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Cardiovascular Drugs Our Patients Take

Course Number: 581

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 underlie 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 (Rank/300)Mechanisms of ActionCommon Indications
Class IC antiarrhythmics
• Flecainide (188)
Block voltage-gated Na+ channels in ventricular myocytes
• Sustained ventricular tachycardia
• Paroxysmal supraventricular tachycardia
• Paroxysmal atrial fibrillation/flutter

Class II antiarrhythmics
• Propranolol (88)
Block β1-adrenoceptors in SA and AV nodal cells
• Supraventricular and ventricular arrhythmias precipitated by sympathetic stimulation
Class III antiarrhythmics
• Amiodarone (198)
• Sotalol (296)
Block K+ channels and prolong repolarization

Sotalol exhibits both β-adrenoreceptor blocking and cardiac action potential duration prolongation
• Recurrent and unstable ventricular arrhythmias
• Maintain normal sinus rhythm in patients with symptomatic atrial flutter or atrial fibrillation
Class IV antiarrhythmics
• Diltiazem (76)
• Verapamil (151)
Block voltage-gated L-type Ca2+ channels and thereby
• Decrease excitability of SA nodal cel
• Prolong AV nodal conduction

• Paroxysmal supraventricular tachycardias
Cardiac glycosides
• Digoxin (237)
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
 o Atrial flutter
 o Atrial fibrillation
 o Paroxysmal atrial tachycardia