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8 Cards in this Set

  • Front
  • Back
what are the classes of antiarrythmic drugs and their actions?
class I: depress rate of depolarization of phase 0 via inibition of fast Na+ channels; local anesthetic action
Class II: block beta adrenergic receptors
Class III (K channel blockers): prolong action potential repolarization
Class IV (Ca channel blockers): depresses phases 2 and 3 of AP by blocking slow Ca channels
What are the differences b/w the class I antiarrythmics?
Class IA: moderate phase 0 depolarization, prolonged repolarization, increased AP duration
Class IB: weak phase 0 depolarization block, shortened repolarization, decreased AP duration
Class IC: strong phase 0 depolarization block, no effect on repolarization, no effect on AP duration
How is Quinidine used?
1) Tx of supraventricular* and ventricular arrythmias
2) effective w/ cardioversion in restoration of sinus rhythm in atrial flutter/fibrillation
3) effective in preventing recurrence of a-fib/flutter, extrasystoles
Quinidine's mechanism of action?
inhibition of the fast Na channel and inhibition of repolarization
quinidine's extracardiac effects?
adrenergic receptor blocking properties--hypotension and reflex increase SA rate
2)antimalarial, antipyretic, oxytocic properties
adverse effects of quinidine?
1)antimuscarinic actions: overcome membrane effects, increase sinus rate and AV conduction
2)quinidine syncope: lightheadedness, fainting
3)diarrhea, nausea, vomiting (most common)
4)cinchonism: headache, dizziness, tinnitus
5)increases digoxin plasma levels, may ppt digitalis toxicity
6)prolonged Q-T interval
7)widening of QRS complex
procainamide used?
1)Tx of atrial and ventricular ectopic beats
2)tx of ventricular tachyarrthmias not repsonsive to lidocaiane or quinidine
*similar to quinidine*
advantage of procainamide over lidocaine?
less susceptible to hydrolysis, can be administered by mouth or parenterally
major metabolite also has antiarrythmic properties