Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 341: What is the drug of choice for paroxysmal supraventricular tachycardia?

A. Adenosine (Correct Answer)
B. Digitalis
C. Procainamide
D. Mexiletine

Explanation: **Explanation:** **Adenosine** is the drug of choice (DOC) for the acute termination of Paroxysmal Supraventricular Tachycardia (PSVT) [1], specifically those involving the AV node (AVNRT). **Why Adenosine is correct:** Adenosine acts on **A1 receptors** in the AV node, causing the opening of potassium channels and inhibition of calcium uptake [1]. This results in profound hyperpolarization and a transient "chemical cardioversion" by blocking AV conduction [1]. Its rapid onset and ultra-short half-life (<10 seconds) make it ideal for emergency termination of tachyarrhythmias without long-term hemodynamic compromise [1]. **Why other options are incorrect:** * **Digitalis (Digoxin):** While it slows AV conduction, its onset of action is too slow (hours) for acute termination of PSVT. It is primarily used for rate control in atrial fibrillation. * **Procainamide:** This is a Class IA antiarrhythmic. While it can be used for WPW syndrome or ventricular arrhythmias, it is not the first-line choice for PSVT due to its side effect profile (hypotension). * **Mexiletine:** This is a Class IB antiarrhythmic, primarily used for ventricular arrhythmias (especially post-MI). It has no significant effect on the AV node and is ineffective in PSVT. **High-Yield Clinical Pearls for NEET-PG:** * **Administration:** Must be given as a **rapid IV bolus** followed by a saline flush due to its short half-life. * **Contraindications:** Avoid in **Asthmatics** (causes bronchospasm via A2B receptors) and patients with **2nd/3rd-degree heart block**. * **Interactions:** **Theophylline/Caffeine** (adenosine receptor antagonists) decrease its effect, while **Dipyridamole** (uptake inhibitor) potentiates it. * **Common Side Effect:** Patients often experience a transient, distressing feeling of "impending doom" or chest heaviness [1] during administration.

Question 342: Calcium channel blockers are used in all of the following conditions, except:

A. Angina
B. Supraventricular tachycardia
C. Sick sinus syndrome (Correct Answer)
D. Hypertension

Explanation: **Explanation:** Calcium Channel Blockers (CCBs), specifically the non-dihydropyridines like **Verapamil and Diltiazem**, exert significant negative chronotropic (heart rate) and negative dromotropic (conduction velocity) effects by blocking L-type calcium channels in the SA and AV nodes. **Why Sick Sinus Syndrome (SSS) is the correct answer:** In SSS, the SA node is already dysfunctional, leading to episodes of bradycardia or sinus arrest. Administering CCBs further suppresses the SA node firing and AV node conduction, which can precipitate severe bradycardia, asystole, or high-grade heart block. Therefore, CCBs are **contraindicated** in SSS (unless a permanent pacemaker is in place). **Analysis of Incorrect Options:** * **Angina:** CCBs are first-line agents. They reduce myocardial oxygen demand (by decreasing afterload and contractility) and increase oxygen supply (by causing coronary vasodilation). * **Supraventricular Tachycardia (SVT):** Verapamil and Diltiazem are drugs of choice for terminating paroxysmal SVT and controlling ventricular rate in atrial fibrillation/flutter due to their potent inhibitory effect on the AV node. * **Hypertension:** Dihydropyridines (like Amlodipine) are first-line antihypertensives that act by reducing peripheral vascular resistance through systemic vasodilation. **High-Yield NEET-PG Pearls:** 1. **Contraindications for Non-Dihydropyridines:** SSS, 2nd or 3rd-degree heart block, and Heart Failure with reduced Ejection Fraction (HFrEF) due to negative inotropic effects. 2. **Drug of Choice:** CCBs are the preferred drugs for **Prinzmetal (Variant) Angina** and Raynaud’s phenomenon. 3. **Side Effects:** Amlodipine commonly causes **ankle edema** (due to precapillary vasodilation), while Verapamil is notorious for causing **constipation**.

Question 343: Platelet aggregation is inhibited by all agents except?

