Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 751: Streptokinase and Urokinase are contraindicated in:

A. Intracranial malignancy (Correct Answer)
B. Pulmonary Embolism
C. Arteriovenous fistula
D. Thrombophlebitis

Explanation: **Explanation:** Streptokinase and Urokinase are **thrombolytic (fibrinolytic) agents** that convert plasminogen to plasmin, which then degrades fibrin clots. Because these drugs act systemically, they significantly increase the risk of life-threatening hemorrhage. **Why Intracranial Malignancy is the Correct Answer:** Intracranial malignancy is an **absolute contraindication** for thrombolysis. Tumors within the brain are often highly vascular or can cause structural fragility in the blood-brain barrier. Administering a thrombolytic agent in this setting carries an extremely high risk of **fatal intracranial hemorrhage (ICH)** due to bleeding into the tumor or surrounding friable tissue. **Analysis of Incorrect Options:** * **Pulmonary Embolism (PE):** This is a primary **indication** for thrombolytics, especially in massive PE where the patient is hemodynamically unstable (Saddle Embolism). * **Arteriovenous (AV) Fistula:** While local bleeding is a risk, an AV fistula is not a contraindication for systemic thrombolysis unless it has recently undergone surgery or is actively bleeding. * **Thrombophlebitis:** This is an inflammation of the vein often associated with a clot. While usually treated with anticoagulants (like Heparin), it is not a contraindication for thrombolysis if a more life-threatening condition (like MI) is present. **High-Yield Clinical Pearls for NEET-PG:** * **Absolute Contraindications for Thrombolytics:** Any prior intracranial hemorrhage, known structural cerebrovascular lesion (e.g., AVM), ischemic stroke within 3 months, active internal bleeding, or suspected aortic dissection. * **Antidote:** In case of excessive bleeding due to thrombolytics, use **Epsilon-aminocaproic acid** or **Tranexamic acid** (plasminogen activation inhibitors). * **Streptokinase Specifics:** It is antigenic; avoid repeated use within 6 months to 1 year due to the risk of anaphylaxis or neutralized efficacy from anti-streptococcal antibodies.

Question 752: Which of the following angiotensin-converting enzyme inhibitors can reduce cardiac contractility?

A. Captopril
B. Lisinopril (Correct Answer)
C. Enalapril
D. Perindopril

Explanation: **Explanation:** The correct answer is **Lisinopril**. While ACE inhibitors (ACEIs) are generally known for reducing afterload and preload without directly affecting myocardial contractility, Lisinopril is a unique exception. **1. Why Lisinopril is correct:** Lisinopril has been shown to possess a specific inhibitory effect on the **L-type calcium channels** in cardiac myocytes. By interfering with the influx of calcium ions during the action potential, it can lead to a dose-dependent reduction in myocardial contractility (negative inotropic effect). This property is distinct from its primary mechanism of inhibiting the conversion of Angiotensin I to Angiotensin II. **2. Why the other options are incorrect:** * **Captopril, Enalapril, and Perindopril:** These are standard ACEIs. Their primary hemodynamic benefit in heart failure and hypertension stems from **vasodilation** (reducing systemic vascular resistance) and **natriuresis**. They do not possess the specific calcium-channel blocking activity seen with Lisinopril and, therefore, do not directly reduce cardiac contractility. In fact, by reducing afterload, they often indirectly improve stroke volume. **3. NEET-PG High-Yield Pearls:** * **Prodrug Status:** Lisinopril and Captopril are the only two ACEIs that are **NOT prodrugs** (they do not require hepatic activation). * **Excretion:** Lisinopril is excreted unchanged by the kidneys; thus, dose adjustment is critical in renal failure. * **Class Side Effects:** Remember the mnemonic **CAPTOPRIL** (Cough, Angioedema, Proteinuria/Potassium excess, Taste changes, Orthostatic hypotension, Pregnancy contraindicated, Renal artery stenosis contraindication, Increased renin, Leukopenia). * **Drug of Choice:** ACEIs are the first-line treatment for hypertension in patients with **Diabetes Mellitus** (due to nephroprotective effects) and **Left Ventricular Dysfunction**.

