Cardiology Practice Questions

Q: What is the first-line drug of choice for acute pulmonary edema?

Furosemide. **Explanation:** **Furosemide (Option A)** is the first-line drug of choice for acute pulmonary edema because it addresses the primary pathology: fluid overload and increased pulmonary capillary wedge pressure. It works via a dual mechanism [1]: 1. **Immediate Venodilation:** Within 5–15 minutes of IV administration, it increases venous capacitance, reducing preload and shifting fluid away from the lungs [2]. 2. **Diuresis:** It inhibits the Na-K-2Cl symporter in the thick ascending limb of the Loop of Henle, promoting the excretion of excess fluid [1]. **Analysis of Incorrect Options:** * **Morphine (Option B):** Previously a mainstay for its venodilatory and anxiolytic effects, it is no longer first-line. Recent guidelines (ESC/AHA) caution against its routine use as it is associated with increased rates of mechanical ventilation and ICU admissions. * **Aminophylline (Option C):** A phosphodiesterase inhibitor used historically for "cardiac asthma" to relieve bronchospasm. It is rarely used today due to its narrow therapeutic index and pro-arrhythmic potential. * **Oxygen (Option D):** While essential for patients with hypoxemia ($SpO_2 < 90\%$), it is a supportive measure rather than a definitive pharmacological treatment to resolve the underlying edema. **High-Yield Clinical Pearls for NEET-PG:** * **L-M-N-O-P Mnemonic:** The classic management sequence is **L**asix (Furosemide), **M**orphine (selective use), **N**itrates (to reduce preload/afterload), **O**xygen, and **P**ositioning (propped up). * **Nitroglycerin:** If the patient is hypertensive, IV Nitroglycerin is often the most effective co-intervention alongside Furosemide [2]. * **Nesiritide:** A recombinant B-type natriuretic peptide (BNP) that can be used in refractory cases for its vasodilatory and natriuretic effects [1].

Q: What is true about the third heart sound (S3)?

Heard in mitral regurgitation. **Explanation:** The **third heart sound (S3)**, also known as a ventricular gallop, occurs during the **early phase of diastole** (rapid ventricular filling phase) [2]. It is caused by the sudden deceleration of blood flow into a dilated or non-compliant left ventricle. **1. Why Option A is Correct:** In **Mitral Regurgitation (MR)**, there is a volume overload of the left ventricle. During diastole, the ventricle receives both the normal venous return and the regurgitated volume from the previous systole. This massive influx of blood into a dilated ventricle creates the S3 [4]. It is a hallmark of volume overload states and heart failure. **2. Why the Other Options are Incorrect:** * **Option B:** S3 is a **diastolic sound**, occurring just after S2. Systolic sounds include S1 and ejection clicks [3]. * **Option C:** S3 is a **low-pitched sound** (thud-like) [1]. It is best heard with the **bell** of the stethoscope at the apex in the left lateral decubitus position [1]. High-pitched sounds (like S1, S2, or MR murmurs) are heard better with the diaphragm. * **Option D:** While S3 can be physiological in children, young adults (<40 years), and pregnant women, it is **pathological in older adults**, where it usually signifies congestive heart failure (CHF). **Clinical Pearls for NEET-PG:** * **S3 Sequence:** S1–S2–S3 (resembles the cadence of the word "Kentucky"). * **Most Common Cause:** Left ventricular failure (decreased EF). * **Differential Diagnosis:** S3 is also seen in high-output states like anemia, thyrotoxicosis, and pregnancy. * **S4 vs. S3:** S4 (atrial gallop) occurs in late diastole and is associated with **pressure overload** (e.g., Hypertension, Aortic Stenosis) and stiff ventricles.

Q: What is the treatment for orthostatic hypotension?

