Cardiovascular Drugs Practice Questions

Q: A patient has been taking digoxin for several years and is about to receive atropine for some other indication. A common side effect of digoxin that can be blocked by atropine is:

Increased PR interval on the ECG. Explanation:The correct answer is C. Increased PR interval on the ECG.Mechanism of Action:Digoxin exerts its effects through two primary mechanisms: inhibition of the Na+/K+ ATPase pump (leading to positive inotropy) and parasympathomimetic (vagomimetic) action. By increasing vagal tone, digoxin slows conduction through the Atrioventricular (AV) node. On an ECG, AV nodal delay is represented by an increased PR interval [1]. Since atropine is a muscarinic antagonist (parasympatholytic), it blocks the vagal effects of digoxin on the AV node, thereby preventing or reversing the prolongation of the PR interval.Analysis of Incorrect Options: A. Decreased appetite: This is a common early sign of digoxin toxicity caused by direct stimulation of the Chemoreceptor Trigger Zone (CTZ). It is not mediated by the vagus nerve and thus cannot be blocked by atropine. B. Increased cardiac contractility: This is the therapeutic goal of digoxin, achieved by increasing intracellular calcium via Na+/K+ ATPase inhibition. This mechanical effect is independent of the autonomic nervous system and is not affected by atropine. D. Tachycardia: Digoxin typically causes bradycardia due to its vagomimetic effects. Tachycardia (specifically atrial tachycardia with AV block) is a sign of toxicity, but atropine would likely worsen a tachycardia rather than block it.High-Yield Clinical Pearls for NEET-PG: ECG Changes with Digoxin: Earliest change is a decreased QT interval [1]; most characteristic is the "reverse tick" or "sagging" ST-segment depression (Salvador Dali sign). Vagal Effect: Digoxin is used in Atrial Fibrillation primarily to control ventricular rate by increasing the refractory period of the AV node via the vagus nerve. Antidote: For life-threatening toxicity, the treatment of choice is Digoxin-specific antibody fragments (DigiFab). Atropine is specifically used to treat digoxin-induced symptomatic bradycardia or high-grade AV block.

Q: Which of the following drugs does not increase the QT interval?

Digitalis. **Explanation:** The correct answer is **Digitalis (Digoxin)**. **Why Digitalis is correct:** Digitalis acts by inhibiting the $Na^+/K^+$ ATPase pump, which leads to an increase in intracellular calcium. Electrophysiologically, Digitalis **shortens the action potential duration (APD)** and the **QT interval**. It is well-known for causing "ST-segment sagging" (reverse tick sign) and a shortened QT interval, which is a classic finding on an ECG of a patient on Digoxin. **Why the other options are incorrect:** * **Amiodarone (Class III Antiarrhythmic):** Its primary mechanism is blocking potassium channels, which prolongs Phase 3 of the action potential, thereby increasing the QT interval. * **Quinidine (Class IA Antiarrhythmic):** It blocks both sodium and potassium channels. By blocking potassium channels, it prolongs repolarization and increases the QT interval. It is a notorious cause of *Torsades de Pointes*. * **Amitriptyline (Tricyclic Antidepressant):** TCAs have "quinidine-like" effects on the heart. They block myocardial sodium and potassium channels, leading to QRS widening and QT interval prolongation, especially in overdose. **High-Yield Clinical Pearls for NEET-PG:** * **QT Prolonging Drugs (Mnemonic: ABCDE):** **A**ntiarrhythmics (Class IA, III), **B**iotics (Macrolides, Fluoroquinolones), **C**an't-be-depressed (TCAs, Antipsychotics), **D**efective electrolytes (Hypokalemia, Hypomagnesemia, Hypocalcemia), **E**metics (Ondansetron). * **Digitalis ECG Changes:** Shortened QT, ST-segment depression (scooped appearance), T-wave inversion, and PR interval prolongation. * **Torsades de Pointes:** A polymorphic ventricular tachycardia associated with a prolonged QT interval. Interestingly, while Amiodarone prolongs the QT, it has a lower risk of causing Torsades compared to other Class III drugs.

Q: A hypertensive patient is taking tablet atenolol 200 mg/day in divided doses. After anesthesia, their heart rate fell from 50 beats/min to 40 beats/min. What is the appropriate treatment to improve the heart rate?

