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Pharm 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What is procainamide’s mechanism of action?

A
  • potassium and sodium channel blocker
  • depresses automaticity by decrease slope of phase 0 depolarization
  • prevents reentry by converting unidirectional to bidirectional block
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2
Q

What are indications for use of procainamide?

A
  • atrial fibrillation
  • PVCs
  • SVT
  • VT
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3
Q

What are signs of procainamide toxicity?

A
  • heart block
  • hypotension
  • myocardial depression
  • QRS complex
  • QT prolongation
  • ventricular ectopy
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4
Q

What is the half life of procainamide?

A
  • 3-4 hours
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5
Q

What is the metabolite of procainamide?

A
  • N-acetyl procainamide (NAPA)
  • half life of metabolite is 6-10 hours
  • renally eliminated
  • increased risk of side effects and QT prolongation
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6
Q

What are indications for use of quinidine?

A
  • atrial fibrillation
  • atrial flutter
  • ventricular fibrillation
  • ventricular tachycardia
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7
Q

What class does quinidine belong to?

A
  • class 1A
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8
Q

What are signs and symptoms of quinidine toxicity?

A
  • cinchonism
  • loose stools
  • QT prolongation
  • thrombocytopenia
  • ventricular tachycardia
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9
Q

What is the half life of quinidine?

A
  • 6-8 hours
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10
Q

Quinidine is a potent ___________ inhibitor.

A
  • CYP2D6
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11
Q

What class does disopyramide belong to?

A
  • class 1A

- similar to quinidine without alpha effects

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12
Q

What are indications for use of disopyramide?

A
  • atrial arrhythmias

- ventricular tachyarrhythmias

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13
Q

What are signs and symptoms of disopyramide toxicity?

A
  • anticholinergic side effects (most significant)
  • heart failure exacerbation
  • QT prolongation
  • thrombocytopenia
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14
Q

What is the half life of disopyramide?

A
  • 6-7 hours

- renally eliminated

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15
Q

What class does lidocaine belong to?

A
  • class 1B
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16
Q

What are indications for use of lidocaine?

A
  • ventricular arrhythmias (especially re-entry dysrhythmias)
  • ineffective against supraventricular arrhythmias
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17
Q

What are signs and symptoms of lidocaine toxicity?

A
  • bradycardia
  • CNS depression
  • LV depression in patients with pre-existing disease
  • nystagmus (early sign)
  • seizure
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18
Q

What is the half life of lidocaine?

A
  • 8 minutes
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19
Q

When should you use a reduced dose of lidocaine?

A
  • CHF

- liver disease

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20
Q

True or False

Lidocaine undergoes significant first pass metabolism.

A
  • true
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21
Q

What class does phenytoin belong to?

A
  • 1B
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22
Q

What are indications for use of phenytoin?

A
  • paradoxical ventricular tachycardia or torsades prolonged with prolonged QTc interval
  • suppression of ventricular dysrhythmias associated with digitalis toxicity
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23
Q

What are signs and symptoms of phenytoin toxicity?

A
  • death
  • drowsiness
  • nausea
  • nystagmus
  • respiratory arrest
  • severe hypotension
  • ventricular ectopy
  • vertigo
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24
Q

What class does flecainide belong to?

A
  • 1C
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25
Q

What are indications for treatment with flecainide?

A
  • atrial tachyarrythmias
  • PVCs
  • WPW
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26
Q

What are the side effects of flecainide?

A
  • difficulty with visual accommodation
  • moderate negative inotropic effect
  • vertigo
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27
Q

When should you avoid treatment with flecainide?

A
  • CAD
  • LV failure
  • ventricular tachycardia
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28
Q

What are indications for treatment with beta blockers?

A
  • atrial tachyarrhythmias
  • slow ventricular response to atrial fibrillation and flutter
  • SVT
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29
Q

What are signs and symptoms of beta blocker toxicity?

A
  • acute bronchospasm
  • asystole
  • LV failure
  • profound bradycardia
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30
Q

What class does amiodarone belong to?

A
  • class III
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31
Q

What are indications for treatment with amiodarone?

