Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 171: Which of the following is an antiarrhythmic drug?

A. Phentolamine
B. Phenobarbitone
C. Procainamide (Correct Answer)
D. Pentamidine

Explanation: **Explanation:** **Procainamide** is the correct answer as it is a classic **Class IA antiarrhythmic drug**. It works by blocking voltage-gated sodium channels (Phase 0) and, to a lesser extent, potassium channels (Phase 3). This action slows conduction velocity, prolongs the action potential duration (APD), and increases the effective refractory period (ERP) in both atrial and ventricular myocardial cells. It is clinically used for both supraventricular and ventricular arrhythmias. **Analysis of Incorrect Options:** * **Phentolamine (Option A):** A non-selective **alpha-adrenergic blocker** used primarily in the management of pheochromocytoma and hypertensive crises. * **Phenobarbitone (Option B):** A **barbiturate** that acts as a sedative-hypnotic and antiepileptic by enhancing GABA-mediated chloride channel opening. * **Pentamidine (Option C):** An **antiprotozoal** agent used to treat *Pneumocystis jirovecii* pneumonia and leishmaniasis. Interestingly, it can actually *cause* arrhythmias (QT prolongation) as a side effect. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolism:** Procainamide is metabolized via **acetylation** (by N-acetyltransferase) into **NAPA** (N-acetylprocainamide). NAPA has Class III antiarrhythmic properties. * **Side Effect:** A classic exam favorite is **Drug-Induced Lupus Erythematosus (DILE)**, seen more commonly in "slow acetylators." Unlike systemic lupus, DILE usually spares the kidneys and is associated with **anti-histone antibodies**. * **ECG Changes:** Class IA drugs cause widening of the QRS complex and prolongation of the QT interval.

Question 172: Digoxin increases cardiac contractility by directly engaging in which of the following mechanisms?

A. Inhibiting myocardial Na+/Ca2+-ATPase
B. Activating L-type Ca2+ channels
C. Inhibiting cardiac phosphodiesterase
D. Inhibiting myocardial Na+/K+-ATPase (Correct Answer)

Explanation: **Explanation:** Digoxin, a cardiac glycoside, increases cardiac contractility (positive inotropy) through a well-defined sequence of ionic shifts. **Mechanism of Action (Why D is correct):** The primary molecular target of Digoxin is the **Na+/K+-ATPase pump** located on the sarcolemma of myocardial cells. By binding to the extracellular alpha subunit of this pump, Digoxin inhibits the active transport of Na+ out of the cell and K+ into the cell. This leads to an **increase in intracellular Na+**. The rise in intracellular Na+ reduces the concentration gradient that drives the **Na+/Ca2+ exchanger (NCX)**. Consequently, the efflux of Ca2+ is diminished, leading to increased intracellular Ca2+ levels. This excess Ca2+ is sequestered into the Sarcoplasmic Reticulum (SR) and released during subsequent action potentials, enhancing actin-myosin cross-bridge formation and force of contraction. **Analysis of Incorrect Options:** * **A. Inhibiting myocardial Na+/Ca2+-ATPase:** There is no such enzyme as Na+/Ca2+-ATPase; the Na+/Ca2+ exchanger (NCX) is a secondary active transporter, not a primary ATPase. * **B. Activating L-type Ca2+ channels:** This is the mechanism for drugs like Bay K 8644. Digoxin does not directly act on these channels. * **C. Inhibiting cardiac phosphodiesterase:** This is the mechanism of **Milrinone and Inamrinone**, which increase cAMP levels to improve contractility. **High-Yield NEET-PG Pearls:** * **ECG Changes:** Digoxin causes the characteristic "reverse tick" or "hockey stick" ST-segment depression (Salvador Dali sign). * **Electrolyte Interactions:** **Hypokalemia** predisposes to Digoxin toxicity because K+ and Digoxin compete for the same binding site on the Na+/K+-ATPase pump. * **Antidote:** Digibind (Digoxin-specific Fab fragments). * **Therapeutic Range:** Narrow (0.5–2 ng/mL). Toxicity often presents with gastrointestinal symptoms and xanthopsia (yellow-green vision).