IV atropine. ### Explanation **Correct Option: B. IV Atropine** The patient is experiencing symptomatic bradycardia (HR 40 bpm) likely due to the high dose of **Atenolol** (a cardioselective $\beta_1$ blocker) exacerbated by anesthesia. * **Mechanism:** Beta-blockers reduce heart rate by decreasing sympathetic drive to the SA node. In such cases, the primary treatment for hemodynamically significant bradycardia is **IV Atropine**. * Atropine is a muscarinic antagonist that blocks the parasympathetic (vagal) input to the heart. By inhibiting the "brake" (vagus nerve), it allows the heart rate to increase, effectively counteracting the beta-blocker-induced bradycardia. **Why Other Options are Incorrect:** * **A. IV Adrenaline:** While it increases heart rate, it is generally reserved for cardiac arrest or severe anaphylaxis. In a patient on beta-blockers, adrenaline can cause "unopposed alpha-stimulation," leading to severe hypertension and reflex bradycardia. * **C. IV Isoprenaline:** This is a non-selective beta-agonist. While it can increase heart rate, its effect is competitively inhibited by the high dose of Atenolol already present in the patient's system, making it less effective. * **D. Dobutamine:** This is primarily an inotrope used in cardiogenic shock. Like isoprenaline, its efficacy is reduced in the presence of beta-blockade. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for Beta-blocker Overdose:** If atropine fails, the specific antidote is **IV Glucagon**. Glucagon increases cAMP in the myocardium via independent receptors, bypassing the blocked beta-receptors. * **Atenolol Dosing:** The standard dose is 25–100 mg/day. 200 mg/day is a high dose, increasing the risk of profound bradycardia and loss of cardioselectivity. * **Vagal Tone:** Anesthesia often increases vagal tone; when combined with beta-blockers, it significantly predisposes patients to intraoperative bradyarrhythmias.

Q: All of the following are true about digoxin except:

It is 95% plasma protein bound. **Explanation:** The correct answer is **C** because Digoxin has **low plasma protein binding (approximately 20–25%)**. This is a high-yield pharmacokinetic fact; most of the drug is sequestered in skeletal muscle (its primary reservoir) rather than bound to albumin. **Analysis of Options:** * **Option A (True):** Digoxin exerts a **vagomimetic effect** on the SA and AV nodes. By increasing vagal tone, it slows the heart rate (negative chronotropy) and decreases conduction velocity through the AV node, making it useful in controlling ventricular rate in atrial fibrillation. * **Option B (True):** The primary mechanism of action is the inhibition of the **Na+/K+ ATPase pump** on the sarcolemma. This leads to an increase in intracellular Na+, which subsequently slows the Na+/Ca2+ exchanger, increasing intracellular Ca2+ levels and resulting in increased contractility (**positive inotropy**). * **Option D (True):** Digoxin is primarily eliminated **unchanged by the kidneys** via glomerular filtration. Its clearance is directly proportional to the Creatinine Clearance (CrCl), necessitating dose adjustments in renal failure. **High-Yield NEET-PG Pearls:** * **Volume of Distribution (Vd):** Digoxin has a very large Vd (~6–7 L/kg) because it binds extensively to skeletal muscle. * **Therapeutic Window:** It has a narrow therapeutic index (0.5–2.0 ng/mL). * **Toxicity:** Hypokalemia predisposes to digoxin toxicity because K+ and digoxin compete for the same binding site on the Na+/K+ ATPase pump. * **Antidote:** Digoxin-specific antibody fragments (**DigiFab**). * **ECG Changes:** Characterized by the "reverse tick" or "sagging" ST-segment depression (Salvador Dali mustache sign).

Q: Which antiarrhythmic drug is known to cause hypothyroidism?

Amiodarone. **Explanation:** **Amiodarone** is the correct answer because it is a Class III antiarrhythmic drug with a unique chemical structure containing approximately **37% iodine by weight**. Each 200 mg tablet provides about 75 mg of iodine, which is significantly higher than the daily requirement. The high iodine content can lead to thyroid dysfunction via two mechanisms: 1. **Hypothyroidism:** Occurs due to the **Wolff-Chaikoff effect**, where an iodine overload inhibits the synthesis of thyroid hormones. This is more common in iodine-sufficient areas. 2. **Hyperthyroidism:** Occurs via the **Jod-Basedow phenomenon** (excess iodine acting as a substrate for hormone synthesis) or through destructive thyroiditis. **Analysis of Incorrect Options:** * **B. Amrinone:** A phosphodiesterase-3 (PDE3) inhibitor used in heart failure. Its primary side effect is **thrombocytopenia**, not thyroid dysfunction. * **C. Digoxin:** A cardiac glycoside used for rate control in atrial fibrillation. Common toxicities include gastrointestinal upset, visual disturbances (xanthopsia), and various arrhythmias. * **D. Procainamide:** A Class IA antiarrhythmic. Its most characteristic high-yield side effect is **Drug-Induced Lupus Erythematosus (DILE)**, especially in slow acetylators. **High-Yield Clinical Pearls for NEET-PG:** * **Amiodarone Side Effects:** Remember the mnemonic **"6 P's"**: **P**ulmonary fibrosis (most serious), **P**hotosensitivity, **P**igmentation (Blue-gray skin), **P**eripheral neuropathy, **P**rolonged QT interval, and **P**arent (Thyroid) dysfunction. * **Monitoring:** Baseline and periodic Thyroid Function Tests (TFTs) and Liver Function Tests (LFTs) are mandatory for patients on long-term Amiodarone. * **Half-life:** Amiodarone has an exceptionally long half-life (approx. 3–8 weeks) due to its high lipid solubility.

