Cardiovascular Drugs Practice Questions

Q: Which antiarrhythmic drug decreases both the rate of depolarization (phase 0) and the rate of repolarization of myocardial fibres?

Quinidine. **Explanation** The question describes the characteristic electrophysiological profile of **Class IA antiarrhythmics**. **1. Why Quinidine is Correct:** Quinidine belongs to **Class IA** of the Vaughan-Williams classification. Its mechanism involves: * **Sodium Channel Blockade (Phase 0):** It binds to open sodium channels, decreasing the slope of phase 0 (depolarization), which slows conduction velocity. * **Potassium Channel Blockade (Phase 3):** It blocks outward K+ channels, thereby prolonging the action potential duration (APD) and the effective refractory period (ERP). This manifests as a **decrease in the rate of repolarization**. * On an ECG, this corresponds to a widened QRS complex and a prolonged QT interval. **2. Why the other options are incorrect:** * **Verapamil (Class IV):** A calcium channel blocker. It primarily affects the SA and AV nodes by slowing Phase 0 of the nodal action potential (calcium-dependent), not the myocardial fiber depolarization. * **Propranolol (Class II):** A beta-blocker. It acts by decreasing sympathetic activity and slowing the heart rate; it does not significantly block sodium or potassium channels in myocardial fibers at standard doses. * **Lignocaine (Class IB):** While it blocks sodium channels (Phase 0), it actually **shortens** repolarization (Phase 3) or leaves it unchanged, unlike Class IA drugs which prolong it. **High-Yield NEET-PG Pearls:** * **Class IA Mnemonic:** "**P**olice **D**epartment **Q**uarters" (**P**rocainamide, **D**isopyramide, **Q**uinidine). * **Quinidine Side Effects:** Cinchonism (tinnitus, headache), thrombocytopenia, and *Torsades de Pointes* (due to QT prolongation). * **Drug Interaction:** Quinidine increases plasma levels of **Digoxin** by displacing it from tissue binding sites and reducing renal clearance.

Q: Supraventricular tachycardia can be managed best by:

Adenosine. **Explanation:** **Adenosine** is the drug of choice for the acute termination of Paroxysmal Supraventricular Tachycardia (PSVT), including those involving accessory pathways (WPW syndrome). It works by activating A1 receptors in the AV node, leading to increased potassium efflux and inhibition of calcium current. This results in profound hyperpolarization and a transient "chemical cardioversion" by blocking AV nodal conduction. Its ultra-short half-life (<10 seconds) makes it ideal for emergency use with minimal prolonged side effects. **Analysis of Incorrect Options:** * **Digitalis (Digoxin):** While it can be used for rate control in atrial fibrillation by increasing vagal tone, its onset of action is too slow (hours) for the acute management of SVT. * **Disopyramide & Quinidine:** These are Class IA antiarrhythmics. They are rarely used for SVT today due to their potential for pro-arrhythmia and significant side effects (e.g., anticholinergic effects of disopyramide, cinchonism with quinidine). Furthermore, they can paradoxically increase ventricular rate in atrial flutter/fibrillation by improving AV conduction. **High-Yield Clinical Pearls for NEET-PG:** * **Administration:** Adenosine must be given as a **rapid IV bolus** (usually 6mg, followed by 12mg) through a large-bore peripheral vein, followed by a saline flush, due to its rapid metabolism by erythrocytes and endothelial cells. * **Contraindications:** Avoid in **Asthmatics** (can cause bronchospasm via A2B receptors) and patients with **high-grade heart block**. * **Interactions:** Its effects are antagonized by **Theophylline/Caffeine** (adenosine receptor antagonists) and potentiated by **Dipyridamole**. * **Side Effects:** Patients often experience a transient, distressing sense of "impending doom," chest pain, or flushing.

Q: Which of the following drugs has been used in the treatment of angina by the inhalation route with a very rapid onset and short duration of action?

