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ELECTROPHYSIOLOGY > ANTI-ARRHYTHMIC DRUGS > Flashcards

ANTI-ARRHYTHMIC DRUGS Flashcards

1
Q

How many phases are there in the cardiac action potential?

A

5 phases
Phase 0,1,2,3 and 4

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2
Q

What is the current flow in phase 0 of the action potential?

A

Phase 0 begins with fast inward sodium current that taken the membrane potential from resting (-85 mV) to above zero

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3
Q

What is current flow in phase 1 of the action potential?

A

In phase 1 there is an outward sodium current that causes the action potential to “dip” a little

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4
Q

What are the currents in phase 2 of the action potential?

A

Phase 2 is the plateau phase marked by a balance between an inward calcium and outward potassium current

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5
Q

What are the currents in phase 3 of the action potential?

A

In phase 3 there is an outward potassium current which leads to repolarization

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6
Q

What is phase 4 of the action potential?

A

Phase 4 in non-pacemaker cells is flat but in pacemaker cells there is slow depolarization due to funny sodium channels “If” channels

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7
Q

Surface electrocardiogram is a summation of which action potentials?

A

ECG is a summation of all the action potentials in the heart cells, i.e atrial mycocytes, SA/AV nodes, His Bundles, Purkinjie fibers and ventricular myocytes

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8
Q

Are all cardiac cell actions potentials the same?

A

No
Different cells have slightly different action potentials

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9
Q

Which classification is used for anti-arrhythmic drugs?

A

Vaughan Williams classification

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10
Q

What is Class I drugs in the Vaughan Williams classification?

A

These are sodium channel blockers
They slow the conduction velocty by blocking Na channels of phase 0

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11
Q

Class I drugs will prolong which interval on the ECG?

A

QRS interval
They will slow conduction velocity of phase 0 by blocking fast Na channels

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12
Q

What are the three states of the sodium channels?

A

Resting: Na channels are closed in this state and the membrane potential is at the resting potential
Activated: Na channels are open when the membrane potential reaches threshold potential causing a rapid influx on sodium ions
Inactivated: As the membrane potential depolarizes, Na channels close again in this state and remain closed till membrane potential is restored

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13
Q

What are the subclassification of Class I drugs?

A

Type 1A
Type 1B
Type 1C

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14
Q

Drugs in Type 1A?

A

Quinidine
Procainamide (IV)
Disopyramide

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15
Q

Effects of Type 1A drugs?

A

Block sodium channels
Also prolong action potential duration
Strong negative inotropes

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16
Q

Main uses of Class IA drug Quinidine?

A

Quinidine has a niche use in Brugada syndrome (ito blockade)

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17
Q

Side effects of Class IA drug Quinidine?

A

Diarrhea, torsades, thrombocytopenia/leukopenia, drug interactions, hypersensitivity

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18
Q

Main uses of Class IA drug Procainamide?

A

Pre-excited atrial fibrillation
Terminating monomorphic VT
Inducing Brugada ECG pattern (diagnostic purposes)

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19
Q

Unique metabolite of procainamide and it’s effects?

A

Procainamide is metabolized to NAPA (N-acetyl procainamide) by plasma acetylation and has Class III properties and can cause LQTS/Torsades

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20
Q

Side effects of Class IA drug Procainamide?

A

Lupus like syndrome
Torsades
Agranulocytosis

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21
Q

Main use of Class IA drug Disopyramide?

A

Niche use in HCM and vagally mediated atrial fibrillation

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22
Q

Side effects of Class IA drug Disopyramide?

A

Anticholinergic effects such as dry mouth, urinary retention and avoid in BPH and glaucoma
Strong negative inotrope effect and avoid in HFrEF

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23
Q

Type 1 B drugs?

A

Lidocaine (IV)
Mexiletine (PO)

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24
Q

Effects of Type 1B drugs?

