Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 361: Which of the following is associated with a systolic murmur?

A. Ejection click (Correct Answer)
B. Opening snap
C. S4
D. Pericardial knock

Explanation: **Explanation:** The correct answer is **A. Ejection click**. **Understanding the Concept:** Systolic murmurs and associated sounds occur between the first heart sound (S1) and the second heart sound (S2). An **ejection click** is a high-pitched, sharp sound that occurs in early systole, shortly after S1 [1]. It is caused by the sudden opening of a stenotic but mobile semilunar valve (Aortic or Pulmonary stenosis) or the rapid distension of a dilated great vessel (Aorta or Pulmonary artery) [1]. Because it occurs during the ventricular ejection phase, it is inherently a systolic event [3]. **Analysis of Incorrect Options:** * **B. Opening Snap:** This is a high-pitched sound heard in early **diastole**, typically associated with Mitral Stenosis [1]. It occurs due to the sudden opening of a thickened mitral valve. * **C. S4 (Fourth Heart Sound):** This is a low-pitched sound occurring in **late diastole** (presystole). It is caused by atrial contraction against a stiff, non-compliant ventricle (e.g., in LV hypertrophy). * **D. Pericardial Knock:** This is a high-pitched sound heard in early **diastole**, characteristic of Constrictive Pericarditis. It occurs when rapid ventricular filling is suddenly halted by a rigid pericardium. **NEET-PG High-Yield Pearls:** * **Aortic Ejection Clicks:** Best heard at the apex; they do not vary with respiration [1]. * **Pulmonary Ejection Clicks:** Best heard at the left upper sternal border; they are the **only** right-sided sound that **decreases** in intensity during inspiration. * **Midsystolic Clicks:** Associated with Mitral Valve Prolapse (MVP), often followed by a late systolic murmur [1]. * **Rule of Thumb:** If a sound occurs after S2 but before S1, it is diastolic. If it occurs after S1 but before S2, it is systolic [2].

Question 362: In stable angina, what is the typical finding regarding cardiac markers?

A. CK-MB is elevated
B. Troponin I is elevated
C. Myoglobin is elevated
D. The levels of cardiac markers remain unchanged (Correct Answer)

Explanation: The hallmark of **Stable Angina Pectoris** is reversible myocardial ischemia [1]. This occurs when myocardial oxygen demand exceeds supply (usually due to a fixed atherosclerotic plaque), but the stress is insufficient to cause permanent cell death [2]. **Why the correct answer is right:** Cardiac markers (Troponin I/T, CK-MB, Myoglobin) are intracellular proteins released into the bloodstream only when there is **irreversible myocardial necrosis** (cell death) [3]. In stable angina, the ischemia is transient and does not result in the rupture of the myocyte membrane. Therefore, cardiac biomarkers remain within the normal reference range. **Why the incorrect options are wrong:** * **Options A, B, and C:** Elevation of CK-MB, Troponin I, or Myoglobin indicates **Acute Myocardial Infarction (AMI)**. * **Troponins** are the most sensitive and specific markers for necrosis [3]. * **CK-MB** is useful for detecting re-infarction due to its shorter half-life [3]. * **Myoglobin** is the earliest marker to rise but lacks cardiac specificity. If these markers were elevated in a patient with chest pain at rest, the diagnosis would shift to NSTEMI or STEMI [3]. **NEET-PG High-Yield Pearls:** * **Stable Angina:** Chest pain brought on by exertion, relieved by rest or nitroglycerin, lasting <20 minutes, with a **normal** EKG (at rest) and **normal** biomarkers [1]. * **Unstable Angina:** Characterized by increased frequency/severity or pain at rest, but crucially, **biomarkers remain negative** [3]. * **NSTEMI vs. Unstable Angina:** The differentiating factor is the elevation of cardiac troponins in NSTEMI [3]. * **Gold Standard:** Coronary Angiography remains the definitive investigation to assess the extent of CAD.

Question 363: A patient suffering from atherosclerosis. Which of the following is the most beneficial drug for prevention of stroke in this patient?

