| Term 
 
        | What is Class 1 action? What are the effects of Class Ia agents on conduction velocity, action potential duration (APD) and what speed are the kinetics? |  | Definition 
 
        | Class 1 - Na+ channel blockers.  Ia - slow conduction, prolong RP, prolong APD, intermediate kinetics |  | 
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        | Term 
 
        | What is Class 1 action? What are the effects of Class Ib agents on conduction velocity, refractory period, action potential duration (APD) and what speed are the kinetics? |  | Definition 
 
        | Class 1 - Na+ channel blockers. Ib - shorten APD in some tissues, rapid kinetics |  | 
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        | Term 
 
        | What is Class 1 action? What are the effects of Class Ic agents on conduction velocity, action potential duration (APD) and what speed are the kinetics? |  | Definition 
 
        | Class 1 - Na+ channel blockers, Ic - minimal effects on APD, slow kinetics |  | 
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        | Term 
 | Definition 
 
        | sympatholytic, antagonize adrenergic recepts |  | 
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        | Term 
 
        | What is Class III action? |  | Definition 
 
        | III - prolong repolarization,  prolong APD, most block Krapid |  | 
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        | Term 
 | Definition 
 
        | IV - block Ca2+, slows conduction in regions where AP upstroke depends on Ca - nodes |  | 
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        | Term 
 
        | Pro-Dis-Quin is which class? |  | Definition 
 | 
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        | Term 
 
        | name the drug: blocks Na and Kr (secondary). Which class? |  | Definition 
 | 
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        | Term 
 
        | name the drug: slows conduction velocity and pacemaker rate, prolongs APD and dissociates with intermediate kinetics, direct depressant effects on SA and AV nodes |  | Definition 
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        | Term 
 
        | What are the clinical applications of procainamide? |  | Definition 
 
        | most atrial and ventricular arrhythmias, drug of second choice for most sustained V-arrhythmias associated with acute MI |  | 
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        | Term 
 
        | name the drug: oral, IV, IM, eliminated by hepatic metabolism to NAPA and renal elimination, NAPA implicated in torsad de pointes in pts with renal failure, tox: hypotension, long term --> lupus-like reversible symptoms |  | Definition 
 | 
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        | Term 
 
        | how does disopyramide compare to procainamide? |  | Definition 
 
        | similar but significant antimuscarinic effects, may precipitate heart failure |  | 
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        | Term 
 
        | how does quinidine compare to procainamide? |  | Definition 
 
        | similar but more toxic - cinchronism, TdP, rarely used |  | 
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        | Term 
 
        | Which class is lidocaine? What's the MOA? |  | Definition 
 
        | Ib, sodium channel blockade |  | 
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        | Term 
 
        | Name the drug: blocks activated and inactivated Na channels with rapid kinetics, does not prolong and may shorten AP |  | Definition 
 | 
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        | Term 
 
        | What are the clinical applications for lidocaine? |  | Definition 
 
        | terminate V-tachycardias and prevent V-fib after cardioversion |  | 
        |  | 
        
        | Term 
 
        | Name the drug: IV, first pass hepatic metabolism, reduce dose in pts with heart failure or liver disease, Tox: Neuro symptoms |  | Definition 
 | 
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        | Term 
 
        | how does mexiletine compare to lidocaine? |  | Definition 
 
        | orally active congener, used in V-arrhythmias, chronic pain syndromes |  | 
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        | Term 
 
        | What class is flecainide? What is the MOA? |  | Definition 
 | 
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        | Term 
 | Definition 
 | 
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        | Term 
 
        | What class is flec-prop-mor? |  | Definition 
 | 
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        | Term 
 
        | Name the drug: dissociates from Na channel with slow kinetics, no change in APD |  | Definition 
 | 
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        | Term 
 
        | What are the clinical applications of flecainide? |  | Definition 
 
        | supraventricular arrhythmias in pts with normal heart, do not use in ischemic conditions (post-MI) |  | 
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        | Term 
 
        | Name the drug: Oral, hepatic and kidney metabolism, half life ~20hrs, Tox: proarrhythmic |  | Definition 
 | 
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        | Term 
 