A

Little effect on atrial tissue
Greatest effect on diseased ventricular myocytes

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25
Q

Main use of Class B drugs?

A

These are used in ventricular arrhythmias

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26
Q

Main use of Class IB drug Lidocaine (IV)

A

Terminate/prevent VT especially post MI
Torsades de pointes
Note: Not used prophylactically after MI

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27
Q

Main side effects of Class IB drug lidocaine?

A

Neurologic/CNS
Sinus node slowing
Increased risk in CHF and shock
Lower levels with hepatic enzyme inducers (phenytoin, rifampin, barbituates)

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28
Q

Main uses of Class IB drug Mexilitine (oral)?

A

Niche use in ICD shocks
congential LQT3

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29
Q

Main excretion/clearence of Class IB drug mexilitine?

A

Hepatic clearence (90%)

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30
Q

Main side effects of Class IB drug mexilitine?

A

Neurologic/CNS and GI symptoms

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31
Q

Type 1 C drugs?

A

Flecanide
Propafenone

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32
Q

Effects of Type 1 C drugs?

A

Most potent Na blocking drugs (Can prolong QRS on ECG)
Negative inotropes

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33
Q

Main use of Class IC drugs?

A

Atrial arrhythmias
Idiopathic VT

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34
Q

Class IC drugs are contraindicated in?

A

CAD
HFrEF
These are strong negative inotropes

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35
Q

Main uses of Class IC drug Flecanide?

A

Atrial fibrillation
SVT
WPW syndrome
Idiopathic VT

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36
Q

What did flecanide show in the CAST (Cardiac arrhythmia suppression) trial?

A

Flecanide use doubled mortality after MI including VT and should not be used in MI.
Don’t use in patients with structural heart disease

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37
Q

Unique side effect of flecanide and how to treat it?

A

Flecanide can cause afib to change to atrial flutter with 1:1 conduction. Give with a beta-blocker or calcium channel blocker

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38
Q

Use dependence of flecanide?

A

At higher heart rates, flecanide’s effects increase and can cause rate dependent AV block

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39
Q

Side effects of Flecanide?

A

Parasthesias
Diplopia
Chest pain

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40
Q

Main uses of Propafenone?

A

Atrial fibrillation
SVT

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41
Q

Propafenone is contraindicated in?

A

MI & structural heart disease
Note: It wasn’t used in the CAST trial but results apply to it as it is similar to flecanide.

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42
Q

Unique effect of Propafenone?

A

Propafenone has some intrinsic beta blocker activity

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43
Q

What is Class II drugs in the Vaughan Williams classification?

A

These are Beta-adrenergic blockers

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44
Q

Examples of drugs in Class II?

A

Metoprolol
Atenalol
Propranolol
Carvedilol
Esmolol

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45
Q

Mechanism of action of Class II drugs?

A

They decrease cytosolic calcium

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46
Q

Effects of Class II drugs?

A

Slow sinus rate
Prolong AV conduction and refractoriness
Inhibit automaticity
Block cardiac sympathetic innervation and effects of circulating catecholamines

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47
Q

Class II drugs effects of ECG?

A

Increase P-P interval (SA Node)
Increase PR interval (AV node)

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48
Q

Main use of Class II drugs?

A

Beta-blockers are useful in:
Mortality benefit and anti-arrhythmic effect post MI and chronic CHF
Control of ventricular rate in atrial fibrillation
Useful in VT storm (without cardiogenic shock)

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49
Q

Use of Class II beta-blockers in torsades?

A

Beta-blockers are useful in preventing torsades in patients with congenital LQTS but not drug induced LQTS (these are bradycardia dependent)

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50
Q

Main side effects of Class II drugs?

A

Bradycardia
Hypotension

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51
Q

What is Class III drugs in the Vaughan Williams classification?

A

These are Potassium channel blockers

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52
Q

Drugs in Class III?

