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Anti-arrhythmics
USMLE Step 1
| Drug | MOA & ADRs |
|---|---|
| 4 classes of anti-arrhythmics | Silly (Na) Bunnies (Beta) Punch (K) Cats (Ca) |
| Class 1A antiarrhythmic: Quinidine | MOA: Na channel blocker used for both atrial & ventricular tachycardias (slow phase 0 depolarization, increase AP duration), for ectopic arrhythmias; ADRs: hypoTN & QT prolongation, potentiates digitoxin toxicity b/c displaces digitoxin from albumin |
| Class 1A antiarrhythmic: Procainamide | MOA: Na channel blocker used for ventricular & supraventricular tachycardias, increase AP duration & slow phase 0 depolarization, used for ectopic arrhythmias; ADRs: hypoTN & QT prolongation, reversible lupus erythematosus if taken on a chronic basis |
| Class 1B antiarrhythmic: Phenytoin | MOA: Na channel blocker that decreases AP duration & slows phase 0 depolarization, used for acute ventricular flutter/fib & digitalis induced arrhythmias, *Note rarely used as an antiarrhythmic*; ADRs: gingiva hyperplasia |
| Class 1B antiarrhythmic: Lidocaine | MOA: Na channel blocker used for ventricular tachycardia or ventricular fib (mildly slow phase 0 while significantly shortening phase 3 repolarization, thus good for abnml arrythmias), used for digitalis induced arrhythmias |
| Class 1C antiarrhythmic: Flecainide | MOA: Na channel blocker effective in minimizing the chance of ectopic beats in the ventricle (effect on phase 0 is more profound, no effect on AP duration), used as a 'broad spectrum' antiarrhythmic; ADRs: pro-arrhythmic = risk of causing death |
| Class 2 antiarrhythmic: Propranolol | MOA: beta-1 antagonist used post-MI due to #1 cause of post-MI death is arrythmia, slow the HR in case of A fib & flutter, suppresses phase 4, particularly suited in symp-driven tachyarrythmias (i.e. AV nodal re-entrant tachy) |
| Class 2 antiarrhythmic: Metoprolol | MOA: beta-1 antagonist more preferred b/c specific, used post-MI due to #1 cause of post-MI death is arrythmia, slow the HR in case of A fib & flutter, suppresses phase 4, particularly suited in symp-driven tachyarrythmias (i.e. AV nodal re-entrant tachy) |
| Class 3 antiarrhythmic: Bretylium | MOA: K channel blocker that is rarely used, but increases phase 3 depolarization leading to phase 0 remains unchanged to control arrhythmia (however can also induce an arrhythmia), used for severe unresponsive ventricular arrhythmias |
| Class 3 antiarrhythmic: Amidarone | MOA: K channel blocker that is a 1st line agent for many ventricular and supraventricular arrhythmias, used 4 severe unresponsive ventricular arrhythmias, ADRs: most notable when used long term include pulmonary fibrosis as well as thyroid fx derangements |
| Class 1C antiarrhythmic: Encainide | MOA: Na channel blocker (effect to slow phase 0 depolarization, no effect on AP duration), used as a 'broad spectrum' antiarrhythmic; ADRs: pro-arrhythmic = risk of causing death and for this reason taken off the market 12/16/91 by Bristol-Myers Squibb |
| Class 4 antiarrhythmic: Verapamil | MOA: Ca channel blocker use 2 ways 1) slow Ca in those that are highly dependent like the AV node & 2) slow phase 4 = prolonged AP, thus phase 2 plateau is lost, used in controlling ventricular rate in A fib, also used in atrial tachy & flutter |
| Class 4 antiarrhythmic: Diltiazem | Ca channel blocker use 2 ways 1) slow Ca in those that are highly dependent like the AV node & 2) slow phase 4 = prolonged AP, thus phase 2 plateau is lost, used in controlling ventricular rate in A fib |
Created by:
jerrica_08
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