A. Aspirin
B. Clopidogrel
C. Thromboxane A2 (Correct Answer)
D. Eptifibatide

Explanation: **Explanation:** The question asks for the agent that does **not** inhibit platelet aggregation. To answer this, one must distinguish between antiplatelet drugs and physiological platelet activators. **Why Thromboxane A2 (TXA2) is the correct answer:** TXA2 is a potent **platelet agonist** and vasoconstrictor produced by activated platelets via the cyclooxygenase-1 (COX-1) pathway. It binds to TP receptors on the platelet surface, leading to a conformational change in the GP IIb/IIIa receptors, which promotes platelet aggregation. Therefore, TXA2 **promotes** rather than inhibits aggregation. **Analysis of Incorrect Options:** * **Aspirin:** It is an irreversible inhibitor of the **COX-1 enzyme**. By blocking COX-1, it prevents the synthesis of TXA2, thereby inhibiting platelet aggregation for the lifespan of the platelet (7–10 days). * **Clopidogrel:** This is a P2Y12 receptor antagonist. It prevents **ADP (Adenosine Diphosphate)** from binding to its receptor on platelets, which is a crucial step in platelet activation and subsequent aggregation. * **Eptifibatide:** This is a **GP IIb/IIIa receptor antagonist**. Since GP IIb/IIIa is the "final common pathway" for platelet aggregation (where fibrinogen binds to link platelets), blocking it provides potent inhibition of aggregation. **High-Yield Clinical Pearls for NEET-PG:** * **Final Common Pathway:** GP IIb/IIIa receptor (Inhibitors: Abciximab, Eptifibatide, Tirofiban). * **Phosphodiesterase Inhibitors:** Dipyridamole and Cilostazol also inhibit aggregation by increasing intra-platelet cAMP levels. * **P2Y12 Inhibitors:** Clopidogrel and Prasugrel are prodrugs (irreversible), while **Ticagrelor** is a direct-acting drug (reversible). * **Prostacyclin (PGI2):** Unlike TXA2, PGI2 is a potent endogenous **inhibitor** of platelet aggregation produced by vascular endothelium.

Question 344: What is the first symptom of digoxin overdose?

A. Gastrointestinal disturbance (Correct Answer)
B. U-wave on ECG
C. Ectopic beats on ECG
D. Fainting spells

Explanation: **Explanation:** Digoxin has a narrow therapeutic index, making toxicity a common clinical scenario. The **earliest (first) symptoms** of digoxin toxicity are almost always **gastrointestinal (GI)** in nature. **1. Why Gastrointestinal Disturbance is Correct:** The initial manifestation of digoxin overdose involves anorexia, nausea, and vomiting. These symptoms occur due to the direct stimulation of the **Chemoreceptor Trigger Zone (CTZ)** in the area postrema of the medulla and through vagal stimulation. In clinical practice, a sudden loss of appetite in a patient on digoxin is often the first warning sign of impending toxicity. **2. Why the other options are incorrect:** * **U-wave on ECG:** This is a classic sign of **hypokalemia**, not digoxin toxicity. While hypokalemia *predisposes* a patient to digoxin toxicity (as they compete for the same binding site on the Na+/K+ ATPase pump), the U-wave itself is not caused by digoxin. * **Ectopic beats on ECG:** While cardiac arrhythmias (most commonly ventricular bigeminy or PVCs) are the **most common serious/life-threatening** signs of toxicity, they usually appear *after* the initial GI symptoms. * **Fainting spells:** These may occur due to high-grade AV block or bradycardia caused by digoxin, but they are late-stage manifestations rather than the initial symptom. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common arrhythmia:** Ventricular Bigeminy (PVCs). * **Most characteristic arrhythmia:** Atrial Tachycardia with AV block. * **Visual disturbance:** Xanthopsia (yellow-green halos around lights) is a specific but later sign. * **Antidote:** Digoxin Immune Fab (Digibind). * **Electrolyte interaction:** Hypokalemia, hypomagnesemia, and hypercalcemia all increase the risk of digoxin toxicity.

Question 345: All of the following arrhythmias can be treated with Adenosine, except?

