Antiarrhythmic Drugs — MCQs

10 questions

Which electrolyte imbalance causes prolonged QT interval?

Which of the following is a late inward sodium channel blocker?

Which class of antihypertensive drugs is known to cause erectile dysfunction?

QT shortening is associated with which electrolyte imbalance?

Which of the following are CYP3A inhibitors?

Which of the following antiarrhythmic drugs is contraindicated in a patient with interstitial lung disease?

What is the drug of choice in paroxysmal supraventricular tachycardia?

Q10

Which one of the following was traditionally considered the drug of choice for ventricular tachycardia in myocardial infarction?

Antiarrhythmic Drugs Indian Medical PG Practice Questions and MCQs

Question 1: Which electrolyte imbalance causes prolonged QT interval?

A. Hypernatremia
B. Hyperkalemia
C. Hypocalcemia (Correct Answer)
D. Hyponatremia

Explanation: ***Hypocalcemia*** - **Hypocalcemia** prolongs the **repolarization phase** of the action potential in cardiac myocytes, leading to a lengthened **QT interval** on an electrocardiogram. - This increased duration of repolarization places the heart at higher risk for **Torsades de Pointes** and other life-threatening arrhythmias [2], [3]. *Hypernatremia* - **Hypernatremia** primarily affects neurological function and can cause symptoms like **confusion** and **seizures**. - It does not typically lead to a **prolonged QT interval**; instead, it can sometimes be associated with a shortened QT interval or other non-specific ECG changes. *Hyperkalemia* - **Hyperkalemia** primarily causes peaked T waves, a widened QRS complex, and eventually **bradycardia** and **asystole** [1]. - While it drastically alters cardiac conduction, it typically **shortens** rather than prolongs the QT interval. *Hyponatremia* - **Hyponatremia** is associated with cerebral edema and neurological symptoms such as **headaches**, **nausea**, and **altered mental status**. - It generally does not cause a **prolonged QT interval**; significant hyponatremia can sometimes be associated with non-specific ECG changes [1] but not a specific lengthening of the QT interval.

Question 2: Match the following antiarrhythmic drugs with their mechanism of action: | Mechanism of action | Drug | | :-- | :-- | | 1. Na+ channel blocker | A. Quinidine | | 2. K+ channel blocker | B. Digoxin | | 3. Na+K+ ATPase inhibitor | C. Esmolol | | 4. Beta-blocker | D. Ibutilide |

A. 1-D, 2-B, 3-A, 4-C
B. 1-A, 2-D, 3-B, 4-C (Correct Answer)
C. 1-A, 2-C, 3-D, 4-B
D. 1-D, 2-C, 3-A, 4-B

Explanation: ***1-A, 2-D, 3-B, 4-C*** - **Quinidine** is a Class IA antiarrhythmic drug that primarily blocks **sodium channels**, prolonging the action potential duration and refractoriness. - **Ibutilide** is a Class III antiarrhythmic drug that blocks **potassium channels**, leading to delayed repolarization and increased effective refractory period. - **Digoxin** inhibits the **Na+/K+ ATPase pump**, increasing intracellular calcium and affecting AV nodal conduction. - **Esmolol** is a **beta-blocker** (Class II antiarrhythmic) that reduces heart rate and contractility by blocking β1-adrenergic receptors. *1-A, 2-C, 3-D, 4-B* - This option incorrectly matches **Esmolol** (a beta-blocker) with **K+ channel blocker** and **Ibutilide** (K+ channel blocker) with **Na+K+ ATPase inhibitor**. - It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**. *1-D, 2-C, 3-A, 4-B* - This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**. - It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**. *1-D, 2-B, 3-A, 4-C* - This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and **Digoxin** (Na+K+ ATPase inhibitor) with **K+ channel blocker**. - It also incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**.

Question 3: Which of the following is a late inward sodium channel blocker?

A. Ranolazine (Correct Answer)
B. Fasudil
C. Ivabradine
D. Trimetazidine

Explanation: ***Ranolazine*** - **Ranolazine** selectively inhibits the **late inward sodium current (I_Na)** in cardiac myocytes. - By reducing this current, it helps to decrease intracellular **sodium and calcium overload**, thereby improving myocardial relaxation and reducing angina and ischemia. *Ivabradine* - **Ivabradine** is a selective **funny channel (If) inhibitor** in the sinoatrial node. - It slows down the heart rate by reducing the rate of diastolic depolarization, primarily used for **chronic stable angina** and **heart failure**. *Fasudil* - **Fasudil** is a **rho-kinase inhibitor** used primarily in Japan and China for **cerebral vasospasm** following subarachnoid hemorrhage. - It works by inhibiting the phosphorylation of myosin light chain, leading to **vasodilation**. *Trimetazidine* - **Trimetazidine** is an **anti-ischemic metabolic agent** that inhibits the enzyme 3-ketoacyl-CoA thiolase, shifting cardiac metabolism from fatty acid oxidation to glucose oxidation. - This improves myocardial glucose utilization, which is more efficient in **ischemic conditions**, thereby reducing angina symptoms.

