Category: Fundamentals In normal tissues, the action potential is shortened and conduction velocity shows little change with lidocaine. However, in depolarized fibers or in fibers damaged by ischemia, lidocaine prolongs the action potential and slows conduction.
Category: Fundamentals Lidocaine is a class IB antiarrhythmic. However, its electrophysiologic effects are different in that it is selective to ischemic tissue, and especially to active fast sodium channels in the bundle of His, Purkinje fibers and ventricular myocardium.
Category: Fundamentals The class IB antiarrhythmics include lidocaine and mexiletine. These agents decrease automaticity, conduction velocity and shorten refractoriness. These drugs primarily exert their electrophysiologic effects on the ventricular myocardium.
Category: Fundamentals Disopyramide slows conduction velocity (phase 0), prolongs refractoriness (phase 3) and decreases automaticity (phase 4). These effects are manifested as a prolonged QT interval and a slightly prolonged QRS complex on the ECG.
Category: Fundamentals Procainamide widens the QRS complex, prolongs the QT interval and prolongs the PR interval on the ECG. NAPA, the major metabolite of procainamide, blocks outward potassium currents and thereby has class III electrophysiologic properties.
Category: Fundamentals Procainamide has the same electrophysiologic effects as quinidine, except it does not have the anticholinergic activity. Procainamide slows conduction velocity (phase 0), prolongs refractoriness (phase 3) and decreases automaticity (phase 4).
Category: Fundamentals The most common adverse effects associated with quinidine are gastrointestinal (nausea, vomiting and diarrhea). As with other class IA drugs, quinidine can cause proarrhythmia, specifically torsades de pointes.
Category: Fundamentals Quinidine has potent anticholinergic properties that affect the SA and AV nodes. It can increase SA nodal discharge and AV nodal conduction. Consequently, in AF, these anticholinergic effects may lead to a more rapid ventricular rate.
Category: Fundamentals Quinidine is a broad-spectrum antiarrhythmic drug that may be used to treat supraventricular and ventricular arrhythmias. This drug slows conduction velocity (phase 0), prolongs refractoriness (phase 3) and decreases automaticity (phase 4).
Category: Fundamentals Antiarrhythmic drugs (AAD) are organized into four classes, I (Ia, Ib, Ic), II, III and IV. Although the Vaughan Williams classification system is the most widely used method for grouping AADs based on their electrophysiologic actions.
Category: Fundamentals Conditions that may cause arrhythmias are electrolyte imbalances, drug overdose, renal failure, thyroid disorders, metabolic acidosis, pulmonary embolism, tension pneumothorax, hypoxemia and valvular or congenital defects in the heart.
Category: Fundamentals Ventricular arrhythmias originate in the ventricles or the bundle of His. These types of arrhythmias are usually symptomatic and may cause loss of consciousness or death. Therefore, arrhythmias in this category require immediate intervention.
Category: Fundamentals Supraventricular and AV nodal arrhythmias are not usually life threatening. However, they may become troublesome and lead to reduced cardiac output related to decreased ventricular filling.
Category: Fundamentals Arrhythmias evolve either above or below the ventricles. Supraventricular arrhythmias evolve above the ventricles in the atria, SA node or AV node. Arrhythmias can be either tachy/brady-cardia or with regularity or irregularity.
Category: Fundamentals The sinoatrial node has the most rapid rate of depolarization during diastole and reaches threshold first. Cells of the atrioventricular node and His-Purkinje system have automaticity but a slower rate of phase 4 depolarization.
