Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 1101: Which of the following antiarrhythmic drugs is contraindicated in a patient with interstitial lung disease?

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

Explanation: ***Amiodarone*** - **Amiodarone** is contraindicated in patients with interstitial lung disease due to its well-known and potentially severe pulmonary toxicity, which can exacerbate or induce **pulmonary fibrosis**. - Its long half-life means that drug accumulation and persistent adverse effects, including **ILD exacerbation**, are significant concerns. *Sotalol* - **Sotalol** primarily carries risks of **prolonged QT interval** and **torsades de pointes** because it has both beta-blocking and Class III antiarrhythmic properties. - While it has cardiac and minor non-cardiac side effects, it is not specifically known to cause or worsen **interstitial lung disease**. *Lignocaine* - **Lignocaine** (lidocaine) is a Class Ib antiarrhythmic primarily used for **ventricular arrhythmias**, especially in acute settings. - Its adverse effects are mainly **neurological** (e.g., dizziness, seizures at high doses) and **cardiovascular** (e.g., hypotension, bradycardia), with no significant association with lung disease. *Quinidine* - **Quinidine** is a Class Ia antiarrhythmic that can cause a variety of side effects, including **gastrointestinal upset**, **cinchonism** (tinnitus, blurred vision), and **cardiac rhythm disturbances**. - While it can rarely cause a hypersensitivity pneumonitis, it is not a primary concern or contraindication in existing **interstitial lung disease** compared to amiodarone.

Question 1102: In acute left ventricular failure with pulmonary edema, which drug can be administered for immediate management?

A. Morphine (Correct Answer)
B. Amlodipine
C. Epinephrine
D. Propranolol

Explanation: ***Morphine*** - **Morphine** is a key drug in the **acute management of left ventricular failure with pulmonary edema** - It provides **anxiolysis**, reduces **sympathetic drive**, and decreases **preload** through venodilation - Reduces **oxygen demand** and **work of breathing** in acute decompensation - Standard dose: **2-5 mg IV**, can be repeated as needed - Caution needed for **respiratory depression** and **hypotension**, but benefits outweigh risks in severe pulmonary edema *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that is **contraindicated in acute/decompensated heart failure** - Beta-blockers **reduce contractility** and can worsen acute cardiac output - While certain beta-blockers (carvedilol, metoprolol, bisoprolol) are used in **chronic stable heart failure**, propranolol is NOT a guideline-recommended agent for heart failure management - In acute settings, beta-blockers would precipitate or worsen decompensation *Amlodipine* - **Amlodipine** is a **dihydropyridine calcium channel blocker** used for hypertension and angina - **Not recommended in heart failure** as it can cause **negative inotropic effects** and peripheral edema - Does not provide mortality benefit and may worsen outcomes in LV dysfunction - Other vasodilators (nitrates, ACE inhibitors) are preferred *Epinephrine* - **Epinephrine** is a potent **catecholamine** with alpha and beta effects - Increases **heart rate**, **contractility**, and **systemic vascular resistance** - Would dramatically increase **myocardial oxygen demand** and **afterload** in LV failure - Reserved for **cardiac arrest** or **cardiogenic shock requiring inotropic support**, not routine LV failure management - Risk of **arrhythmias** and **ischemia**

Question 1103: Statins act on:

A. HMG CoA synthetase
B. HMG CoA reductase (Correct Answer)
C. HMG CoA hydratase
D. Squalene epoxidase

Explanation: ***HMG CoA reductase*** - **HMG-CoA reductase inhibitors** (statins) are the most effective and widely used class of hypolipidemic agents [1, 2, 3]. - This enzyme is the **rate-limiting step** in cholesterol biosynthesis in the liver [1, 2, 3]. *HMG CoA synthetase* - HMG-CoA synthetase is involved in the synthesis of **HMG-CoA** from acetyl-CoA and acetoacetyl-CoA. - This enzyme precedes the HMG-CoA reductase step and is **not the primary target** for cholesterol-lowering drugs. *Squalene epoxidase* - Squalene epoxidase is an enzyme involved in the later stages of the **cholesterol synthesis pathway**, specifically in converting squalene to squalene epoxide. - While inhibition of this enzyme would reduce cholesterol synthesis, it is **not the main target** of current widely used hypolipidemic agents. *HMG CoA hydratase* - HMG-CoA hydratase (also known as HMG-CoA lyase) is involved in the breakdown of HMG-CoA into **acetyl-CoA and acetoacetate** in ketogenesis. - It is **not directly involved** in the main pathway of cholesterol synthesis that is targeted by current hypolipidemic drugs.

