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6
Q

What can change the rate of the SA node?

A

Nerves innervating the heart

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7
Q

What is the function of the AV node?

A
  • Electrical connection btwn atria and ventricles

- Delays action potential by 0.1 second to allow atria to contract and ventricles to fill

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8
Q

AV node spontaneously discharges _____ beats per min

A

40-60

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9
Q

What is the function of conduction fibres?

A

To excite ventricular mass as near simultaneously as possible

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10
Q

Purkinje fibres spontaneously discharge _____ beats per min

A

20-40

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11
Q

What is the path of an action potential in the heart?

A

SA node pacemaker -> conduction to atria -> AV -> bundle of His and Purkinje fibres -> ventricular myocardium -> contraction

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12
Q

What is the P wave?

A

Atrial depolarization

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13
Q

What is the QRS complex?

A

Ventricular depolarization

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14
Q

What is the T wave?

A

Ventricular repolarization

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15
Q

What is the PR interval?

A

Conduction time from atria to ventricles

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16
Q

What is the QRS interval?

A

Time for all ventricular cells to be activated

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17
Q

What is the QT interval?

A

Duration of ventricular action potential

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18
Q

What causes the differences btwn action potentials?

A

Different ion channels expressed in myocytes

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19
Q

Which anti-arrhythmic drugs block Na channels?

A
  • Procainamide
  • Lidocaine
  • Flecanide
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20
Q

Which anti-arrhythmic drugs block beta-adrenergic receptors?

A
  • Propranolol
  • Metoprolol
  • Esmolol
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21
Q

Which anti-arrhythmic drugs block K channels?

A
  • Amiodarone

- Sotalol

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22
Q

Which anti-arrhythmic drug blocks Ca channels?

A

Verapamil

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23
Q

Which anti-arrhythmic drugs work via other mechanisms?

A
  • Magnesium
  • Adenosine
  • Digoxin
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24
Q

What occurs during each phase of an action potential from non-pacemaker cells?

A 
0 = Na+ influx
1 = Cl- influx
2 = Ca2+ influx and K+ efflux
3 = K+ efflux
4 = K+ efflux
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25
Q

Is the resting potential more negative in pacemaker cells or non-pacemaker cells?

A

Non-pacemaker cells

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26
Q

What happens when the threshold is reached in non-pacemaker cells?

A

“Active” voltage gated Na channels open, causing rapid depolarization

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27
Q

What happens if all Na channels are in the “inactive” state?

A

Myocyte can’t depolarize, so is in an absolute refractory period

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28
Q

What if some Na channels are in the “inactive” state?

A

Myocyte may depolarize, but a less rapid depolarization; called relative refractory period

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29
Q

What does rapid depolarization of a cell result in?

A

Strong and rapid transmission of the impulse to surrounding fibres

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30
Q

What does rapid depolarization of the resting membrane potential of a cell cause?

A
  • Decreased # of sodium channels available
  • Decrease rate of depolarization
  • Decreased strength and speed of impulse
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31
Q

What can cause slow depolarization of resting membrane potential?

A
  • Hyperkalemia
  • Ischemia
  • Drugs blocking sodium channels
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32
Q

Sufficient sodium channels must be _____ to allow an action potential to be evoked

A

Activated

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33
Q

What occurs during the funny current in pacemaker cells?

A

Increased Na+ influx

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34
Q

What happens when the threshold is reached in pacemaker cells?

A

Voltage gated L-type Ca channels open, causing rapid depolarization

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35
Q

What happens in phase 3 of an action potential in pacemaker cells?

A

Voltage gated K channels open and membrane repolarizes

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36
Q

Where do fast response times occur in the heart? What is the resting membrane potential of these cells? Do they send off automatic signals?

A
  • Atria, purkinje fibers, ventricles
  • -80 to -95 mV
  • Purkinje fibers can send off automatic signals; atria and ventricles can’t
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37
Q

Where do slow response times occur in the heart? What is the resting membrane potential of these cells? Do they send off automatic signals?

