Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 1111: Which local anesthetic is considered the most cardiotoxic?

A. Procaine
B. Prilocaine
C. Ropivacaine
D. Bupivacaine (Correct Answer)

Explanation: ***Bupivacaine*** - **Bupivacaine** is an amide-type local anesthetic associated with significant **cardiotoxicity** due to its high lipid solubility and slow dissociation from cardiac sodium channels. - This can lead to severe **arrhythmias** and myocardial depression, making it particularly dangerous in systemic overdose. *Procaine* - **Procaine** is an ester-type local anesthetic with a relatively low potential for cardiotoxicity. - Its rapid metabolism by **plasma pseudocholinesterase** limits systemic exposure and reduces the risk of cardiac effects. *Prilocaine* - **Prilocaine** is an amide-type local anesthetic that is generally less cardiotoxic than bupivacaine. - Its primary concern is the potential to cause **methemoglobinemia** at higher doses, a side effect not directly related to cardiotoxicity. *Ropivacaine* - **Ropivacaine** is an amide-type local anesthetic developed as an alternative to bupivacaine with a reduced cardiotoxicity profile. - It exhibits a more favorable **therapeutic index** for cardiac effects due to its chemical structure and faster dissociation from cardiac sodium channels.

Question 1112: Which drug is primarily known for inhibiting cardiac remodeling in congestive heart failure (CHF)?

A. ACE inhibitors (Correct Answer)
B. Digitalis
C. Diuretics
D. Vasodilators

Explanation: ***ACE inhibitors*** - **Angiotensin-converting enzyme (ACE) inhibitors** prevent the conversion of angiotensin I to angiotensin II, reducing detrimental effects like **vasoconstriction**, **aldosterone secretion**, and **cardiac hypertrophy**. - By inhibiting the **renin-angiotensin-aldosterone system (RAAS)**, ACE inhibitors effectively reduce cardiac preload and afterload, leading to the prevention or reversal of **cardiac remodeling**. *Digitalis* - Digitalis primarily acts as a **positive inotrope**, increasing the force of myocardial contraction, and slowing the heart rate, particularly in **atrial fibrillation**. - While it improves symptoms, it does not directly prevent or reverse **cardiac remodeling** and can have a narrow therapeutic index. *Diuretics* - Diuretics primarily reduce **fluid overload** and congestion in CHF by increasing **sodium and water excretion**, thereby decreasing preload. - They alleviate symptoms like **edema** and **dyspnea** but do not directly target or inhibit the underlying processes of **cardiac remodeling**. *Vasodilators* - Vasodilators (such as nitrates and hydralazine) reduce **cardiac preload** and/or **afterload**, improving symptomatic relief. - While they can improve hemodynamics, their primary action is not focused on preventing the cellular and structural changes associated with **cardiac remodeling**.

Question 1113: The drug of choice for prompt relief of an ongoing attack of angina precipitated by exercise or emotional stress is:

A. Propranolol
B. Verapamil
C. Sublingual nitroglycerin (Correct Answer)
D. Sublingual nifedipine

Explanation: ***Sublingual nitroglycerin*** - **Sublingual nitroglycerin** acts rapidly (within 1-3 minutes) by causing **vasodilation**, primarily of veins, which reduces **preload** and myocardial oxygen demand, providing prompt relief of anginal symptoms. - It works by releasing **nitric oxide**, leading to **smooth muscle relaxation** in blood vessels, which is critical for acute attack termination. *Propranolol* - **Propranolol** is a **beta-blocker** used for long-term prevention of angina by reducing heart rate and contractility, thereby decreasing oxygen demand. - It is **not suitable for acute relief** as its onset of action is not rapid enough to abort an ongoing anginal attack. *Verapamil* - **Verapamil** is a **calcium channel blocker** that reduces heart rate, contractility, and causes vasodilation, making it useful for angina prevention. - While it can improve oxygen supply, its onset of action is **too slow** for acute symptomatic relief of an ongoing anginal attack. *Sublingual nifedipine* - **Nifedipine** is a **dihydropyridine calcium channel blocker** predominantly used for hypertension and stable angina, primarily causing arterial vasodilation. - Sublingual nifedipine can cause a **rapid and substantial drop in blood pressure**, which can lead to reflex tachycardia and potentially worsen angina or cause adverse cardiovascular events; therefore, it is **not recommended for acute anginal relief**.