Fludrocortisone. **Explanation:** Orthostatic hypotension (OH) is defined as a sustained reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within 3 minutes of standing [1]. The primary goal of treatment is to increase intravascular volume and peripheral vascular resistance. **Why Fludrocortisone is correct:** **Fludrocortisone** is a potent synthetic mineralocorticoid and the first-line pharmacological treatment for symptomatic OH [2]. It works by promoting renal sodium reabsorption, thereby expanding the extracellular fluid volume and increasing the sensitivity of alpha-adrenergic receptors to circulating catecholamines, which enhances vasoconstriction. **Why the other options are incorrect:** * **Dopamine (A):** This is an intravenous inotrope/vasopressor used in acute shock or critical care settings. It is not practical or indicated for the chronic management of orthostatic hypotension. * **Diuretics (B):** These agents (e.g., Furosemide) promote fluid loss and decrease blood volume, which would significantly worsen orthostatic hypotension [3]. * **Calcium Channel Blockers (D):** These drugs (e.g., Amlodipine) cause peripheral vasodilation and are used to treat hypertension; they would exacerbate the drop in blood pressure upon standing. **High-Yield Clinical Pearls for NEET-PG:** * **Non-pharmacological measures:** Always the first step (e.g., increasing salt/water intake [2], using compression stockings, and avoiding sudden postural changes). * **Midodrine:** An alpha-1 agonist often used as a second-line agent or in combination with fludrocortisone. * **Droxidopa:** A precursor of norepinephrine used specifically in neurogenic orthostatic hypotension (e.g., Parkinson’s, MSA). * **Side effect alert:** Monitor for hypokalemia and supine hypertension when using Fludrocortisone.

Q: Dressler's syndrome is due to:

Myocardial infarction. **Explanation:** **Dressler’s Syndrome** (also known as post-myocardial infarction syndrome) is a form of secondary **pericarditis** that occurs as a late complication following a **Myocardial Infarction (MI)**. 1. **Why Myocardial Infarction is correct:** The underlying mechanism is an **immune-mediated (Type III hypersensitivity)** response. Following an MI, cardiac antigens are released into the circulation due to myocardial necrosis. The body forms anti-myocardial antibodies, leading to an inflammatory reaction involving the pericardium, pleura, and sometimes the lungs. It typically presents **2 to 6 weeks** after the acute event with fever, pleuritic chest pain, and pericardial effusion. 2. **Why the other options are incorrect:** * **Cor pulmonale:** This refers to right-sided heart failure due to chronic lung disease (e.g., COPD). It does not trigger the specific autoimmune pericarditis seen in Dressler’s. * **Mitral stenosis:** This is a valvular heart disease. While it leads to left atrial enlargement and pulmonary congestion, it is not an inflammatory or necrotic trigger for post-cardiac injury syndrome. * **Pulmonary embolism:** While PE can cause pleuritic chest pain and pleural effusion, it does not cause the systemic autoimmune pericarditis characteristic of Dressler’s syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Timeline:** Unlike "Early Post-infarction Pericarditis" (which occurs within 1–3 days due to direct inflammation), Dressler’s is a **late** complication (weeks later). * **Triad:** Fever, pleurisy, and pericardial effusion. * **Treatment:** The mainstay of treatment is **Aspirin** or **NSAIDs** plus **Colchicine**. Steroids are reserved for refractory cases [1]. * **ECG Finding:** Diffuse ST-segment elevation with PR-segment depression (typical of pericarditis) [1].

Q: What is the initial pharmacological treatment for sinus bradycardia in the context of myocardial infarction?

