Cardiovascular Drugs Practice Questions

Q: Which of the following agents decreases cardiac afterload?

Nicorandil. **Explanation:** The correct answer is **Nicorandil** because of its unique dual mechanism of action. To understand this, we must distinguish between **preload** (venous return/venous dilation) and **afterload** (systemic vascular resistance/arterial dilation). 1. **Why Nicorandil is correct:** Nicorandil acts as both a **Nitrate-like vasodilator** and a **K+ATP channel opener**. While the nitrate component causes venodilation (reducing preload), the opening of ATP-sensitive potassium channels leads to significant hyperpolarization of vascular smooth muscle cells in the **arterioles**. This results in potent arterial dilation, which directly decreases systemic vascular resistance, thereby **decreasing cardiac afterload**. 2. **Why other options are incorrect:** * **Glyceryl trinitrate (GTN) & Isosorbide dinitrate:** These are organic nitrates that primarily act on the venous capacitance vessels at therapeutic doses. Their main effect is reducing **preload**. While they can cause some arterial dilation at very high doses, their clinical hallmark is venodilation. Therefore, they are not the primary agents for afterload reduction compared to Nicorandil. **High-Yield Clinical Pearls for NEET-PG:** * **Dual Action:** Nicorandil is the only drug in this list that targets both preload and afterload. * **Cardioprotection:** It mimics "ischemic preconditioning" by opening mitochondrial K+ATP channels, protecting the myocardium during ischemia. * **Side Effect Alert:** A classic, high-yield side effect of Nicorandil is **persistent mucosal ulcerations** (anal, oral, or GI ulcers). * **Contraindication:** Like other nitrates, it should not be co-administered with Sildenafil (PDE-5 inhibitors) due to the risk of severe hypotension.

Q: Which of the following drugs does NOT reduce myocardial remodelling in Congestive Heart Failure?

Digoxin. **Explanation:** The goal of modern Heart Failure (HF) management is to block the neurohormonal compensatory mechanisms (Sympathetic and RAAS activation) that lead to **myocardial remodelling**—the structural changes (hypertrophy, fibrosis, and ventricular dilation) that worsen cardiac function over time. **Why Digoxin is the correct answer:** Digoxin is a positive inotropic agent that inhibits the Na+/K+ ATPase pump. While it improves symptoms and reduces the rate of hospitalization by increasing cardiac contractility, it has **no effect on the neurohormonal pathways** responsible for structural remodeling. Consequently, Digoxin does not reduce mortality in heart failure patients. **Analysis of other options:** * **Carvedilol (Beta-blocker):** Blocks the chronic effects of catecholamines, preventing apoptosis and cardiac hypertrophy. Beta-blockers are cornerstones in reducing mortality and reversing remodeling. * **Enalapril (ACE Inhibitor):** Prevents the formation of Angiotensin II, a potent stimulus for myocyte growth and collagen deposition. ACE inhibitors are the first-line agents for preventing remodeling. * **Spironolactone (Mineralocorticoid Receptor Antagonist):** Blocks aldosterone, which is directly responsible for myocardial and vascular fibrosis. It significantly reduces mortality in NYHA Class II-IV heart failure. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs reducing mortality in HF:** ACE inhibitors, ARBs, Beta-blockers (specifically Carvedilol, Metoprolol succinate, Bisoprolol), Aldosterone antagonists, and SGLT2 inhibitors. * **Drugs improving symptoms but NOT mortality:** Digoxin and Diuretics (Furosemide). * **Digoxin Toxicity:** Characterized by gastrointestinal symptoms, xanthopsia (yellow vision), and any arrhythmia (most common: PVCs; most specific: PAT with block).

Q: Digoxin is contraindicated in which of the following conditions?

Hypertrophic obstructive cardiomyopathy. **Explanation:** **Hypertrophic Obstructive Cardiomyopathy (HOCM)** is the correct answer because Digoxin is strictly contraindicated in this condition. In HOCM, there is asymmetrical septal hypertrophy that creates a dynamic sub-aortic outflow tract obstruction. Digoxin is a **positive inotrope**; by increasing the force of myocardial contraction, it narrows the outflow tract further during systole, worsening the obstruction and potentially leading to sudden cardiac collapse. **Analysis of Incorrect Options:** * **A & B (SVT and Atrial Fibrillation):** Digoxin is used in these supraventricular arrhythmias due to its **vagomimetic action**. It slows conduction through the AV node (negative dromotropy), which helps control the ventricular rate. * **C (Congestive Heart Failure):** Digoxin is indicated in chronic HFrEF (Heart Failure with reduced Ejection Fraction), especially when accompanied by atrial fibrillation. It improves symptoms and reduces hospitalization rates, though it does not decrease overall mortality. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Inhibits Na+/K+ ATPase pump → increases intracellular Na+ → decreases Na+/Ca2+ exchange → increases intracellular Ca2+ → positive inotropy. * **Other Contraindications:** Ventricular tachycardia/fibrillation, WPW syndrome (can lead to preferential conduction through the accessory pathway), and Hypokalemia (increases risk of digoxin toxicity). * **Toxicity Sign:** The most common initial symptom is anorexia/nausea; the most characteristic ECG finding is the "reverse tick" or "Sagging ST segment." * **Antidote:** Digibind (Digoxin-specific Fab fragments).