Amyl nitrite. **Explanation:** **Amyl nitrite** is the correct answer because it is a highly volatile liquid administered via **inhalation**. It is supplied in glass ampoules that are crushed and inhaled, leading to a very rapid onset of action (within 30 seconds) but a very short duration of effect (3–5 minutes). While it was historically used for acute angina, its primary clinical relevance today is in the emergency management of **cyanide poisoning** due to its ability to induce methemoglobinemia. **Why the other options are incorrect:** * **Isosorbide dinitrate (ISDN):** Primarily administered sublingually or orally. While sublingual ISDN has a rapid onset (2–5 minutes), it is not administered by inhalation and has a longer duration of action (1–2 hours) compared to Amyl nitrite. * **Isosorbide mononitrate (ISMN):** This is the active metabolite of ISDN. It has high oral bioavailability and a long half-life, making it suitable for the **prophylaxis** of angina, not for acute termination via inhalation. * **Nitroglycerin (Glyceryl Trinitrate):** The drug of choice for acute angina. It is typically administered sublingually (tablet or spray) or intravenously. While a lingual spray exists, it is not an "inhalational" drug that reaches the alveoli like Amyl nitrite. **High-Yield NEET-PG Pearls:** * **Cyanide Poisoning:** Amyl nitrite is used because it converts hemoglobin to **methemoglobin**, which has a high affinity for cyanide, forming non-toxic cyanmethemoglobin. * **Diagnostic Use:** In cardiology, Amyl nitrite inhalation is used to differentiate heart murmurs; it **increases** the intensity of the murmur in Hypertrophic Obstructive Cardiomyopathy (HOCM) and Mitral Regurgitation by decreasing systemic vascular resistance. * **Storage:** Organic nitrates (especially Nitroglycerin) must be stored in dark, tightly sealed glass containers because they are sensitive to light and can adsorb to plastic.

Q: Which antihistamine is associated with an increased risk of cardiac arrhythmias when co-administered with erythromycin or ketoconazole?

Terfenadine. **Explanation:** **Correct Option: D (Terfenadine)** Terfenadine is a second-generation H1-antihistamine that acts as a **pro-drug**. It is normally metabolized by the hepatic cytochrome **CYP3A4** enzyme into its active, non-toxic metabolite, fexofenadine. When co-administered with CYP3A4 inhibitors like **Erythromycin** (macrolide) or **Ketoconazole** (azole antifungal), the metabolism of terfenadine is blocked. This leads to high plasma levels of the parent drug, which blocks the delayed rectifier potassium channels ($I_{Kr}$) in the heart. This action prolongs the QT interval, potentially leading to a life-threatening polymorphic ventricular tachycardia known as **Torsades de Pointes**. Due to this risk, terfenadine was withdrawn from the market and replaced by fexofenadine. **Incorrect Options:** * **A & B (Diphenhydramine & Clemastine):** These are first-generation antihistamines. While they have sedative and anticholinergic side effects, they do not significantly block cardiac potassium channels or interact with CYP3A4 to cause Torsades de Pointes. * **C (Loratadine):** This is a second-generation antihistamine. While it is metabolized by CYP3A4, it does not possess the same potent cardiac potassium channel-blocking activity as terfenadine, making it much safer regarding cardiotoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Astemizole** is another second-generation antihistamine withdrawn for the same reason (QT prolongation). * **Fexofenadine** is the active metabolite of terfenadine; it is safe because it does not block cardiac $K^+$ channels. * **Mnemonic for QT-prolonging drugs:** "ABCDE" – **A**ntiarrythmics (Class IA, III), **B**iotics (Macrolides, Quinolones), **C**ant Psychotics (Haloperidol), **D**epressants (TCAs), **E**metics (Ondansetron).

Q: Which of the following decreases defibrillation threshold?

