Antiarrhythmics MCQ — NEET PG Practice Question | NEETPGAI
Antiarrhythmics
medium
pill Pharmacology
A 68-year-old man with a history of dilated cardiomyopathy presents with sustained ventricular tachycardia. He is initiated on intravenous procainamide. Which of the following best explains the antiarrhythmic mechanism of procainamide in this patient?
A. Slowing of AV nodal conduction via adenosine receptor activation
B. Inhibition of fast sodium channels with slowing of phase 0 depolarization
C. Blockade of L-type calcium channels with negative inotropic effect
D. Prolongation of action potential duration through potassium channel blockade
Explanation
Procainamide Mechanism of Action
Key Point
Procainamide is a Class IA antiarrhythmic agent that exerts its primary antiarrhythmic effect through blockade of fast sodium channels in the cardiac myocyte membrane.
Sodium Channel Blockade (Primary Mechanism)
Procainamide inhibits the inward fast sodium current (INa) during phase 0 of the cardiac action potential. This results in:
1.
Slowing of phase 0 depolarization — the rate of rise of the action potential is decreased
2.
Increased conduction time — particularly in tissues dependent on fast sodium channels (ventricular myocardium, Purkinje fibers, atrial muscle)
3.
Widening of the QRS complex on the ECG — a hallmark of Class I activity
Secondary Mechanism: Potassium Channel Blockade
Procainamide also possesses Class III properties (potassium channel blockade), which:
Prolongs the action potential duration (APD)
Extends the effective refractory period (ERP)
Increases the QT interval on ECG
This dual action (Class IA + III) makes procainamide effective for both atrial and ventricular arrhythmias.
Clinical Application in Ventricular Tachycardia
In sustained ventricular tachycardia (as in this patient with dilated cardiomyopathy), the sodium channel blockade:
Slows conduction velocity in the reentrant circuit
Increases the refractory period
Breaks the reentrant loop or prevents its perpetuation
Clinical Pearl
Procainamide is particularly useful in VT because it combines sodium channel blockade (slows conduction) with potassium channel blockade (prolongs refractoriness) — a synergistic effect for terminating reentrant arrhythmias.
Why Class IA, Not Class IB or IC?
Table
Class
Primary Effect
Secondary Effect
Example
IA
Na+ channel block
K+ channel block (prolongs APD)
Procainamide, Quinidine
IB
Na+ channel block
K+ channel activation (shortens APD)
Lidocaine, Mexiletine
IC
Na+ channel block (marked)
Minimal effect on APD
Flecainide, Propafenone
Procainamide's prolongation of APD (via K+ blockade) is the distinguishing feature that makes it Class IA.
High-YieldNEET PG
On the NEET PG exam, remember: Class IA = Na+ block + K+ block (APD prolongation). This dual action is why procainamide and quinidine are effective for both atrial and ventricular arrhythmias, unlike Class IB agents.