Question 1104: Clonidine is used as an antihypertensive agent, but if used as a fast intravenous injection, it can increase blood pressure due to:

A. Agonistic action on vascular Alpha 2 adrenergic receptors (Correct Answer)
B. Cardiac stimulation
C. Stimulation of the vasomotor center leading to increased sympathetic output
D. Release of noradrenaline from adrenergic nerve endings

Explanation: ***Agonistic action on vascular Alpha 2 adrenergic receptors*** - When administered rapidly intravenously, clonidine initially acts as an agonist on **postsynaptic α2-adrenergic receptors** in the vascular smooth muscle. - This direct peripheral vasoconstrictive effect occurs before central effects dominate, leading to a transient increase in blood pressure. *Stimulation of the vasomotor center leading to increased sympathetic output* - Clonidine's primary antihypertensive effect is through **central α2-receptor agonism**, which *decreases* sympathetic outflow from the vasomotor center. - It would not stimulate the vasomotor center to *increase* sympathetic output, as this contradicts its fundamental mechanism of action. *Cardiac stimulation* - Clonidine is known for its **cardiac depressant effects** due to reduced sympathetic outflow, leading to decreased heart rate and contractility. - It does not directly stimulate the heart, and any initial blood pressure rise is due to vascular effects, not increased cardiac output. *Release of noradrenaline from adrenergic nerve endings* - Clonidine is an **α2-adrenergic agonist**, and activation of presynaptic α2-receptors typically *inhibits* the release of noradrenaline. - It does not cause a direct release of noradrenaline but rather modulates its release in the opposite direction.

Question 1105: Dobutamine mainly acts on which receptor:

A. Beta 1 (Correct Answer)
B. Beta 2
C. Alpha 1
D. Alpha 2

Explanation: ***Beta 1*** - **Dobutamine** is a direct-acting **beta-1 adrenergic agonist**, which means it primarily stimulates beta-1 receptors. - Stimulation of **beta-1 receptors** in the heart leads to increased **cardiac contractility** (positive inotropy) and heart rate (positive chronotropy), making it useful in conditions like **heart failure**. *Beta 2* - **Beta-2 receptors** are primarily found in the lungs and **vascular smooth muscle**. - Stimulation of **beta-2 receptors** causes **bronchodilation** and **vasodilation**, effects that are not the primary therapeutic goal of dobutamine. *Alpha 1* - **Alpha-1 receptors** are mainly located in **vascular smooth muscle** and cause **vasoconstriction** when stimulated. - While dobutamine may have some weak effects on alpha-1 receptors at higher doses, its dominant action is on beta-1 receptors, and significant vasoconstriction is not its primary clinical effect. *Alpha 2* - **Alpha-2 receptors** are largely presynaptic and act to inhibit the release of **norepinephrine**. - **Dobutamine** has minimal to no significant activity at **alpha-2 receptors**.

Question 1106: All of the following are centrally acting antihypertensive drugs except:

A. Methyldopa
B. Clonidine
C. Guanabenz
D. Trimethoprim (Correct Answer)

Explanation: ***Trimethoprim*** - **Trimethoprim** is an **antibiotic** and is not used as an antihypertensive drug. - It works by inhibiting **dihydrofolate reductase**, an enzyme involved in bacterial folate synthesis. *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. *Clonidine* - **Clonidine** is a **centrally acting alpha-2 adrenergic agonist** that stimulates alpha-2 receptors in the brainstem. - This stimulation reduces sympathetic outflow, leading to vasodilation and decreased heart rate. *Guanabenz* - **Guanabenz** is also a **centrally acting alpha-2 adrenergic agonist**. - It acts similarly to clonidine by stimulating central alpha-2 receptors to decrease sympathetic tone and lower blood pressure.

Question 1107: Most common digoxin-induced arrhythmia is

A. Ventricular bigeminy
B. Atrial Flutter
C. Ventricular Premature Beats (Correct Answer)
D. Ventricular Fibrillation

Explanation: ***Ventricular Premature Beats (VPBs)*** - **Most common** digoxin-induced arrhythmia overall, occurring in up to 50-90% of digoxin toxicity cases. - Digoxin increases intracellular calcium through Na+/K+-ATPase inhibition, leading to **increased automaticity** and **delayed afterdepolarizations** that trigger ventricular ectopy. - **Hypokalemia** (common with concurrent diuretic use) significantly increases the risk by enhancing digoxin binding to Na+/K+-ATPase and further elevating intracellular calcium. - VPBs can manifest in various patterns including isolated beats, couplets, or organized patterns like ventricular bigeminy. *Ventricular bigeminy* - While ventricular bigeminy (every other beat is a VPB) is highly **characteristic** and specific for digoxin toxicity, it is a specific *pattern* of VPBs rather than the most common arrhythmia overall. - Represents severe ventricular irritability and indicates significant digoxin effect, but occurs less frequently than isolated VPBs. - When present, it strongly suggests digoxin toxicity and warrants immediate attention. *Ventricular Fibrillation* - A rare but **life-threatening** complication of severe digoxin toxicity. - Usually preceded by other ventricular arrhythmias (VPBs, ventricular tachycardia) and represents advanced toxicity. - Not common enough to be considered the "most common" digoxin-induced arrhythmia. *Atrial Flutter* - Digoxin can cause various atrial arrhythmias, but atrial flutter is relatively uncommon. - The most characteristic **atrial** arrhythmia in digoxin toxicity is **paroxysmal atrial tachycardia (PAT) with AV block**, not atrial flutter. - Digoxin's primary atrial effect is to slow AV nodal conduction, which may actually help control atrial flutter rather than cause it.