A
  • SA node, AV node
  • -40 to -65 mV
  • Yes, send off automatic signals
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38
Q

What is the phase 0 current for non-pacemaker and pacemaker cells?

A
  • Non-pacemaker = sodium

- Pacemaker = calcium

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39
Q

What are arrhythmias related to?

A

Abnormal pacemaker/conduction and/or muscle depolarization

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40
Q

Arrhythmias must be _____ in order to be treated

A

Symptomatic

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41
Q

What are bradyarrhythmias?

A

HR less than 50-60 bpm

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42
Q

How are bradyarrhythmias treated?

A

W/ pacemaker, not normally w/ drugs

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43
Q

What can cause bradyarrhythmias?

A
  • Sick sinus syndrome

- Atrio-ventricular conduction block

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44
Q

What are tachyarrhythmias?

A

HR over 100 bpm

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45
Q

What is a paroxysmal tachycardia?

A
  • HR between 150 and 250 bpm

- Paroxysm = rapid onset

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46
Q

What is an atrial flutter?

A

Atria beat at 250-350 bpm, but regular heart rhythm

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47
Q

What is atrial fibrillation?

A

Atria beat up to 500 bpm, irregular rhythm, and uncoordinated contraction

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48
Q

What is ventricular fibrillation?

A
  • Irregular rhythm w/ uncoordinated contraction

- Immediate cause of death

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49
Q

What is torsade de pointes?

A

Long QT syndrome

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50
Q

What can cause torsade de pointes?

A
  • Genetics

- Drug induced

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51
Q

What are causes of an arrhythmia?

A
  • Insufficient oxygen to myocardial cells
  • Acidosis or accumulation of waste products
  • Electrolyte disturbances
  • Structural damage of conduction pathway
  • Drugs (ex: antipsychotics, antihistamines)
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52
Q

What are the most important ions for an action potential in pacemaker cells?

A

Calcium and potassium

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53
Q

What are the most important ions for an action potential in non-pacemaker cells?

A

Sodium, calcium, and potassium

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54
Q

What can cause abnormal automaticity of the heart?

A
  • Altered regular pacemaker activity in SA node

- Pacemaker of abnormal origin (ectopic foci)

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55
Q

What can cause abnormal impulse formation?

A

1) Abnormal automaticity

2) Triggered activity

56
Q

What is triggered activity?

A

Slow and poorly conducted action potential in atria or ventricles

57
Q

What can cause abnormal conduction?

A
  • Impaired AV node (causes bradyarrhythmias)

- Re-entry/circus conduction (causes tachyarrhythmias)

58
Q

What does enhanced activity of spontaneous pacemakers (AV node, Purkinje fibers) cause?

A
  • Decrease in phase 4 K conductance => increased spontaneous depolarization
  • Inactivation of Na+ channels in depolarized cells => converts fast cells to ectopic pacemakers
  • Localized supersensitivity to catecholamines following ischemia
59
Q

What is the relationship btwn rate of depolarization and heart rate?

A

Direct relationship (increase in rate of depolarization causes increased HR)

60
Q

What is the relationship btwn resting membrane potential and heart rate?

A

More depolarized RMP = increased HR; more hyperpolarized RMP = decreased HR)

61
Q

What is the relationship btwn AP threshold potential and heart rate?

A

More negative threshold = increased heart rate; more positive threshold = decreased HR (inverse relationship?)

62
Q

What releases acetylcholine and what does it act on?

A
  • Released from para nerves
  • Acts on muscarinic receptors; phase 4, so slows depolarization rate, decreases automaticity in SA node, and slows conduction in AV node
63
Q

What releases norepinephrine and what does it act on?

A
  • Released from symp nerves
  • Acts on beta receptors; phase 4, so increases depolarization rate and reduces AP firing threshold, increases automaticity in SA node, and increases conduction in AV node
64
Q

What determines how calcium and sodium channels can be depolarized again?

