Antiarrhythmic

• Decrease automaticity in SA node by
• -shifting the threshold to more positive potentials
• -decreasing the slope of phase 4

• Decrease the likelihood of re-entry by
• -decreasing the conduction velocity
• -increasing the refractory period (class 1A)

• Quinidine
• Procainamide
• Disopyramide

• -A moderate block on Na+ channels
• -Also block K+ channels (increase refractory period)
• -Decrease the phase 0 upstroke velocity, which decreases conduction velocity through the myocardium
• -Have some degree of anticholinergic effects *significant clinically b/c it can increase conduction velocity through the AV node

Class IA Antiarrhythmic

• Adverse Effects:  diarrhea, torsade de pointes (prolonged QT), syncope (fainting) secondary to reduction in CO and BP, cinchonism, tinnitus, blurred vision
• *Quinidine-induced digoxin toxicity - increases serum levels of digoxin by inhibiting Pgp

Occasionally to suppress atrial flutter, atrial fibrillation, supraventricular and ventricular arrhythmias

-If patient has atrial fibrillation - first treat with drug that decreases AV node conduction (digoxin) and then give quinidine

• -Long term uses causes lupus erythematosus (is reversible)
• -Indications: atrial flutter, Afib, ventricular tachycardia, paroxysmal atrial tachycardia

• -Orally to prevent life-threatening sustained ventricular tachycardia
• -Has greater negative inotropic and anticholinergic effects than other class IAs and therefore should be used with caution in patiens with heart failure and in the elderly

• Lidocaine
• Mexiletine
• Phenytoin

• -Preferentially bind to both open and inactivated Na+ channels (I>O)
• -Fast dissociation from Na+ channels
• -Exhibit use-dependent block
• -Increases ventricular fibrillation threshold

Used most commonly to treat ventricular arrhythmias (ventricular fibrillation & ventricular tachycardia) in emergency situations associated with myocardial ischemia

High concentrations can cause confusion, dizziness, seizure

Cimetidine (or other drugs that inhibits P450 enzymes) can precipitate lidocaine toxicity

• -Analog of lidocaine
• -Primary indication: life-threatening ventricular tachycardia
• -dose related nausea and tremo

• -Considered an antiepileptic med
• -Supresses digoxin-induced delayed after depolatization
• -ventricular tachycardia
• -Induces hepatic enzymes (P450 3A4)

• Flecainide
• Propafenone

• -Preferentially bind to both open and inactivated Na+ channels (I=O)
• -Most potent Na+ channel blockers
• Little/no effect on AP duration
• -Prevent paroxysmal supraventricular tachycardia and atrial fibrillation
• -Depressive effects on cardiac function

• -Various Atrial and ventricular arrhythmias, except those associated with MI (increased mortalitiy rate)
• Adverse effects:  bronchospasm, leukopenia, thrombocytopenia, seizures

• -Treat various atrial and ventricular arrhythmia
• -Potential ventricular arrhythmias and several hemotologic abnormalities, including agranulocytosis, anemia, and thrombocytopenia

• Esmolol
• Metoprolol
• Propranolol

• -Decrease automaticity by decreasing the slope of phase 4
• -Decreases the incidence of re-entry by slowing electrical conduction at the AV node
• -The AV node is more sensitive than the SA node to the effects of B-blockers
• -The most frequently used agents in the treatment of supraventricular and ventricular arrhythmias precipitate by sympathetic stimulation

• Amiodarone
• Dofetilide
• Ibutilide
• Sotalol

• -Block K+ channels
• -Prolongs AP
• +Decreases the incidence of re-entry by increasing the effective refractory period
• -Increase the likelihood of developing early afterdepolarization and torsade de pointes

• -Mainly class III
• -Also Class I, II, IV
• -Alters lipid membrane in which ion channels and receptors are located
• -decreases re-entry by prolonging AP duration
• -decreases the rate of firing in pacemarke cells as class I
• -Class II activity by noncomp. antatgonizing B-receptors
• -Cna cause significant AV block and bradycardia

Adverse effects:  hypotension, AV block, various arrhythmias, blue-gray skin discoloration, thyroid abnormalities, fatal pulmonary fibrosis

Also corneal deposits, blurred vision, photosensitivity, and GI disturbances

Inhibits metabolism of digoxin, flecainide, phenytoin, procainamide, warfarin

• Used to terminate AFib and atrial flutter
• -Adverse effects:  torsades de points, may requrie electrical cardioversion

• Mixed Class II and III
• -Used for patients that cannot tolerate amiodarone
• -Prevents recurrent atrial flutter/fib
• -Causes fatigue, bradycardia, and can induce torsades de pointes

• Diltiazem
• Verapamil

• -Block cardiac Ca channels
• -Act preferentially on SA and AV nodal tissues
• -Slows AP upstroke in AV node, leading to slowed conduction velocity through the AV node
• -Use to treat re-entrant paroxysmal sypraventricular tachycardia that involves AV node

• -opens a G protein-coupled K+ channel
• -inhibits SA nodal, atrial, and
• AV nodal conduction
• -also inhibits the potentiation of Ca2+ channel
• activity by cAMP
• -has a plasma half-life of less than 10 sec
• -often used as the first-line agent for
• converting narrow-complex paroxysmal supraventricular tachycardia
• -adverse effects include headache,
• flushing, chest pain, and excessive AV or SA nodal inhibition

• -Indirectly increase vagal tone and slows AV node conduction and increases AV node refractory period
• -Use to slow the ventricular rate in patients with AFib (b-blockers and CCB are usually preferred b/c of their more rapid onset of action and greater degree of AV node blockade)

• -Mg is second most common intracellular cation
• -deficiency can cause arrhythmias, CHF, and GI/renal disorders
• -Mag sulfate IV suppresses drug-induced torsades de pointes to treat digitalis-induced ventricular arrhythmias
• -Also treats supraventricular arrhythmias associated with Mag deficiency