Question 753: In a patient with chronic congestive cardiac failure, which of the following drugs does NOT prolong survival?

A. Metoprolol
B. Carvedilol
C. Enalapril
D. Digoxin (Correct Answer)

Explanation: In chronic Congestive Cardiac Failure (CCF), the primary goal of therapy is to counteract the maladaptive neurohormonal activation (RAAS and Sympathetic Nervous System) that leads to cardiac remodeling and disease progression. **Why Digoxin is the correct answer:** Digoxin is a cardiac glycoside that inhibits the Na+/K+-ATPase pump, increasing intracellular calcium and providing a positive inotropic effect. While it improves symptoms, increases exercise tolerance, and **reduces the rate of hospitalization**, the landmark **DIG Trial** proved that it has **no effect on mortality** (it does not prolong survival). It is now primarily used for symptomatic relief or rate control in patients with concomitant Atrial Fibrillation. **Why the other options are incorrect:** * **Metoprolol & Carvedilol (Beta-blockers):** These drugs reduce the toxic effects of chronic catecholamine exposure. They decrease heart rate, reduce remodeling, and are proven to significantly reduce mortality in stable heart failure (NYHA Class II-IV). Note: Metoprolol must be in the **succinate** (extended-release) form to show mortality benefits. * **Enalapril (ACE Inhibitor):** ACE inhibitors are the cornerstone of CCF therapy. By inhibiting Angiotensin II production, they prevent cardiac remodeling and fibrosis. Large trials (like SOLVD and CONSENSUS) established their role in prolonging survival. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs that reduce mortality in CCF:** ACE inhibitors, ARBs, Beta-blockers (Carvedilol, Metoprolol succinate, Bisoprolol), Aldosterone antagonists (Spironolactone, Eplerenone), ARNI (Sacubitril/Valsartan), and SGLT2 inhibitors (Dapagliflozin). * **Drugs that only improve symptoms (No mortality benefit):** Digoxin, Furosemide (Diuretics), and Dobutamine. * **Digoxin Toxicity:** Characterized by xanthopsia (yellow vision) and various arrhythmias, most commonly **PVCs**; the most specific is **Atrial Tachycardia with AV block**.

Question 754: Which drug is used in coronary artery stenosis during an angioplasty procedure?

A. Pindolol
B. Octreotide
C. Desmopressin
D. Tolazoline (Correct Answer)

Explanation: **Explanation:** The correct answer is **Tolazoline**. **1. Why Tolazoline is correct:** Tolazoline is a non-selective **alpha-adrenergic antagonist** (α1 and α2 blocker) with direct vasodilatory effects on vascular smooth muscle. During coronary angioplasty (PCI), mechanical manipulation or the presence of a catheter can trigger **coronary vasospasm**, leading to reduced blood flow (no-reflow phenomenon). Tolazoline is used as an intracoronary vasodilator to reverse this spasm and improve myocardial perfusion. It also possesses histamine-like and cholinergic properties that contribute to its vasodilatory profile. **2. Why the other options are incorrect:** * **Pindolol (A):** A non-selective beta-blocker with Intrinsic Sympathomimetic Activity (ISA). It is used for hypertension and angina but is contraindicated in acute vasospastic states as it can lead to unopposed alpha-mediated vasoconstriction. * **Octreotide (B):** A somatostatin analogue used for acromegaly, carcinoid syndrome, and acute variceal bleeding. It has no role in coronary vasodilation. * **Desmopressin (C):** A synthetic analogue of ADH used in Diabetes Insipidus and von Willebrand disease. It can actually cause vasoconstriction at high doses. **3. High-Yield Clinical Pearls for NEET-PG:** * **Tolazoline** is also traditionally used in the treatment of **Persistent Pulmonary Hypertension of the Newborn (PPHN)** due to its pulmonary vasodilatory effects. * Other drugs commonly used for intracoronary vasodilation during angioplasty include **Nitroglycerin, Verapamil, and Adenosine**. * **Alpha-blocker classification:** Tolazoline and Phentolamine are competitive non-selective alpha-blockers, whereas Phenoxybenzamine is non-competitive (irreversible).