Question 173: What is the drug of choice for paroxysmal supraventricular tachycardia?

A. Verapamil (Correct Answer)
B. Digitalis
C. Quinidine
D. Diphynylhydantoin

Explanation: **Explanation:** **Verapamil** is a non-dihydropyridine Calcium Channel Blocker (CCB) and is considered a drug of choice for terminating an acute episode of **Paroxysmal Supraventricular Tachycardia (PSVT)** [2], [3]. PSVT most commonly arises from an AV nodal re-entrant circuit. Verapamil acts by blocking L-type calcium channels in the AV node, which slows conduction and increases the refractory period, effectively breaking the re-entrant circuit and restoring sinus rhythm [2]. **Analysis of Incorrect Options:** * **Digitalis:** While it increases vagal tone and slows AV conduction, its onset of action is too slow for the acute termination of PSVT. It is primarily used for rate control in chronic atrial fibrillation. * **Quinidine:** This is a Class IA antiarrhythmic. It is rarely used for PSVT because it has antimuscarinic effects that can actually paradoxically increase AV conduction, potentially worsening the tachycardia. * **Diphenylhydantoin (Phenytoin):** This is a Class IB antiarrhythmic. It is specifically the drug of choice for **Digitalis-induced arrhythmias**, not for standard PSVT. **High-Yield Clinical Pearls for NEET-PG:** * **Adenosine vs. Verapamil:** In modern clinical practice, **Adenosine** is the first-line drug of choice for acute PSVT due to its ultra-short half-life (<10 seconds) [2]. However, if Adenosine is not an option or if the question follows classic pharmacological guidelines, Verapamil is the standard answer [3]. * **Contraindication:** Never give Verapamil to patients with Wide QRS Tachycardia or WPW syndrome with atrial fibrillation, as it can lead to ventricular fibrillation [1]. * **Vagal Maneuvers:** Always remember that the initial management step for a stable PSVT patient is a vagal maneuver (e.g., Carotid sinus massage or Valsalva).

Question 174: What is the renal dose of dopamine?

A. 2.5 mcg/kg/min
B. 5-10 mcg/kg/min
C. 10-20 mcg/kg/min
D. 1-2 mcg/kg/min (Correct Answer)

Explanation: **Explanation:** Dopamine is a unique sympathomimetic amine because its pharmacological effects are strictly **dose-dependent**. It acts on different receptors based on the infusion rate, which is a high-yield concept for NEET-PG. 1. **Low Dose (1–2 mcg/kg/min):** This is the **"Renal Dose."** At this concentration, dopamine selectively stimulates **D1 receptors** in the renal, mesenteric, and coronary beds. This leads to vasodilation, increased renal blood flow, and increased glomerular filtration rate (GFR). 2. **Intermediate Dose (2–10 mcg/kg/min):** This is the **"Inotropic Dose."** It primarily stimulates **β1 receptors** in the heart, increasing myocardial contractility and cardiac output. 3. **High Dose (>10 mcg/kg/min):** This is the **"Pressor Dose."** It predominantly stimulates **α1 receptors**, causing systemic vasoconstriction and increasing blood pressure. **Analysis of Options:** * **Option D (1-2 mcg/kg/min):** Correct. It targets D1 receptors to improve renal perfusion. * **Option B (5-10 mcg/kg/min):** Incorrect. This range targets β1 receptors (Cardiac effect). * **Option C (10-20 mcg/kg/min):** Incorrect. This range targets α1 receptors (Vasoconstrictor effect). * **Option A (2.5 mcg/kg/min):** Incorrect. While close to the threshold, it begins to transition into β-receptor activity. **High-Yield Clinical Pearls:** * **The "Renal Dose" Myth:** While low-dose dopamine increases urine output, clinical trials (like the SOAP II trial) have shown it **does not** prevent or treat acute renal failure or improve survival. * **Fenoldopam:** A selective D1 agonist used for hypertensive emergencies; it provides renal vasodilation without the β or α effects of dopamine. * **Adverse Effect:** High doses can cause tachycardia and arrhythmias due to β1 stimulation.