A. Aspirin (Correct Answer)
B. Warfarin
C. Low dose subcutaneous heparin
D. Digoxin

Explanation: ### Explanation **Correct Answer: A. Aspirin** **Why Aspirin is the Correct Choice:** Atherosclerosis is a chronic inflammatory process characterized by the formation of fibro-fatty plaques. The primary mechanism behind acute ischemic events (like stroke or myocardial infarction) in these patients is **plaque rupture**, which leads to platelet adhesion, activation, and aggregation. **Aspirin** is an antiplatelet agent that irreversibly inhibits the enzyme **Cyclooxygenase-1 (COX-1)**, thereby blocking the synthesis of Thromboxane A2 (a potent platelet aggregator) [1]. In patients with established atherosclerosis, low-dose aspirin is the gold standard for the secondary prevention of thromboembolic strokes [2] by preventing the formation of white thrombi at the site of arterial injury. **Why Other Options are Incorrect:** * **B. Warfarin:** This is an oral anticoagulant that inhibits Vitamin K-dependent clotting factors. It is primarily used for preventing embolic strokes in patients with **Atrial Fibrillation** or prosthetic heart valves, but it is not the first-line choice for preventing strokes caused specifically by atherosclerosis. * **C. Low dose subcutaneous heparin:** This is typically used for the prophylaxis of **Deep Vein Thrombosis (DVT)** and pulmonary embolism in hospitalized or immobilized patients. It does not provide long-term secondary prevention for arterial stroke. * **D. Digoxin:** This is a cardiac glycoside used in the management of heart failure and rate control in atrial fibrillation. It has no antiplatelet or anticoagulant properties and does not prevent stroke. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Prevention:** Aspirin is no longer routinely recommended for primary prevention in elderly patients without established CVD due to bleeding risks. * **Secondary Prevention:** For non-cardioembolic ischemic stroke, antiplatelets (Aspirin, Clopidogrel) are superior to anticoagulants [3]. * **Dual Antiplatelet Therapy (DAPT):** Aspirin + Clopidogrel is often used for a short duration (21–90 days) following a Minor Stroke or TIA to further reduce recurrence risk.

Question 364: Which of the following statements regarding cardiac tamponade is true?

A. Kussmaul sign is positive
B. Enlargement of the cardiac silhouette is present (Correct Answer)
C. Prominent y descent is observed
D. Electrical alternans is seen

Explanation: **Explanation:** Cardiac tamponade occurs when fluid accumulation in the pericardial space increases intrapericardial pressure, leading to impaired diastolic filling and reduced cardiac output [1]. **Why Option B is Correct:** In cardiac tamponade, the pericardial sac expands to accommodate the fluid. On a chest X-ray, this manifests as an **enlargement of the cardiac silhouette**, often described as a **"Water-bottle heart"** or "Money-bag" appearance [1]. This is a classic radiological finding, though it requires at least 200ml of fluid to be visible. **Analysis of Incorrect Options:** * **A. Kussmaul sign:** This is a paradoxical rise in JVP during inspiration. It is a hallmark of **Constrictive Pericarditis**, not tamponade [2]. In tamponade, the rigid pericardium is absent, allowing the negative intrathoracic pressure to still be transmitted to the heart. * **C. Prominent y descent:** In tamponade, the high intrapericardial pressure prevents rapid ventricular filling during early diastole. Therefore, the **y descent is characteristically absent or blunted**. A prominent y descent is seen in Constrictive Pericarditis (Friedreich’s sign) [2]. * **D. Electrical alternans:** While this is a specific sign of tamponade (caused by the heart swinging in fluid), it is **not always present** [1]. It is a late finding and less common than silhouette enlargement. (Note: In some exam contexts, this is a "distractor" because while true, B is the more fundamental physiological/radiological expectation). **NEET-PG High-Yield Pearls:** * **Beck’s Triad:** Hypotension, JVP distension, and muffled heart sounds. * **Pulsus Paradoxus:** A drop in systolic BP >10 mmHg during inspiration (most sensitive physical sign). * **ECG:** Low voltage complexes and electrical alternans [1]. * **Treatment:** Immediate ultrasound-guided pericardiocentesis [1].

Question 365: Osler's nodes are typically seen in which one of the following conditions?

A. Chronic candida endocarditis
B. Acute staphylococcal endocarditis (Correct Answer)
C. Pseudomonas endocarditis
D. Libman-Sacks endocarditis

Explanation: **Explanation:** **Osler’s nodes** are painful, erythematous, pea-sized nodules typically found on the pads of the fingers and toes. Pathophysiologically, they represent **immune complex deposition** (Type III hypersensitivity) in the dermal vessels, leading to localized vasculitis [1]. 1. **Why Option B is Correct:** While Osler’s nodes were historically associated with subacute bacterial endocarditis (SBE), they are frequently seen in **Acute Infective Endocarditis (IE)** caused by *Staphylococcus aureus*. In the context of this question, *S. aureus* is the most common cause of acute IE, and the rapid immune response can trigger these peripheral stigmata. 2. **Why Other Options are Incorrect:** * **Options A & C:** While fungal (Candida) and Gram-negative (Pseudomonas) endocarditis can cause peripheral emboli, they are less classically associated with the specific immunological phenomenon of Osler’s nodes compared to staphylococcal or streptococcal infections. * **Option D:** Libman-Sacks endocarditis is a non-bacterial verrucous endocarditis seen in **Systemic Lupus Erythematosus (SLE)**. It typically presents with sterile vegetations and lacks the embolic/immunological skin manifestations seen in infective endocarditis. **High-Yield Clinical Pearls for NEET-PG:** * **Osler’s Nodes vs. Janeway Lesions:** * **O**sler’s = **O**uch (Painful), Immunological. * **J**aneway = **J**ust fine (Painless), Microabscesses/Embolic. * **Roth Spots:** Retinal hemorrhages with central clearing (pale centers), also an immunological phenomenon of IE. * **Duke’s Criteria:** Remember that these peripheral stigmata (Osler’s nodes, Roth spots, Rheumatoid factor) fall under the **Minor Criteria** for the diagnosis of IE.

Question 366: All of the following heart sounds occur shortly after S2, except?

