Mechanism of action
Increases intracellular calcium and allows more calcium to enter the myocardial cell during depolarization via a sodium-potassium pump
mechanism; this increases force of contraction (positive inotropic effect), increases renal perfusion (seen as diuretic effect in patients
with CHF), decreases heart rate (negative chronotropic effect), and decreases AV node conduction velocity.

Indications

CHF
Atrial fibrillation
Atrial flutter
Paroxysmal atrial tachycardia

Contraindications/cautions

Contraindicated in allergy to digitalis preparations,
ventricular tachycardia,
ventricular fibrillation,
heart block,
sick sinus syndrome,
IHSS,
acute MI,
renal insufficiency and
electrolyte abnormalities (decreased K+, decreased Mg++, increased Ca++).

Use caution in the presence of pregnancy and lactation.

Adverse effects

CNS: Headache, weakness, drowsiness, visual disturbances
GI: GI upset, anorexia
CV: Arrhythmias

Quinidine
From Wikipedia, the free encyclopedia.

Quinidine is a pharmaceutical agent that acts as a class I antiarrhythmic agent in the heart.

Like all other class I antiarrhythmic agents, quinidine primarily works by blocking the fast inward sodium current (INa). Quinidine's effect on INa is known as a use dependant block. This means that at higher heart rates, the block increases, while at lower heart rates the block decreases. The effect of blocking the fast inward sodium current causes the phase 0 depolarization of the cardiac action potential to decrease (decreased Vmax).

Quinidine also blocks the slowly inactivating tetrodoxin-sensitive Na current, the slow inward calcium current (ICa), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito.

The effect of quinidine on the ion channels is to prolong the cardiac action potential, thereby prolonging the QT interval on the surface EKG.