Question 175: What is the antihypertensive of choice in a patient with diabetes mellitus and proteinuria?

A. Enalapril (Correct Answer)
B. Propranolol
C. Hydralazine
D. Minoxidil

Explanation: **Explanation:** **Enalapril (Option A)** is an ACE inhibitor and the drug of choice for patients with diabetes mellitus (DM) and proteinuria. The underlying medical concept is **renoprotection**. In diabetic nephropathy, there is preferential constriction of the efferent arteriole mediated by Angiotensin II, leading to increased intraglomerular pressure. ACE inhibitors (and ARBs) cause vasodilation of the efferent arteriole, which reduces intraglomerular capillary pressure, decreases the glomerular filtration rate (GFR) slightly, and significantly reduces protein excretion (proteinuria), thereby slowing the progression of chronic kidney disease. **Why the other options are incorrect:** * **Propranolol (Option B):** A non-selective beta-blocker. It is generally avoided as a first-line agent in diabetics because it can mask the autonomic symptoms of hypoglycemia (like tachycardia and tremors) and may delay recovery from hypoglycemic episodes. * **Hydralazine (Option C):** A direct vasodilator primarily used in pregnancy-induced hypertension or in combination with nitrates for heart failure. It does not offer specific renoprotective benefits. * **Minoxidil (Option D):** A potent vasodilator reserved for refractory hypertension. It causes significant salt and water retention and reflex tachycardia, requiring concomitant use of diuretics and beta-blockers. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** ACE inhibitors/ARBs are DOC for hypertension in DM, CKD with proteinuria, and Heart Failure. * **Side Effects:** Watch for a dry cough (due to bradykinin accumulation) and hyperkalemia. * **Contraindications:** ACE inhibitors are strictly contraindicated in pregnancy (teratogenic) and bilateral renal artery stenosis. * **Monitoring:** A rise in serum creatinine up to 30% after starting an ACE inhibitor is considered acceptable.

Question 176: What is the mechanism of action of aspirin as an antiplatelet drug, specifically its inhibitory action on which substance?

A. Prostacyclins
B. PGF 2 alpha
C. Thromboxane A2 (Correct Answer)
D. Phospholipase C

Explanation: **Mechanism of Action** Aspirin (Acetylsalicylic acid) acts as an antiplatelet agent by **irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1)**. It achieves this by acetylating a serine residue at the enzyme's active site. In platelets, COX-1 is responsible for converting arachidonic acid into **Thromboxane A2 (TXA2)**. TXA2 is a potent vasoconstrictor and a key mediator of platelet aggregation. Since platelets are anucleated and cannot synthesize new enzymes, the inhibition lasts for the entire lifespan of the platelet (approx. 7–10 days). **Analysis of Options** * **Option A (Prostacyclins):** While aspirin can inhibit Prostacyclin (PGI2) synthesis in vascular endothelial cells, PGI2 is a vasodilator and *inhibitor* of aggregation. At low doses, aspirin selectively inhibits TXA2 more than PGI2, which is the basis for its therapeutic antiplatelet effect. * **Option B (PGF 2 alpha):** This is a prostaglandin involved in uterine contraction and bronchoconstriction; it is not the primary target for aspirin’s antiplatelet therapy. * **Option D (Phospholipase C):** This enzyme is involved in the IP3/DAG signaling pathway. Aspirin does not directly inhibit this enzyme; its target is downstream in the arachidonic acid cascade. **High-Yield NEET-PG Pearls** * **Low-dose Aspirin (75–150 mg):** Exhibits antiplatelet effects. Higher doses are required for analgesic and anti-inflammatory effects. * **Primary/Secondary Prevention:** Used in Myocardial Infarction (MI) and Ischemic Stroke. * **Side Effect:** Can cause **Reye’s Syndrome** in children with viral infections; hence, it is contraindicated in that population. * **Aspirin Resistance:** Some patients may not show adequate TXA2 suppression, increasing the risk of recurrent thrombotic events.