A
  • Sodium channels must be switched from inactive to resting through repolarization
  • Calcium channels are based on time
65
Q

What do class 1 and class 3 antiarrhythmic drugs do?

A

Block potassium channels

66
Q

What can cause calcium channels to be ready before sodium channels?

A

Prolonged action potential duration (QT interval)

67
Q

What can early afterdepolarization (EAD) trigger?

A

Torsade de pointes

68
Q

What do torsade de pointes show up as on ECG?

A
  • Twisting of isoelectric points

- Prolonged QT interval

69
Q

What can torsade de pointes cause?

A
  • Ventricular fibrillation

- Sudden death

70
Q

What is the tx for torsade de pointes?

A

Magnesium

71
Q

Which drugs can cause an increased QT interval?

A
  • Antiarrhythmics (class 1a and 3)
  • Antihistamines
  • Anti-psychotics
  • Antibiotics
72
Q

What is required for reentry (circus conduction) to occur?

A
  • Available circuit (closed conduction loop)
  • Unidirectional block
  • Different conduction speed in limbs of circuit (conduction time > effective refractory period)
73
Q

What are some causes of circus conduction?

A
  • Ischemia
  • Congenital
  • Hyperkalemia
74
Q

What can circus conduction occur?

A

Any part of the heart (AV node; btwn SA node and atria; btwn atria and ventricles)

75
Q

____ accounts for most tachyarrhythmias in cardiac patients

A

Circus conduction

76
Q

How can circus conduction be stopped?

A

By converting unidirectional block tissue to bi-directional block (can be done w/ drugs that block Na+ channels in non-pacemaker cells)

77
Q

What is paroxysmal supraventricular tachycardia?

A

Re-entry in the AV node

78
Q

How is paroxysmal supraventricular tachycardia treated?

A

Drugs that depress AV conduction, causing bidirectional block (Ca channel blockers, beta blockers, adenosine)

79
Q

What is Wolff-Parkinson-White syndrome?

A

Re-entry in the AV node through an abnormal electrical pathway (conducts from ventricles to atria)

80
Q

How is Wolff-Parkinson-White syndrome treated?

A
  • Catheter ablation of abnormal electrical pathway

- Amiodarone first choice to stabilize heart rate

81
Q

When should AV node blockers NOT be used for Wolff-Parkinson-White syndrome? What should be used instead?

A
  • If atrial fibrillation or flutter

- Use beta blocker, calcium antagonist, adenosine, or digoxin

82
Q

What are the 3 mechanisms of action of antiarrhythmic drugs?

A

1) Reduce automaticity
2) Block re-entry mechanisms
3) Normalize ventricular rate by slowing conduction through AV node

83
Q

How can you reduce triggered activity?

A

Block inactivated Na+ or Ca2+ channels in depolarized tissues (prevent conversion to resting state)

84
Q

How can you reduce pacemaker activity?

A
  • Hyperpolarize resting membrane potential

- Increase membrane threshold potential for activation of Na+ or Ca2+ channels

85
Q

How can you reduce automaticity?

A

Reduce triggered activity or pacemaker activity

86
Q

How can you block re-entry mechanisms?

A

1) Reduce phase 0 depolarization, which converts region of unidirectional block to bidirectional block
2) Prolong action potential depolarization, which increases effective refractory period enough that it is greater than conduction time, so re-entry is blocked

87
Q

What happens when you reduce ventricular rate?

A

Increases time for ventricular filling from atrium, so increase stroke volume and cardiac output, which improves hemodynamics

88
Q

What do class 1 antiarrhythmic drugs do? What are some examples?

A
  • Block Na channels

- Procainamide, lidocaine, flecainide

89
Q

What do class 2 antiarrhythmic drugs do? What are some examples?

A
  • Block beta-adrenergic receptors

- Propranolol, metoprolol, esmolol

90
Q

What do class 3 antiarrhythmic drugs do? What are some examples?

