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- W90383406 abstract "Class I antiarrhythmic drugs block the cardiac sodium channel. The magnitude of sodium channel block depends on heart rate, membrane potential, and the physicochemical characteristics of each drug that determine the rate of onset and recovery from block. 1 2 This has led to a subclassification of antiarrhythmic drug effects based on the magnitude of their effects on cardiac conduction. Class IA drugs, quinidine, procainamide, and disopyramide, have an intermediate effect on sodium channel block and generally only cause significant prolongation of conduction in cardiac tissue at more rapid heart rates. Class IB drugs, lidocaine and mexiletine, have minimal effects on the sodium channel in normal tissue but cause significant conduction slowing in depolarized tissue. Class IC drugs, flecainide and propafenone, cause significant prolongation of conduction in cardiac tissue, and this effect may manifest as an increase in the QRS complex duration of the electrocardiogram at normal heart rates. Many of these drugs have effects on other ion channels and/or membrane receptors through which some of their electrophysiologic effects are mediated ( Table 99-1 ). 1 2 Although these drugs were developed predominantly to treat ventricular arrhythmias, their use has been limited in patients with structural heart disease because of the risk of ventricular proarrhythmia. 3 4 At present, class IA and class IC drugs are used predominantly to treat supraventricular tachyarrhythmias. 5 6 7 8" @default.
- W90383406 created "2016-06-24" @default.
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- W90383406 date "2004-01-01" @default.
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- W90383406 title "Class I Antiarrhythmic Drugs: Quinidine, Procainamide, Disopyramide, Lidocaine, Mexiletine, Flecainide, and Propafenone" @default.
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- W90383406 doi "https://doi.org/10.1016/b0-7216-0323-8/50102-0" @default.
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