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Explore classes, mechanisms of action, indications, treatment principles, patient variables, and education on antiarrhythmic agents. Stay informed on guidelines, evidence-based recommendations, monitoring, and safety elements.
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Chapter 21 Antiarrhythmic Agents
Drug Overview • Class I • IA: quinidine, procainamide • IB: lidocaine, mexiletine, tocainide • IC: flecainide, propafenone • Class II • β-Adrenergic blockers: propranolol, acebutolol
Drug Overview • Class III • amiodarone, sotalol, ibutilide, dofetilide • Class IV • Calcium channel blockers: verapamil, diltiazem • Other • digoxin, adenosine
Indications • Paroxysmal Supraventricular Tachycardia • Atrial Fibrillation • Premature Ventricular Contractions
Mechanism of Action • Antiarrhythmic Drugs Act to Reduce Electrical Irregularity of the Heart by Altering the Action Potential of Cardiac Cells • All Antiarrhythmics Have the Potential to Cause Arrhythmias
Mechanism of Action • Class IA Drugs Depress Rapid Depolarization (Phase 0) of the Action Potential • Class IB Drugs Exert Less Effect on Sodium Channels at Rest but Are More Prominent During Depolarization, so Their Effect on Phase 0 Is Only Slight
Mechanism of Action • Class IC Drugs Markedly Depress Phase 0 and Profoundly Slow Conduction • Class II Antiarrhythmics Work by Inhibiting Sympathetic Stimulation • Class III Drugs Prolong Phase 3 Repolarization by Blocking Potassium Channels • The QT interval thus is prolonged on the ECG • Prolongation also increases the risk of torsades de pointes • Amiodarone is the exception
Mechanism of Action • Class IV Drugs (Nondihydropyridine Calcium Channel Blockers) • Inhibit calcium ion influx through slow channels into conductile and contractile myocardial cells and vascular smooth muscle cells • Slow AV conduction • Prolong the effective refractory period within the AV node
Mechanism of Action • Digoxin Suppresses AV Node Conduction to Increase the Effective Refractory Period and Decrease Conduction
Treatment Principles • Standardized Guidelines • ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation J Am Coll Cardiol 48(4):e149-e246, 2006 • Evidence-Based Recommendations • digoxin • diltiazem • verapamil
Treatment Principles • Cardinal Points of Treatment • The cardiologist determines the appropriate medication and begins treatment • Once stable, the patient may be turned over to the primary care provider for long-term monitoring
Treatment Principles • Pharmacologic Treatment • Prophylaxis of PSVT • digoxin, β-blockers • verapamil • Atrial fibrillation • Control of rate • Control of rhythm • Control of thromboembolic events
Treatment Principles • Pharmacologic Treatment (cont’d) • PVCs • Criteria for treatment
How to Monitor • Therapeutic Effect • Toxicity • digoxin • quinidine • amiodarone
Patient Variables • Geriatrics • At increased risk for adverse reactions to medications • May require decreased dosage because of possible impaired renal or hepatic function • amiodarone • Healthy subjects older than 65 years show lower clearances of amiodarone than do younger subjects, as well as an increased half-life (20 to 47 days)
Patient Variables • Pediatrics • Safety and efficacy of these drugs have not been established • Pregnancy and Lactation • Category B: lidocaine • Category C: quinidine, procainamide, mexiletine, tocainide, flecainide, propafenone, propranolol, metoprolol, verapamil, diltiazem, digoxin, and adenosine • Category D: amiodarone, propranolol, metoprolol (second/third trimesters [expert opinion]), atenolol • Drugs are excreted in breast milk
Patient Education • Wear a Medical Alert Bracelet and Carry a Medical Identification Card Specifying That You Are Taking an Antiarrhythmic Drug • Report Any New or Uncomfortable Symptoms to Your Health Care Provider • amiodarone • digoxin
amiodarone (Cordarone) • Contraindications • Warnings/precautions • Pharmacokinetics • Adverse Effects • Drug Interactions