A. Atrial flutter
B. Paroxysmal atrial tachycardia
C. Supraventricular tachycardia
D. Arrhythmia with aberrant pathways (Correct Answer)

Explanation: **Explanation:** **Adenosine** is a short-acting nucleoside that acts as a potent vasodilator and depressant of the AV node [1]. Its primary mechanism involves activating $A_1$ receptors, leading to the opening of potassium channels and inhibition of calcium current, which causes significant hyperpolarization and a transient "chemical heart block" [1]. **Why Option D is Correct:** In arrhythmias involving **aberrant pathways** (such as WPW syndrome with pre-excitation), Adenosine can be dangerous. By blocking the AV node, Adenosine may paradoxically facilitate conduction through the accessory pathway. In cases of atrial fibrillation/flutter with an accessory pathway, blocking the AV node can lead to a rapid ventricular response, potentially degenerating into **Ventricular Fibrillation**. Therefore, it is generally avoided in pre-excited tachycardias [2]. **Analysis of Incorrect Options:** * **C & B (SVT/PAT):** Adenosine is the **drug of choice** for terminating Paroxysmal Supraventricular Tachycardia (PSVT) involving the AV node (AVNRT/AVRT) [1]. It breaks the re-entry circuit by acutely slowing AV conduction. * **A (Atrial Flutter):** While Adenosine does not typically *terminate* Atrial Flutter, it is used **diagnostically**. By transiently blocking the AV node, it "unmasks" the underlying flutter waves (saw-tooth pattern) on an ECG, allowing for a definitive diagnosis. **High-Yield Clinical Pearls for NEET-PG:** * **Half-life:** Extremely short (<10 seconds); must be given as a **rapid IV bolus** followed by a saline flush [1]. * **Antagonism:** Effects are blocked by **Theophylline/Caffeine** (adenosine receptor antagonists). * **Potentiation:** Effects are prolonged by **Dipyridamole** (inhibits adenosine uptake). * **Side Effects:** Flushing, chest pain (dyspnea), and a transient sense of "impending doom" [1]. * **Contraindication:** Avoid in **Asthmatics** (can cause bronchoconstriction via $A_2/A_3$ receptors).

Question 346: Which calcium channel blocker is typically used in subarachnoid hemorrhage?

A. Nimodipine (Correct Answer)
B. Diltiazem
C. Verapamil
D. Flunarizine

Explanation: **Explanation:** **Nimodipine** is the drug of choice for preventing and treating delayed cerebral ischemia caused by **vasospasm** following a subarachnoid hemorrhage (SAH). The underlying medical concept is its high **lipid solubility**, which allows it to cross the blood-brain barrier effectively. Once in the cerebral circulation, it exhibits a high affinity for L-type calcium channels in cerebral blood vessels, leading to vasodilation and neuroprotection. Clinical trials have shown that Nimodipine significantly improves neurological outcomes and reduces mortality in SAH patients. **Analysis of Incorrect Options:** * **Diltiazem (Benzothiazepine):** Primarily used for rate control in atrial fibrillation and hypertension. It has intermediate effects on both the heart and blood vessels but lacks the cerebrovascular specificity required for SAH. * **Verapamil (Phenylalkylamine):** A potent negative inotrope and chronotrope. It is used for supraventricular tachycardia (SVT) and hypertrophic cardiomyopathy but is not indicated for cerebral vasospasm. * **Flunarizine:** A non-selective calcium channel blocker used primarily for **migraine prophylaxis** and vertigo. It is not used in the acute management of SAH. **High-Yield Pearls for NEET-PG:** * **Nimodipine Protocol:** Usually started within 96 hours of SAH onset and continued for 21 days. * **Clevidipine:** An ultra-short-acting IV dihydropyridine used for hypertensive emergencies. * **Nifedipine:** Associated with "reflex tachycardia" and is used in chronic hypertension and Raynaud’s phenomenon. * **Drug of Choice for SAH Vasospasm:** Nimodipine. * **Drug of Choice for Prophylaxis of Migraine:** Flunarizine or Propranolol.

Question 347: Which of the following is NOT an arteriolar dilator?