A
  • recurrent ventricular fibrillation or unstable ventricular tachycardia in patients unresponsive to other agents
  • suppression of tachydysrhthmias associated with WPW
  • termination of ventricular and supraventricular arrhythmias
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32
Q

What is the half life of amiodarone?

A
  • prolonged to weeks to months in patients on oral agents
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33
Q

What drug interactions can occur with amiodarone?

A
  • CYP3A4 substrate

- CYP3A4, CYP2C9 and PGP inhibitor

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34
Q

What are signs and symptoms of amiodarone toxicity?

A
  • CV: bradycardia, dysrhythmias, heart block, heart failure, hypotension, sinus arrest
  • Endo: hypothyroidism or hyperthyroidism
  • Heme: coagulation abnormalities
  • Hepatic: increased LFTs, liver failure
  • Other: peripheral neuropathy, muscle weakness
  • Respiratory: ARDS, pulmonary fibrosis
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35
Q

When is dronedarone contraindicated?

A
  • Permanent atrial fibrillation
  • decompensated heart failure
  • medications that inhibit CYP3A4 or prolong QTc
  • pregnancy
  • significant liver disease
  • second/third degree heart block
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36
Q

When is treatment with dronedarone indicated?

A
  • atrial fibrillation
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37
Q

What class does verapamil belong to?

A
  • class IV
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38
Q

What are indications for use of verapamil?

A
  • slow ventricular rate in atrial fibrillation and flutter

- SVT

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39
Q

What are signs and symptoms of verapamil toxicity?

A
  • asystole
  • AV block
  • bradycardia
  • hypotension
  • myocardial depression
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40
Q

What is diltiazem’s mechanisms of action?

A
  • slow Ca+ channel blocking prolongs AV nodal conduction and refractoriness
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41
Q

What are indications for use of diltiazem?

A
  • ventricular rate control in atrial fibrillation or atrial flutter
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42
Q

What are signs and symptoms of diltiazem toxicity?

A
  • bradycardia
  • constipation
  • edema
  • hypotension
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43
Q

What drug interactions can occur with diltiazem?

A
  • potent CYP3A4 inhibitors, so MANY drug interactions
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44
Q

What are indications for use of digoxin?

A
  • ventricular rate control in atrial fibrillation and flutter
  • SVT
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45
Q

What is digoxin’s mechanism of action?

A
  • inhibits sodium and potassium ATPase
  • directly prolongs the effective refractory period in the AV node
  • slows ventricular response rate in atrial fibrillation
  • enhances conduction through accessory pathways
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46
Q

What are signs and symptoms of digoxin toxicity?

A
  • can see any known rhythm disturbance
  • PVCs common
  • cardiac toxicity is enhanced with hypokalemia
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47
Q

What is adenosine’s mechanism of action?

A
  • activates potassium channels that hyperpolarize nodal tissue causing a transient third degree AV block
  • depression of the action potential in the AV and SA node
  • Inhibits effects of increased cAMP, reduces calcium currents to increase AV note refractoriness
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48
Q

What are indications for use of adenosine?

A
  • treatment of paroxysmal SVT that involves accessory pathways
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49
Q

What is the half life of adenosine?

A
  • 1.5 seconds
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50
Q

What are signs and symptoms of adenosine toxicity?

A
  • chest pressure (most common)
  • dyspnea
  • facial flushing
  • can exacerbate bronchoconstriction in asthmatic patients
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51
Q

What are prodysrhythmic effects of antiarrhythmics?

A
  • brady or tachyarrhythmias that represent new cardiac dysrhythmias associated with chronic antidysrhythmic drug treatment
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52
Q

How to antiarrhythmics promote torsades de pointes?

A
  • potassium channel blockade may prolong QT interval and induce triggered activity in the ventricle
  • class 1A and class III drugs block potassium channels and prolong QTc
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53
Q

Describe phase 0 of the action potential

A
  • rapid depolarization
  • increase in sodium conductance through ion channels
  • leads to ventricular contraction
  • ends with sodium channels becoming inactive at 65 mV
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54
Q

Describe phase 1 of the action potential

A
  • sodium permeability is rapidly inactivated
  • cell starts to repolarize
  • potassium channels open and begin transient efflux
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55
Q

Describe phase 2 of the action potential

A
  • plateau
  • repolarization is delayed by an increase in conduction of calcium influx
  • potassium channels open and maintain plateau through potassium efflux
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56
Q

Describe phase 3 of the action potential

A
  • rapid repolarization
  • complete repolarization due to inactivation of calcium conduction and increase in potassium permeability
  • no significant movement of calcium or sodium
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57
Q

Describe phase 4 of the action potential

A
  • spontaneous depolarization

- ATP dependent pumps move Ca+ and K+ ions to regain balance

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58
Q

How do action potentials vary between the muscle cell and the SA cell?