Q: Which of the following drugs is NOT used to reverse cardiac remodeling in congestive cardiac failure?

Digoxin. **Explanation:** Cardiac remodeling is the structural change in the heart (hypertrophy, fibrosis, and chamber dilation) driven by chronic neurohumoral activation. To reverse or prevent this, a drug must inhibit the **Sympathetic Nervous System (SNS)** or the **Renin-Angiotensin-Aldosterone System (RAAS)**. **Why Digoxin is the correct answer:** Digoxin is a positive inotrope that acts by inhibiting the Na+/K+ ATPase pump. While it improves symptoms and reduces hospitalization rates in heart failure (HF), it has **no effect on cardiac remodeling** and does not reduce mortality. It is primarily used for rate control in patients with concomitant Atrial Fibrillation or for symptomatic relief in refractory HF. **Why the other options are incorrect:** * **ACE Inhibitors (e.g., Enalapril):** These are the gold standard for reversing remodeling. They decrease Angiotensin II levels, reducing fibroblast proliferation and cardiac hypertrophy. * **Beta Blockers (e.g., Carvedilol, Metoprolol):** They counteract the toxic effects of chronic catecholamine exposure, allowing the heart to recover its systolic function over time (reverse remodeling). * **Aldosterone Antagonists (e.g., Spironolactone):** These prevent aldosterone-induced myocardial fibrosis and collagen deposition, significantly reducing mortality in NYHA Class II-IV heart failure. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mortality-Reducing Drugs in HF:** ACEIs, ARBs, Beta-blockers, Aldosterone antagonists, and ARNIs (Sacubitril/Valsartan). 2. **Digoxin Toxicity:** Characterized by xanthopsia (yellow vision) and various arrhythmias; the most characteristic is **Paroxysmal Atrial Tachycardia with AV block**. 3. **ARNI:** Currently considered superior to ACEIs for reversing remodeling in HFrEF.

Q: What is the mechanism of action of Aspirin in myocardial infarction?

Thromboxane A2 synthesis inhibition. **Explanation:** **Mechanism of the Correct Answer (A):** Aspirin (Acetylsalicylic acid) acts as an antiplatelet agent by **irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1)**. In platelets, COX-1 is responsible for converting arachidonic acid into Prostaglandin H2, which is then converted into **Thromboxane A2 (TXA2)**. TXA2 is a potent vasoconstrictor and a mediator of platelet aggregation. By inhibiting its synthesis, Aspirin prevents platelet plug formation, thereby reducing the risk of further coronary artery occlusion during a myocardial infarction (MI). **Analysis of Incorrect Options:** * **Option B:** Stimulating TXA2 synthesis would promote clot formation and worsen ischemia, which is the opposite of the desired therapeutic effect. * **Option C:** Antagonism of adenosine is a characteristic of Methylxanthines (like Theophylline or Caffeine), not Aspirin. Adenosine itself is used for supraventricular tachycardia (SVT). * **Option D:** While Aspirin affects the prostaglandin pathway, its primary cardioprotective benefit in MI is derived from TXA2 inhibition, not the stimulation of PGF2. **High-Yield Clinical Pearls for NEET-PG:** * **Irreversibility:** Aspirin acetylates a serine residue in the active site of COX-1. Since platelets lack a nucleus, they cannot synthesize new enzymes; thus, the effect lasts for the **entire lifespan of the platelet (7–10 days)**. * **Dose-Dependency:** At low doses (75–150 mg), Aspirin is selective for COX-1 (antiplatelet). At higher doses, it inhibits COX-2 (anti-inflammatory). * **Emergency Protocol:** In acute MI, the patient should **chew** the tablet (usually 325 mg) to ensure rapid buccal absorption and faster onset of action. * **Primary Side Effect:** Gastric ulceration and GI bleeding due to the inhibition of protective prostaglandins (PGE2) in the stomach.

Q: All of the following drugs cause QT prolongation except?