A

Sotalol
Dofelitide
Ibutilide
Amiodarone
Dronedarone

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53
Q

Why are amiodarone and dronedarone unique drugs?

A

They have properties of all 4 Classes!

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54
Q

Effects of Class III drugs?

A

They block potassium channels and therefore outward potassium current (phase 3) causing slowing of repolarization and increase in action potential duration.

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55
Q

ECG effect of Class III drugs?

A

They will prolong the QT interval

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56
Q

Main uses of Class III drug Sotalol?

A

Atrial fibrillation
Ventricular tachycardia in patients with ICDs

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57
Q

Unique effect of Sotalol?

A

Sotalol has mild beta blocker effect Class II

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58
Q

Side effects of Class III drug Sotalol?

A

Major risk is LQTS/Torsades due to reverse use dependence
May lower DFT

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59
Q

Excretion of Sotalol?

A

Mostly renal

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60
Q

Main uses of Class III drug Dofelitide?

A

Persistent atrial fibrillation
(on the basis of the DIAMOND studies)

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61
Q

Side effects of Class III drug Dofelitide?

A

LQTS/Torsades
May lower DFT

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62
Q

Excretion of Class III drug Dofelitide?

A

Renal

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63
Q

Main use of Class III drug Ibutilide?

A

Atrial fibrillation
Atrial flutter
Note: Converts 30-60% of afib and flutter. Conversion better for flutter than fibrillation. Can facilitate DCCV of afib

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64
Q

How is Class III drug Ibutilide administered?

A

1 mg given over 10 minutes and may repeat x 1

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65
Q

Side effect of Class III drug Ibutilide?

A

Risk of LQTS/Torsades
(Maybe reduced with magnesium pre-treatment)

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66
Q

Main use of Class III drug Amiodarone?

A

Most effective for recurrent AF
Most effective for VT/VF causing ICD shocks
Occasionally used for SVTs

67
Q

Side effects of Class III drug Amiodarone?

A

May raise DFT slightly
Cardiac: AV block, bradycardia, LQTS/torsades
Pulmonary: Fibrosis, bronchiolitis obliterans
Thyroid: Hypo>Hpyer
Gastrointestinal: Hepatitis, transaminitis, nausea
Neurologic: Ataxia, tremor, neuropathy
Ocular: Corneal deposits, retinopathy
Skin: Photosensitivity, blue skin

68
Q

Unique effect of Amiodarone?

A

Has all Class effects I-IV

69
Q

Main uses of Class III drug Dronedarone?

A

Approved for AF/Flutter only

70
Q

Class III drug Dronedarone is not indicated in?

A

VT or VF

71
Q

Class III drug Dronedarone is contraindicated for?

A

Systolic heart failuire (ANDROMEDA trial)
Permanent AF (PALLAS trial)

72
Q

What is Class IV drugs in the Vaughan Williams classification?

A

These are the calcium channel blockers

73
Q

Drugs in class IV?

A

Verapamil and Diltiazem

74
Q

Mechanism of action of Class IV drugs?

A

Block L type calcium channels causing decrease in cytosolic calcium

75
Q

Effects of Class IV drugs?

A

Prolong AV node conduction and refractoriness
Mild effect on SA node

76
Q

Main use of Class IV Calcium channel blockers?

A

Greatest effect on AV node > Sinus node
Rate control of AF
Termination and chronic suppression of PSVT
Note: IV verapamil as effective as adenosine for PSVT

77
Q

Side effects of Class IV calcium channel blockers?

A

Hypotension, constipation, peripheral edema, negative inotropy (don’t use in systolic HF)
May raise digoxin levels
Synergistic bradycardic effects with beta-blockers

78
Q

What is the concept of use dependence?

A

Greater drug effect at faster HR

79
Q

Which drugs show use dependence and whats the benefit and drawback?

