Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 1041: Which beta blocker contains a d-isomer responsible for its action?

A. Nebivolol (Correct Answer)
B. Timolol
C. Esmolol
D. Propranolol

Explanation: ***Nebivolol*** - **Nebivolol** is unique among beta-blockers because its **d-isomer (SRRR-nebivolol)** is responsible for its highly selective beta-1 adrenergic receptor antagonism. - The **l-isomer (RSSS-nebivolol)** of nebivolol causes **vasodilation** via nitric oxide release. *Timolol* - **Timolol** is a non-selective beta-blocker that lacks intrinsic sympathomimetic activity and membrane-stabilizing effects. - It exists as a **racemic mixture**, but its beta-blocking activity does not specifically rely on a d-isomer for its primary action. *Esmolol* - **Esmolol** is an ultra-short-acting, cardioselective beta-1 blocker, primarily used intravenously in acute settings due to its rapid metabolism. - Its beta-blocking activity is not attributed to a specific d-isomer; it is a straightforward competitive antagonist. *Propranolol* - **Propranolol** is a non-selective beta-blocker that inhibits both beta-1 and beta-2 adrenergic receptors [1]. - It is often formulated as a **racemic mixture** (a 50:50 mixture of d- and l-isomers), but its beta-blocking effects primarily reside with the l-isomer [1].

Question 1042: Which of the following changes in ECG is most commonly associated with Digitalis use?

A. Tall T waves
B. ST segment elevation
C. Prolonged QT interval
D. Prolonged PR interval (Correct Answer)

Explanation: ***Prolonged PR interval*** - Digitalis increases **parasympathetic tone** and slows **AV nodal conduction**, leading to a prolonged PR interval [1], [2]. - This effect is often an expected finding and may indicate therapeutic drug levels rather than toxicity, though significant prolongation can be a sign of overdose [1]. *Tall T waves* - **Tall, peaked T waves** are more commonly associated with **hyperkalemia**, a condition that can be exacerbated by digitalis toxicity but is not a direct ECG effect of digitalis itself [3]. - Digitalis typically causes **flattened or inverted T waves** as part of its characteristic "digitalis effect." *ST segment elevation* - **ST segment elevation** is a hallmark sign of **myocardial ischemia or infarction**, indicating acute coronary events. - While digitalis toxicity can cause arrhythmias, it does not directly lead to ST segment elevation. *Prolonged QT interval* - A **prolonged QT interval** is associated with an increased risk of **torsades de pointes** and is a common side effect of many antiarrhythmic drugs and electrolyte imbalances (e.g., hypokalemia, hypomagnesemia). - Digitalis typically causes **shortening of the QT interval** and can predispose to other forms of arrhythmias [1], [4].

Question 1043: A patient who is a known case of hypertension on multiple anti-hypertensive medications came to OPD. His ECG finding is given below. Which of the following drugs is responsible for the ECG finding? (Image of ECG finding)

A. Prazosin
B. Metoprolol
C. Hydrochlorothiazide
D. Spironolactone (Correct Answer)

Explanation: ***Spironolactone*** - The ECG shows a **tall, peaked T wave**, which is characteristic of **hyperkalemia**. - **Spironolactone** is a **potassium-sparing diuretic**, and its use, especially in combination with other medications or in patients with **renal impairment**, can lead to **hyperkalemia**. *Prazosin* - Prazosin is an **alpha-1 adrenergic blocker** used for **hypertension**. - It does **not directly affect potassium levels** and is not associated with the ECG changes seen in hyperkalemia. *Metoprolol* - Metoprolol is a **beta-blocker** primarily used for **hypertension**, **angina**, and **arrhythmias**. - It does **not significantly cause hyperkalemia** or the characteristic ECG changes shown. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** that typically causes **hypokalemia**, not hyperkalemia, by **increasing potassium excretion**. - The ECG findings associated with hypokalemia would include **flattened T waves** or **prominent U waves**.

Question 1044: Skin blood flow is decreased by ?

A. Noradrenaline (Correct Answer)
B. Isoprenaline
C. Dopamine
D. Acetylcholine

Explanation: ***Noradrenaline*** - **Noradrenaline** (norepinephrine) is a potent **vasoconstrictor**, particularly in the skin, which **decreases blood flow** by stimulating alpha-1 adrenergic receptors. - This vasoconstrictive action redirects blood flow to more vital organs during stress or sympathetic activation. *Dopamine* - At low doses, dopamine can cause **renal and mesenteric vasodilation**, while at higher doses it acts similarly to noradrenaline causing **vasoconstriction**. - Its effects on skin blood flow are variable and dose-dependent; it is not primarily known for consistently decreasing skin blood flow like noradrenaline. *Isoprenaline* - **Isoprenaline** (isoproterenol) is a non-selective **beta-adrenergic agonist** that primarily causes **vasodilation** in most vascular beds, thereby **increasing blood flow**. - It would typically **increase skin blood flow** rather than decrease it, due to its strong beta-2 receptor agonism. *Acetylcholine* - **Acetylcholine** is the primary neurotransmitter for **sympathetic innervation of sweat glands** in the skin, but it also causes **vasodilation** when released by parasympathetic nerves. - In the skin, its overall effect on blood flow is typically **vasodilation**, contributing to heat dissipation.