Question 1114: ACE inhibitors, when used for a long time in hypertensive patients, cause

A. Rightward shift in Renal pressure natriuresis curve
B. Reduction in filtration fraction (Correct Answer)
C. Significant increase in heart rate
D. No change in the compliance of large arteries

Explanation: **Reduction in filtration fraction** - ACE inhibitors cause **vasodilation of the efferent arteriole** in the glomerulus. - This vasodilation leads to a **decrease in glomerular filtration pressure**, thereby reducing the filtration fraction. *Rightward shift in Renal pressure natriuresis curve* - A rightward shift in the renal pressure natriuresis curve indicates that a **higher blood pressure is required to excrete the same amount of sodium and water**. - ACE inhibitors typically cause a **leftward shift of this curve** by improving sodium and water excretion at lower pressures. *Significant increase in heart rate* - ACE inhibitors typically cause a **decrease or no significant change in heart rate**, as they interfere with the renin-angiotensin-aldosterone system (RAAS), which can affect sympathetic tone. - A significant increase in heart rate is **not a common or expected side effect** of long-term ACE inhibitor use. *No change in the compliance of large arteries* - Long-term use of ACE inhibitors can actually **improve arterial compliance** by remodeling the vessel walls and reducing stiffness. - This effect contributes to their **beneficial cardiovascular outcomes** beyond just blood pressure reduction.

Question 1115: All of the following are seen in digitalis toxicity except:

A. Ventricular bigeminy
B. Regularization of atrial fibrillation
C. Bidirectional ventricular tachycardia
D. Paroxysmal atrial tachycardia with fast ventricular rate (Correct Answer)

Explanation: ***Paroxysmal atrial tachycardia with fast ventricular rate*** - Digitalis toxicity typically causes **bradyarrhythmias** or **tachyarrhythmias** with AV block, leading to a slow or normal ventricular rate. - A **fast ventricular rate** in the presence of paroxysmal atrial tachycardia (PAT) suggests that the AV node is conducting impulses unimpeded, which is less likely in digitalis toxicity due to its negative dromotropic effects. *Ventricular bigeminy* - This is a **classic arrhythmia** seen in digitalis toxicity, characterized by alternating normal and premature ventricular beats. - Digitalis increases intracellular calcium and can lead to **delayed afterdepolarizations**, initiating ventricular ectopy. *Regularization of atrial fibrillation* - Digitalis can **slow AV nodal conduction** and increase ventricular refractoriness, which may lead to regularization of the ventricular response in atrial fibrillation. - While not a complete reversal of atrial fibrillation, the **ventricular rhythm becomes more regular** due to increased AV nodal block. *Bidirectional ventricular tachycardia* - This is a highly specific but **rare arrhythmia** associated with severe digitalis toxicity, characterized by alternating QRS complexes in opposite directions. - It results from enhanced automaticity and altered conduction properties in the **His-Purkinje system**.