A

Type 1C drugs such as flecanide and proafenone
We want them to work more when there is a tachyardia so thats the benefit
Negative is that they can cause rate dependent AV block by being too efecacious

80
Q

What is the concept of reverse use dependence?

A

Greater drug effect at slower heart rates

81
Q

Which drugs show reverse use dependence and what is the drawback?

A

Type III drugs such as dofelitide and sotalol
At slower heart rates they can cause prolonged QT and precipitate LQT/Torsades

82
Q

Major pro-arrhythmic effects of Class I drugs?

A

Rate dependent AV block (type 1c)
Promote monomorphic VT in patients with cardiomyopathy

83
Q

Major pro-arrhythmic effects of Class III drugs?

A

Brady-dependent LQTS/Torsades

84
Q

What causes QT prolongation?

A

Results from prolongation of action potential duration

85
Q

Which drug classes can prolong QT?

A

Class 1A drugs
Class III drugs

86
Q

What other factors can cause QT prolongation?

A

Low Mg, Low K
Using drugs that prolong QT
(Chloroquine, chlorpromazine, droperidol, erythromycin, haloperdol, methadone, pentamidine, moxifloxacin)
Using drugs that inhibit metabolism of AADs

87
Q

What is Torsades de pointes?

A

Tdp is a polymorphic VT that occurs in the setting of a long QT interval.
Usually we have a baseline normal sinus rhythm with a prolonged QT and PVCs where a PVC can trigger polymorphic VT which then degenerates to v-fib

88
Q

Treatment of torsades de pointes

A

Withdraw offending agent
Magnesium IV
Correct hypokalemia
Isoproterenol or pacing at 90-100 bpm to reduce QT interval
IV lidocaine
Don’t use amiodarone or procainamide as they can prolong QT
No beta blockers due to reverse use dependence
If degenerates to v-fib then defibrillate

89
Q

Which AADs increase ICD defibrillation thresholds and pacing thresholds?

A

Sodium channel blockers
Mexilitine
Flecanide/propafenone
Amiodarone (has all 4 class properties)

90
Q

Which AADs decrease ICD defibrillation thresholds and pacing thresholds?

A

Potassium channel blockers such as sotalol and dofelitide

91
Q

Which AADs can bring out a latent Brugada pattern?

A

Type 1 AADs
Note: Here we see Type 1 pattern come out after 15 minutes of Type 1 AAD. Initially we have a Type III pattern
Can be used as a diagnostic tool

92
Q

What is a unique effect of Type Ic drugs on atrial fibrillation?

A

Type 1C drugs, especially flecanide can cause atrial fibrillation to organize to slow atrial flutter with 1-1 AV conduction

93
Q

How can we prevent the risk of atrial fibrillation slowing to atrial flutter with 1:1 conduction with Type 1c drugs?

A

Give beta-blockers or calcium channel blockers with Type 1c drugs such as flecanide

94
Q

What are some pro-arrhythmic effects of digoxin?

A

Atrial tachycardia or atrial fibrillation with 2nd or 3rd degree AV block
Bidirectional VT
Ventricular fibrillation

95
Q

Which AADs are excreted renally?

A

Sotalol
Dofelitide
Digoxin
Note: Reduce dose in CKD

96
Q

Which drugs are excreted by liver?

A

Lidocaine
Propafenone
Amiodarone
Reduce dose or avoid in liver disease

97
Q

AAD drug elimination

A
98
Q

What is the interaction between amidarone and Warfarin?

A

Amiodarone inhibits CYP 2C9 and leads to higher levels of Warfarin

99
Q

What is the interaction between Verapamil and Droedarone?

A

Verapamil inhibits CYP3A4 and can increase dronaderone levels

100
Q

CYP drug interactions?

A
101
Q

What is the P-glycoprotein pathyway?

A

This is an excretion pathway where drugs are attached to the P glycoprotein which transports drugs and is found in GI tract, liver and kidney

102
Q

What is the P-glycoprotein pathyway?

