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Clinical pharmacy 2024/2025 Level 3 Pharm D Pharmacology 1 (PO 502)

Mechanism of action

Class Mechanism of action

 Moderate block Na+ channels → slows phase 0
Quinidine, depolarization, ↓ conductivity
IA Procainamide  Block K+ channels→ Prolong re-polarization
(I.V only)
↑ APD, ERP

 Marked effect on phase 4 (↓ automaticity)
IB Lidocaine  May activate K channel→ Shortens phase 3
+
repolarization (↓ERP)

IC Flecainide, Propafenone  Marked slow phase 0 depolarization (↓ conductivity)

 Competitively block catecholamine induced
II Propranolol stimulation of Beta-receptor
 Decrease phase 4 depolarization, ↓ automaticity

Amiodarone,
III Dronedarone,  Prolong phase 3 repolarization (increase ERP)

sotalol
 Shortens action potential (increase refractory Period
IV Verapamil
AV node)

1- Class I - Sodium-channel blockers

Quinidine

➢ Binds to sodium channels and prevents sodium influx, thus slowing the rapid upstroke
during phase 0, inhibits potassium channels, and because of these actions, it slows
conduction velocity.
➢ In addition, it has α- blocking action.

Therapeutic Quinidine is used in the treatment of a wide variety of arrhythmias,
uses including atrial, AV junctional, and ventricular tachyarrhythmias.
➢ Quinidine may increase the effects of antihypertensive,

anticoagulant drugs.
Drug-drug
➢ Phenobarbital and phenytoin reduce the effect of quinidine.
interaction ➢ Digoxin-Quinidine increases the effects of digoxin

(decrease 50% digoxin dose) since it is an inhibitor hepatic enzyme

➢ SA block or arrest, high grade AV block, ventricular tachycardia

and hypotension.
Adverse effects

➢ Large doses of quinidine may induce the symptoms of cinchonism
(blurred vision, tinnitus, headache, disorientation, and psychosis).

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