Antiarrhythmics

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Causes of Arrhythmias

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Abnormal AP formation
Abnormal AP conduction

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Class I Antiarrhythmic Drugs

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Quinidine
Procainamide
Lidocaine
Flecainide

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Class I Antiarrhythminc Drugs

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All inhibit sodium channels
Binds more readily to open or inactivated Na channels(rather than resting)

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Class IA Antiarrhythmics

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Quinidine, Procainamide
Slow rate of rise of phase 0 of AP (slow conduction velocity)
Also inhibit phase 3 K channels to increase AP duration and ERP

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Class IB Antiarrhythmics

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Less inhibition of phase 0 Na channels
Less slowing effect on rate of rise of phase 0
Therefore, decrease AP duration and ERP

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Class IC Antiarrhythmics

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Markedly inhibit phase 0 Na currents
Markedly decrease rate of rise of phase 0
Marked slowing of conduction velocity

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Quinidine

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Class IA
Mainly inhibits Na channels
Also inhibits K channels
Versitile: Used for Various arrhythmias (ectopic atrial, supraventricular and ventricular), restore cardiac rhythm ,BRAUNWALDS heart disease
ADE: can cause other arrhythmias (TdP due to prolonged QT), NVD, INCREASED DIG levels! can have alpha-adrenergic effect (decrease BP and increase sinus rate)

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Procainamide

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Class IA
Inhibit Na channels less than quinidine
A portion is acetylated in the liver to NAPA (little effect on phase 0, but prolongs AP (inhibits K channels))
ADE: Lupus, CNS, GI and alpha block(less than with quinidine)

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Lidocaine

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Class IB
Rapidly interact with phase 0 Na channels
Shortens phase 3 repolarization (decreasing AP duration and ERP) due to inhibition of a small population of late opening Na channels during AP plateau
Uses: Ventricular arrhythmias during MI
IV ONLY
ADR: CNS, no negative ionotropic effect

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Flecainide

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Class IC
interact more slowly with Na channels
Markedly suppresses phase 0 in all Na dependent fibers
Also inhibits some K channeds, but also block late opening Na channels
Reduced abnormal AP FORMATION because it increases the threshold for phase 0
Use: reserved for severe arrhythmias resistant to other drugs
ADR: negative ionotropic effects effects can aggravate CHF, CNS, aggravate pre-existing arrhythmias or induce tachycardia aggravated by hyperkalemia. INCREASED MORTALITY

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Class II antiarrhythmics

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B-adgrenergic receptor antagonist
Block B receptor actions on Ca channels (decrease inward Ca currents))
Depress phase 4 especially in nodal tissues
Used for arrhythmias caused by increased sympathetic neural activity or excess catecholamine presence
Als used for atrial flutter and fibrillation
Avoid use with Ca channel blockers! (too much suppression of normal cardiac function)

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Propranolol

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Class II Beta Blocker
Reduce sudden arrhythmic death after MI
Has membrance stabilizing properties

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Acebutolol

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Class II Beta Blocker
B-1 specific
Partial agoinst activity may decrease risk of to much suppression of normal cardiac function

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Esmolol

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Class II Beta Blocker
Very short acting used IV in arrhythmias during SURGERY or EMERGENCY situations

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Class III Antiarrhythmics

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Primarily inhibi phase 3 K channels
Prolongs repolarization (phase 3), AP duration and ERP without altering other phases or phase 4

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Amiodarone

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Class III
Complex effects (shows class I, II, III and IV activity)
Decreases conduction velocity by cell-to-cell coupling
Uses: Severe refractory (resistant) suprventricular and ventricular tachyarrhythmia, and in patients who have implantable defibrillators for controlling arrhythmias (drug lowers how aften ICD must deliver shocks)
Concentrates in tissues for several weeks
ADR: Pulmonary fibrosis, thyroid problems, iodine accumulation is skin

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Dofetilide

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Class III
Inhibits only K channels
Mostly supraventricular arrhythmias
Good for Atrial fibrillation
ADR: Ventricular Tdp

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Class IV Antiarrhythmic Drugs

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Block voltage-sensitive L-type Ca channels (decrase inward Ca current in phase 0, 2 and 4)
Prolongs AP duration and ERP

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Verapamil and Diltiazem

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Class IV
Bind to Ca channels to decrease inward Ca current, thus decreaseing slopes of phae 0 and 4 (slows conduction and automaticity)