Atropine. **Explanation:** **Why Atropine is the Correct Answer:** Sinus bradycardia is common in the early stages of acute myocardial infarction (MI), particularly in **inferior wall MI**, due to increased vagal tone or ischemia of the SA node. [3] **Atropine** is the first-line pharmacological treatment because it is a competitive antagonist of acetylcholine at muscarinic receptors. By blocking vagal inhibition, it increases the heart rate and improves cardiac output. It is indicated if the bradycardia is symptomatic (e.g., hypotension, altered mental status, or ischemic chest pain). [3] **Why the Other Options are Incorrect:** * **B. Digoxin:** This is a positive inotrope but a negative chronotrope. It increases vagal tone and slows the heart rate, which would worsen bradycardia. * **C. Calcium Channel Blockers (e.g., Verapamil, Diltiazem):** These agents have negative chronotropic and dromotropic effects. They are contraindicated in bradycardia as they further suppress the SA and AV nodes. [1] * **D. Propranolol:** This is a non-selective beta-blocker. [2] Beta-blockers decrease the heart rate and are contraindicated in the acute phase of MI if the patient is already bradycardic or has heart block. [1] **Clinical Pearls for NEET-PG:** * **Drug of Choice:** Atropine (0.5 mg IV, repeatable up to 3 mg) is the initial drug for symptomatic bradycardia. [3] * **Inferior Wall MI Connection:** Sinus bradycardia is most frequently associated with Inferior MI (Right Coronary Artery occlusion) due to the **Bezold-Jarisch reflex**. [3] * **Next Step:** If Atropine fails, the next steps include transcutaneous pacing or infusions of Dopamine or Epinephrine. [3] * **Caution:** Use Atropine cautiously in MI; excessive increases in heart rate can increase myocardial oxygen demand and worsen ischemia.

Q: A 73-year-old woman has had episodes of chest pain during the past week. She is afebrile. Her pulse is 80/min, respirations are 16/min, and blood pressure is 110/70 mm Hg. On auscultation of the chest, heart sounds seem distant, but the lung fields are clear. Neck veins are distended to the angle of the jaw, even while sitting. There is a darkly pigmented, irregular, 1.2-cm skin lesion on the right shoulder. A chest radiograph shows prominent borders on the left and right sides of the heart. Pericardiocentesis yields bloody fluid. Laboratory findings include a serum troponin I level of 0.3 ng/mL. Which of the following lesions is the most likely cause of these findings?

Epicardial metastases. **Explanation:** The clinical presentation describes **Beck’s Triad** (distended neck veins, distant heart sounds, and hypotension/narrow pulse pressure), which is pathognomonic for **Cardiac Tamponade** [1]. The chest radiograph showing "prominent borders" (globular heart) and the aspiration of **bloody pericardial fluid** further confirm a hemorrhagic pericardial effusion [1]. The key diagnostic clue is the **darkly pigmented, irregular skin lesion**, which is highly suggestive of **Malignant Melanoma**. Melanoma is notorious for metastasizing to the heart (epicardium/myocardium) [1]. These metastases can cause hemorrhagic effusions and subsequent tamponade [1]. While the troponin is slightly elevated (0.3 ng/mL), this reflects myocardial irritation or direct invasion by the tumor rather than a primary ischemic event. **Analysis of Incorrect Options:** * **A & D (Calcific Aortic Stenosis / Mitral Valvulitis):** These are valvular pathologies. While they cause heart failure or murmurs, they do not typically cause hemorrhagic pericardial effusions or sudden tamponade. * **B (Coronary Atherosclerosis):** While a myocardial infarction (MI) can lead to free wall rupture and hemopericardium [1], this usually occurs 3–7 days post-MI and presents with acute, catastrophic collapse. The presence of a suspicious skin lesion and a week-long history makes malignancy a more likely etiology. **NEET-PG High-Yield Pearls:** * **Most common primary tumor of the heart:** Myxoma (usually left atrium). * **Most common secondary (metastatic) tumor of the heart:** Lung cancer, Breast cancer, and Melanoma. * **Hemorrhagic Pericardial Effusion:** Think of Malignancy [1], Tuberculosis [2], or Uremia. * **Beck’s Triad:** Hypotension, JVD, and Muffled heart sounds (Cardiac Tamponade).

Q: A 45-year-old man presents with central chest pain for 4 hours. Troponin I is 0.8 ng/dL. What is the diagnosis?

