class I drugs

1. Mechanism. Class I drugs block fast Na1 channels, thereby reducing the rate of phase
0 depolarization, decreasing conduction velocity, prolonging the effective refractory
period, increasing the threshold of excitability, and reducing the rate of phase 4
depolarization
(see Fig. 4.4). These drugs also have local anesthetic properties.
a. Class IA drugs prolong the refractory period and slow conduction.
b. Class IB agents shorten the duration of the refractory period.
c. Class IC drugs slow conduction.

2. Class IA
a. Quinidine (Quinidex, Duraquin, Cardioquin)
(1) Effects and pharmacologic properties
(a) At therapeutic levels, direct electrophysiologic effects predominate, including
depression of the pacemaker rate and depressed conduction and excitability,
prolongation of QT interval, and heart block. At low doses, anticholinergic
(vagolytic) effects predominate; they may increase conduction velocity in the
AV node and accelerate heart rate.
(b) Quinidine is administered orally and is rapidly absorbed from the GI tract.
(c) Quinidine is hydroxylated in the liver and has a t1/2 of approximately 512
hours, which is longer in hepatic or renal disease and in heart failure.
(2) Therapeutic uses
(a) Quinidine is used for supraventricular and ventricular arrhythmias, especially
if
caused by ectopia, and it is used to maintain sinus rhythm after conversion of
atrial flutter or fibrillation by digoxin, propranolol, or verapamil.
(b) Quinidine is used to prevent frequent premature ventricular complexes and
ventricular tachycardia. Paradoxical tachycardia may be seen.
(c) As the dextrorotary isomer of quinine, quinidine also exhibits antimalarial,
antipyretic, and oxytoxic actions.