Cetrizine. **Explanation:** The correct answer is **Cetirizine**. **1. Why Cetirizine is the correct answer:** QT prolongation is primarily caused by the blockade of the **hERG (human Ether-à-go-go-Related Gene) potassium channels** in the heart, which delays ventricular repolarization. While many first-generation and early second-generation antihistamines affect these channels, **Cetirizine** (a second-generation H1 antagonist and metabolite of hydroxyzine) does not significantly block hERG channels at therapeutic doses. It is considered "non-cardiotoxic" and does not cause clinically significant QT prolongation or Torsades de Pointes (TdP). **2. Why the other options are incorrect:** * **Cisapride:** A prokinetic agent formerly used for GERD. It was withdrawn from many markets because it is a potent blocker of the hERG K+ channel, leading to fatal arrhythmias. * **Quinidine:** A Class IA antiarrhythmic. By definition, Class IA drugs block fast sodium channels and potassium channels, inherently prolonging the action potential duration and the QT interval. * **Terfenadine:** The first non-sedating antihistamine. It was withdrawn because it is a prodrug metabolized by CYP3A4. If metabolism is inhibited (e.g., by erythromycin or grapefruit juice), the parent compound accumulates and causes life-threatening QT prolongation. (Fexofenadine is its safe active metabolite). **High-Yield Clinical Pearls for NEET-PG:** * **The "ABCDE" of QT Prolongation:** **A**ntiarrhythmics (Class IA, III), **B**iotics (Macrolides, Fluoroquinolones), **C**isapride/Antipsychotics (Haloperidol), **D**epressants (TCAs), **E**metics (Ondansetron). * **Safe Antihistamines:** Fexofenadine, Cetirizine, and Loratadine are generally considered safe regarding the QT interval. * **Risk Factor:** Hypokalemia and hypomagnesemia potentiate drug-induced QT prolongation.

Q: What is the primary treatment for torsades de pointes?

Magnesium sulfate (MgSO4). **Explanation:** **Torsades de Pointes (TdP)** is a specific form of polymorphic ventricular tachycardia characterized by a "twisting of points" around the isoelectric line. It is typically associated with a prolonged QT interval. **Why Magnesium Sulfate (MgSO4) is the Correct Answer:** Intravenous Magnesium sulfate is the **drug of choice** for both the treatment and prevention of recurrences of TdP, regardless of the patient's baseline magnesium levels. It works by stabilizing the cardiac cell membrane and suppressing the **Early Afterdepolarizations (EADs)** that trigger the arrhythmia. It achieves this by blocking L-type calcium channels and reducing the influx of calcium, thereby shortening the action potential duration in the Purkinje fibers. **Analysis of Incorrect Options:** * **A. Propranolol:** While beta-blockers are used in Congenital Long QT Syndrome (LQTS) to prevent episodes, they are not the primary acute treatment for an active episode of TdP. * **B. Calcium channel blockers:** These are generally contraindicated as they can worsen bradycardia or hypotension, potentially exacerbating the arrhythmia. * **D. Lignocaine:** This is a Class IB antiarrhythmic used for stable ventricular tachycardia but is ineffective in TdP and does not address the underlying QT prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **Immediate Management:** If MgSO4 fails and the patient is hemodynamically unstable, **unsynchronized cardioversion** (defibrillation) is required. * **Heart Rate Management:** Increasing the heart rate via **isoprenaline** or **cardiac pacing** can help shorten the QT interval and "overdrive" suppress TdP. * **Avoidance:** Class IA (Quinidine, Procainamide) and Class III (Sotalol, Amiodarone) antiarrhythmics must be avoided as they further prolong the QT interval and can worsen TdP.

Q: Which of the following calcium channel blockers is useful in the treatment of supraventricular tachycardia by suppressing AV node conduction?

Verapamil. Explanation: Calcium channel blockers (CCBs) are broadly classified into two categories: **Dihydropyridines (DHPs)** and **Non-Dihydropyridines (Non-DHPs)** [1]. **Why Verapamil is correct:** Verapamil is a Non-DHP CCB with significant **cardioselective** properties. It primarily acts on the L-type calcium channels in the myocardium and the conduction system [3]. By blocking these channels in the **Atrioventricular (AV) node**, it increases the refractory period and slows down conduction velocity (negative dromotropy) [3]. This makes it highly effective for terminating and controlling the ventricular rate in **Supraventricular Tachycardia (SVT)** [3]. **Why the other options are incorrect:** * **Amlodipine and Nifedipine:** These are Dihydropyridines. They are **vasoselective**, acting primarily on smooth muscles of the peripheral blood vessels to cause vasodilation [1]. They have minimal effect on the AV node at clinical doses and may even cause reflex tachycardia, making them unsuitable for arrhythmias [4]. * **Nimodipine:** This is a DHP with high lipid solubility and selectivity for **cerebral blood vessels**. It is specifically used to prevent cerebral vasospasm following subarachnoid hemorrhage, not for cardiac arrhythmias [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Adenosine is the DOC for acute paroxysmal SVT; Verapamil is an alternative [3]. * **Contraindication:** Never give Verapamil in wide-complex tachycardia of unknown origin or in WPW syndrome with Atrial Fibrillation, as it may precipitate ventricular fibrillation [2]. * **Side Effects:** Constipation is the most common side effect of Verapamil [2]. * **Diltiazem:** Another Non-DHP CCB (Benzothiazepine) that acts on both the heart and blood vessels, also used in SVT [3].