A
  • pacemaker cells lack phase 1 and phase 2

- In muscle cells, phase 0 is mediated by Na+. In pacemaker cells, phase 0 is mediated by Ca+

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59
Q

What is the role of calcium channels in the action potential?

A
  • responsible for phase 0 in SA and AV nodes
  • contributes to phase 2 in ventricular contractile cells and prolongs refractory period
  • affects phase 4 spontaneous depolarization
  • facilitated by catecholamines
60
Q

What is the role of sodium channels in the action potential?

A
  • fast channels are sodium mediated
  • responsible for phase 0
  • rapid conduction velocity
61
Q

What is impulse generation?

A
  • automaticity

- cells that undergo spontaneous phase 4 depolarization are automatic and capable of impulse generation

62
Q

Where can re-entry arrhythmias occur?

A
  • SA node: SA nodal re-entry
  • atrium: atrial tachycardia or flutter
  • AV node: AV nodal re-entry and tachycardia mediated by accessory pathways
  • ventricle: ventricular tachycardia
63
Q

Where are sodium channels located in the heart?

A
  • atria

- ventricles

64
Q

Where are calcium channels located in the heart?

A
  • AV node

- SA node

65
Q

What are the 4 types of antiarrhythmics drugs?

A
  • type I: sodium channel blockers
  • type II: beta blockers
  • type III: potassium channel blockers
  • type IV: calcium channel blockers
66
Q

What is the mechanism of action of sodium channel blockers?

A
  • slows conduction

- prolongs QRS complexes in atria and ventricles

67
Q

What is the mechanism of action of calcium channel blockers?

A
  • slows the atrial rate

- slows conduction through the AV node (prolonging the PR interval)

68
Q

What is the mechanism of action of potassium channel blockers?

A
  • interrupts re-entry by slowing conduction or increasing the refractory period
  • prolongs the QT interval
  • induces triggered activity in the ventricle causing torsades de pointes
69
Q

What are the 3 subclasses of class I (sodium channel blockers)?

A
  • 1A
  • 1B
  • 1C
70
Q

What drugs are class III antiarrhythmics?

A
  • amiodarone
  • bretylium
  • dofetilide
  • dronedarone
  • ibutilide
  • sotalol
71
Q

What drugs are class IV of antiarrhythmics?

A
  • diltiazem

- verapamil

72
Q

What drugs are included in class II of the antiarrhythmics?

A
  • beta blockers (except sotalol)
73
Q

What drugs are included in class 1A of the antiarrhythmics?

A
  • disopyramide
  • moricizine
  • procainamide
  • quinidine
74
Q

What drugs are included in class 1B of the antiarrhythmics?

A
  • lidocaine
  • mexilitine
  • Phenytoin
75
Q

What drugs are included in class 1C of the antiarrhythmics?

A
  • flecainide

- propafenone

76
Q

What is the effect of class 1A antiarrhythmics on the action potential?

A
  • slows phase 0

- prolonged phase 3

77
Q

What is the effect of class 1B antiarrhythmics on the action potential?

A
  • slows phase 0

- shortens phase 3

78
Q

What is the effect of class 1C antiarrhythmics on the action potential?

A
  • creates a very slow phase 0

- no effect on phase 3

79
Q

What is the effect of class II antiarrhythmics on the action potential?

A
  • reduces slope of phase 4
80
Q

What is the effect of class III antiarrhythmics on the action potential?

A
  • prolongs phase 3
81
Q

What is the effect of class IV antiarrhythmics on the action potential?

A
  • reduces slope of phase 4
82
Q

What is the mechanism of action of class 1 antiarrhythmics?