Question 1045: Which of the following drugs can be given in patients of primary pulmonary hypertension?

A. Icatibant
B. Bosentan (Correct Answer)
C. Sodium nitroprusside
D. Labetalol

Explanation: ***Bosentan*** - **Bosentan** is an **endothelin receptor antagonist** that blocks the vasoconstrictive and proliferative effects of endothelin-1, a key mediator in the pathogenesis of **pulmonary hypertension**. - It is an FDA-approved medication specifically used for the treatment of **pulmonary arterial hypertension (PAH)**, improving exercise capacity and delaying clinical worsening. *Icatibant* - **Icatibant** is a **bradykinin B2 receptor antagonist** used in the treatment of **hereditary angioedema**. - It has no known role or efficacy in the management of **primary pulmonary hypertension**. *Labetalol* - **Labetalol** is a **beta-blocker** with **alpha-1 adrenergic blocking activity** used primarily for systemic **hypertension** and **hypertensive emergencies**. - Beta-blockers are generally **contraindicated** in pulmonary hypertension as they can worsen right heart function and lead to clinical deterioration. *Sodium nitroprusside* - **Sodium nitroprusside** is a **direct arterial and venous vasodilator** used in hypertensive crises and severe heart failure by reducing both preload and afterload. - While it can lower systemic blood pressure, its use in pulmonary hypertension is **limited** due to the risk of **systemic hypotension** and the lack of selective pulmonary vasodilation compared to other agents.

Question 1046: What is the primary mechanism of action of beta-blockers in the management of hypertension?

A. Decreasing heart rate and contractility to reduce cardiac output. (Correct Answer)
B. Direct relaxation of vascular smooth muscle.
C. Vasodilation through alpha-adrenergic blockade.
D. Inhibition of the renin-angiotensin-aldosterone system (RAAS).

Explanation: ***Decreasing heart rate and contractility to reduce cardiac output.*** - Beta-blockers primarily work by blocking **beta-1 adrenergic receptors** in the heart, leading to a decrease in **heart rate** and **myocardial contractility** [1], [2]. - This reduction in cardiac output directly lowers **blood pressure**, making it a key mechanism in hypertension management [1], [2]. *Direct relaxation of vascular smooth muscle.* - While ultimately leading to lower blood pressure, beta-blockers do not achieve this through **direct relaxation** of vascular smooth muscle. - This mechanism is more characteristic of **calcium channel blockers** or **direct vasodilators** like hydralazine. *Vasodilation through alpha-adrenergic blockade.* - Some beta-blockers, like carvedilol and labetalol, also have **alpha-1 adrenergic blocking properties** which cause vasodilation [1], [3]. - However, the primary mechanism of *most* beta-blockers in hypertension is through their **beta-blocking effects** on the heart, not primarily alpha-blockade [1]. *Inhibition of the renin-angiotensin-aldosterone system (RAAS).* - Beta-blockers can indirectly reduce **renin release** from the kidneys by blocking beta-1 receptors, which is part of the RAAS [1], [2]. - However, direct and primary inhibition of the entire **RAAS** is the mechanism of action for drugs like **ACE inhibitors** and **ARBs**, not beta-blockers.

Question 1047: Which drug is most classically associated with QT interval prolongation?

A. Magnesium Sulfate
B. Lignocaine
C. Quinidine (Correct Answer)
D. Amiodarone

Explanation: ***Quinidine*** - **Quinidine** is a Class IA antiarrhythmic drug that is the **classic textbook example** of drug-induced QT interval prolongation. - It blocks **sodium channels** and **potassium channels**, specifically delayed rectifier potassium channels (IKr). - This blockade of potassium channels **slows repolarization** of the cardiac myocyte, thereby prolonging the **QT interval** and increasing the risk of **Torsades de Pointes**. - Historically, quinidine has been the **prototype drug** used to teach this adverse effect in medical education. *Magnesium Sulfate* - **Magnesium sulfate** is used to **treat Torsades de Pointes**, a polymorphic ventricular tachycardia often associated with **QT prolongation**, but it does not primarily cause QT prolongation itself. - Its mechanism involves stabilizing the cardiac membrane and reducing abnormal electrical activity, rather than lengthening the **QT interval**. *Lignocaine* - **Lignocaine** (Lidocaine) is a Class IB antiarrhythmic drug that primarily blocks **sodium channels**, shortening the action potential duration in some cardiac tissues. - It does **not** significantly prolong the **QT interval**; in some cases, it can even shorten it, making it safer in patients with pre-existing QT prolongation. *Amiodarone* - **Amiodarone** is a Class III antiarrhythmic drug that blocks multiple channels, including **potassium channels**, leading to significant **QT interval prolongation**. - While amiodarone does prolong the QT interval considerably, the question asks for the **"most classically associated"** drug, which is quinidine—the historical prototype for this adverse effect. - The associated risk of **Torsades de Pointes** with amiodarone is lower than with Class IA agents like quinidine due to its **less proarrhythmic** profile, making quinidine the more classic teaching example.