Anterior wall, NSTEMI. ***Anterior wall, NSTEMI*** - **Elevated troponin I (0.8 ng/dL)** indicates myocardial necrosis, confirming myocardial infarction rather than unstable angina. - **Anterior wall localization** suggests involvement of **LAD territory** with likely **ST depression or T-wave inversions in V1-V4** without ST elevation, characteristic of NSTEMI. *Anterior wall, STEMI* - Would require **ST elevation ≥1mm in V1-V4** on ECG, which is not mentioned in this case. - **Troponin elevation** alone without ST elevation cannot diagnose STEMI. *Unstable Angina* - Characterized by **normal cardiac biomarkers** including troponin levels within normal range. - **Elevated troponin I (0.8 ng/dL)** definitively rules out unstable angina and confirms myocardial infarction. *Prinzmetal angina* - Caused by **coronary artery vasospasm** typically occurring at rest, often with **transient ST elevation**. - **Troponin levels remain normal** as there is no myocardial necrosis in typical vasospastic episodes.

Question 1

What is the first-line drug of choice for acute pulmonary edema?

Accepted Answer

Furosemide

Answer

Morphine

Answer

Aminophylline

Answer

Oxygen

Question 2

Which of the following is an absolute contraindication for exercise testing?

Accepted Answer

Aortic stenosis

Answer

Peripheral vascular disease

Answer

Unstable angina

Answer

One week post-myocardial infarction

Question 3

What is true about the third heart sound (S3)?

Accepted Answer

Heard in mitral regurgitation

Answer

A systolic sound

Answer

A high-pitched sound

Answer

Normal in adults

Question 4

What is the treatment for orthostatic hypotension?

Accepted Answer

Fludrocortisone

Answer

Dopamine

Answer

Diuretics

Answer

Calcium channel blockers

Question 5

Dressler's syndrome is due to:

Accepted Answer

Myocardial infarction

Answer

Cor pulmonale

Answer

Mitral stenosis

Answer

Pulmonary embolism

Question 6

What is the initial pharmacological treatment for sinus bradycardia in the context of myocardial infarction?

Accepted Answer

Atropine

Answer

Digoxin

Answer

Calcium channel blocker

Answer

Propranolol

Question 7

A 73-year-old woman has had episodes of chest pain during the past week. She is afebrile. Her pulse is 80/min, respirations are 16/min, and blood pressure is 110/70 mm Hg. On auscultation of the chest, heart sounds seem distant, but the lung fields are clear. Neck veins are distended to the angle of the jaw, even while sitting. There is a darkly pigmented, irregular, 1.2-cm skin lesion on the right shoulder. A chest radiograph shows prominent borders on the left and right sides of the heart. Pericardiocentesis yields bloody fluid. Laboratory findings include a serum troponin I level of 0.3 ng/mL. Which of the following lesions is the most likely cause of these findings?

Accepted Answer

Epicardial metastases

Answer

Calcific aortic stenosis

Answer

Coronary atherosclerosis

Answer

Mitral valvulitis

Question 8

Which of the following statements is TRUE in diastolic dysfunction of the left ventricle?

Accepted Answer

Tachycardia will improve the symptoms

Answer

It presents as dyspnea on exertion

Answer

Uncontrolled hypertension is an important cause

Answer

Ischemic heart disease is a cause

Question 9

A 45-year-old man presents with central chest pain for 4 hours. Troponin I is 0.8 ng/dL. What is the diagnosis?

Accepted Answer

Anterior wall, NSTEMI

Answer

Anterior wall, STEMI

Answer

Unstable Angina

Answer

Prinzmetal angina

Question 10

All of the following are true about Atrial Fibrillation, except?

Accepted Answer

Anticoagulation is not required

Answer

Increased risk of thromboembolism

Answer

Digoxin is used for treatment

Answer

Aspirin is given

Cardiology — MCQs

Cardiology — MCQs

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