Question 1116: Atenolol is indicated in all except:

A. Hypertension
B. Hypertrophic obstructive cardiomyopathy
C. Classical angina
D. Partial heart block (Correct Answer)

Explanation: ***Partial heart block*** - Beta-blockers like atenolol are **contraindicated** in patients with **partial heart block** (second- or third-degree AV block) as they can further depress AV nodal conduction, worsening the block and potentially leading to **bradycardia** or complete heart block [3]. - This adverse effect is due to their action on beta-1 adrenergic receptors in the heart, which reduces heart rate and conduction velocity [3]. *Hypertension* - Atenolol is a **beta-1 selective blocker** commonly used in the treatment of hypertension [1]. - It lowers blood pressure by reducing cardiac output and inhibiting **renin release** from the kidneys [1]. *Hypertrophic obstructive cardiomyopathy* - Beta-blockers, including atenolol, are often used in **hypertrophic obstructive cardiomyopathy (HOCM)** to reduce the **left ventricular outflow tract (LVOT)** obstruction. - They achieve this by increasing **diastolic filling time** and reducing myocardial contractility. *Classical angina* - Atenolol is effective in managing **classical angina** (stable angina) by reducing **myocardial oxygen demand** [2]. - It decreases heart rate, contractility, and blood pressure, thereby alleviating anginal symptoms [2].

Question 1117: The positive inotropic effect of digitalis is due to inhibition of Na+/K+ ATPase pump in cardiac muscle cell membrane leading to:

A. Increased intracellular Na+ decreasing the activity of Ca++ pump in the sarcoplasmic reticulum
B. Increased intracellular Na+ causing increased efflux of Na+ and increased influx of Ca++ through Na+/Ca++ exchanger in the sarcolemma
C. Decreased efflux of Na+ leading to less negative resting membrane potential and opening of voltage gated Ca++ channels on the T tubules
D. Decreased activity of Na+/Ca++ exchanger causing decreased influx of sodium and decreased efflux of Ca++ in the sarcolemma (Correct Answer)

Explanation: ***Decreased activity of Na+/Ca++ exchanger causing decreased influx of sodium and decreased efflux of Ca++ in the sarcolemma*** - Inhibition of the **Na+/K+-ATPase pump** by **digitalis** leads to an increase in intracellular sodium ([Na+]i). - This elevated [Na+]i reduces the electrochemical gradient for the **Na+/Ca++ exchanger (NCX)**, which normally extrudes Ca++ from the cell in exchange for Na+ influx. - With reduced Na+ gradient, the NCX becomes **less active**, resulting in **decreased Na+ influx** and **decreased Ca++ efflux** through this exchanger. - The net effect is an **increase in intracellular Ca++**, which enhances myocardial contractility (positive inotropic effect). *Increased intracellular Na+ causing increased efflux of Na+ and increased influx of Ca++ through Na+/Ca++ exchanger in the sarcolemma* - This statement is incorrect because an **increased intracellular Na+** would actually reduce the efflux of Na+ via the NCX, not increase it. - The primary action of NCX is to extrude Ca++ in exchange for Na+ influx; a reduced gradient for Na+ influx would mean **less Ca++ efflux**, not increased Ca++ influx. - The direction described here is opposite to what actually occurs with digitalis. *Increased intracellular Na+ decreasing the activity of Ca++ pump in the sarcoplasmic reticulum* - An increase in **intracellular Na+** does not directly decrease the activity of the **sarcoplasmic reticulum Ca++-ATPase (SERCA) pump**. - SERCA pump activity is primarily regulated by intracellular Ca++ levels and phospholamban, not Na+ levels. - This mechanism is not the primary pathway for digitalis's inotropic effect. *Decreased efflux of Na+ leading to less negative resting membrane potential and opening of voltage gated Ca++ channels on the T tubules* - While inhibition of the **Na+/K+-ATPase** does lead to **decreased Na+ efflux** and can depolarize the membrane slightly, this is not the primary mechanism of digitalis's positive inotropic effect. - The main inotropic effect is mediated by increased intracellular Ca++ due to the **NCX exchanger's reduced activity**, rather than sustained opening of voltage-gated Ca++ channels at rest. - Voltage-gated Ca++ channels open during the action potential, not at rest due to minor depolarization.

Question 1118: Which drug is primarily associated with QT prolongation?