Sotalol. ### Explanation **Concept: Defibrillation Threshold (DFT)** The Defibrillation Threshold is the minimum electrical energy required to successfully terminate ventricular fibrillation. Drugs that **increase** DFT make it harder to defibrillate a patient, while drugs that **decrease** DFT make the heart more sensitive to electrical cardioversion. **Why Sotalol is Correct:** Sotalol is a Class III antiarrhythmic agent with potent potassium channel-blocking properties. By blocking the delayed rectifier potassium current ($I_{Kr}$), it prolongs the action potential duration (APD) and the effective refractory period (ERP). This increase in cardiac refractoriness lowers the energy required to terminate re-entrant circuits, thereby **decreasing the defibrillation threshold**. This property makes it particularly useful in patients with Implantable Cardioverter Defibrillators (ICDs). **Analysis of Incorrect Options:** * **Amiodarone:** Unlike Sotalol, chronic administration of Amiodarone is well-known to **increase** the DFT. This is a critical clinical consideration for patients with ICDs, as it may necessitate increasing the device's energy output settings. * **Verapamil and Diltiazem:** These are Class IV antiarrhythmics (Calcium Channel Blockers). While they affect the AV node and heart rate, they have **no significant effect** on the defibrillation threshold. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs that Decrease DFT (Make defibrillation easier):** Sotalol, Dofetilide, and Bretylium. * **Drugs that Increase DFT (Make defibrillation harder):** Amiodarone, Lidocaine, Mexiletine, and Phenytoin. * **Sotalol Side Effect:** Being a Class III agent, the most feared complication of Sotalol is **Torsades de Pointes** due to QT interval prolongation. * **Amiodarone vs. Sotalol:** Remember that while both are Class III, they have opposite effects on DFT. Amiodarone increases it; Sotalol decreases it.

Q: Which of the following drugs has the longest half-life?

Amiodarone. **Explanation:** The correct answer is **Amiodarone**. **1. Why Amiodarone is correct:** Amiodarone is a Class III antiarrhythmic drug known for its exceptional lipophilicity and extensive tissue distribution. It accumulates significantly in the adipose tissue, liver, and lungs. Due to this massive volume of distribution ($V_d$), it has an extraordinarily long elimination half-life, typically ranging from **25 to 60 days** (averaging several weeks). This necessitates the use of a loading dose to achieve steady-state plasma concentrations quickly. **2. Why the other options are incorrect:** * **Quinidine (Option B):** A Class IA antiarrhythmic with a half-life of approximately **6 to 8 hours**. * **Diltiazem (Option C):** A Class IV antiarrhythmic (Calcium Channel Blocker) with a relatively short half-life of **3 to 4.5 hours**, often requiring sustained-release formulations for long-term management. * **Procainamide (Option D):** A Class IA antiarrhythmic with a very short half-life of **3 to 4 hours**. Its active metabolite, N-acetylprocainamide (NAPA), has a longer half-life (6–10 hours) but is still significantly shorter than Amiodarone. **3. High-Yield Clinical Pearls for NEET-PG:** * **Iodine Content:** Amiodarone contains about 37% iodine by weight, leading to thyroid dysfunction (Hypothyroidism/Wolff-Chaikoff effect or Hyperthyroidism/Jod-Basedow phenomenon). * **Adverse Effects:** Due to its long half-life, toxicities take a long time to resolve. Key side effects include **pulmonary fibrosis** (most serious), corneal micro-deposits, bluish-grey skin discoloration, and hepatotoxicity. * **Monitoring:** Patients on long-term Amiodarone require regular Pulmonary Function Tests (PFTs), Liver Function Tests (LFTs), and Thyroid Function Tests (TFTs).

Q: A 23-year-old pregnant woman presents with features of dilated cardiomyopathy. Which of the following drugs should NOT be given for her treatment?