Q: Which antiarrhythmic drug decreases both the rate of depolarization (phase 0) and the rate of repolarization of myocardial fibres?

Quinidine. **Explanation** The question describes the characteristic electrophysiological profile of **Class IA antiarrhythmics**. **1. Why Quinidine is Correct:** Quinidine belongs to **Class IA** of the Vaughan-Williams classification. Its mechanism involves: * **Sodium Channel Blockade (Phase 0):** It binds to open sodium channels, decreasing the slope of phase 0 (depolarization), which slows conduction velocity. * **Potassium Channel Blockade (Phase 3):** It blocks outward K+ channels, thereby prolonging the action potential duration (APD) and the effective refractory period (ERP). This manifests as a **decrease in the rate of repolarization**. * On an ECG, this corresponds to a widened QRS complex and a prolonged QT interval. **2. Why the other options are incorrect:** * **Verapamil (Class IV):** A calcium channel blocker. It primarily affects the SA and AV nodes by slowing Phase 0 of the nodal action potential (calcium-dependent), not the myocardial fiber depolarization. * **Propranolol (Class II):** A beta-blocker. It acts by decreasing sympathetic activity and slowing the heart rate; it does not significantly block sodium or potassium channels in myocardial fibers at standard doses. * **Lignocaine (Class IB):** While it blocks sodium channels (Phase 0), it actually **shortens** repolarization (Phase 3) or leaves it unchanged, unlike Class IA drugs which prolong it. **High-Yield NEET-PG Pearls:** * **Class IA Mnemonic:** "**P**olice **D**epartment **Q**uarters" (**P**rocainamide, **D**isopyramide, **Q**uinidine). * **Quinidine Side Effects:** Cinchonism (tinnitus, headache), thrombocytopenia, and *Torsades de Pointes* (due to QT prolongation). * **Drug Interaction:** Quinidine increases plasma levels of **Digoxin** by displacing it from tissue binding sites and reducing renal clearance.

Question 1

A patient has been taking digoxin for several years and is about to receive atropine for some other indication. A common side effect of digoxin that can be blocked by atropine is:

Accepted Answer

Increased PR interval on the ECG

Answer

Decreased appetite

Answer

Increased cardiac contractility

Answer

Tachycardia

Question 2

Which of the following drugs does not increase the QT interval?

Accepted Answer

Digitalis

Answer

Amiodarone

Answer

Quinidine

Answer

Amitriptyline

Question 3

A hypertensive patient is taking tablet atenolol 200 mg/day in divided doses. After anesthesia, their heart rate fell from 50 beats/min to 40 beats/min. What is the appropriate treatment to improve the heart rate?

Accepted Answer

IV atropine

Answer

IV adrenaline

Answer

IV isoprenaline

Answer

Dobutamine infusion intravenously

Question 4

Lignocaine is used in which of the following conditions?

Accepted Answer

Ventricular tachycardia

Answer

Atrial fibrillation

Answer

Atrial flutter

Answer

PSVT

Question 5

All of the following are true about digoxin except:

Accepted Answer

It is 95% plasma protein bound

Answer

Causes bradycardia due to increased vagal tone

Answer

Acts by inhibiting Na+K+ ATPase in myocardial fibres

Answer

Primarily excreted unchanged by glomerular filtration

Question 6

Which antiarrhythmic drug is known to cause hypothyroidism?

Accepted Answer

Amiodarone

Answer

Amrinone

Answer

Digoxin

Answer

Procainamide

Question 7

A 45-year-old female patient with essential hypertension was started on ramipril, furosemide, and aspirin. Two weeks later, she presented with well-controlled blood pressure but developed a persistent dry cough. Which alteration should be made to manage her cough without affecting her controlled blood pressure?

Accepted Answer

Replace ramipril with other angiotensin receptor blockers like valsartan.

Answer

Replace aspirin with clopidogrel.

Answer

Replace all drugs with beta blockers.

Answer

Replace furosemide with other diuretics.

Question 8

What is the drug of choice for ventricular tachycardia in a patient with myocardial ischemia?

Accepted Answer

Lignocaine

Answer

Propranolol

Answer

Diltiazem

Answer

Digoxin

Question 9

Alpha-methyldopa is primarily used for which of the following conditions?

Accepted Answer

Pregnancy-induced hypertension

Answer

Renovascular hypertension

Answer

First-line agent in hypertension

Answer

Refractory hypertension

Question 10

Which antiarrhythmic drug decreases both the rate of depolarization (phase 0) and the rate of repolarization of myocardial fibres?

Accepted Answer

Quinidine

Answer

Verapamil

Answer

Propranolol

Answer

Lignocaine

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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