Question 1108: Effects of beta blockers on the heart are all of the following except:

A. Decreases duration of systole (Correct Answer)
B. Decrease in heart rate
C. May decrease cardiac output initially.
D. May precipitate heart failure in acute settings.

Explanation: ***Decreases duration of systole*** - Beta-blockers primarily prolong the **duration of systole** by extending the **ejection time** and slowing ventricular relaxation. - They also increase the **diastolic filling time** by reducing heart rate, impacting overall cardiac cycle duration. *Decrease in heart rate* - Beta-blockers block **beta-1 adrenergic receptors** in the heart, leading to a decrease in **sympathetic stimulation** and thus a reduced heart rate. - This effect is beneficial in conditions like **tachycardia** and **angina**, as it reduces myocardial oxygen demand. *May decrease cardiac output initially.* - By reducing heart rate and contractility, beta-blockers can initially decrease **cardiac output**, especially in patients with pre-existing **ventricular dysfunction**. - This effect is often transient, as chronic use can lead to beneficial remodeling and improved efficiency in some conditions. *May precipitate heart failure in acute settings.* - In patients with acutely decompensated heart failure or severe left ventricular dysfunction, beta-blockers can acutely worsen cardiac function due to their **negative inotropic effects**. - Therefore, beta-blockers are typically initiated cautiously at low doses in stable heart failure patients and are contraindicated in acute decompensation.

Question 1109: Cardiac hyperaemia/vasodilation is due to which mediator?

A. Acetylcholine
B. Adrenaline
C. Dopamine
D. Adenosine (Correct Answer)

Explanation: ***Adenosine*** - **Adenosine** is a potent endogenous vasodilator in the heart, released in response to increased myocardial oxygen demand or ischemia. - It acts on **A2A receptors** in vascular smooth muscle, leading to relaxation and increased coronary blood flow (hyperemia). *Acetylcholine* - **Acetylcholine** primarily causes vasodilation in skeletal muscle and some other vascular beds, mediated by nitric oxide release from endothelial cells. - In the heart, it mainly acts as a **negative chronotropic** and **dromotropic** agent, slowing heart rate and conduction, with variable direct effects on coronary vessels. *Adrenaline* - **Adrenaline** (epinephrine) typically causes vasoconstriction via **alpha-1 receptors** in many vascular beds, but can cause vasodilation via **beta-2 receptors** in some, such as skeletal muscle. - In the heart, its primary effect is positive chronotropy and inotropy, and it can cause **coronary vasoconstriction** or dilation depending on receptor distribution and dose. *Dopamine* - **Dopamine** has complex effects on the vasculature, depending on the dose and receptor subtypes activated. - At low doses, it can cause **renal and mesenteric vasodilation** via D1 receptors, but at higher doses, it can cause generalized vasoconstriction via alpha-adrenergic receptors.

Question 1110: HMG-CoA reductase is inhibited by:

A. Lovastatin (Correct Answer)
B. Gemfibrozil
C. Nicotinic acid
D. Clofibrate

Explanation: ***Lovastatin*** - **Lovastatin** is part of the statin class of drugs, which are potent competitive inhibitors of **HMG-CoA reductase**. - By inhibiting this enzyme, statins reduce the synthesis of **mevalonate**, a precursor to **cholesterol**, thereby lowering LDL-cholesterol levels. *Gemfibrozil* - **Gemfibrozil** is a **fibrate**, a class of drugs that primarily act by activating **peroxisome proliferator-activated receptor alpha (PPAR-α)**. - Its main effect is to decrease **triglyceride** levels and increase **HDL cholesterol**, not directly inhibit HMG-CoA reductase. *Clofibrate* - **Clofibrate** is also a **fibrate** and operates similarly to gemfibrozil by activating **PPAR-α**. - It primarily reduces **triglycerides** and has a modest effect on increasing HDL, but does not inhibit HMG-CoA reductase. *Nicotinic acid* - **Nicotinic acid** (niacin or vitamin B3) reduces hepatic synthesis of **VLDL** and inhibits the release of **fatty acids** from adipose tissue. - This leads to a decrease in **LDL cholesterol** and triglycerides, and an increase in **HDL cholesterol**, but it does not directly inhibit HMG-CoA reductase.

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

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