Question 177: Cardioselective beta blockers are contraindicated in which of the following conditions?

A. COPD
B. II & III degree heart block (Correct Answer)
C. Asthma
D. Tachycardia

Explanation: **Explanation:** The core pharmacological action of beta-blockers involves the inhibition of $\beta_1$ receptors in the heart, leading to negative inotropic (force), chronotropic (rate), and dromotropic (conduction velocity) effects. **Why Option B is Correct:** In **II and III-degree heart blocks**, the conduction of impulses from the atria to the ventricles is already impaired. Beta-blockers further depress the **Atrioventricular (AV) node** conduction. This can exacerbate the block, potentially leading to complete heart block, severe bradycardia, or asystole. Therefore, they are strictly contraindicated regardless of their selectivity. **Why Other Options are Incorrect:** * **A & C (COPD and Asthma):** While *non-selective* beta-blockers are contraindicated due to $\beta_2$ blockade causing bronchospasm, **cardioselective** ($\beta_1$ specific) blockers (e.g., Metoprolol, Atenolol) can be used with extreme caution in stable COPD or mild asthma if the cardiac benefit outweighs the risk. They are not an absolute contraindication compared to heart block. * **D (Tachycardia):** Beta-blockers are actually a **treatment** for tachycardia (especially sinus tachycardia and supraventricular arrhythmias) because they reduce the heart rate. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cardioselective ($\beta_1$) blockers:** *"New Beta Blockers Are Very Exclusive"* (Nebivolol, Betaxolol, Bisoprolol, Acebutolol, Atenolol, Valolol, Esmolol, Metoprolol). * **Esmolol** is the shortest-acting beta-blocker (half-life ~9 mins), used IV for hypertensive emergencies. * **Absolute Contraindications:** Severe bradycardia, cardiogenic shock, overt heart failure, and advanced heart block. * **Prinzmetal Angina:** Beta-blockers are contraindicated as they can cause unopposed alpha-mediated coronary vasoconstriction.

Question 178: Which of the following antihypertensives was once used as an antipsychotic?

A. Atenolol
B. Propranolol
C. Clonidine
D. Reserpine (Correct Answer)

Explanation: **Explanation:** **Reserpine** is the correct answer. It is an alkaloid derived from the plant *Rauwolfia serpentina*. * **Mechanism:** Reserpine irreversibly blocks the **Vesicular Monoamine Transporter (VMAT)**. This prevents the storage of neurotransmitters like norepinephrine, dopamine, and serotonin in synaptic vesicles, leading to their depletion. * **Clinical Use:** By depleting norepinephrine, it acts as an antihypertensive. By depleting dopamine and serotonin in the CNS, it was historically used as an **antipsychotic** to treat schizophrenia. However, its use is now obsolete due to the severe side effect of **suicidal depression**. **Incorrect Options:** * **Atenolol:** A selective $\beta_1$ blocker. It is hydrophilic, does not cross the blood-brain barrier effectively, and has no antipsychotic properties. * **Propranolol:** A non-selective $\beta$ blocker. While it is lipophilic and used for performance anxiety, essential tremors, and prophylaxis of migraine, it has never been used as an antipsychotic. * **Clonidine:** An $\alpha_2$ agonist that decreases sympathetic outflow. It is used in ADHD and opioid withdrawal but lacks antipsychotic efficacy. **High-Yield Pearls for NEET-PG:** 1. **Reserpine-induced Depression:** The observation that reserpine caused depression led to the "Monoamine Hypothesis" of depression. 2. **VMAT Inhibition:** Unlike Cocaine or TCAs (which act on reuptake transporters like NET/DAT), Reserpine acts on the **vesicular** transporter. 3. **Contraindication:** Never give reserpine to a patient with a history of mental depression or peptic ulcer disease (as it increases gastric acid secretion).

Question 179: Which antihypertensive is not used in the management of pregnancy-induced hypertension (PIH)?