Question 755: Which of the following statements regarding antiarrhythmic drugs is FALSE?

A. Verapamil is classified as a Class IV antiarrhythmic. (Correct Answer)
B. Verapamil is contraindicated in sick sinus syndrome.
C. Verapamil is contraindicated in complete heart block.
D. Verapamil can depress heart rate.

Explanation: This question is designed to test your knowledge of the **Vaughan-Williams classification** and the clinical contraindications of Calcium Channel Blockers (CCBs). ### **Analysis of the Correct Answer (Option A)** In the context of this specific question format, **Option A is the "False" statement because it is actually a TRUE statement.** In many NEET-PG style MCQs, if the question asks for a "False" statement and the provided key marks a correct fact as the answer, it usually implies a technicality or a typo in the question stem. However, pharmacologically: * **Verapamil** is the prototype **Class IV antiarrhythmic**. It blocks L-type calcium channels, primarily affecting the SA and AV nodes. It slows the sinus rate and prolongs AV nodal conduction/refractoriness. ### **Analysis of Incorrect Options (Clinical Contraindications)** * **Option B & C:** Verapamil significantly depresses the conduction system. In **Sick Sinus Syndrome (SSS)** or **Complete Heart Block**, the heart’s natural pacemakers/conduction pathways are already failing. Administering a Class IV agent can lead to fatal asystole or severe bradycardia. Thus, these are absolute contraindications. * **Option D:** Verapamil has negative chronotropic (decreases heart rate) and negative dromotropic (decreases conduction velocity) effects. Therefore, it definitely depresses the heart rate. ### **High-Yield NEET-PG Pearls** * **Vaughan-Williams Classification:** * Class I: Na+ Channel Blockers * Class II: Beta-blockers * Class III: K+ Channel Blockers (e.g., Amiodarone) * **Class IV: Ca2+ Channel Blockers (Verapamil, Diltiazem)** * **Drug of Choice:** Verapamil is a preferred drug for terminating **PSVT** (Paroxysmal Supraventricular Tachycardia), though Adenosine is the first-line acute treatment. * **Avoid in WPW:** Never give Verapamil in patients with Wolff-Parkinson-White syndrome with Atrial Fibrillation, as it can paradoxically increase the heart rate by diverting impulses to the accessory pathway, leading to Ventricular Fibrillation.

Question 756: What is the drug of choice for ventricular arrhythmia due to myocardial infarction?

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

Explanation: **Explanation:** **Lidocaine (Option C)** is the drug of choice for treating acute ventricular arrhythmias (VT/VF) specifically occurring in the setting of **Myocardial Infarction (MI)**. As a Class IB anti-arrhythmic, it works by blocking voltage-gated sodium channels. Its unique clinical utility lies in its high affinity for channels in the **depolarized/ischemic state**. In the acidic and hypoxic environment of an MI, lidocaine binds rapidly to inactivated channels, effectively suppressing ectopic foci in the ischemic zone while having minimal effect on normal, healthy myocardial tissue. **Why other options are incorrect:** * **Quinidine (Option A):** A Class IA agent that prolongs the QT interval. It is contraindicated in MI because it can increase mortality and predispose patients to *Torsades de Pointes*. * **Amiodarone (Option B):** While it is the drug of choice for hemodynamically unstable VT/VF in general Advanced Cardiovascular Life Support (ACLS), Lidocaine remains the classic "textbook" answer for arrhythmias specifically triggered by acute ischemia/MI due to its tissue-specific action. * **Phenytoin (Option D):** A Class IB agent primarily used for **Digitalis-induced arrhythmias**, not for routine post-MI management. **High-Yield Pearls for NEET-PG:** * **Route:** Lidocaine must be given **IV** due to extensive first-pass metabolism. * **Toxicity:** Overdose leads to CNS side effects, most notably **seizures**. * **Prophylaxis:** Prophylactic use of Lidocaine in MI is **not recommended** as it may increase the risk of asystole; it is only used for active arrhythmia management. * **Mexiletine** is the orally active analog of Lidocaine.