Question 4: Which class of antihypertensive drugs is known to cause erectile dysfunction?

A. Calcium channel blocker
B. ACE inhibitors
C. AT1 receptor antagonists
D. Beta-blockers (Correct Answer)

Explanation: ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients

Question 5: Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |

A. A-1, B-3, C-2, D-4
B. A-4, B-1, C-3, D-2 (Correct Answer)
C. A-3, B-2, C-4, D-1
D. A-2, B-4, C-1, D-3

Explanation: ***A-4, B-1, C-3, D-2*** - **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms. - **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes. - **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development. - **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation. *A-1, B-3, C-2, D-4* - This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications. - It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy. *A-3, B-2, C-4, D-1* - This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications. - It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation. *A-2, B-4, C-1, D-3* - This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications. - It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.

Question 6: QT shortening is associated with which electrolyte imbalance?

A. Hypercalcemia (Correct Answer)
B. Hypokalemia
C. Hypocalcemia
D. Hyperkalemia

Explanation: ***Hypercalcemia*** - **Elevated calcium levels** lead to a shortened **plateau phase of the cardiac action potential**, which manifests as a **shortened QT interval** on an ECG. - This imbalance increases the risk of ventricular arrhythmias, although profound shortening can lead to **QRS widening** with further increase in calcium. *Hypokalemia* - **Low potassium** levels typically cause **QT prolongation**, usually due to prominent U waves and T wave flattening. - It does not cause QT shortening; instead, it is associated with an **increased risk of Torsades de Pointes**. *Hypocalcemia* - **Low calcium** levels cause **QT prolongation** by lengthening the **plateau phase of the cardiac action potential**, increasing the duration of ventricular repolarization. - ECG findings include prolonged ST segment and can increase the risk of arrhythmias, including Torsades de Pointes. *Hyperkalemia* - **High potassium** levels primarily cause **peaked T waves**, a **widened QRS complex**, and a **prolonged PR interval**, potentially leading to asystole or ventricular fibrillation. - It does not cause QT shortening; instead, severe hyperkalemia can lead to **loss of P waves** and a **sine wave pattern**.

Question 7: Which of the following are CYP3A inhibitors?

A. Ritonavir
B. Amiodarone
C. Verapamil
D. Both a and c (Correct Answer)

Explanation: ***Both a and c (Ritonavir and Verapamil)*** - **Ritonavir** is a **potent CYP3A4 inhibitor**, one of the strongest known, commonly used as a pharmacokinetic booster for other protease inhibitors to increase their bioavailability - **Verapamil** is a **calcium channel blocker** that acts as a **moderate CYP3A4 inhibitor**, leading to clinically significant drug interactions requiring dose adjustments - Both drugs have **clinically relevant and well-established** CYP3A4 inhibitory effects *Ritonavir alone* - While correct that Ritonavir is a potent CYP3A4 inhibitor, this option is incomplete as it excludes Verapamil - Ritonavir's inhibitory effect is so strong that it can increase plasma concentrations of co-administered CYP3A4 substrates by several-fold *Amiodarone* - Amiodarone is primarily a **potent inhibitor of CYP2C9, CYP2D6, and P-glycoprotein** - While it does have **weak to moderate CYP3A4 inhibitory activity**, this effect is **less clinically significant** compared to its effects on other CYP enzymes - In the context of clinically important CYP3A4 inhibitors, Ritonavir and Verapamil are more relevant examples *Verapamil alone* - While correct that Verapamil is a CYP3A4 inhibitor, this option is incomplete as it excludes Ritonavir - Verapamil can increase plasma concentrations of drugs like simvastatin, cyclosporine, and other CYP3A4 substrates

Question 8: Which of the following antiarrhythmic drugs is contraindicated in a patient with interstitial lung disease?

