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- 3. ANTIARRHYTHMIC DRUGS
- BG Katzung & MM Scheinman
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- I. General principles of arrhythmia treatment
- II. Drug selection <select3>
- III. Adverse reactions and drug interactions <tox3>
- Tables
- Group IA <tab3-1>
- Group IB, IC <tab3-2>
- Group II, III, IV <tab3-3>
- Miscellaneous <tab3-4>
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- 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.
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- 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.
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- 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.
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- 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.
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- Nevertheless, all antiarrhythmic drugs
- are potentially arrhythmogenic or proarrhythmic. The membrane
- actions of the major antiarrhythmic drugs are summarized in
- <tab3-1a>. The most important clinical effects of the agents
- are listed in <tab3-2a>. Furthermore, all antiarrhythmic
- agents are, to some extent, negatively inotropic, a factor of
- considerable importance in patients with marginal cardiac
- output.
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- Pharmacokinetics and Dosage
- These drugs are chemically heterogeneous and therefore
- vary markedly in their pharmacokinetic properties:
- For Group IA drugs (quinidine, procainamide,etc) <tab3-1>
- For Groups IB and IC (lidocaine, flecainide, etc) <tab3-2>
- For Groups II, III, and IV (ß-blockers, calcium channel
- blockers, etc) <tab3-3>
- For drugs with multiple actions (amiodarone, etc) <tab3-4>
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- 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.
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