Blocks Na⁺ channels which slows the upstroke potential, slows conduction, and prolongs the QRS duration. Also prolongs APD by nonspecific blockade of K⁺ channels. Direct depressant effect on SA and AV nodes.

Excessive APD prolongation, QT interval prolongation, and induction of torsade de pointes arrhythmia and syncope

Long term therapy produces lupus-like symptoms

Agranulocytosis

Most atrial and ventricular arrhythmias

Drug of 2^nd choice for most ventricular arrhythmias associated with acute MI

Similar to other Class 1A drugs but with significant antimuscarinic effects

May precipitate heart failure

Administered with a drug that slows AV conduction when treating atrial flutter or fibrillation

Blocks Na+ channels which slows the upstroke potential, slows conduction, and prolongs the QRS. Prolongs APD by blockade of K⁺ channels.

Torsade de pointes arrhythmia, GI  effects, cinchonism (a syndrome of headache, dizziness and tinnitus)

Altered color vision

Rarely used because of adverse effects

Blocks activated and inactivated Na⁺ channels, but block is rapidly reversed during diastole when channel recovers to resting state (-85mv).  Gradual depolarization due to ischemia ↑ time for unblocking resulting in selective suppression of depolarized “sick” tissue.  Effects on Purkinje and ventricular cells > atrial cells.

Neurologic – paresthesias, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions

Termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in acute ischemia

Similar electrophysiologic and antiarrhythmic actions are similar to lidocaine

Neurologic – tremor, blurred vision, lethargy

Ventricular arrhythmias

Anticonvulsant drug that has similar eletrophysiologic effects and has been used as an antiarrhythmic

(See CH 24) diplopia, ataxia, gingival hyperplasia, hirsutism, neuropathy

Typically used for generalized tonic-clonic seizures, partial seizures

Potent blocker of Na⁺ and K⁺ channels with slow unblocking kinetics. (Although it blocks K⁺ channels, it does not prolong the action or QT interval)

Severe exacerbation of arrhythmia in patients with preexisting ischemic heart conditions

Supraventricular arrhythmias in patients with otherwise normal hearts

Block β adrenoceptor; direct membrane effects (Na⁺ channel block) and prolongation of APD; slow SA node automaticity and AV node conduction velocity

Bradycardia, asthmatic attack,

Depression, Bronchoconstriction, Fatigue with exercise

Atrial arrhythmias and prevention of recurrent infarction and sudden death in patients recovering from acute MI

Prolongs APD by blockade of I_Kr, I_Ks during chronic treatment, and inactivated Na⁺ channels. Also has weak adrenergic and Ca⁺² channel blocking actions.  Slows HR and AV nodal conduction. 

Hepatic toxicity, pulmonary fibrosis, optic neuritis, pigmentation changes

Serious ventricular arrhythmias, supraventricular arrhythmias (such as atrial fibrillation)

Blocks rapid component of the delayed rectifier potassium current, I_Kr, which also ↑ hypokalemia. (No blockade of other K⁺ channels or Na⁺).  Prolongs APD and refractory period.

Torsade de pointes

Maintenance or restoration of sinus rhythm in atrial fibrillation

Calcium channel (I_Ca-L type) blockade; slows SA node automaticity and AV nodal conduction velocity (depend exclusively on Ca⁺² current) , ↓ cardiac contractility, ↓ BP

(See CH 12) AV block, acute heat failure, constipation, edema

Supraventricular tachycardias

Activation of an inward rectifier K⁺ current and inhibition of Ca⁺² current causing hyperpolarization and suppression of Ca⁺² dependent action potentials; inhibits AV nodal conduction and refractory period

Flushing, shortness of breath/chest burning

Short-lived AV block, atrial fibrillation

paroxysmal supraventricular tachycardia