Abstract
Treatment of arrhythmias is best understood if viewed from 2 major electrophysiologic standpoints: disturbances of impulse formation and disturbances of impulse conduction, or both. Arrhythmias secondary to enhanced automaticity are best controlled by agents depressing diastolic depolarization (quinidine, lidocaine and propranolol). Arrhythmias secondary to depressed conduction can be terminated by (1) enhancing conduction velocity by hyperpolarization (bretylium) or increase in membrane responsiveness (diphenylhydantoin) or (2) by further depressing conduction (quinidine and propranolol). Simple prolongation of the effective refractory period can also interrupt reentry. Direct antifibrillatory effects of high levels of potassium are demonstrated. Specific effects on intraatrial, intranodal and subnodal conduction and ineffectiveness of certain antiarrhythmic agents such as lidocaine in the presence of low levels of potassium are also discussed.
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