ACE inhibitors. **Explanation:** The management of heart failure or dilated cardiomyopathy in pregnancy requires careful consideration of fetal safety. **1. Why ACE Inhibitors are Contraindicated:** ACE inhibitors (e.g., Enalapril, Lisinopril) and Angiotensin Receptor Blockers (ARBs) are strictly **contraindicated (Category X/D)** during pregnancy, especially in the second and third trimesters. They interfere with the fetal renin-angiotensin system, leading to **fetal renal dysgenesis**, oligohydramnios, pulmonary hypoplasia, intrauterine growth restriction (IUGR), and cranial ossification defects. If a patient is on these drugs and becomes pregnant, they must be switched to safer alternatives immediately. **2. Analysis of Other Options:** * **Digoxin:** It is considered safe during pregnancy (Category C) and is often used to control heart rate or improve contractility in maternal heart failure. * **Diuretics (e.g., Furosemide):** While used cautiously to avoid placental hypoperfusion due to volume depletion, they are not absolute contraindications and are frequently used to manage acute pulmonary edema in pregnant patients. * **Hydralazine and Nitrates:** These are the preferred vasodilators for afterload reduction in pregnant women with heart failure instead of ACE inhibitors. **Clinical Pearls for NEET-PG:** * **Teratogenic effect of ACEIs:** "Fetal Renal Tubular Dysgenesis" is a high-yield keyword. * **Safe Antihypertensives in Pregnancy:** Remember the mnemonic **"Better Mother Love Her Child"** — **B**eta-blockers (Labetalol), **M**ethyldopa (Drug of choice for chronic HTN), **L**abetalol, **H**ydralazine, **C**alcium Channel Blockers (Nifedipine). * **Peripartum Cardiomyopathy:** Usually occurs in the last month of pregnancy or within 5 months postpartum; Bromocriptine is sometimes used in its management.

Question 1

What is the drug of choice for ventricular tachycardia in a patient with myocardial ischemia?

Accepted Answer

Lignocaine

Answer

Propranolol

Answer

Diltiazem

Answer

Digoxin

Question 2

Alpha-methyldopa is primarily used for which of the following conditions?

Accepted Answer

Pregnancy-induced hypertension

Answer

Renovascular hypertension

Answer

First-line agent in hypertension

Answer

Refractory hypertension

Question 3

Which antiarrhythmic drug decreases both the rate of depolarization (phase 0) and the rate of repolarization of myocardial fibres?

Accepted Answer

Quinidine

Answer

Verapamil

Answer

Propranolol

Answer

Lignocaine

Question 4

Supraventricular tachycardia can be managed best by:

Accepted Answer

Adenosine

Answer

Digitalis

Answer

Disopyramide

Answer

Quinidine

Question 5

Which of the following drugs has been used in the treatment of angina by the inhalation route with a very rapid onset and short duration of action?

Accepted Answer

Amyl nitrite

Answer

Isosorbide dinitrate

Answer

Isosorbide mononitrate

Answer

Nitroglycerin

Question 6

Which antihistamine is associated with an increased risk of cardiac arrhythmias when co-administered with erythromycin or ketoconazole?

Accepted Answer

Terfenadine

Answer

Diphenhydramine

Answer

Clemastine

Answer

Loratadine

Question 7

Which of the following decreases defibrillation threshold?

Accepted Answer

Sotalol

Answer

Amiodarone

Answer

Verapamil

Answer

Diltiazim

Question 8

Which of the following drugs has the longest half-life?

Accepted Answer

Amiodarone

Answer

Quinidine

Answer

Diltiazem

Answer

Procainamide

Question 9

A 23-year-old pregnant woman presents with features of dilated cardiomyopathy. Which of the following drugs should NOT be given for her treatment?

Accepted Answer

ACE inhibitors

Answer

Digoxin

Answer

Diuretics

Answer

Diuretics

Question 10

A patient presents to the casualty department in an unconscious state with a blood pressure of 220/110 mm Hg. What is the most suitable drug for this patient to rapidly decrease the blood pressure?

Accepted Answer

Intravenous infusion of sodium nitroprusside

Answer

Sublingual nifedipine

Answer

Intramuscular injection of hydralazine

Answer

Intravenous injection of clonidine

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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