A. Hydralazine
B. Propranolol (Correct Answer)
C. Labetalol
D. Alpha-methyldopa

Explanation: **Explanation:** The management of Pregnancy-Induced Hypertension (PIH) requires drugs that are both effective for the mother and safe for the fetus. **Propranolol** (Option B) is generally avoided in pregnancy because it is a non-selective beta-blocker associated with **Intrauterine Growth Retardation (IUGR)**. It can also cause fetal bradycardia and neonatal hypoglycemia by interfering with the fetus's metabolic response to stress. **Analysis of Options:** * **Alpha-methyldopa (Option D):** Historically the **drug of choice** for chronic hypertension in pregnancy. It has a long-standing safety profile with no known teratogenic effects. * **Labetalol (Option C):** Currently the **first-line agent** for both acute and maintenance management of PIH. It is a combined alpha and beta-blocker that maintains placental perfusion better than pure beta-blockers. * **Hydralazine (Option A):** A potent vasodilator used primarily in the management of **hypertensive emergencies** (Preeclampsia/Eclampsia) during pregnancy. **NEET-PG High-Yield Pearls:** 1. **Drug of Choice (Acute/Emergency PIH):** I.V. Labetalol (Hydralazine is an alternative). 2. **Drug of Choice (Maintenance/Chronic PIH):** Oral Labetalol or Alpha-methyldopa. 3. **Absolute Contraindications in Pregnancy:** ACE Inhibitors (e.g., Enalapril) and ARBs (e.g., Losartan) due to risk of fetal renal dysgenesis and skull defects (teratogenicity). 4. **Diuretics** are generally avoided as they can further reduce placental perfusion by decreasing plasma volume.

Question 180: Which of the following drugs is MOST suitable for a 45-year old diabetic with blood pressure 150/95 mmHg?

A. Lisinopril (Correct Answer)
B. Amlodipine
C. Propranolol
D. Hydrochlorothiazide

Explanation: **Explanation:** The correct answer is **Lisinopril (Option A)**. **Why Lisinopril is the drug of choice:** In patients with **Diabetes Mellitus (DM)** and hypertension, **ACE inhibitors (ACEIs)** like Lisinopril or **Angiotensin Receptor Blockers (ARBs)** are the first-line treatment [1]. The primary medical concept here is **Renoprotection**. ACEIs dilate the efferent arteriole more than the afferent arteriole in the kidney, reducing intraglomerular pressure. This action slows the progression of diabetic nephropathy and reduces albuminuria, regardless of the blood pressure-lowering effect. **Analysis of Incorrect Options:** * **B. Amlodipine:** While Calcium Channel Blockers (CCBs) are metabolically neutral and effective antihypertensives, they do not offer the same level of specific renal protection as ACEIs in diabetic patients [2]. * **C. Propranolol:** Non-selective beta-blockers are generally avoided in diabetics because they can mask the warning signs of hypoglycemia (tachycardia/tremors) and may worsen insulin sensitivity. * **D. Hydrochlorothiazide:** Thiazide diuretics can potentially cause hyperglycemia and hyperlipidemia, making them less ideal as a first-line monotherapy in a diabetic patient compared to ACEIs. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC):** ACEIs/ARBs are DOC for HTN with DM, Chronic Kidney Disease (CKD), and Heart Failure. * **Side Effect:** The most common side effect of ACEIs is a **dry cough** (due to increased bradykinin); if this occurs, switch the patient to an ARB (e.g., Losartan). * **Contraindication:** ACEIs and ARBs are strictly **contraindicated in pregnancy** (teratogenic) and in patients with bilateral renal artery stenosis.

Practice by Chapter

Antihypertensive Agents

Practice Questions

Drugs for Heart Failure

Practice Questions

Antiarrhythmic Drugs

Practice Questions

Antianginal Agents

Practice Questions

Lipid-Lowering Drugs

Practice Questions

Anticoagulants and Antiplatelet Drugs

Practice Questions

Thrombolytic Agents

Practice Questions

Drugs Used in Pulmonary Hypertension

Practice Questions

Drugs Used in Shock

Practice Questions

Cardiovascular Effects of Non-Cardiovascular Drugs

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