Prolong repolarization

Glass lA Antiarrhythmic Agents. Class lA antiarrhythmic agents decrease automaticity, ie, depress pacemaker rates, especially ectopic foci rates produce moderate depression of phase 0 depolarization and thus slow conduction in atria, A-V node, His-Purkinje system, and ventricles prolong repolarization, ie, lengthen action potential duration increase refractoriness and depress excitabiHty. These electrophysiological effects are manifested in the ECG by increases in the PR, QRS, and QT intervals. 

Glass IG Antiarrhythmic Agents. Class IC antiarrhythmic agents have marked local anesthetic effects. They slow the rapid inward sodium current producing marked phase 0 depression and slow conduction. Action potential duration of ventricular muscle is increased, ie, prolonged repolarization, but decreased in the His-Purkinie system by these agents. The effects on the ECG are increased PR interval, marked prolongation of the... 

Fleca.inide, Elecainide acetate, a fluorobenzamide, is a derivative of procainamide, and has been reported to be efficacious in suppressing both supraventricular and ventricular arrhythmias (26—29). The dmg is generally reserved for patients with serious and life-threatening ventricular arrhythmias. Elecainide depresses phase 0 depolarization of the action potential, slows conduction throughout the heart, and significantly prolongs repolarization (30). The latter effect indicates flecainide may possess some Class III antiarrhythmic-type properties (31). 

The Vaughan-Williams classification of antiarrhythmic drugs has been criticized for a number of reasons. The classification is based on the effects of drugs on normal, rather than diseased, myocardium. In addition, many of the drugs may be placed into more than one class. For example, the class IA drugs prolong repolarization/refractoriness, either via the parent drug8,9 or an active metabolite,10 and therefore also maybe placed in class III. Sotalol is also a 3-blocker, and therefore fits into class II. Amiodarone inhibits sodium and potassium channels, is a non-competitive inhibitor of 3-receptors, and inhibits calcium... 

Procainamide (Class IA antiarrhythmic drug) is an effective agent for ventricular tachycardia. Its mechanism of action involves blockade of the fast Na+ channels responsible for phase 0 in the fast response tissue of the ventricles. Therefore, its effect is most pronounced in the Purkinje fibers. The effects of this drug s activity include a decrease in excitability of myocardial cells and in conduction velocity. Therefore, a decrease in the rate of the phase 0 upstroke and a prolonged repolarization are observed. As a result, duration of the action potential and the associated refractory period is prolonged and the heart rate is reduced. These effects are illustrated by an increase in the duration of the QRS complex. 

I88-E89. The answers arc 188-g 189-b. (Hardman, pp 858-859, 864-865.) It is widely accepted that anti arrhythmic drugs are best classified according to their electro physio logic attributes. This is best accomplished by relating the effects of the different drugs to their actions on Na and Ca channels, which are reflected by changes in the monophasic action potential. Amiodarone blocks Na, Ca, and K currents and markedly prolongs repolarization, particularly in depolarized cells. Hecainide is related... 

Quinidine also prolongs repolarization in Purkinje fibers and ventricular muscle, increasing the duration of the action potential. As in atrial muscle, quinidine administration results in postrepolarization refractoriness, that is, an extension of refractoriness beyond the recovery of the resting membrane potential. The indirect (anticholinergic) properties of quinidine are not a factor in its actions on ventricular muscle and the His-Purkinje system. 

In general, drugs that block the sodium channel and shorten the action potential tend to increase the defibrillation threshold. Drugs that prolong repolarization also tend to decrease this threshold. These changes have obvious important ramifications for patients with ICDs. 

Mechanism of Action A selective potassium channel blocker that prolongs repolar-ization without affecting conduction velocity by blocking one or more time-dependent potassium currents. Dofetilide has no effect on sodium channels or adrenergic alpha or beta receptors. Therapeutic Effect Terminates reentrant tachyarrhythmias,... 

By prolonging repolarization, AP is widened and ERP is increased, so the tissues remain refractory even after full repolarization. 

Class III drugs currently in use include amiodarone, bretylium, dofetilide, and ibutilide (see Table 23-2). These drugs all exert their primary effects by prolonging repolarization in cardiac cells. Amiodarone, however, also appears to have some properties similar to drugs in other classes, and may help control arrhythmias by inhibiting sodium channel function (class I effect), by beta blockade (class II effect), or even by blocking calcium channels (class IV effect).5... 

Class III antiarrhythmic drug, which prolongs repolarization by inhibition of the delayed rectifier potassium current (lkr) and by selective enhancement of the slow inward sodium current, Ibutilide has no known negative inotropic effects (53),... 

A. Quinidine prolongs repolarization and the effective refractory period. 

Prolong repolarization Medications that extend the time when the electrical impulse returns to normal and is ready to fire again. Commonly prescribed prolonged repolarizations are ... 

Class III Prolongs repolarization during Adenosine (Adenocard) (Facial flushing,... 

Prolong repolarization ventricular dysrhythmias shortness of breath,/dyspnea) Amiodarone HC1... 

Acute treatment of TdP is different from treatment for the more common acute monomorphic ventricular tachycardia (or polymorphic VT with a normal QT interval). For an acute episode of TdP, most patients will require and respond to DCC. However, TdP tends to the paroxysmal in nature and often will recur rapidly after countershock. Therefore, after the initial restoration of a stable rhythm, therapy designed to prevent recurrences of TdP should be instituted. Drugs that further prolong repolarization such as intravenous procainamide are absolutely contraindicated. Lidocaine usually is inef-... 

T action potential duration (APD) and effective refractory period (ERP) Also blocks K+ channel (prolongs repolarization)... 

Slows conduction prolongs repolarization Slows conduction and shortens repolaiization... 

Prolongs repolarization during ventricular dysrhythmias. Prolongs action potential duration. 

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