A

This is an excretion pathway where drugs are attached to the P glycoprotein which transports drugs and is found in GI tract, liver and kidney

103
Q

What are the substrates for the P-glycoprotein pathway?

A

Digoxin
Dabigatran
Anti-neoplastic drugs

104
Q

What are inducers of P glycoprotein pathway?

A

Rifampin
HIV protease inhibitors
Note: These drugs will decrease levels of substrates (digoxin and dabigatran)

105
Q

What are the inhibitors of the P glycoprotein pathway?

A

Amiodarone
Dronedarone
Verapamil
Quinidine
Erythromycin
Ketoconazole
Itraconazole
Cyclosporine
Note: They will increase the levels of the substrates (digoxin, dabigatran)

106
Q

Main uses of digoxin?

A

Major use is in atrial fibrillation with concurrent CHF
Also useful if BB or CCB inadequate

107
Q

Digoxin not useful for which atrial fibrillation?

A

Paroxysmal atrial fibrillation as it does not prevent paroxysms or terminate AF

108
Q

Mechanism of actions for digoxin?

A

Mechanism 1: Blocks NA-K ATPase and increases intracellular Ca increasing contractility
Mechanism 2: Increase vagal tone

109
Q

Main side effects of digoxin?

A

Nausea, vomiting
Visual disturbances
CNS
Proarrrhythmias : AT or AF with AV block, bidirectional VT, VF

110
Q

Treatment for Proarrrhythmias caused by digoxin?

A

Correct K/Mg
Atropine/pacing for bradycardia
Lidocaine for VT/VF
Anti-digoxin Fab antibody fragments (digiband) for refractory VT/VF, hyperkalemia

111
Q

Excretion of Digoxin is via this pathway?

A

P-glycoprotein transporter and excreted via kidneys

112
Q

Half-life of digoxin?

A

1.5 to 3 days

113
Q

What did the DIG trial show?

A

DIG trial was a RCT of 6800 patients with CHF, LVEF <45% who were on digoxin. There was no benefit in mortality.
A secondary analysis showed that there was an increase in mortality with higher digoxin levels >1.1 and serum levels <0.8 were associated with a lower mortality. Therefore, minimize digoxin use but if used keep levels less than or equal to 0.8

114
Q

Which drugs increase digoxin levels?

A

Levels increase with amiodarone, dronedarone, verapamil

115
Q

Mechanism of action of nucleoside adenosine?

A

Binds to adenosine A1 receptor and activated outward potassium current in the atrium. Also has CCB effect

116
Q

Main uses of Adenosine?

A

Terminate SVT (AVNRT, AVRT, AT)

117
Q

How is adenosine administered?

A

Give adenosine 6 mg rapid IV push. If no conversion give 12 mg IV push and can repeat 12 mg dose once more
Note: Try vagal maneuvers first

118
Q

Half life of adenosine?

A

10 seconds

119
Q

Side effects of adenosine?

A

Flushing, headache, chest pain
Asystole
Atrial fibrillation (10-15%)
Bronchospasm (avoid in asthmatics)

120
Q

What blunts adenosine effects?

A

Caffeine
Theophylline

121
Q

What enhances adenosine effects?

A

Dipyridamole
Heart transplant

122
Q

Mechanism of action of Ranolazine?

A

Blocks late sodium current and shortens APD

123
Q

Main use of Ranolazine?

A

FDA approved for chronic stable angina
Also reduced NSVT, SVT, and AF in MERLIN-TIMI-36 trial

124
Q

Ranolazine use for VT/VF?

A

RAID trial in ICD pateints showed ranolzine reduced recurrent VT/VF ICD therapy for treated VT or VF . It did not reduce the primary end point of first treated VT/VF or death.

125
Q

Prevention of VT/VF
What did the cardiac arrhythmia suppression trial show (CAST)?