Q: Ankle edema caused by calcium channel blockers is prevented by which of the following classes of drugs?

ACE inhibitors. **Explanation:** The ankle edema associated with **Dihydropyridine Calcium Channel Blockers (CCBs)** like Amlodipine is not due to fluid overload, but rather a result of **preferential precapillary (arteriolar) vasodilation**. This increases the hydrostatic pressure in the capillaries, causing fluid to leak into the interstitial space. **1. Why ACE inhibitors are correct:** ACE inhibitors (and ARBs) cause **balanced vasodilation** of both the **precapillary (arteriolar)** and **postcapillary (venular)** vessels. By dilating the venules, ACE inhibitors reduce the hydrostatic pressure gradient in the capillary bed, thereby facilitating the reabsorption of fluid back into the vascular compartment and neutralizing the edema caused by CCBs. **2. Why other options are incorrect:** * **Propranolol:** This is a non-selective beta-blocker. While it can be used to treat reflex tachycardia caused by CCBs, it has no significant effect on postcapillary venodilation and does not prevent peripheral edema. * **Adrenaline:** This is a sympathomimetic. It would likely worsen cardiovascular parameters and has no role in managing drug-induced edema. * **Ropinirole:** This is a dopamine agonist used in Parkinson’s disease and Restless Leg Syndrome. Interestingly, Ropinirole itself is known to *cause* peripheral edema as a side effect. **Clinical Pearls for NEET-PG:** * **Mechanism:** CCB-induced edema is "non-pitting" and does not respond to diuretics (like Furosemide) because the total body sodium/water is normal. * **Combination Therapy:** The combination of a CCB and an ACE inhibitor is a "high-yield" clinical strategy because it provides synergistic BP lowering while minimizing the side effect of edema. * **Other CCB side effects:** Gingival hyperplasia, reflex tachycardia (with DHPs), and constipation (specifically Verapamil).

Question 1

Which of the following drugs is known to cause a coronary steal phenomenon?

Accepted Answer

Dipyridamole

Answer

Pyridoxine

Answer

Dihydropyridine

Answer

Trimetazidine

Question 2

Which of the following agents decreases cardiac afterload?

Accepted Answer

Nicorandil

Answer

Glyceryl trinitrate

Answer

Isosorbide dinitrate

Answer

None of the above

Question 3

Which of the following drugs does NOT reduce myocardial remodelling in Congestive Heart Failure?

Accepted Answer

Digoxin

Answer

Carvedilol

Answer

Enalapril

Answer

Spironolactone

Question 4

Digoxin is contraindicated in which of the following conditions?

Accepted Answer

Hypertrophic obstructive cardiomyopathy

Answer

Supraventricular tachycardia

Answer

Atrial fibrillation

Answer

Congestive heart failure

Question 5

Which of the following drugs is NOT used to reverse cardiac remodeling in congestive cardiac failure?

Accepted Answer

Digoxin

Answer

Beta blocker

Answer

ACE inhibitor

Answer

Aldosterone antagonist

Question 6

What is the mechanism of action of Aspirin in myocardial infarction?

Accepted Answer

Thromboxane A2 synthesis inhibition

Answer

Thromboxane A2 synthesis stimulation

Answer

Antagonist of adenosine

Answer

Stimulation of PGF2 synthesis

Question 7

All of the following drugs cause QT prolongation except?

Accepted Answer

Cetrizine

Answer

Cisapride

Answer

Quinidine

Answer

Terfenadine

Question 8

What is the primary treatment for torsades de pointes?

Accepted Answer

Magnesium sulfate (MgSO4)

Answer

Propranolol

Answer

Calcium channel blocker

Answer

Lignocaine

Question 9

Which of the following calcium channel blockers is useful in the treatment of supraventricular tachycardia by suppressing AV node conduction?

Accepted Answer

Verapamil

Answer

Amlodipine

Answer

Nimodipine

Answer

Nifedipine

Question 10

Ankle edema caused by calcium channel blockers is prevented by which of the following classes of drugs?

Accepted Answer

ACE inhibitors

Answer

Propranolol

Answer

Adrenaline

Answer

Ropinirole

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?