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

Explanation: ***Quinidine*** - **Quinidine** is a Class IA antiarrhythmic drug that blocks **sodium channels** and also prolongs the **repolarization** phase of the action potential by blocking potassium channels, leading to **QT prolongation**. - Significant **QT prolongation** can predispose to **Torsades de pointes**, a polymorphic ventricular tachycardia. *Magnesium Sulfate* - **Magnesium sulfate** is used to treat **Torsades de pointes**, not cause it, as it stabilizes cardiac membranes and reduces arrhythmogenic activity. - While it can affect cardiac conduction, its primary effect is not **QT elongation** in a proarrhythmic way. *Lignocaine* - **Lignocaine** (Lidocaine) is a Class IB antiarrhythmic drug that primarily blocks **sodium channels** and **shortens** the action potential duration in some cardiac tissues. - It typically **does not cause QT prolongation** and is often used for ventricular arrhythmias without significant risk of Torsades de pointes. *Amiodarone* - **Amiodarone** is a Class III antiarrhythmic drug that causes **QT prolongation** by blocking potassium channels. - While it can prolong the QT interval, **Quinidine** is more classically and primarily associated with this effect, especially in causing **Torsades de pointes** as a side effect.

Question 1119: Which of the following is a contraindication for the use of beta blockers?

A. Asthma (Correct Answer)
B. Myocardial infarction
C. Arrhythmia
D. Hypertension

Explanation: ***Asthma*** - Beta-blockers can cause **bronchoconstriction** by blocking beta-2 adrenergic receptors in the lungs, worsening asthma symptoms. - This effect can precipitate or exacerbate an **asthma attack**, making it a significant contraindication, especially for non-selective beta-blockers. *Myocardial infarction* - Beta-blockers are often **indicated** in the post-myocardial infarction setting to reduce myocardial oxygen demand, heart rate, and risk of future events. - They improve survival by preventing remodeling and reducing the incidence of **ventricular arrhythmias**. *Hypertension* - Beta-blockers are a common and effective treatment for **hypertension**, lowering blood pressure by reducing heart rate and cardiac output. - They are particularly useful when hypertension is accompanied by **angina** or **migraines**. *Arrhythmia* - Beta-blockers are frequently used to treat various **arrhythmias**, such as **atrial fibrillation** and **supraventricular tachycardia**. - They decrease the heart rate and conduction velocity through the AV node, helping to **control ventricular response**.

Question 1120: Which of the following is a late inward sodium channel blocker?

A. Ranolazine (Correct Answer)
B. Fasudil
C. Ivabradine
D. Trimetazidine

Explanation: ***Ranolazine*** - **Ranolazine** selectively inhibits the **late inward sodium current (I_Na)** in cardiac myocytes. - By reducing this current, it helps to decrease intracellular **sodium and calcium overload**, thereby improving myocardial relaxation and reducing angina and ischemia. *Ivabradine* - **Ivabradine** is a selective **funny channel (If) inhibitor** in the sinoatrial node. - It slows down the heart rate by reducing the rate of diastolic depolarization, primarily used for **chronic stable angina** and **heart failure**. *Fasudil* - **Fasudil** is a **rho-kinase inhibitor** used primarily in Japan and China for **cerebral vasospasm** following subarachnoid hemorrhage. - It works by inhibiting the phosphorylation of myosin light chain, leading to **vasodilation**. *Trimetazidine* - **Trimetazidine** is an **anti-ischemic metabolic agent** that inhibits the enzyme 3-ketoacyl-CoA thiolase, shifting cardiac metabolism from fatty acid oxidation to glucose oxidation. - This improves myocardial glucose utilization, which is more efficient in **ischemic conditions**, thereby reducing angina symptoms.

Practice by Chapter

Antihypertensive Agents

Practice Questions

Drugs for Heart Failure

Practice Questions

Antiarrhythmic Drugs

Practice Questions

Antianginal Agents

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Lipid-Lowering Drugs

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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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