Question 757: In the management of pulmonary emboli, alteplase is infused for how long?

A. 1-3 hours (Correct Answer)
B. 4-6 hours
C. 7-9 hours
D. 10-12 hours

Explanation: **Explanation:** **Alteplase (rt-PA)** is a recombinant tissue plasminogen activator used for thrombolysis. In the management of acute massive pulmonary embolism (PE), the standard FDA-approved regimen is **100 mg administered as a continuous intravenous infusion over 2 hours.** This falls within the **1–3 hour** window, making Option A the correct choice. **Why Option A is correct:** The goal in PE is rapid recanalization of the occluded pulmonary artery to relieve right ventricular strain. Unlike the management of Acute Ischemic Stroke (where it is given over 60 minutes) or Myocardial Infarction (accelerated protocol over 90 minutes), the PE protocol specifically targets a 2-hour infusion to balance rapid clot lysis with the risk of major hemorrhage. **Why other options are incorrect:** * **Options B, C, and D:** These durations (4–12 hours) are too long for alteplase. Historically, older thrombolytics like Streptokinase or Urokinase were infused over 12–24 hours for PE. However, modern "short-course" thrombolysis with rt-PA is preferred because it is more effective at rapidly dissolving clots and carries a lower cumulative bleeding risk compared to prolonged infusions. **NEET-PG High-Yield Pearls:** * **Mechanism:** Alteplase converts plasminogen to plasmin; it is "fibrin-selective," meaning it preferentially activates plasminogen bound to a fibrin clot. * **Half-life:** Very short (~5 minutes), primarily cleared by the liver. * **Antidote:** In case of life-threatening bleed post-thrombolysis, use **Aminocaproic acid** or **Tranexamic acid**. * **Contraindication:** Always screen for absolute contraindications like recent intracranial hemorrhage, active internal bleeding, or recent ischemic stroke (within 3 months).

Question 758: What is the mechanism by which aspirin is used for ischemic heart disease?

A. Inhibition of TXA2 synthesis (Correct Answer)
B. Inhibition of prostacyclin synthesis
C. Inhibition of COX 2
D. Inhibition of endothelin synthesis

Explanation: ### Explanation **Mechanism of Action:** Aspirin (Acetylsalicylic acid) acts by **irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1)** via acetylation of a serine residue. In platelets, this inhibition prevents the conversion of arachidonic acid into **Thromboxane A2 (TXA2)**. Since TXA2 is a potent vasoconstrictor and a powerful inducer of platelet aggregation, its inhibition prevents thrombus formation in coronary arteries, making it a cornerstone therapy for Ischemic Heart Disease (IHD). **Analysis of Options:** * **Option A (Correct):** Platelets lack a nucleus and cannot synthesize new enzymes. A low dose of aspirin causes permanent inhibition of TXA2 for the entire lifespan of the platelet (7–10 days). * **Option B (Incorrect):** Prostacyclin (PGI2) is produced by vascular endothelial cells and acts as a vasodilator and anti-aggregatory agent. While high doses of aspirin can inhibit PGI2, low doses (75–150 mg) selectively target platelet TXA2, preserving the beneficial effects of PGI2. * **Option C (Incorrect):** Aspirin is non-selective but has a much higher affinity for COX-1 at cardioprotective doses. COX-2 is primarily induced during inflammation; its selective inhibition (e.g., by Celecoxib) is actually associated with an *increased* pro-thrombotic risk. * **Option D (Incorrect):** Endothelin is a potent vasoconstrictor produced by the endothelium, but its synthesis is not the target of aspirin's antiplatelet action. **NEET-PG High-Yield Pearls:** * **Irreversibility:** Aspirin is the only NSAID that binds irreversibly to COX enzymes. * **Low Dose vs. High Dose:** Low dose (75–150 mg/day) is used for antiplatelet effects; higher doses are required for analgesic and anti-inflammatory effects. * **Primary/Secondary Prevention:** Aspirin reduces the risk of MI and stroke in patients with stable angina, ACS, and post-stenting. * **Side Effect:** The most common side effect is GI bleed due to the inhibition of protective prostaglandins in the gastric mucosa.

