Antiarrythmics

Drug Class Actions Therapeutic Uses Pharmacokinetics Adverse Effects Other

Quinidine IA -Binds to open and inactivated Na+ -Atrial tachyarrhythmias -Rapidly and completely -Polymorphic ventricular -Has class III activity
channels Prevents NA+ influx -Av-junctional absorbed after oral tachyarrhythmias as well
Slowing rapid upstroke during tachyarrhythmias administration (torsades de pointes) -Cardiotoxic effects
Phase 0 -Ventricular arrhythmias -Extensive metabolism -SA and AV block are exacerbated by
-Decreases the slope of Phase 4 -Maintains sinus rhythm by CYP450 -Asystole hyperkalemia
spontaneous depolarization after direct-current -Toxic: ventricular -Increases steady-
-Inhibits K+ channels cardioversion tachycardia state concentration of
-Mild α-adrenergic blocking action -Prevent frequent -Nausea DIGOXIN by displacing
-Atropine-like effect ventricular tachycardia -Vomiting it from tissues and
-Diarrhea decreasing its renal
-Cinchonism (blurred clearance
vision, tinnitus, headache,
disorientation, psychosis)
Procainamide IA -Binds to open and inactivated Na+ -Well absorbed after -SLE –like syndrome -Dosage needs to be
channels Prevents NA+ influx oral administration -Asystole adjusted in patients
Slowing rapid upstroke during -1/2 life: 2-3 hours -Ventricular arrhythmias with renal failure
Phase 0 -Acetylated in liver to -Depression
-NAPA: prolongs the duration of the NAPA -Hallucination
action potential (class III actions) -NAPA eliminated via -Psychosis
kidneys
Disopyramide IA -Binds to open and inactivated Na+ -Ventricular arrhythmias -50% excreted in urine -Dry mouth -Has Class III activity
channels Prevents NA+ influx unchanged -Urinary retention
Slowing rapid upstroke during -30% of the drug -Blurred vision
Phase 0 converted by liver to -Constipation
-Negative inotropic effect (decrease in mono-N-dealkylated
contractility) is stronger than metabolite
QUINDINE and PROCAINAMIDE
-Peripheral vasoconstriction
Lidocaine IB -Rapidly associates and dissociates -Ventricular arrhythmias -Given via IV due to -Drowsiness -Local anesthetic
from NA+ channels arising during extensive 1st pass -Slurred speech -Dose should be
-Actions are manifested when cardiac myocardial ischemia metabolism -Paresthesia adjusted in people
cell is depolarized or firing rapidly -Wide therapeutic index -Agitation with liver dysfunction
-Shortens Phase 3 repolarisation and -Confusion
decreases the duration of AP -Convulsions
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-Cardiac arrhythmias
Mexiletine IB -Shortens Phase 3 repolarisation and -Mexiletine: chronic tx -Tocainide: pulmonary
Tocainide decreases the duration of AP of ventricular toxicity leading to
arrhythmias associated pulmonary fibrosis
w/ previous MI
Tocainide: tx of
ventricular
tachyarrhythmias
Flecainide IC -Slowly dissociate from resting Na+ -Refractory ventricular -Absorbed orally -Dizziness -Negative inotropic
channels arrhythmias -1/2 life: 16-20 hours -Blurred vision effects can aggravate
-Prominent effects even at normal -Prevention of -Headache CHF
heart rates paroxysmal atrial -Nausea
-Suppresses Phase ) upstroke in fibrillation/flutter -Aggravates pre-existing
Purkinje and myocardial fibers  -Paroxysmal arrhythmias
Slowing of conduction in all cardiac supraventricular -Induces ventricular
tissue tachycardia tachycardia
-Automaticity is reduced by an -Suppresses premature
increase in the threshold potential ventricular contraction
Propafenone IC -Slows conduction in all cardiac tissues -Broad spectrum
antiarrhythmic agent
β-Antagonists II -Diminish Phase 4 depolarization  -Tachyarrhythmias -Propranolol: reduces
Propranolol depressing automaticity, prolonging caused by increased incidence ofsudden
Metoprolol AV conduction and decreasing HR and sympathetic activity arrhythmic death
Esmolol contractility -Atrial flutter and after MI
fibrillation -Metoprolol: reduces
-AV-nodal re-entrant the risk of
tachycardia bronchospasm; most
-Esmolol: acute widely used in
arrhythmias during treatment of cardiac
surgery or emergency arrhythmias
situations
Amiodarone III -Prolongs the action potential -Severe refractory -Incompletely absorbed -Interstitial pulmonary -Has Class I, II, IV
duration and the refractory period supraventricular and after oral administration fibrosis actions as well
ventricular -Prolonged ½ life of -GI intolerance -Also has antianginal
tachyarrhythmias several weeks -Tremor actions
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-Extensive distribution -Ataxia

in adipose tissue -Dizziness
-Full clinical effects -Hyper- or hypothyroidism
achieved 6 weeks after -Liver toxicity
initiation of therapy -Photosensitivity
-Neuropathy
-Muscle weakness
-Blue skin discoloration
Sotalol III -Has potent nonselective β-blocker -Prevents recurrence of -Torsade de pointes
activity (suppresses ectopic beats, arrhythmias
reduces myocardial oxygen demand, -Decreased mortality in
antifibrillatory effects ) patients with sustained
-Blocks rapid outward K+ current ventricular tachycardia
(delayed rectifier)  prolongs both
repolarisation and duration of AP 
Lengthening effective refractory
period
Dofetilide III -1st line agent in pts -1/2 life 10 hours -AMIODARONE, β-
with persistent atrial -Excreted in urine BLOCKERS AND
fibrillation and HF DOFETILIDE are the
-CAD w/ impaired LV only antiarrhythmic
function drugs recommended
for tx of atrial
fibrillations
Verapamil IV -Block voltage-sensitive Ca2+ channels -Arrhythmias that -Absorbed well after -Decrease BP -contraindicated in
Diltiazem  Decrease in slow inward current traverse Ca2+ dependent oral administration pts with pre-existing
that triggers cardiac contraction  cardiac tissues -Verapamil: extensively depressed cardiac
Slow conduction and prolong effective -Atrial arrhythmias metabolized by liver function (due to
refractory period -Reentrant negative inotropic
-Bind only to open, depolarized supraventricular effects)
channels, preventing repolarisation tachycardia
until the drug dissociates -Reduce ventricular rate
-Block most effectively when the heart it atrial flutter and
is rapidly beating (use-dependent) fibrillation
-HTN
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-Angina
Digoxin -Shortens the refractory period in -Control ventricular -Ectopic ventricular beats
atrial and ventricular myocardial cells response rate in atrial  Ventricular tachycardia
-Prolongs the effective refractory fibrillation and flutter and fibrillation (treated
period and diminishes conduction with LIDOCAINE OR
velocity in the AV node PHENYTOIN)
Adenosine -Decreases conduction velocity -DOC: abolishing acute -Short duration of -Flushing -Naturally occurring
-Prolongs refractory period supraventricular action: 15 seconds -Chest pain nucleoside
-Decreases automaticity in the AV tachycardia -Hypotension
node

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 Antiarrythmics

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