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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)

MECHANISMS OF ACTION OF DRUGS USED TO TREAT CARDIAC ARRHYTHMIAS
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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 ...

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