A

This was a trial done in patients that were post MI and frequently had reduced EF with PVCs/NSVT and used Class Ic agents like encainide and flecanide. These drugs suppressed PVCs/NSVT BUT

Doubled mortality and could cause VT as well. Therefore, they carry a black box warning and shouldnt be used in patients with MI (and structural heart disease such as low EF).

126
Q

Prevention of VT/VF
Effect of Sotalol on mortality for treatment of VT/VF?

A

Use of sotalol increased mortality when used for VT/VF (SWORD trial Lancet 1996)

127
Q

Prevention of VT/VF
Effect of Dofelitide on mortality for treatment of VT/VF?

A

Neutral (DIAMOND-MI Trial Lancet 2000)

128
Q

Prevention of VT/VF
Effect of Dronedarone on mortality for treatment of VT/VF?

A

Mortality increased (ANDROMEDA NEJM 2008). In Andromeda trial patients had heart failure with reduced ejection fraction. Therefore, dronaderone should not be used in these patients, it is contraindicated

129
Q

Prevention of VT/VF
Effect of Amiodarone on mortality for treatment for VT/VF?

A

Mixed study results but no proven benefit on moratlity

130
Q

Prevention of VT/VF
What was the SCD-HeFT trial?

A

This was a study of about 2500 subjects with LVEF <35% and NYHA II-III symptoms who were randomized to receive amiodarone, placebo or ICD therapy and followed for 48 months

131
Q

Prevention of VT/VF
What did the SCD-HeFT trial show?

A

There was no benefit to amiodarone over placebo. However, ICD showed significant reduction in mortality

132
Q

Treatment of VT/VF arrest
First step in treatment of pulseless VT/VF arrest?

A

Shock

133
Q

Treatment of VT/VF arrest
If pulseless VT or VF arrest refractory to initial shock?

A

Give amiodarone 300 mg IV/IO and can repeat boluses of 150 IV/IO
Note: Lidocaine can be used as an alternative

134
Q

Treatment of VT/VF arrest
What did the ARREST trial show?

A

ARREST trial analyzed 504 patients with out of hospital cardiac arrest refractory to initial shock and use of amiodarone improved % patients surviving to admission

135
Q

Treatment of VT/VF arrest

What did the ALIVE trial show?

A

AlIVE TRIAL analyzed 347 out of hospital cardiac arrest patients refractory to initial shock treat with amiodarone vs lidocaine and showed amiodarone more effacacious than lidocaine.

136
Q

Treatment of sustained monomorphic VT (with a pulse)

A

If patients are relatively stable then IV amiodarone 150 mg IV over 10 minutes and repeat as needed.
Procainamide IV if no severe CHF or MI. 20-50 mg/min until hypotension or QRS duration increased by 50%
Lidocaine can be used but is less effective than procainamide
Beta-blockers/verapamil can be used for idiopathic VT

137
Q

Prevention of ICD shocks
Which AAD is most effective for preventing ICD shocks?

A

Amiodarone is the most effective
Note: Based on the OPTIC trial that compared beta-blocker to sotalol and amiodarone + beta blocker

138
Q

Prevention of ICD shocks
Order of efficacy of AADs in prevention of ICD shocks?

A

Amiodarone > Sotalol > beta-blocker alone

139
Q

Prevention of ICD shocks?
Second line agent is first line agents are not working?

A

Mexilitine

140
Q

Prevention of ICD shocks
When should cathetar ablation be used?

A

For treatment of monomorphic VT

141
Q

Prevention of ICD shocks?

A

First use amiodarone + beta-blocker
Sotalol can be used as well
Mexilitine as second line
Cathetar ablation for monomorphic VT

142
Q

First line treatment of acute termination of regular SVT?

A

Vagal maneuvers or IV adenosine

143
Q

If Vagal maneuvers or IV adenosine don’t work for acute termination of regular SVT and patient is hemodynamically stable?

