Skip to Main Content
Home > Books > Workbook and Casebook for Goodman and Gilman's The Pharmacological Basis of Therapeutics >

Chapter 18: Antiarrhythmic Drugs

++

INTRODUCTION

++

This chapter will be most useful after having a basic understanding of the material in Chapter 29, Anti-Arrhythmic Drugs in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12th Edition. In particular, the reader is directed to the following tables, and to animations available in the online version of Goodman & Gilman’s The Pharmacological Basis of Therapeutics:

  • Table 29-1 Drug-Induced Cardiac Arrhythmias, which shows drugs known to cause arrhythmias (ie, proarrhythmias), the likely arrhythmogenic mechanism, the treatment, and the clinical features of the proarrhythmia

  • Table 29-4 Patient-Specific Anti-arrhythmic Drug Contraindications, which shows conditions and contraindicated drugs

  • Several animations in the online version of Goodman & Gilman’s The Pharmacological Basis of Therapeutics illustrate the electrophysiology of cardiac cells and the mechanism of action of antiarrhythmic drugs

++

LEARNING OBJECTIVES

++

  • Know the principles of cardiac electrophysiology especially the ion channels, exchangers, and pumps that are targets of antiarrhythmic drugs.

  • Understand the mechanisms that cause cardiac arrhythmias.

  • Know the common and important tachyarrhythmias and their mechanisms.

  • Understand the mechanisms and classification of antiarrhythmic drugs.

  • Know the principles of antiarrhythmic drug pharmacotherapy.

  • Know the pharmacological, pharmacokinetic, and adverse effects of specific antiarrhythmic agents.

++

DRUGS IN THIS CHAPTER

  • Adenosine (ADENOCARD)

  • Amiodarone (CORDARONE)

  • Digoxin (LANOXIN; see Chapter 17)

  • Diltiazem (CARDIZEM)

  • Disopyramide (NORPACE)

  • Dofetilide (TIKOSYN)

  • Dronedarone (MULTAQ)

  • Esmolol (BREVIBLOC)

  • Flecainide (TAMBOCOR)

  • Ibutilide (CORVERT)

  • Lidocaine (XYLOCAINE)

  • Mexiletine (MEXITIL)

  • Procainamide (PRONESTYL)

  • Propafenone (RYTHMOL)

  • Propranolol (INDERAL; see Chapter 7)

  • Quinidine (QUINIDEX)

  • Sotalol (BETAPACE)

  • Verapamil (CALAN; see Chapter 16)

++
Table Graphic Jump Location
MECHANISMS OF ACTION OF DRUGS USED TO TREAT CARDIAC ARRHYTHMIAS
View Table|Favorite Table|Download (.pdf)
MECHANISMS OF ACTION OF DRUGS USED TO TREAT CARDIAC ARRHYTHMIAS
ANTIARRHYTHMIC DRUG CLASS DRUG PRIMARY MECHANISM OF ACTION*
Class IA Quinidine, procainamide, disopyramide Na+ channel blocker, prolongs action potential duration (APD)
Class IB Lidocaine, mexiletine Na+ channel blocker, rapid dissociation
Class IC Flecainide, propafenone Na+ channel blocker, slow dissociation
Class II Propranolol, sotalol, esmolol β Adrenergic blocker
Class III Amiodarone, sotalol, ibutilide, dofetilide, dronedarone Prolongs APD (primarily by K+ channel blockade)
Class IV Verapamil, diltiazem Ca2+ channel blocker (nondihydropyridine)
Miscellaneous Adenosine Adenosine receptor agonist
Miscellaneous Digoxin Na+, K+-ATPase inhibitor

*Note: Most antiarrhythmic drugs have multiple mechanisms of action (Table 18-1).

++

THE CARDIAC ACTION POTENTIAL

  • In fast-conducting cardiac myocytes and cells of the conducting system, Phase 0 depolarization is caused by the opening of voltage-gated Na+ channels.

  • In slow-conducting cells of the sinoatrial (SA) node and atrioventricular (AV) node, which have relatively few voltage-gated Na+ channels, Phase 0 depolarization is caused by opening of voltage-gated L-type Ca2+ channels.

  • Phase 3 repolarization is primarily caused by K+ movement out of the cell through voltage-gated K+ channels.

  • Figure 18-1 shows action potentials from different regions of the heart, the ion currents that contribute to these action potentials, and the ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.

This site uses cookies to provide, maintain and improve your experience. MHE Privacy Center Close