Antiarrhythmics Flashcards
Describe the mechanism of action of class IA antiarrhythmics (quinidine and procainamide)
block Na+ channels in normal and depolarized (“sick”) cells; prolong repolarization after the action potential and increasing the refractory period by blocking K+ channels
What are the side effects of class IA antiarrhythmics (quinidine and procainamide)?
Frequent toxicity- fever, diarrhea, arrhythmias like Torsades de Pointes, long AT syndrome
What are the clinical indications for class IA antiarrhythmics (quinidine, procainamide)?
Atrial and ventricular arrhythmias; quinidine suppresses A fib.
When are class IA antiarrhythmics contraindicated?
Only use in EXTREME caution in patients w/ complete AV block
Name the class IB antiarrhythmics.
lidocaine and mexiletine
Describe the mechanism of action of class IB antiarrhythmics (lidocaine and mexiletine).
They block Na+ channels in depolarized (“sick”) cells and increase K+ permeability. Decrease automaticity of Purkinje fibers
What are the side effects of class IB antiarrhythmics (lidocaine and mexiletine)?
Respiratory arrest, convulsion d/t blockage of inhibitory transmission in the brain
What are the clinical indications for class IB antiarrhythmics (lidocaine and mexiletine)?
Ventricular arrhythmias
- mexiletine treats long QT syndrome
- lidocaine can only be given IV
Name the class IC antiarrhythmics.
Flecainide
Describe the mechanism of action of class IC antiarrhythmics (flecainide).
Blocks Na+ channels in normal and depolarized (“sick”) cells with no effect on repolarization.
*the action potential duration increases like class IA drgus but by a different mechanism so they are less likely to cause torsades de pointes
What are the clinical indications for class IC antiarrhythmics (flecainide)?
Ventricular arrhythmias; can suppress PVCs but are shown to increase mortality when used after MI to tx asymptomatic PVCs
Name the class II antiarrhythmics.
Metoprolol
Describe the mechanism of action of class II antiarrhythmics (metoprolol).
Adrenergic beta-blocker; decreases SA nodal rate and AV conduction by blocking sympathetic input
What are the clinical indications for class II antiarrhythmics (metoprolol)?
Atrial tachycardias; proven effective in reducing mortality s/p MI
**DO NOT use in WPW patients
Name the class III antiarrhythmics.
Amiodarone, sotalol
Describe the mechanism of action of class III antiarrhythmics (amiodarone, sotalol).
block K+ efflux during phase 3 and beta receptor blockade
*amiodarone also has a lesser blockade on Ca++ channels, increasing the refractory period
What are the side effects of class III antiarrhythmics (amiodarone, sotalol)?
Prolonged QT that can lead to torsades de pointes.
*amiodarone- also causes pulm fibrosis in 1% of patients, thyroid dysfunction, liver toxicity, photosensitivity from corneal deposits
What possible drug interactions should you watch out for with amiodarone?
Simvastatin (can increase risk of rhabdo b/c amiodarone inhibits the CYP enzyme that metabolizes simvastatin)
What are the clinical indications for amiodarone (class III antiarrhythmic)?
at low doses suppresses A fib; high doses supress ventricular arrhythmias
*drug of choice in cardiac arrest
What are the clinical indications for sotalol (class III antiarrhythmic)?
Supraventricular and ventricular arrhythmias; used for pts w/ ICD
Name the class IV antiarrhythmics.
verapamil, diltiazem
Describe the mechanism of action of class IV antiarrhythmics (verapamil, diltiazem).
Ca++ channel blockers (L-type). Slow the conduction at the SA and AV nodes in depolarized fibers
What are the side effects of class IV antiarrhythmics (verapamil, diltiazem)?
Can cause edema not reflective of cardiac fxn in 33% of pts
What are the clinical indications of class IV antiarrhythmics (verapamil, diltiazem)?
SVT, A fib, A flutter