A. Hydralazine
B. Minoxidil
C. Nitrates (Correct Answer)
D. Nifedipine

Explanation: ### Explanation The classification of vasodilators is based on their site of action: pure arteriolar dilators, pure venodilators, or mixed (balanced) vasodilators. **Why Nitrates are the correct answer:** Nitrates (e.g., Nitroglycerin, Isosorbide dinitrate) are primarily **venodilators**. At therapeutic doses, they increase venous capacitance, which decreases venous return to the heart (preload). This reduces myocardial oxygen demand, making them the mainstay for angina. While they can cause arteriolar dilation at very high doses, their predominant clinical effect is on the venous side. **Analysis of Incorrect Options:** * **Hydralazine:** A direct-acting **pure arteriolar dilator**. It acts by increasing cGMP levels and interfering with calcium release. It is commonly used in pregnancy-induced hypertension. * **Minoxidil:** A potent **pure arteriolar dilator**. It works by opening ATP-sensitive $K^+$ channels, leading to hyperpolarization of smooth muscle. It is reserved for refractory hypertension and is known for causing hypertrichosis. * **Nifedipine:** A Dihydropyridine Calcium Channel Blocker (CCB). These agents act specifically on L-type calcium channels in the vascular smooth muscle of **arterioles**, causing significant peripheral vasodilation. **High-Yield Clinical Pearls for NEET-PG:** * **Mixed Vasodilator:** **Sodium Nitroprusside** is the classic example of a balanced vasodilator (acts on both arteries and veins). * **The Reflex Phenomenon:** Pure arteriolar dilators (Hydralazine, Minoxidil) often cause **reflex tachycardia** and **sodium/water retention**. Therefore, they are usually prescribed alongside a $\beta$-blocker and a diuretic. * **Drug of Choice:** Hydralazine is a preferred agent for **Hypertension in Pregnancy**. * **Side Effect:** Minoxidil can cause pericardial effusion; Hydralazine is associated with **Drug-Induced Lupus Erythematosus** (especially in slow acetylators).

Question 348: Which of the following conditions increases the risk of digoxin toxicity?

A. Administration of quinidine (Correct Answer)
B. Hyperkalemia
C. Hypermagnesemia
D. Hypocalcemia

Explanation: **Explanation** Digoxin has a narrow therapeutic index, making the understanding of drug interactions and electrolyte imbalances crucial for NEET-PG. **Why Quinidine is Correct:** Quinidine increases digoxin levels through two primary mechanisms: 1. **Displacement:** It displaces digoxin from tissue binding sites (skeletal muscle). 2. **Reduced Excretion:** It inhibits **P-glycoprotein (P-gp)** in the renal tubules, significantly reducing the renal clearance of digoxin. When co-administered, the dose of digoxin should typically be halved to prevent toxicity. **Analysis of Incorrect Options:** * **Hyperkalemia (B):** Potassium and digoxin compete for the same binding site on the **Na+/K+ ATPase pump**. Therefore, *hypokalemia* (low K+) increases digoxin binding and toxicity, while hyperkalemia antagonizes digoxin's effects. * **Hypermagnesemia (C):** *Hypomagnesemia* is a known risk factor for toxicity. Magnesium acts as a cofactor for the Na+/K+ ATPase pump; its deficiency sensitizes the heart to digitalis-induced arrhythmias. * **Hypocalcemia (D):** Digoxin works by increasing intracellular calcium. Therefore, **Hypercalcemia** (high Ca2+) synergizes with digoxin, increasing the risk of arrhythmias ("Stone Heart"). Hypocalcemia actually reduces the risk. **High-Yield Clinical Pearls for NEET-PG:** * **Electrolytes predisposing to toxicity:** Hypokalemia, Hypomagnesemia, and Hypercalcemia. * **Other drugs increasing Digoxin levels:** Verapamil, Amiodarone, and Spironolactone (all inhibit P-gp). * **Most common arrhythmia:** Ventricular Bigeminy. * **Most specific arrhythmia:** Atrial Tachycardia with AV block. * **Antidote:** Digoxin Immune Fab (Digibind).

Question 349: Adverse effects of beta-blockers may include which of the following?

