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Back to main menu: ESC Back one screen: left arrow Back to Table of Contents: 3. ANTIARRHYTHMIC DRUGS BG Katzung & MM Scheinman 旼컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴 I. General principles of arrhythmia treatment II. Drug selection III. Adverse reactions and drug interactions Tables Group IA Group IB, IC Group II, III, IV Miscellaneous 읕컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴컴 (PgDn key for more text) I. GENERAL PRINCIPLES OF ARRHYTHMIA TREATMENT Cardiac arrhythmias are among the most common and serious medical emergencies. A few are relatively easy to treat; many are very difficult. All antiarrhythmic drugs are potentially toxic. The pharmacologic management of difficult arrhythmias is most successful if first, the nature of the arrhythmia is properly documented by clinical, electrocardiographic, and electrophysiologic examination; second, the efficacy of the candidate drug (or drugs) is adequately ascertained; and third, the adequacy of dosage is determined by measuring the drug concentration in the blood (see Hondeghem and Mason ref). In most arrhythmias, selection of a drug is empiric and often, several agents must be tried before finding one that is effective and well tolerated by the patient. (PgDn key for more text) Pathophysiology. Arrhythmias that are associated with organic heart disease and/or significant symptoms are generally considered for treatment. The major mechanisms of arrhythmias include: * Abnormal conduction, especially reentry, which probably causes atrial and ventricular flutter and fibrillation, supraventricular tachycardia involving accessory pathways or nodal reentry, and many ventricular tachycardias. * Abnormal automaticity, which probably causes many atrial and ventricular tachycardias, and catecholamine- and digitalis- induced arrhythmias. Triggered arrhythmia is a form of abnormal repetitive firing that resembles automaticity. * Combinations of the above, which are probably responsible for many post-infarction arrhythmias. (PgDn key for more text) Therapeutic Rationale * Prevention of deterioration from a nonfatal into a fatal arrhythmia, eg, from ventricular tachycardia into ventricular fibrillation. * Improvement of hemodynamic function, by slowing and regularizing the cardiac rhythm, or by synchronizing atrial and ventricular contractions. * Prevention of intrachamber clotting that would otherwise result from stasis (in atrial fibrillation). * Relief of symptoms, eg those due to premature ventricular depolarizations or supraventricular tachycardia. Mechanisms of Drug Action * Selective Depression: Useful antiarrhythmic drugs are usually depressants of cardiac function. Safe and effective therapy requires depression of the arrhythmic tissue with minimal interference with normal tissue. Fortunately, most sites of arrhythmogenesis are more susceptible than normal myocardium to antiarrhythmic drugs by virtue of depolarization, rapid discharge, or both. (PgDn key for more text) Nevertheless, all antiarrhythmic drugs are potentially arrhythmogenic or proarrhythmic. The membrane actions of the major antiarrhythmic drugs are summarized in . The most important clinical effects of the agents are listed in . Furthermore, all antiarrhythmic agents are, to some extent, negatively inotropic, a factor of considerable importance in patients with marginal cardiac output. Pharmacokinetics and Dosage These drugs are chemically heterogeneous and therefore vary markedly in their pharmacokinetic properties: For Group IA drugs (quinidine, procainamide,etc) For Groups IB and IC (lidocaine, flecainide, etc) For Groups II, III, and IV (-blockers, calcium channel blockers, etc) For drugs with multiple actions (amiodarone, etc) (PgDn key for references) References: 1. Cheitlin MD, Abbott JA: Cardiac emergencies. In: Current Emergency Diagnosis & Treatment, Mills J et al, eds, Lange, 1985,pp 490-500. 2. Heger JJ, et al: Amiodarone. Clinical efficacy and electrophysiology during long-term therapy for recurrent ventricular tachycardia or ventricular fibrillation. N Engl J Med 1981; 305:539. 3. Hondeghem LM, Mason JW: Agents used in cardiac arrhythmias. In: Basic & Clinical Pharmacology, BG Katzung, ed, Lange, 1987, pp 151-168. 4. Somberg, J: Antiarrhythmic drug therapy. Recent advances and current status. Cardiology 1985; 72: 329. 5. Schmidt, G, et al: Long term efficacy of class I antiarrhythmic agents and amiodarone in patients with malignant ventricular arrhythmias. Drugs 1985; 29 (Suppl 3):37. 6. Woosley, RL, Echt DS, Roden DM: Treatment of ventricular arrhythmias in the failing heart: Pharmacologic and clinical considerations. Rational Drug Therapy 1985; 19: 1. (Home to return to top of file)


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