Which of the following drugs is associated with QT prolongation?

Explanation

## Correct Answer: B. Quinidine Quinidine is a Class IA antiarrhythmic drug that is a potent blocker of cardiac potassium channels (particularly the rapid component of the delayed rectifier potassium current, IKr). This inhibition delays repolarization, prolonging the action potential duration and the QT interval on the ECG. Quinidine's mechanism involves both sodium channel blockade (Class I effect) and potassium channel blockade, making it one of the most QT-prolonging antiarrhythmics. This property is therapeutically useful for suppressing ectopic activity in conditions like atrial fibrillation, but it carries a significant risk of torsades de pointes—a potentially fatal polymorphic ventricular tachycardia—especially in the setting of electrolyte abnormalities (hypokalemia, hypomagnesemia) or concurrent use of other QT-prolonging drugs. In Indian clinical practice, quinidine is less commonly used than amiodarone for atrial fibrillation, but it remains an important teaching point because it exemplifies the Class IA antiarrhythmic profile. The QT prolongation is dose-dependent and requires ECG monitoring during initiation and dose adjustment. ## Why the other options are wrong **A. Lignocaine** — Lignocaine (lidocaine) is a Class IB antiarrhythmic that actually *shortens* the action potential duration and QT interval, not prolongs it. Class IB drugs enhance potassium channel activity, accelerating repolarization. While lignocaine can cause CNS and cardiac toxicity at high doses, QT prolongation is not its characteristic effect. This is a common NBE trap pairing local anesthetics with antiarrhythmics. **C. Magnesium sulfate** — Magnesium sulfate is used therapeutically to *prevent* and treat torsades de pointes caused by QT-prolonging drugs—it does not prolong QT itself. In fact, magnesium is a natural potassium channel opener and stabilizes cardiac electrolytes. It is given IV in acute settings (e.g., polymorphic VT) and is part of Indian ICU protocols for arrhythmia management. Confusing it with QT-prolonging agents is a classic distractor. **D. All of the above** — This is incorrect because lignocaine shortens QT and magnesium sulfate does not prolong QT. The 'all of the above' trap is designed to catch students who either misremember lignocaine's Class IB profile or conflate magnesium's therapeutic role in treating torsades with causing QT prolongation. Only quinidine among the three is a true QT-prolonging agent. ## High-Yield Facts - **Class IA antiarrhythmics** (quinidine, procainamide, disopyramide) prolong QT interval by blocking both sodium and potassium channels; Class IB (lignocaine, mexiletine) shorten QT; Class IC (flecainide, propafenone) have minimal QT effect. - **Quinidine-induced torsades de pointes** risk increases with hypokalemia, hypomagnesemia, female sex, bradycardia, and concurrent QT-prolonging drugs (macrolides, antipsychotics, antifungals). - **Magnesium sulfate** is the first-line acute treatment for torsades de pointes (2 g IV bolus over 5–20 minutes, then infusion) regardless of serum magnesium level. - **QT prolongation** is defined as QTc >450 ms in males and >460 ms in females; risk of arrhythmia increases significantly when QTc exceeds 500 ms. - **Lignocaine** is Class IB and used for acute VT/VF post-MI in Indian hospitals; it does NOT prolong QT and has a wide therapeutic window compared to Class IA drugs. ## Mnemonics **Class I Antiarrhythmics: QT Effect** **IA** = Increases QT (Quinidine, Procainamide, Disopyramide); **IB** = Decreases QT (Lignocaine, Mexiletine); **IC** = Minimal QT change (Flecainide, Propafenone). Memory: IA = 'I Add' potassium blockade → QT ↑; IB = 'I Block' potassium → QT ↓. **Torsades de Pointes Triggers (ABCDE)** **A**ntiarrhythmics (Class IA, III), **B**radycardia, **C**hannel blockers (Ca²⁺, K⁺), **D**rugs (macrolides, antipsychotics), **E**lectrolyte abnormalities (↓K⁺, ↓Mg²⁺). Use when assessing QT-prolonging drug risk in Indian ICU patients. ## NBE Trap NBE pairs lignocaine (a Class IB that shortens QT) with quinidine (Class IA that prolongs QT) to test whether students confuse antiarrhythmic classes by their sodium-blocking potency rather than their potassium-channel effects. The 'all of the above' option exploits this confusion and the false belief that magnesium causes QT prolongation. ## Clinical Pearl In Indian tertiary care, quinidine has largely been replaced by amiodarone for chronic atrial fibrillation due to amiodarone's broader efficacy and lower torsades risk at therapeutic doses. However, quinidine remains the teaching prototype for Class IA QT prolongation and is still encountered in board exams and in patients on older regimens. Always check baseline QTc and electrolytes before starting any Class IA agent. _Reference: KD Tripathi Pharmacology Ch. 31 (Antiarrhythmics); Harrison Principles of Internal Medicine Ch. 226 (Arrhythmias)_