        | how does propafenone compare to flecainide? |  | Definition 
 
        | orally active, weak B blocking, supraventric arrhythmias, hepatic metabolism |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | Class 1c, phenothiazine derivative, orally active, ventricular arrhythmias, proarrhythmic, withdrawn in US |  | 
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        | Term 
 
        | Propanolol - which class? MOA? |  | Definition 
 | 
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        | Term 
 
        | Name the drug: direct membrane effects (Na channel block), and prolongation of APD, slows SA node automaticity and AV nodal conduction velocity |  | Definition 
 | 
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        | Term 
 
        | What are the applications for propranolol? |  | Definition 
 
        | atrial arrhythmias and prevention of recurrent infarction and sudden death |  | 
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        | Term 
 
        | How does esmolol compare to propranolol? |  | Definition 
 
        | short acting, IV only, used for intra-op and other acute arrhythmias |  | 
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        | Term 
 
        | Amiodarone: which class? MOA? |  | Definition 
 
        | class 3, blocks Kr, Na, Ca-L channels, B adrenoreceptors |  | 
        |  | 
        
        | Term 
 
        | name the drug: prolongs APD and QT interval, slows HR and AV conduction, low incidence of TdP |  | Definition 
 | 
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        | Term 
 
        | what are the applications for amiodarone? |  | Definition 
 
        | serious ventricular arrhythmias and supraventricular arrhythmias |  | 
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        | Term 
 
        | name the drug: oral, IV, variable absorption and tissue accumulation, hepatic metabolism, elimination complex and slow, tox: bradycardia and heart block in diseased heart, peripheral vasodilation, pulm and hepatic tox, hyper or hypothyroidism, interactions are many- based on CYP |  | Definition 
 | 
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        | Term 
 
        | name the drug: oral, parenteral, duration 4-6h, tox: asthma, AV blockade, acute heart failure, interactions with other cardiac depressants and hypotensive drugs |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | prolongs AP, effective refractory period |  | 
        |  | 
        
        | Term 
 
        | what are the clinical applications for dofetilide? |  | Definition 
 
        | maintenance or restoration of sinus rhythm in A-fib |  | 
        |  | 
        
        | Term 
 
        | name the drug: oral, renal excretion, tox: TdP, additive with other QT-prolonging drugs |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | class 3, b-blocker, direct AP prolongation, use for ventric arrhythmias and a-fib |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | class 3, K channel blocker, may activate inward current, IV, use for conversion in a-flutter and a-fib |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | class 3, investigational, multichannel actions, reduces mortality in pts with a-fib |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | investigational, multichannel actions in atria, prolongs atrial refractoriness, effective in a-fib |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | class 4, L type Ca channel blocker |  | 
        |  | 
        
        | Term 
 
        | name the drug: slows SA node automaticity and AV nodal conduction velocity, decreases cardiac contractility, reduces BP |  | Definition 
 | 
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        | Term 
 
        | what are the applications for verapamil? |  | Definition 
 
        | supraventricular tachycardias |  | 
        |  | 
        
        | Term 
 
        | verapamil - oral or IV? metabolism? caution in which pts? |  | Definition 
 
        | oral and IV, hepatic, hepatic dysfunction |  | 
        |  | 
        
        | Term 
 
        | diltiazem is equivalent to... |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Name the drug: activates K, blocks Ca, very brief effects, usually complete AV blockade, used for paroxysmal supraventricular tachycardias, IV only, tox: flushing, dizziness, chest tightness |  | Definition 
 | 
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        | Term 
 
        | name the drug: poorly understood MOA, interacts with Na/K/ATPase and K and Ca channels, used for TdP, digitalis-induced arrhythmias, IV, duration depends on dose, tox:  muscle weakness in overdose |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | name the drug: increases K permeability, K currents, slows ectopic pacemakers, slows conduction velocity, used for digitalis-induced arrhythmias, arrhythmias assoc with hypokalemia, oral, IV, tox: reentrant arrhythmias, fibrillation or arrest in overdose |  | Definition 
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