Drugs that Regulate Cardiac Rhythm

The heart is both a mechanical and an electrical organ. The electrical component controls the rhythm of the heart. Under the influence of the autonomic nervous system, the sinoatrial (SA) node initiates action potentials, i.e., paces the heart at normal resting rates between 60 and 100 beats per minute.¹ Other pacemaker cell are found in the atrioventricular (AV) node, and the ventricular conducting system. Abnormal impulse generation and/or impulse conduction lead to cardiac arrhythmias.^6,7

The most common cause of cardiac arrhythmias is chronic coronary artery disease; less commonly, arrhythmias may be related to cardiomyopathies, valvular and congenital heart disease, primary electrophysiological disorders, and genetically determined ion-channel abnormalities.^1,7 Drugs in the top 300 that regulate cardiac rhythm (Table 4) include: (1) Na+ channel blockers, (2) β₁-adrenoceptor antagonists, (3) K⁺ channel blockers, (4) Ca²⁺ channel blockers, and (5) cardiac glycosides.^6,7,10

Table 4. Drugs that Affect Cardiac Rhythm and Cardiac Contractility^2,^6-8,¹⁰

Drugs	Mechanisms of Action	Common Indications
Class IC antiarrhythmics Flecainide	Block voltage-gated Na+ channels in ventricular myocytes	Sustained ventricular tachycardia Paroxysmal supraventricular tachycardia Paroxysmal atrial fibrillation
Class II antiarrhythmics β₁-adrenoceptor antagonists (see Table 3)	Block β₁-adrenoceptors in SA and AV nodal cells	Supraventricular and ventricular arrhythmias precipitated by sympathetic stimulation
Class III antiarrhythmics Sotalol Amiodarone	Block K⁺ channels and prolong repolarization	Recurrent and unstable ventricular arrhythmias Maintain normal sinus rhythm in patients with symptomatic atrial flutter or atrial fibrillation
Class IV antiarrhythmics Ca²⁺ channel blocking agents (see Table 3)	Block Ca²⁺ channels Decrease excitability of SA nodal cell Prolong AV nodal conduction	Paroxysmal supraventricular tachycardias
Cardiac glycosides Digoxin	Inhibit Na⁺/K⁺-ATPase leading to increased Ca²⁺ concentration in myocytes Positive inotropic effect Prolong refractory period at AV node Slow conduction velocity	Systolic heart failure Supraventricular arrhythmias Atrial flutter Atrial fibrillation Paroxysmal atrial tachycardia

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