A. Congestive heart failure
B. Blunting of sympathetic response to oral hypoglycemic agents
C. Bronchial asthma
D. All of the above (Correct Answer)

Explanation: **Explanation:** Beta-blockers act by antagonizing $\beta_1$ and $\beta_2$ receptors, leading to various physiological effects that can manifest as adverse reactions depending on the patient's underlying condition. * **Congestive Heart Failure (Option A):** Beta-blockers have negative inotropic (decreased contractility) and negative chronotropic (decreased heart rate) effects. In patients with compensated heart failure or borderline cardiac reserve, the sudden withdrawal of sympathetic drive can precipitate acute cardiac decompensation. (Note: While they are used chronically to improve survival in CHF, they must be started at very low doses). * **Blunting of Sympathetic Response (Option B):** In diabetic patients, tachycardia and tremors are "warning signs" of hypoglycemia mediated by the sympathetic nervous system. Beta-blockers mask these symptoms, leading to "hypoglycemia unawareness." Additionally, $\beta_2$ blockade inhibits glycogenolysis in the liver, further delaying recovery from hypoglycemia. * **Bronchial Asthma (Option C):** Non-selective beta-blockers (like Propranolol) block $\beta_2$ receptors in the bronchial smooth muscle, leading to bronchoconstriction. This can trigger life-threatening bronchospasm in patients with asthma or COPD. **Conclusion:** Since all three conditions are recognized adverse effects or contraindications, **Option D** is correct. **High-Yield Clinical Pearls for NEET-PG:** * **Cardioselectivity:** $\beta_1$ selective blockers (e.g., Metoprolol, Atenolol) are safer in asthma/diabetes but lose selectivity at high doses. * **Lipid Profile:** Beta-blockers can increase triglycerides and decrease HDL levels. * **Peripheral Vascular Disease:** They can worsen Raynaud's phenomenon due to unopposed alpha-mediated vasoconstriction. * **Drug of Choice:** Beta-blockers are the drug of choice for hypertrophic obstructive cardiomyopathy (HOCM) and prophylaxis of variceal bleeding.

Question 350: All of the following drugs are Class I anti-arrhythmic drugs EXCEPT?

A. Quinidine
B. Procainamide
C. Flecainide
D. Sotalol (Correct Answer)

Explanation: **Explanation:** The classification of anti-arrhythmic drugs is based on the **Vaughan-Williams classification**, which categorizes drugs according to their primary mechanism of action on the cardiac action potential. **Why Sotalol is the correct answer:** Sotalol is a **Class III anti-arrhythmic drug**. While it possesses non-selective beta-blocking properties (Class II), its primary anti-arrhythmic effect is the **blockade of potassium (K+) channels**. This action prolongs the phase 3 repolarization, thereby increasing the action potential duration (APD) and the effective refractory period (ERP). **Why the other options are incorrect:** Class I drugs are primarily **Sodium (Na+) channel blockers**. They are further subdivided based on their effect on the action potential duration: * **A (Quinidine) & B (Procainamide):** These are **Class IA** drugs. they moderately block Na+ channels and also have some K+ channel blocking activity, leading to a prolonged APD. * **C (Flecainide):** This is a **Class IC** drug. It is a potent Na+ channel blocker with a slow rate of dissociation, significantly slowing conduction (decreased slope of phase 0) with minimal effect on APD. **High-Yield NEET-PG Pearls:** * **Class IB (e.g., Lidocaine):** Shortens the APD and is the drug of choice for post-MI ventricular arrhythmias. * **Sotalol Paradox:** Despite being a Class III drug, it carries a high risk of **Torsades de Pointes** due to QT interval prolongation. * **Mnemonic for Class I:** "**D**ouble **Q**uarter **P**ounder (IA: Disopyramide, Quinidine, Procainamide), **L**ettuce **M**ayo **T**omato (IB: Lidocaine, Mexiletine, Tocainide), **F**ries **P**lease (IC: Flecainide, Propafenone)."

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Antihypertensive Agents

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Drugs for Heart Failure

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Antiarrhythmic Drugs

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Antianginal Agents

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Anticoagulants and Antiplatelet Drugs

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Thrombolytic Agents

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Drugs Used in Pulmonary Hypertension

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Drugs Used in Shock

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Cardiovascular Effects of Non-Cardiovascular Drugs

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