A
  • Block K channels

- Amiodarone, sotalol

91
Q

What do class 4 antiarrhythmic drugs do? What are some examples?

A
  • Block Ca channels

- Verapamil

92
Q

What do class 5 antiarrhythmic drugs do? What are some examples?

A
  • Work via other mechanisms

- Magnesium, adenosine, digoxin

93
Q

What is the main function of procainamide (class 1A)?

A
  • Moderately depresses phase 0 and slows conduction
  • Prolongs repolarization
  • Also blocks K+ channels in phase 3 (prolongs QT interval)
94
Q

What is the main function of lidocaine (class 1B)?

A
  • Minimally depresses phase 0 and slows conduction

- Shortens repolarization

95
Q

What is the main function of flecainide (class 1C)?

A
  • Greatly depresses phase 0 and slows conduction

- Little effect on repolarization

96
Q

Which class 1 antiarrhythmic has the strongest Na+ channel blockade?

A

Flecainide (class 1C)

97
Q

Where are class 1A antiarrhythmics active?

A

Depolarized cells (active, ischemic)

98
Q

When are class 1A antiarrhythmics used?

A
  • Ventricular tachycardia
  • Atrial fibrillation/flutter
  • Generally more limited use
99
Q

Why does procainamide have a limited use?

A
  • Depresses hemodynamics
  • Blocks K+ channels, so prolongs QT interval and may cause Torsade de Pointes
  • May cause lupus like syndrome
100
Q

Where are class 1B antiarrhythmics active?

A
  • Normal tissue, especially atria b/c action potential duration is short
  • Block increased in depolarized tissue (ischemic)
101
Q

What does reduced propagation of action potentials and automaticity result in?

A

Reduced ectopic pacemaker activity, especially in ischemic depolarized tissues

102
Q

When are class 1B antiarrhythmics used? How are they administered?

A
  • Ventricular arrhythmias associated w/ myocardial infarction
  • Administered IV
103
Q

What are some adverse effects of lidocaine?

A
  • Tremor, nausea, lightheadedness
  • Hearing disturbances
  • Slurred speech
  • Convulsions
104
Q

What are contraindications for class 1C antiarrhythmics?

A

Px w/ previous MI, highly arrhythmogenic (b/c of increased re-entry)

105
Q

When are class 1C anti-arrhythmics used?

A
  • Tx of supraventricular (atrial fib and flutter) and life-threatening ventricular arrhythmias
  • *Only in px w/ structurally normal hearts
106
Q

Why are beta-blockers used for arrhythmias?

A
  • Reduce phase 4 slope in pacemaker cells by reducing pacemaker current
  • Reduce AV conduction velocity by reducing voltage-gated Ca2+ current
  • Prolong refractory period in nodal tissues
107
Q

When are beta-blockers used for arrhythmias?

A
  • Control ventricular rate in supraventricular tachycardias
  • Terminate and prevent recurrence of paroxysmal supraventricular tachycardia
  • Reduce mortality after acute MI
108
Q

What are contraindications to beta blockers?

A
  • Bradycardia and heart block
  • Px w/ pulmonary problems
  • Decompensated congestive heart failure
  • Diabetics
  • Wolff-Parkinson-White syndrome
109
Q

Which beta-blocker can be used in cases where beta-blockers are normally contraindicated? Why?

A

Esmolol b/c has a very short duration of action (half life = 10 min)

110
Q

Amiodarone is a ___ spectrum antiarrhythmic

A

Wide

111
Q

What are the functions of amiodarone?

A
  • Blocks K+ ion channel in phase 3, prolonging cardiac AP duration *main function
  • Blocks inactivated Na+ ion channels
  • Blocks Ca2+ ion channels
  • Modestly blocks beta receptors
112
Q

What are the functions of sotalol?