A
  • blocks fast sodium channels with or without potassium channel blockade
  • decreases depolarization rate and conduction velocity
83
Q

What is the mechanism of action of class 1A antiarrhythmics?

A
  • lengthens action potential duration and effective refractory period (sodium channel blockade)
  • lengthens repolarization (potassium channel blockade)
84
Q

What is the mechanism of action of class 1B antiarrhythmics?

A
  • less powerful sodium channel blocker

- shortens the action potential duration and refractory period in normal cardiac ventricular muscle

85
Q

What is the mechanism of action of class 1C antiarrhythmics?

A
  • potent sodium channel blockers
  • decreases rate of phase 0 depolarization and speed of conduction of cardiac impulses
  • shortens duration of action potential in Purkinje fibers
  • more prodysrhythmic effects
86
Q

What is the mechanism of action of class II antiarrhythmics?

A
  • decrease rate of spontaneous phase 4 depolarization
  • slows conduction of cardiac impulses through atrial tissue
  • slows heart rate
  • prolongs PR interval
87
Q

What is the mechanism of action of class III antiarrhythmics?

A
  • blocks potassium ion channels

- prolongs cardiac depolarization, action potential duration and effective refractory period

88
Q

What is the mechanism of action of class IV antiarrhythmics?

A
  • calcium channel blockers

- inhibit inward slow calcium currents

89
Q

What factors reduce automaticity?

A
  • vagal influences
  • digitalis drugs
  • parasympathomimetic drugs
  • halothane
90
Q

True or False

Factors that reduce automaticity at higher pacemaker sites will passively favor the movement of the pacemaker to the lower sites.

A
  • true
91
Q

Amiodarone and sotalol block what receptors?

A
  • sodium channels
  • beta blockade
  • calcium channel blockade
92
Q

What type of syndrome is possible with chronic administration of procainamide?

A
  • systemic lupus erythematous
93
Q

What effect can digoxin have on WPW?

A
  • can increase the ventricular response in WPW

- enhances conduction through accessory pathways

94
Q

When does adenosine not work?

A
  • no effect on arrhythmias originating distal to the AV node
  • not effective in treatment of atrial fibrillation or flutter
95
Q

Disopyramide is similar to _____, but without the ____ effects

A
  • Quinidine

- Alpha

96
Q

Calcium channel blockers reduce slope of phase ____

A

4

97
Q

What is more common with amiodarone toxicity, hypo or hyper thyroidism?

A

Hypothyroidism

98
Q

T/F

Amiodarone has an antiadrenergic effect that causes competitive blockade of alpha and beta receptors.

A

FALSE

causes noncompetitive blockade of alpha and beta receptors

99
Q

T/F

Beta blockers can only be used for atrial arrhythmias

A

True

100
Q

What is an advantage of MULTAQ over amiodarone?

A

Has no iodine, so no risk of thyroid abnormalities

101
Q

T/F

Adenosine may exacerbate bronchoconstriction in asthmatic patients

A

True

102
Q

What non-cardiac med has the highest risk of torsades?

A

Haldol

Antipsychotics are #1
Antibiotics are #2

103
Q

What are 2 drawbacks to using Ibutilide/Dofetilide?

A
  • Very expensive (so tight dispensing laws

- Very high incidence of torsades and ventricular arrhythmias

104
Q

Which subclass of Class I antidysrhythmics is the least powerful sodium channel blockers?

A

IB

IC is the most powerful (so assoc. with more prodysrhythmic effects)

105
Q

Which two meds are basically “phase all” bc they work everywhere on the action potential?

A

Amiodarone and sotalol

106
Q

Which class IA med has some evidence of alpha blockade and vagal inhibitor?

A

Quinidine

107
Q

____ is basically “mini quinidine” and used in the treatment of pseudobulbular effect and alzheimers

A

Neudexa

108
Q

What is the most significant side effect of disopyramide?

A

Anticholinergic effects

109
Q

Disopyramide is similar to quinidine but without the ____ effects

A

alpha

110
Q

What class is the most pro-arrhythmic of all anti-arrhythmics?

A

1C

111
Q

Which anti-arrhythmic has the highest risk of arrhythmias?

