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