A
  • Blocks K+ ion channel in phase 3, prolonging cardiac AP duration
  • Also a beta blocker
113
Q

Can class 3 antarrhythmics be used in px w/ structural heart disease?

A

Yes

114
Q

When is amiodarone used? What is starting to replace it?

A
  • Used for supraventricular and ventricular tachycardia

- Being replaced by implanted cardioinverter

115
Q

What are the adverse effects of amiodarone?

A
  • Highly lipid soluble, so accumulates in liver, lungs, skin, and other tissues
  • Pulmonary toxicity
  • Hepatotoxicity
  • Hyper and hypothyroidism (b/c contains iodine)
  • Sinus bradycardia
  • Photosensitivity
116
Q

When is sotalol used?

A
  • Supraventricular tachycardia (equally as effective as amiodarone)
  • Ventricular tachycardia (less effective than amiodarone, but preferred when amiodarone toxicity a concern)
117
Q

What are the adverse effects of sotalol?

A
  • May accumulate in px w/ renal disease
  • Bradycardia, so contraindicated in px w/ sick sinus syndrome
  • Bronchospasm
  • Greater risk of Torsade de Pointes than amiodarone
118
Q

What is the function of verapamil?

A
  • Block L-type Ca2+ channels in plasma membrane

- Slows conduction in AV node

119
Q

When is verapamil used?

A
  • To reduce ventricular rate in supraventricular tachycardias
  • Acute paroxysmal supraventricular tachycardia
120
Q

What is a contraindication for verapamil?

A

Wolff-Parkinson-White syndrome

121
Q

When is magnesium a first line agent?

A

For Torsade de Pointes, even when magnesium levels are normal

122
Q

What is the mode of action for adenosine?

A
  • Increases K+ conductance (hyperpolarizes)
  • Depresses slow inward Ca2+ current
  • Slows phase 4 of AV pacemaker AP
123
Q

When is adenosine used?

A

Given IV for supraventricular tachycardia due to AV node re-entry

124
Q

What are drug interactions w/ adenosine?

A

Methylxanthines (caffeine, theophylline)

125
Q

What is the mode of action for digoxin?

A

Decreases AV node conduction (releases ACh and inhibits calcium currents and activates K+ currents)

126
Q

When is digoxin used?

A

Atrial fibrillation, atrial flutter, and supraventricular tachycardia w/ rapid ventricular response

127
Q

What is a contraindication for digoxin?

A

Wolff-Parkinson-White syndrome (may cause death)

128
Q

What is the tx for a symptomatic/severe tachycardia?

A

Immediate cardioversion (electrical or pharmacological)

129
Q

What is the tx for paroxysmal tachycardia?

A
  • IV adenosine/verapamil/beta-blocker
  • For WPW, procainamide, flecainide, or amiodarone
  • If area of tissue responsible for arrhythmia can be identified, radiofrequency ablation is preferred
130
Q

What is the tx for atrial fibrillation?

A
  • For rate control - verapamil, beta-blocker, digoxin, or amiodarone
  • For rhythm control - procainamide, flecainamide, amiodarone, or sotalol
131
Q

What is the tx for ventricular fibrillation?

A
  • Transthoracic defibrillation

- IV amiodarone, lidocaine, or magnesium may be used as adjunct

132
Q

What is the tx for ventricular tachycardia?

A
  • To terminate episode in unconscious or hypotensive px - cardioversion
  • To terminate episode in px w/ stable hemodynamics - IV lidocaine, flecainide, amiodarone, or sotalol
133
Q

What is the tx for Torsade de Pointes?

A

IV magnesium

134
Q

What is the tx for chronic therapy of ventricular tachycardia?

A

Cardioverter defibrillator

135
Q

What are the side effects to an implantable cardioverter defibrillator (ICD)?

A
  • Anxiety, depression, PTSD

- Amiodarone may be used in conjunction to reduce prevalance of accidental ICD shocks

Pharmacology - Winter (18 decks)

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