Antiarrhythmics Flashcards
Sotalol
Class III (also a β-blocker)
MOA: K+ channel blocker, decreases SA and AV nodal conduction
Effect: increase AP and ERP
Use: life-threatening ventricular tachycardia or A-fib
SE: torsade (and class II cautions - asthmatics, peripheral vascular dz, DM)
Procainamide
Class 1A
MOA: metabolized by N-acetyltransferase to NAPA an active metabolite which blocks active Na+ channels
Effect: prolong QT
SE: SLE-like syndrome d/t anti-histone Ab, torsades
Class IV Antiarrhythmic Drugs
MOA: Ca2+ channel blockers cardiospecific non-dihydropyridines
Verapamil / Diltiazim
Class II Antiarrhythmic Drugs
MOA: β-blockers
Propranolol / Metoprolol / Esmolol
Esmolol / Metoprolol / Propranolol
Class II
MOA: β-adrenergic blocker, decreases phase 4 of the nodal AP
Effect: slows SA and AV node firing
Use: prevent ventricular arrhythmias s/p MI, used in SVT to protect ventricles from fast atrial rate
Lidocaine / Mexiletine
Class 1B
MOA: blocks inactive Na+ channels
Effect: decreased Na+/K+ ATPase activity
Use: s/p MI, in Digoxin toxicity, open heart surgery
Dofetilide
Class III
MOA: K+ channel blocker
Effect: prolongs QT and converts A-fib or flutter to NSR
SE: torsades (only administered in hospital setting)
Adenosine
Class V MOA: AV nodal blockade via A1 (Gi) on SA and AV node, A2A (Gs) vasodilation including coronaries PK: t1/2 about 30 seconds DOC: paroxysmal SVT (PSVTs) Use: s/p MI increases survival
Digoxin (antiarrhythmic)
MOA: inhibition of cardiac Na+/K+ ATPase in
Effect: increased intracellular Na+ depolarizes cell
Use: CHF, SVTs, A-fib
SE: N/V/D, visual disturbances (halos or color changes)
CI: WPW
Drug interactions: displaced by Amiodarone, Quinidine, Verapamil, Propafenone (increasing toxicity)
Class III Antiarrhythmic Drugs
MOA: K+ channel blockers
Effect: inhibit repolarization
(Amiodarone / Sotalol / Dofetilide)
Quinidine / Procainamide / Disopyramide
Class IA
Magnesium
Class V
Ca2+ antagonist
Use: tx Torsades de pointes, Digoxin-induced arrhythmia, prophylaxis of arrhythmia in acute MI
Heparin (IV)
Use: unstable pt who require immediate cardioversion
Quinidine
Concomitant Class III activity (block K+ channels)
Class I Antiarrhythmics
MOA: Fast Na+ channel blockers
1A: Quinidine, Procainamide, Disopyramide
1B: Lidocaine, Mexiletine
1C: Fecainide, Propafenone
Warfarin (oral)
In stable pt cardioversion should be delayed only for 3-4 wks until adequate anticoagulation has been achieved
*continue oral anticoags at least 4 wks s/p procedure
Disopyramide
MOA: blocks active Na+ channels
Effect: stronger anticholinergic
Amiodarone
Class III (w/ Class 1A, II and IV activity too) MOA: block delayed rectifier K+ current Effect: delay repolarzation, prolongation of AP and ERP, increase QRS, prolong QT Metabolism: high tissue protein binding SE: pulmonary fibrosis, hepatotoxicity, blue-gray discoloration of skin, thyroid dysfunction, QT prolongation
Flecainide / Propafenone
Class 1C
MOA: inhibitors of fast Na+ channels
Use: life-threatening V-tach, fibrillation, refractory SVTs (second-line for all uses)
SE: can increase sudden cardiac death by decreasing LV function
Mexiletine PK
Available orally for Class 1B antiarrhythmic properties
S
Lidocaine MOA:
Blocks inactive Na+ channels, used as anti-arrhythmic or as local anesthetic
*least cardiotoxic of all conventional antiarrhythmics
Verapamil / Diltiazem
Class IV
MOA: non-dihydropyridine Ca2+ channel blockers (cardioselective)
Effect: decrease phase 0 and phase 4 in SA and AV node (slow AV nodal conduction to protect ventricles from fast atrial rhythm)
Use: SVTs
Verapamil SE: constipation, gingival hyperplasia, displaces Digoxin (increasing concentration and toxicity)
Esmolol
β-1 selective, available IV
Effect: decrease phase 4 b/c slowing node by decreasing SANS input
Atropine
Use: bradyarrhythmias to decrease vagal tone
