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Pharmacology of Anti-arrhythmic Agents

  • Peter S. FischbachEmail author
  • Srikant Das

Abstract

Cardiac arrhythmias result from alterations in the orderly sequence of depolarization and repolarization in the heart (Chap.  2). The clinical severity of disordered cardiac activation ranges from asymptomatic palpitations to lethal arrhythmias. Clinicians have a number of therapeutic options from which to choose in an effort to suppress or eliminate the sources or structures that support the arrhythmias, as well as to convert the heart to normal rhythm if other therapies fail. While recent technological advances have led to an increase in the use of non-pharmacological strategies including transcatheter radiofrequency or cryothermal ablation, intraoperative cryoablation as well as implantable pacemakers and defibrillators, pharmacological therapy remains a valuable tool for monotherapy or as adjunctive therapy in combination with device therapy. Anti-arrhythmic medications exert direct effects on cardiac cells by inhibiting the function of specific ion channels or ion pumps or by altering the autonomic input into the heart resulting in alteration of the electrophysiologic properties of the cardiac conduction system. Additionally, several widely used cardiovascular therapies such as angiotensin-converting enzyme, hydroxy-methyl-glutaryl (HMG) Co-A reductase inhibitors, dexmedetomidine, and others also appear to exert important anti-arrhythmic effects. Physicians caring for patients with arrhythmias, therefore, must understand and appreciate the benefits and risks provided by each therapeutic agent, what is the indication for each, and how they interact.

Keywords

Class IA drugs: procainamide, quinidine Class IB drugs: lidocaine, mexiletine Class IC drugs: flecainide, propafenone Class II drugs: atenolol, esmolol, nadalol, propranolol Class III drugs: amiodarone, dofetilide, dronedarone, ibutilide, ranolazine, sotalol, vernakalant Class IV drugs: diltiazem, verapamil Calcium channel blockers Potassium channel blockers Sodium channel blockers DFTs Drug/device interactions Pharmacology Vaughan Williams classification 

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Copyright information

© Springer Science+Business Media, New York 2015

Authors and Affiliations

  1. 1.Sibley Heart Center, Children’s Healthcare of Atlanta, Department of PediatricsEmory University School of MedicineAtlantaUSA
  2. 2.Department of Pediatric Cardiology, Arkansas Children’s HospitalUniversity of Arkansas for Medical SciencesLittle RockUSA

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