A. Amiodarone (Correct Answer)
B. Lignocaine
C. Sotalol
D. Quinidine

Explanation: ***Amiodarone*** - **Amiodarone** is contraindicated in patients with interstitial lung disease due to its well-known and potentially severe pulmonary toxicity, which can exacerbate or induce **pulmonary fibrosis**. - Its long half-life means that drug accumulation and persistent adverse effects, including **ILD exacerbation**, are significant concerns. *Sotalol* - **Sotalol** primarily carries risks of **prolonged QT interval** and **torsades de pointes** because it has both beta-blocking and Class III antiarrhythmic properties. - While it has cardiac and minor non-cardiac side effects, it is not specifically known to cause or worsen **interstitial lung disease**. *Lignocaine* - **Lignocaine** (lidocaine) is a Class Ib antiarrhythmic primarily used for **ventricular arrhythmias**, especially in acute settings. - Its adverse effects are mainly **neurological** (e.g., dizziness, seizures at high doses) and **cardiovascular** (e.g., hypotension, bradycardia), with no significant association with lung disease. *Quinidine* - **Quinidine** is a Class Ia antiarrhythmic that can cause a variety of side effects, including **gastrointestinal upset**, **cinchonism** (tinnitus, blurred vision), and **cardiac rhythm disturbances**. - While it can rarely cause a hypersensitivity pneumonitis, it is not a primary concern or contraindication in existing **interstitial lung disease** compared to amiodarone.

Question 9: What is the drug of choice in paroxysmal supraventricular tachycardia?

A. Amiodarone
B. Quinidine
C. Adenosine (Correct Answer)
D. Lidocaine

Explanation: ***Adenosine*** - **Adenosine** is the drug of choice for acute termination of most paroxysmal supraventricular tachycardias (PSVT) due to its rapid onset and short duration of action [1]. - It works by transiently blocking the **atrioventricular (AV) node**, interrupting the re-entrant circuit common in PSVT [1]. *Amiodarone* - **Amiodarone** is a potent antiarrhythmic primarily used for both supraventricular and ventricular arrhythmias, but it is not the first-line agent for acute PSVT due to a slower onset of action and more significant side effects. - It is typically reserved for **refractory arrhythmias** or for maintaining sinus rhythm in patients with recurrent atrial fibrillation or flutter. *Lidocaine* - **Lidocaine** is primarily used for **ventricular arrhythmias**, particularly in the setting of acute myocardial infarction. - It has little to no efficacy in treating **supraventricular tachycardias** because its main action is on ventricular sodium channels. *Quinidine* - **Quinidine** is a Class IA antiarrhythmic drug used for various supraventricular and ventricular arrhythmias, but it is not the first-line treatment for acute PSVT. - Its use has declined due to a high incidence of side effects like **QT prolongation**, torsades de pointes, and gastrointestinal upset.

Question 10: Which one of the following was traditionally considered the drug of choice for ventricular tachycardia in myocardial infarction?

A. Xylocaine (Correct Answer)
B. Digitalis
C. Quinidine
D. Disopyramide

Explanation: ***Xylocaine/Lidocaine*** - **Lidocaine (Xylocaine)** is a **Class IB antiarrhythmic drug** [2] that was historically the drug of choice for suppressing ventricular arrhythmias, including ventricular tachycardia, in the setting of **myocardial ischemia and infarction** [1]. - It works by **blocking sodium channels** and shortening the action potential duration, thereby reducing excitability and automaticity in ischemic myocardial tissue [1]. - **Current guidelines**: Lidocaine is now considered a **second-line agent**, with **amiodarone** being the preferred first-line antiarrhythmic for hemodynamically stable VT in acute MI, and electrical cardioversion for unstable VT. *Digitalis* - **Digitalis** (e.g., digoxin) is primarily used for **supraventricular arrhythmias** like atrial fibrillation or flutter, and for heart failure due to its positive inotropic effect. - It can **aggravate ventricular arrhythmias** in the setting of acute myocardial infarction and is generally contraindicated for ventricular tachycardia. *Quinidine* - **Quinidine** is a **Class IA antiarrhythmic drug** that prolongs the action potential and is effective against a variety of arrhythmias. - However, it can cause **hypotension** and has a **proarrhythmic effect**, increasing the risk of Torsades de Pointes, making it less favorable as a first-line agent, especially in acute MI. *Disopyramide* - **Disopyramide** is also a **Class IA antiarrhythmic drug** with similar mechanisms to quinidine. - It has significant **negative inotropic effects** and can worsen heart failure [3], which is a common complication in acute myocardial infarction, making it less suitable.

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