A

Flecainide

112
Q

What is a major side effect with Verapamil toxicity?

A

Hypotension

113
Q

Adenosine affects ___ in the ___ node and ___ in the heart cells

A
  • calcium
  • AV
  • potassium
114
Q

What EKG change would be seen after giving adenosine?

A

Third degree heart block

115
Q

T/F

Amiodarone causes acute renal failure and electrolyte abnormalities

A

FALSE

it DOES NOT cause ARF and lyte abnormalities

116
Q

During the action potential, sodium channels go from ___ to ___ to ____

A
  • “closed”
  • “open”
  • “inactive”
117
Q

The action potential ends with sodium channels becoming “inactive” at ___ mV

A

+65mV

118
Q

In cardiac pacemaker cells (SA and AV), phase O is mediated by ____

A
  • Calcium
119
Q

In cardiac muscle cells (atrium and ventricle), phase 0 is mediated by ____

A
  • Sodium
120
Q

What percentage of patients become ANA positive from Procainamide?

A

50-80%

121
Q

T/F

Procainamide is a myocardial depressant

A

True

122
Q

T/F

Quinidine is a potent CYP2D6 inhibitor and can lead to a build up of dextromorphan

A

True

123
Q

What EKG change will you see with all 1a’s?

A

QT prolongation

124
Q

What is the most common indication for beta blockers?

A

Afib

125
Q

What electrolyte mediates beta blockers?

A

Calcium

126
Q

What EKG changes will you see with amiodarone?

A

Prolongs PR, QRS, and QT intervals

127
Q

What are 2 respiratory problems assoc. with amiodarone?

A

Pulmonary fibrosis and ARDS

128
Q

What clinical presentation would see if you from iodine buildup with Amiodarone?

A

Tips of ears and nose turn blue

Esp if already taking synthroid

129
Q

T/F

In rate vs rhythm control for Afib, there is no difference in mortality outcomes in using rhythm control with amiodarone and ???

A

True

130
Q

T/F

If you use verapamil on a pt with accessory pathways, you can exacerbate an re-entry arrhythmia

A

True

Verapamil has NO effect on accessory tracts

131
Q

What is the most common sign of digoxin toxicity?

A

PVC’s

132
Q

Cardiac toxicity from Digoxin is enhanced with _____

A

hypokalemia

133
Q

T/F

Digoxin can be used to convert Afib to NSR

A

FALSE

Digoxin will only slow the rate down, will not convert

134
Q

What receptor does Adenosine work on in the heart?

A

A1 (Adenosine receptor)

135
Q

T/F

Adenosine has effects on arrhythmias originating distal to the AV node

A

FALSE

No effect on arrhythmias originating distal to the AV Node.

136
Q

What are the 3 most common arrhythmias that can be caused by anti-arrhythmics?

A
  • Torsades de pointes.
  • Increased ventricular tachycardias (esp with AV blockers).
  • Wide complex ventricular rhythm.
137
Q

What is the pathophysiology of torsades assoc. with anti-arrhythmics?

A

K channel blockade may prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT or ventricular fibrillation.

138
Q

Which two classes of anti-arrhythmics can most likely cause torsades?

A

IA and III

They both block K+ channels and prolong QTc intervals

139
Q

Torsades occurs in ___% of patients who receive QT prolonging drugs

A

1-8%

140
Q

What two classes of anti-arrhythmics are most likely to precipitate incessant ventricular tachycardia?

A

Ia and Ic

Both have fallen out of favor due to this

141
Q

What two volatile anesthetics are most likely to cause QT prolongation and torsades?

A

Isoflurane and enflurane

142
Q

What class of anti-arrhythmics is most likely to cause wide complex ventricular rhythm?

A

Ic

143
Q

What is the voltage of the action potential at the beginning of phase 0?

A
  • negative 70 mV
144
Q

T/F

In phase 4 of the action potential, ATP-dependent pump moves calcium and potassium ions to regain balance

A

True

145
Q

What 4 conditions predispose a patient to developing torsades?

A
  • Hypomagnesemia
  • Hypokalemia
  • Slow heart rate
  • Preexisting QT prolongation

Pharm 2 (19 decks)

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