Question 1048: Drugs acting on K+ channels include which of the following?

A. Nicorandil (Correct Answer)
B. Methyldopa
C. Amiloride
D. Spironolactone

Explanation: ***Nicorandil*** - **Nicorandil** is a **potassium channel activator** that causes vasodilation by opening ATP-sensitive potassium channels in vascular smooth muscle cells. - This action leads to hyperpolarization of the cell membrane, making it more difficult for calcium influx and thus promoting relaxation and **vasodilation**. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** that works by blocking aldosterone receptors in the renal collecting tubules. - Its main effect is to increase sodium and water excretion while **conserving potassium**, making it a potassium-sparing diuretic, but it does not directly act on potassium channels for its primary mechanism. *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that directly inhibits **epithelial sodium channels (ENaC)** in the collecting duct. - By blocking sodium reabsorption, it indirectly reduces potassium secretion, thus conserving potassium, but it does not directly affect potassium channels. *Methyldopa* - **Methyldopa** is a **centrally acting alpha-2 adrenergic agonist** that reduces sympathetic outflow from the central nervous system. - It decreases peripheral vascular resistance and heart rate, leading to a reduction in blood pressure, and does not directly interact with potassium channels.

Question 1049: What is the drug of choice for treating tachycardia induced by digitalis?

A. Phenytoin (Correct Answer)
B. Lidocaine
C. Reducing the dosage of digoxin
D. Verapamil

Explanation: ***Phenytoin*** - Phenytoin is the traditional drug of choice for **digitalis-induced tachyarrhythmias** as it blocks **sodium channels**, suppresses **automaticity**, and uniquely improves **AV conduction**. - It effectively counteracts digitalis toxicity by stabilizing the **cardiac membrane** and reducing **ectopic ventricular beats** without worsening conduction abnormalities. *Lidocaine* - Though lidocaine is a **Class IB antiarrhythmic** effective for ventricular arrhythmias, it was not the standard answer for this exam question context. - In modern practice, lidocaine may be preferred due to better **safety profile** and **IV availability**, but phenytoin remains the textbook answer for digitalis toxicity. *Reducing the dosage of digoxin* - While reducing digoxin dosage is important in **chronic management** of digitalis toxicity, it does not provide immediate relief from life-threatening arrhythmias. - This approach is too slow for acute situations requiring prompt **pharmacological intervention** to control dangerous tachycardia. *Verapamil* - Verapamil is **contraindicated** in digitalis toxicity as it can worsen **AV block** and exacerbate the **bradycardia** often associated with digitalis intoxication. - It can also increase **digoxin serum levels** by reducing renal clearance, potentially worsening the toxicity rather than treating it.

Question 1050: What type of drug is Sacubitril?

A. ACE inhibitor
B. Neutral endopeptidase inhibitor (Correct Answer)
C. Calcium channel inhibitor
D. Beta adrenergic blocker

Explanation: ***Neutral endopeptidase inhibitor*** - **Sacubitril** is specifically a **neprilysin inhibitor**, which is a type of neutral endopeptidase. - It works by preventing the breakdown of **natriuretic peptides**, leading to vasodilation and natriuresis, beneficial in heart failure. *ACE inhibitor* - **ACE inhibitors** block the conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced aldosterone. - While sacubitril is often given in combination with an **angiotensin receptor blocker (valsartan)**, it is not an ACE inhibitor itself. *Calcium channel inhibitor* - **Calcium channel inhibitors** block the influx of calcium into vascular smooth muscle cells and cardiac myocytes, causing vasodilation and reduced myocardial contractility. - This is a distinct mechanism of action from sacubitril, which affects peptide degradation. *Beta adrenergic blocker* - **Beta-adrenergic blockers** inhibit the effects of catecholamines on beta-adrenergic receptors, reducing heart rate and myocardial contractility. - They are used in various cardiovascular conditions but operate through a different pathway than sacubitril.

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

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free