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8 Cards in this Set
- Front
- Back
what are the classes of antiarrythmic drugs and their actions?
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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 |
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What are the differences b/w the class I antiarrythmics?
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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 |
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How is Quinidine used?
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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 |
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Quinidine's mechanism of action?
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inhibition of the fast Na channel and inhibition of repolarization
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quinidine's extracardiac effects?
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adrenergic receptor blocking properties--hypotension and reflex increase SA rate
2)antimalarial, antipyretic, oxytocic properties |
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adverse effects of quinidine?
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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 |
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procainamide used?
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1)Tx of atrial and ventricular ectopic beats
2)tx of ventricular tachyarrthmias not repsonsive to lidocaiane or quinidine *similar to quinidine* |
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advantage of procainamide over lidocaine?
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less susceptible to hydrolysis, can be administered by mouth or parenterally
major metabolite also has antiarrythmic properties |