A

IV beta blockers
IV Diltiazem or Verapamil
If these fail then cardiovert (synchronized)

144
Q

If Vagal maneuvers or IV adenosine don’t work for acute termination of regular SVT and patient is hemodynamically unstable?

A

Synchronized cardioversion

145
Q

First line treatment for chronic SVT?

A

Ablation

146
Q

Chronic medical therapy if ablation refused or contraindicated?

A

Beta-blockers, Diltiazem, Verapamil (note: if no pre-excitation)

147
Q

Other therapies for chronic medical therapy for SVT?

A

Flecanide. Propafenone (Class IIa)
Amiodarone, Sotalol, Dofelitide (Class IIb)

148
Q

Which drugs can be utilized for acute termination of atrial fibrillation?

A

Class I: Flecanide, propafenone, dofelitide, IV ibutilide
Class IIa: Oral amiodarone

149
Q

Anticoagulation consideration when using AAD for atrial fibrillation?

A

Patients should be anticoagulated three weeks prior and 4 weeks post conversion to normal sinus rhythm (same as DCCV)

150
Q

Pill in pocket approach for acute termination of atrial fibrillation?

A

Class IIa recommendation is to use propafenone or flecanide preferrably with a beta blocker to prevent Aflutter with 1:1 conduction. First dose should be initiated under observation

151
Q

Which AADs can be used for maintenance of sinus rhythm in atrial fibrillation patients with no structural heart disease (no CAD, LVH or HFrEF)?

A

All of them
First line: Dofelitide, Dronaderone, Flecanide, Propafenone, Sotalol
Second line: Amiodarone

Note: Cathetar ablation can also be offered

152
Q

Which AADs can be used for maintenance of sinus rhythm in atrial fibrillation patients with LVH > 1.5 cm?

A

Dronaderone is first line
Amiodarone second line

153
Q

Which AADs can be used for maintenance of sinus rhythm in atrial fibrillation patients with CAD?

A

First line: Dofelitide, Dronaderone, Sotalol
Second line: Amiodarone
Note: Cathetar ablation can be offered as well

154
Q

Which AADs can be used for maintenance of sinus rhythm in atrial fibrillation patients with heart failure with reduced ejection fraction?

A

First line: Amiodarone and Dofelitide
Cathetar ablation can be offered as well

155
Q

What did the Canadian trial of Atrial fibrillation (CTAF) show in terms of maintanence of NSR?

A

Amiodarone most effective when compared to propafenone or sotalol (60% vs 30%)

156
Q

What did the SAFE-T trial show in terms of maintence of sinus rhythm in atrial fibrillation?

A

This trial showed amiodarone was superior to Sotalol

157
Q

What did the DIONYSOS trial show in terms of maintence of sinus rhythm in atrial fibrillation?

A

Amiodarone was superior to Dronaderone

158
Q

Drug of choice in pre-excited atrial fibrillation in patients that are hemodynamically stable?

A

First line: Procainamide and Ibutilide
Avoid beta-blockers, CCBs, adenosine, digoxin and amiodarone as they can degenerate it to VF
Note: If patient is hemodynamically unstable then DCCV

159
Q

Which AADs are safe in pregnancy to use?

A

Adenosine
Metoprolol
Digoxin
Lidocaine
Propranalol

160
Q

These drugs should be avoided in pregnancy?

A

Amiodarone
Atenalol
Dronaderone

161
Q

AADs in prevention of SCD due to VT/VF?

A

No value of AADs for prevention of SCD (except beta-blockers)

162
Q

Drugs of choice in VF/pulseless VT arrest?

A

Amiodarone or Lidocaine

163
Q

Drugs of choice for termination of monomorphic VT with a pulse?

A

Amiodarone or Procainamide

164
Q

Drugs of choice for prevention of ICD shocks?

A

Amiodarone > Sotalol
Second line: Mexilatine

ELECTROPHYSIOLOGY (5 decks)

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