Abstract
Tachycardia triggered by delayed premature depolarizations may result from the cytosolic Ca2+ overload which is often seen in ATP depletion during myocardium ischemia. Tachycardia induced by anatomical or pathological extra circuit may occur when an impulse propagates through more than one pathway between two points in the heart. Atrial or ventricular fibrillation is an extreme case of tachycardia with the uncoordinated muscle fiber contraction. Drugs may be antiarrhythmic if they can suppress the impulse initiation and its propagation. Among those, β blockers are most commonly used to treat DAD-induced arrhythmias. β blockers, and Ca2+ channel blockers are used together to treat atrioventricular reentrant arrhythmias. Isoproterenol and magnesium are used to treat EAD induced by quinidine.
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