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Class I

Sodium channel blockers

Class Ia

increase duration of action potential by slowing phase 0

Class Ib

decrease duration of action potential by shortening phase 3

Class Ic

minimal change in action potential duration; increases threshold potential, thus slowing conduction velocity

Class II

Beta-adrenergic blockers; diminish phase 4, thus depressing automaticity and decreasing heart rate; effective at preventing arrhythmias after an MI; both supraventricular and ventricular tachyarrhythmias respond well

Class III

Potassium channel blockers; extend phase 3

Class IV

Calcium channel blockers; slow SA and AV nodal conduction; decrease rate of phase 4 and thus increase the effective refractory period


Class Ia; for VTach and Supraventricular arrhythmias; Prolongs QT


Class Ia; for ventricular and supraventricular arrhythmias; metabolite has some class III action; LUPUS-like syndrome


Class Ia; for ventricular and supraventricular arrhythmias; causes prostatism and anticholinergic effects


Class Ib; can be used for acute management of ventricular arrhythmias in patients with myocardial infarction, but amiodarone is better; also local anesthetic; nystagmus is early sign of toxicity


Class Ib; for ventricular arrhythmias; can cause pulmonary fibrosis or bone marrow aplasia


Class Ib; for ventricular arrhythmias; blood dyscrasias, nystagmus, leukopenia, agranulocytosis


Class Ib; D.O.C. for treating digoxin-induced atrial and ventricular arrhythmias; anticonvulsant; gingival hyperplasia, serious bone marrow and derm reactions can occur


Class Ic; for treating life-threatening ventricular arrhythmias in patients without myocardial structural abnormalities; used as last-line b/c it can cause arrhythmias; heart block is possible toxicity; blocks Na+ in purkinje shortening AP while blocking K+ in ventricles extending AP-->no change in AP duration


Class Ic; for treating supraventricular and ventricular arrhythmias; similar action as flecainide but also beta blocker activity; hepatic metabolism


Class Ic; for severe ventricular arrhythmias


Class II; very short acting beta blocker; almost always used in treatment of acute surgical arrhythmias


Class III; treats ventricular tachyarrhythmias and supraventricular arrhythmias


Class III; prolongs ventricular action potential and effective refractory period; also blocks norepinephrine release; used to treat refractory VFib and VTach during cardiac arrest; rarely used


Class III; class I-IV activity, but mostly III; adverse effects=pulmonary fibrosis, hepatocellular necrosis, CNS (tremor, ataxia), Photosensitivity, corneal microdeposits, thyroid dysfunction, blue skin discoloration; CHECK PFTs, LFTs, and TFTs


Class III; for atrial flutter and fibrillation; toxicity=torsades de pointes


Class III; used to maintain sinus rhythm in patients w/ atrial fibrillation or flutter; toxicity=torsades de pointes


Inhibits Na/K-ATPase; increases refractory period and decreases conduction time of AV node; for treating supraventricular arrhythmias and CHF; toxicity=atrial of ventricular dysrhythmias (ATach, often); treat toxicity w/ digoxin antibodies.....or phenytoin!!

Magnesium Sulfate

Stabilizes cardiac cell membranes; for treating torsades de pointes


Activates ACh-sensitive K+ channels-->shortened AP duration, hyperpolarization, and decreased automaticity; for diagnosing and terminating paroxysmal supraventricular tachyarrhythmias because of its limited toxicities and rapid onset

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