Antiarrhythmics Flashcards
2 etiologies of arrhythmias
Abnormal impulse formation and alterations in impulse conduction
Most life threatening arrhythmias
Ventricular tachycardia
Class 1 antiarrhythmic drugs
Sodium channel blockers
Class 2 antiarrhythmic drugs
Beta blockers
Class 3 antiarrhythmic drugs
Potassium channel blockers
Class 4 antiarrhythmic drugs
Calcium channel blockers
Fast response fibers
Located in muscle–ventricle and atria
Phase 0 of AP in fast response fibers
Na channels open, rapid depolarization
Class 1 drugs can slow or block phase 0
Phase 1 of AP in fast response fibers
Na+ channels are inactivated
No effect of anti arrhythmic drugs
Phase 2 of AP in fast response fibers
Plateau phase due to L type Ca channels
Inward Ca balanced by outward K
Class III drugs prolong plateau by blocking K channels
Class IV drugs have little effect on this type of Ca channel
Phase 3 of AP in fast response fibers
Repolarization phase due to K leaving and Ca channels inactivated
Class III drugs prolong repolarization
Phase 4 of AP in fast response fibers
Return to resting membrane potential
Due to Na/K pump
Digoxin can be pro-arrhythmic through blockade of phase 4
Slow response fibers
SA and AV nodes
No participation of Na
Class 1 drug has no effect
What is solely responsible for AP in slow response fibers
Ca
Class IV drugs block phase 0
Prolonging action potential duration with antiarrhythmics
Prolongs refractoriness to pathologic stimuli and slows down rhythm
Ischemia causes
Decreased O2 supply–> decreased electron transport chain–> decreased ATP–>Decreased Na/K ATPase–> Na stays in the cell keeping it depolarized causing a large amount of channels in inactive state
Requires anti-arrhythmic drug
Class 1A drugs
Blocks open, activated Na channel
Class 1B drugs
Blocks refractoriness–decreases rate of firing
Class 1C drugs
Blocks open, activated Na channel
Examples of 1A drugs
Quinidine Procainamide Pyramidine Moderate Na binding Increased AP by blocking K+ Used for both ventricular and atrial dysrythmias
Example of 1B drug
Lidocaine
Phenytoin
Mexiletine
Example of 1C drug
Flecainide
Propafenone
1B drugs are specific to
Ischemia
Used for post MI, digoxin toxicity, open heart surgery
Least Na binding; decreased AP
1C drugs used for
life threatening V Tach, fibrillation and refractory SVTs
(A fib)
Strong Na binding
No effect on AP length due to no effect on K+
FDA approved beta blockers for arrhythmias
Metoprolol, Propranolol, Esmolol
Amiodarone
K+ channel blocker
Very long half life of 20-50 days
Main side effects: pulmonary fibrosis, liver toxicity, thyroid dysfunction
Has 1, 2, 3, 4 properties
Calcium channel blockers indicated for arrhythmias
Verapamil and diltiazem
Side effects of calcium channel blockers
Decreased BP, decreased CO, lower extremity edema, constipation
Adenosine
Rapidly acting AV nodal blocker–administered IV
Quick half life of 30 seconds
Drug of choice for paroxysmal supraventricular tachycardia
Digoxin
Inhibits Na/K ATPase inhibitor
Class 2 anti arrhythmic
Beta blocker
Prolongs stage 4 slow depolarization by decreasing Ca depolarization
Treatment of supraventricular arrythmias
Class 3 anti arrhythmic
Blocks K+ channels–delays repolarization and increases AP length
Can treat both atria and ventricular arrhythmias
Sotalol
Class 3 anti arrythmic
Also used as beta blocker
Dofetilide
Class 3 anti arrhythmic
Ibutilide
Class 3 anti arrhythmic
Class 4 anti arrhythmic
Non-dihydropyridine Ca channel blockers
Used for supraventricular arrhythmias especially A fib