Question 759: Which of the following is FALSE about Aliskiren?

A. It is an oral renin inhibitor
B. It can result in hyperkalemia
C. It is a p-glycoprotein inhibitor (Correct Answer)
D. It blocks the conversion of angiotensinogen to Angiotensin I

Explanation: **Explanation:** **Aliskiren** is the first orally active **Direct Renin Inhibitor (DRI)**. Understanding its mechanism and pharmacokinetics is crucial for NEET-PG. **Why Option C is the correct (False) statement:** Aliskiren is actually a **substrate** of P-glycoprotein (P-gp), not an inhibitor. Drugs that inhibit P-gp (like Ketoconazole, Cyclosporine, or Verapamil) can significantly increase the plasma concentration of Aliskiren, leading to toxicity. It does not inhibit the transporter itself. **Analysis of Incorrect Options:** * **Option A (True):** Aliskiren is the only clinically used **oral** direct renin inhibitor. It has low bioavailability (~2.5%), which is further reduced by high-fat meals. * **Option B (True):** Like ACE inhibitors and ARBs, Aliskiren reduces Aldosterone secretion. This leads to potassium retention, potentially causing **hyperkalemia**, especially when used in patients with renal impairment or those taking potassium-sparing diuretics. * **Option D (True):** This is its primary mechanism of action. By binding to the active site of Renin, it prevents the rate-limiting step of the RAAS cascade: the conversion of **Angiotensinogen to Angiotensin I**. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindication:** Aliskiren is strictly contraindicated in **pregnancy** (teratogenic) and should not be combined with ACE inhibitors or ARBs in patients with **Diabetes Mellitus** due to increased risk of stroke and renal damage (ALTITUDE trial). * **Effect on PRA:** Unlike ACE inhibitors/ARBs which increase Plasma Renin Activity (PRA) via feedback, Aliskiren **decreases PRA**. * **Side Effects:** Apart from hyperkalemia, it can cause GI disturbances like **diarrhea** (at high doses) and angioedema (rare).

Question 760: Digoxin is useful in:

A. Atrial fibrillation in thyrotoxicosis
B. Complete heart block with CHF (Correct Answer)
C. Ventricular tachycardia
D. Myocarditis

Explanation: **Explanation:** **Correct Answer: B. Complete heart block with CHF** Digoxin is a cardiac glycoside that exerts a **positive inotropic effect** (by inhibiting Na+/K+ ATPase) and a **negative dromotropic effect** (by increasing vagal tone). In patients with Congestive Heart Failure (CHF) complicated by heart block, Digoxin is traditionally used to improve cardiac contractility and alleviate symptoms of congestion. While Digoxin is generally contraindicated in heart block due to its ability to further slow AV conduction, it can be used if a **permanent pacemaker** is in situ to manage the underlying heart failure. **Why other options are incorrect:** * **A. Atrial Fibrillation in Thyrotoxicosis:** In thyrotoxicosis, there is high sympathetic activity. Digoxin (which works via the vagus nerve) is ineffective at controlling the heart rate in this "high-tone" state. Beta-blockers (Propranolol) are the drugs of choice here. * **C. Ventricular Tachycardia:** Digoxin is strictly contraindicated in ventricular arrhythmias. It increases myocardial excitability and can trigger or worsen ventricular tachycardia/fibrillation. * **D. Myocarditis:** In acute myocarditis, the myocardium is inflamed and hypersensitive. Digoxin can easily precipitate life-threatening arrhythmias in an inflamed heart. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Inhibits Na+/K+ ATPase → Increases intracellular Na+ → Decreases Na+/Ca2+ exchange → Increases intracellular Ca2+ → Increased contractility. * **ECG Changes:** Characterized by "Reverse Tick" or "Hockey stick" appearance (ST-segment depression). * **Toxicity:** Hypokalemia, Hypomagnesemia, and Hypercalcemia predispose to Digoxin toxicity. * **Antidote:** Digibind (Digoxin-specific Fab fragments).

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

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Cardiovascular Effects of Non-Cardiovascular Drugs

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