Antiarrhythmic Agents
Drug
Class
MOA
Indications
Side Effects
Quinidine
1A
Treatment of acute/chronic SVT, WPW
syndrome
N&V, Diarrhea
Interferes with normal neuromuscular transmission
Low therapeutic ratio: heart block, hypotension, proarrhythmia
Procainamide
1A
Inhibit fast Na+ channels – lengthen the action potential duration & effective
refractory period
Decreases the slope of phase 4 depolarization
Alpha blocking drug
Inhibit fast Na+ channels – lengthen the action potential duration & effective
refractory period
Similar to quinidine – less prolongation of QT interval
Decreases the slope of phase 4 depolarization
Used in pts with Afib to suppress ventricular
irritability
Paradoxical vtach
Hypotension d/t myocardial depression
May provoke a lupus-like syndrome, N/V, & lots of other side
effects
Disopyramide
1A
Inhibit fast Na+ channels – lengthen the action potential duration & effective
refractory period
Similar to quinidine - Decreases the slope of phase 4 depolarization
For suppressing atrial and ventricular
tachyarrhythmias
Moricizine
1A
Treatment of sustained ventricular arrhythmias
Lidocaine
1B
Suppression of ventricular arrhythmias (reentry,
PVCs, vtach)
Minimal side effects: in high doses can decrease AV node and
His-Purkinje conduction
Mexiletine
1B
1B
Chronic suppression of ventricular
tachyarrhythmias
No longer available in US (end of story)
Similar to lidocaine – electrophysiologic
Tocainide
Phenytoin
1B
Inhibit fast Na+ channels – lengthen the action potential duration & effective
refractory period
Decreases the fast inward sodium ion current
Decreases automaticity
Inhibit fast Na+ channels – shorten the action potential duration and the
normal ventricular refractory period
Delays rate of phase 4 depolarization
Inhibit fast Na+ channels – shorten the action potential duration and the
normal ventricular refractory period
Inhibit fast Na+ channels – shorten the action potential duration and the
normal ventricular refractory period
Inhibit fast Na+ channels – shorten the action potential duration and the
normal ventricular refractory period
MOA is similar to lidocaine (delays rate of phase 4 depolarization)
Anticholinergic effects cause dry mouth, urinary hesitancy
QT interval prolongation
Paradoxical vtach
Myocardial depression, hypotension, CHF
Proarrhythmic effects occur in 3-15% of patients
CNS disturbances: ataxia, nystagmus, vertigo, slurred speech,
sedation, confusion
Flecainide
1C
Effective in suppressing ventricular arrhythmia
d/t digitalis toxicity
Paradoxical vtach
Torsades de Pointes
Effective in suppression of VPBs and Vtach
Propafenone
1C
Effective oral agent for suppression of
ventricular/atrial tachyarrhythmias
Proarrhythmic in patients with LV dysfunction, preexisting
ventricular arrhythmias, or sustained Vtach
SE: vertigo, blurred vision, taste disturbances
Propranolol
Esmolol
Metoprolol
2
Effective for reducing the arrhythmias provoked
SNS activity (stress, thyrotoxicosis,
pheochromocytoma)
SE: bradycardia, hypotension, myocardial depression,
bronchospasm;
Worsening CHF;
Potentiation of pre-existing conduction blockade (rebound
SVTs)
Upregulation of b-adrenergic receptor density
CNS side effects: mental depression, fatigue
Inhibit fast Na+ channels – potent sodium channel blocker, markedly
decreasing the rate of phase 0 depolarization and conduction speed of
cardiac impulses
Fluorinated local anesthetic analog of procainamide
Delays conduction in bypass tracts (WPW)
Inhibit fast Na+ channels – potent sodium channel blocker, markedly
decreasing the rate of phase 0 depolarization and conduction speed of
cardiac impulses
Has weak B adrenergic and calcium channel-blocking effects
Decrease the rate of spontaneous phase 4 depolarization (↓ ANS activity)
Slow the speed of conduction of impulses through cardiac atrial tissues,
prolonging the PR interval
Proarrhythmic with LV dysfunction
Prolongs QRS by 25% or more
Amiodarone
3
Inhibit potassium channels (phase 3) – resulting in the prolongation of cardiac
myocyte depolarization, action potential duration, and effective refractory
period
Prolongs the refractory period of all cardiac tissues
Exhibits non-competitive blockade of alpha- and beta-receptors
Has potent vasodilating properties
Dilates coronary arteries and increases coronary blood flow
Refractory supraventricular/ventricular
tachycardia:
Tx of: post-cardiac surgery afib, WPW
tachyarrhythmias, decreases mortality after MI
**Amio possesses Class I and Class II effects
Pulm: toxicity:
pulmonary alveolitis (incidence: 5-15%, mortality:
5-15%)
may be r/t & accelerated by high FiO2 exposure
risk may be increased by CPB
*Has a long elimination half time, and a large Vd
CV: QTc interval prolongation, bradycardia, decreased
responsiveness to SNS activity and catecholamines (blockade
of alpha and beta receptors)
Potentiation of myocardial depressant effects of GA,
alpha and beta blockade, calcium channel blockers
Neuro: toxicity – peripheral neuropathy, tremors, sleep
disturbances, HA, proximal muscle weakness
Nausea, diarrhea
Bradycardia, QT prolongation
Increased serum creatinine
Provokation of Torsades d/t QTc prolongation
Dronedarone
3
Noniodinated benzofuran derivative of amiodarone
Blocks sodium, potassium, and calcium channels, and sympatholytic effects
Indicated for tx of resolved/cardioverted
afib/aflutter
Sotalol
3
Non-selective BB at low doses
Prolongs cardiac AP in the atria, ventricles, and accessory pathways
A long-acting BB with L and D isomers
Tx of sustained Vtach of Vfib
Ibutilide
3
Dofetilide
3
Potent, pure potassium channel-blocking agent
Bretylium
Verapamil
Diltiazem
3
4
No longer available in US
Calcium channel blockers (not dihydropyridines)
Inhibit slow calcium channels (phase 4)
Potent AV node depressant effects and decreases the activity of the SA node
Digoxin
Oth
er
Adenosine
Oth
er
Effective for conversion of recent onset
afib/flutter to NSR
Afib, Aflutter
Resolved/Cardioverted Afib/flutter
Also prolongs QT interval
Highly effective in terminating PSVT (a re-entry
tachycardia involving AV node)
Provocation of heart block in patients with conduction system
decrease
Myocardial depression and decreased CO in patients with poor
LV function
Can enhance conduction through accessory pathways (WPW)
increasing the ventricular response rate
Transient AV block
Bronchospasm – antagonized by methylxanthines
(theophylline, caffeine)
Tx/prevention of atrial tachyarrhythmias
Slows conduction of cardiac impulses through the AV node
Electrophysiologic effects resemble verapamil & diltiazem
Stimulation of adeonosine1 receptors increases potassium conductance,
shortens AP duration, and hyperpolarizes cardiac cell membranes
Tx PSVT, WPW
Causes dose-dependent prolongation of QTc