Dronedarone is an antiarrhythmic that is FDA approved for the treatment of atrial fibrillation in patients in sinus rhythm with a history of paroxysmal or persistent atrial fibrillation (AF). Dronedarone is multichannel blocker. Common adverse reactions include abdominal pain, diarrhea, indigestion, nausea, vomiting, asthenia and raised serum creatinine. Dronedarone has potentially important pharmacodynamics interactions: Digoxin: Consider discontinuation or halve dose of digoxin before treatment and monitor; Calcium channel blockers (CCB): Initiate CCB with low dose and increase after ECG verification of tolerability; Beta-blockers: May provoke excessive bradycardia, Initiate with low dose and increase after ECG verification of tolerability.

Ibutilide is a 'pure' class III antiarrhythmic drug, used intravenously against atrial flutter and fibrillation. At a cellular level it exerts two main actions: induction of a persistent Na+ current sensitive to dihydropyridine Ca2+ channel blockers and potent inhibition of the cardiac rapid delayed rectifier K+ current, by binding within potassium channel pores. In other words, Ibutilide binds to and alters the activity of hERG potassium channels, delayed inward rectifier potassium (IKr) channels and L-type (dihydropyridine sensitive) calcium channels. Ibutilide is indicated for the rapid conversion of atrial fibrillation or atrial flutter of recent onset to sinus rhythm. Ibutilide is marketed as Corvert by Pfizer.

Sotalol has both beta-adrenoreceptor blocking and cardiac action potential duration prolongation antiarrhythmic properties. Sotalol inhibits response to adrenergic stimuli by competitively blocking β1-adrenergic receptors within the myocardium and β2-adrenergic receptors within bronchial and vascular smooth muscle. It is FDA approved for the treatment of ventricular arrhythmias, symptomatic atrial fibtillation, symptomatic atriall flutter. Common adverse reactions include bradyarrhythmia, chest pain, lightheadedness, palpitations, rash, nausea, dizziness, headache, dyspnea, fatigue. Proarrhythmic events were more common in sotalol treated patients also receiving digoxin. Sotalol should be administered with caution in conjunction with calcium blocking drugs because of possible additive effects on atrioventricular conduction or ventricular function. Patients treated with sotalol plus a catecholamine depletor should therefore be closely monitored for evidence of hypotension and/or marked bradycardia which may produce syncope.

Flecainide is a potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial arrhythmias and tachycardias. Flecainide has local anesthetic activity and belongs to the membrane stabilizing (Class 1) group of antiarrhythmic agents; it has electrophysiologic effects characteristic of the IC class of antiarrhythmics. Flecainide acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. Flecainide is a sodium channel blocker, binding to voltage gated sodium channels. It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole. Flecainide is sold under the trade name Tambocor (manufactured by 3M pharmaceuticals). Flecainide went off-patent on February 10, 2004. In addition to being marketed as Tambocor, it is also available in generic version and under the trade names Almarytm, Apocard, Ecrinal, and Flécaine.

Mexiletine is a non-selective voltage-gated sodium channel blocker which belongs to the Class IB anti-arrhythmic group of medicines. It is used to treat heart arrhythmias. Mexiletine is also used to treat refractory pain and muscle stiffness resulting in myotonic dystrophy or myotonia congenita. Mexiletine was approved for commercial use in 1985 under the brand name Mexitil, but most marketing efforts have since been discontinued. There has been a continued effort to identify other therapeutic use cases and a number of clinical trials have been conducted including ALS and chronic pain from amputation.

Disopyramide is an antiarrhythmic drug indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia that are life-threatening. In man, Disopyramide at therapeutic plasma levels shortens the sinus node recovery time, lengthens the effective refractory period of the atrium, and has a minimal effect on the effective refractory period of the AV node. Little effect has been shown on AV-nodal and His-Purkinje conduction times or QRS duration. However, prolongation of conduction in accessory pathways occurs. Disopyramide is a Type 1A antiarrhythmic drug (ie, similar to procainamide and quinidine). It inhibits the fast sodium channels. In animal studies Disopyramide decreases the rate of diastolic depolarization (phase 4) in cells with augmented automaticity, decreases the upstroke velocity (phase 0) and increases the action potential duration of normal cardiac cells, decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium, and has no effect on alpha- or beta-adrenergic receptors. It is used for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, ventricular pre-excitation and cardiac dysrhythmias. It is a Class Ia antiarrhythmic drug.

Procainamide is a derivative of procaine with less CNS action. Procainamide hydrochloride injection is indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that, in the judgement of the physician, are life threatening. Because of the proarrhythmic effects of procainamide, its use with lesser arrhythmias is generally not recommended. Treatment of patients with asymptomatic ventricular premature contractions should be avoided. Procainamide (PA) increases the effective refractory period of the atria, and to a lesser extent the bundle of His-Purkinje system and ventricles of the heart. It reduces impulse conduction velocity in the atria, His-Purkinje fibers, and ventricular muscle, but has variable effects on the atrioventricular (A-V) node, a direct slowing action and a weaker vagolytic effect, which may speed A-V conduction slightly. Myocardial excitability is reduced in the atria, Purkinje fibers, papillary muscles, and ventricles by an increase in the threshold for excitation, combined with inhibition of ectopic pacemaker activity by retardation of the slow phase of diastolic depolarization, thus decreasing automaticity especially in ectopic sites. Contractility of the undamaged heart is usually not affected by therapeutic concentrations, although slight reduction of cardiac output may occur, and may be significant in the presence of myocardial damage. Therapeutic levels of PA may exert vagolytic effects and produce slight acceleration of heart rate, while high or toxic concentrations may prolong A-V conduction time or induce A-V block, or even cause abnormal automaticity and spontaneous firing by unknown mechanisms. Procainamide is sodium channel blocker. It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action.

Moricizine is an antiarrhythmic agent previously marketed as Ethmozine. It was used for prophylaxis and treatment of serious and life-threatening ventricular arrhythmias. In 2007 it was withdrawn and discontinued for commercial reasons. Moricizine can be administered intravenously but was more commonly provided as an oral formulation.