A. Opening snap
B. Pericardial knock
C. Ejection click (Correct Answer)
D. Tumor plop

Explanation: ### Explanation The cardiac cycle is divided into systole and diastole. **S2 (Second Heart Sound)** marks the end of ventricular systole and the beginning of diastole [2]. Therefore, sounds occurring "shortly after S2" are **early diastolic sounds**. **Why Ejection Click is the Correct Answer:** An **Ejection Click** is a high-pitched **systolic** sound [1]. It occurs shortly after **S1** (not S2), during the early phase of ventricular ejection. It is caused by the abrupt opening of semilunar valves (Aortic or Pulmonary) or the sudden distension of the great vessels [1]. Since it occurs during systole, it cannot occur after S2. **Analysis of Other Options (Diastolic Sounds):** * **Opening Snap:** Occurs in early diastole due to the forceful opening of a stenotic but mobile Mitral valve (Mitral Stenosis) [1]. It follows S2 after a short interval (S2-OS interval) [1]. * **Pericardial Knock:** A high-pitched sound heard in early diastole in patients with **Constrictive Pericarditis**. It occurs due to the sudden cessation of ventricular filling by a rigid pericardium. * **Tumor Plop:** A sound heard in early-to-mid diastole as an **Atrial Myxoma** (usually left atrial) drops into the mitral orifice during ventricular filling. **Clinical Pearls for NEET-PG:** 1. **S2-OS Interval:** The shorter the interval between S2 and the Opening Snap, the more severe the Mitral Stenosis [1]. 2. **Ejection Click vs. Non-Ejection Click:** Ejection clicks (Aortic/Pulmonary stenosis) occur early in systole; Non-ejection clicks (Mitral Valve Prolapse) occur in mid-to-late systole [1]. 3. **High-Yield Sequence:** The chronological order of diastolic sounds after S2 is: **Opening Snap → Pericardial Knock → S3 → Tumor Plop → S4.**

Question 367: All of the following murmurs may be heard in patients with aortic regurgitation except?

A. High-pitched decrescendo diastolic murmur
B. Soft, low pitched mid diastolic rumbling murmur
C. Mid-systolic ejection flow murmur
D. Pansystolic murmur (Correct Answer)

Explanation: **Explanation** In Aortic Regurgitation (AR), the primary pathology is the backflow of blood from the aorta into the left ventricle (LV) during diastole [1]. This hemodynamic change accounts for three distinct murmurs, while a **pansystolic murmur** is characteristic of AV valve regurgitation (MR/TR) or a VSD, not AR [2]. **Why Option D is correct:** A **pansystolic (holosystolic) murmur** occurs when there is a pressure gradient between two chambers throughout the entirety of systole [2]. In AR, the pathology is diastolic. Therefore, a pansystolic murmur is not a feature of isolated aortic regurgitation. **Why the other options are incorrect:** * **Option A (High-pitched decrescendo diastolic murmur):** This is the **classic murmur** of AR [1]. It is heard best at the left sternal border (Erb’s point) with the patient leaning forward in expiration. It results from the high-pressure regurgitant flow from the aorta to the LV. * **Option B (Austin Flint Murmur):** This is a soft, low-pitched mid-diastolic rumble heard at the apex [1]. It occurs because the regurgitant AR jet displaces the anterior leaflet of the mitral valve, creating "functional" mitral stenosis [1]. * **Option C (Mid-systolic ejection flow murmur):** Patients with chronic AR have a massive stroke volume (due to the combined volume of normal venous return + regurgitant blood). This increased flow across the aortic valve during systole creates a functional flow murmur, even in the absence of true stenosis [1]. **NEET-PG High-Yield Pearls:** * **Severity Marker:** The duration of the decrescendo diastolic murmur correlates better with severity than its intensity. * **Austin Flint vs. Mitral Stenosis:** Austin Flint lacks an opening snap and loud S1. * **Wide Pulse Pressure:** AR is associated with numerous peripheral signs (e.g., Corrigan’s pulse, Quincke’s sign, de Musset’s sign) due to the hyperdynamic circulation.

Question 368: Hepatomegaly with liver pulsation indicates:

A. Tricuspid Regurgitation (Correct Answer)
B. Mitral Regurgitation
C. Pulmonary Hypertension
D. Mitral Stenosis

Explanation: **Explanation:** **Tricuspid Regurgitation (TR)** is the correct answer because of the direct anatomical and hemodynamic relationship between the right atrium and the liver via the inferior vena cava (IVC). In TR, the incompetent tricuspid valve allows blood to backflow from the right ventricle into the right atrium during ventricular systole. Since there are no valves between the right atrium and the IVC, this high-pressure systolic surge is transmitted directly to the hepatic veins, causing the liver to expand and pulsate [2]. This is known as **systolic liver pulsation** (Dressler’s sign). **Why other options are incorrect:** * **Mitral Regurgitation (MR) & Mitral Stenosis (MS):** These are left-sided heart lesions. While they can eventually lead to right heart failure and congestive hepatomegaly, the liver enlargement is typically firm and non-pulsatile because the pressure is buffered by the pulmonary circulation [1]. * **Pulmonary Hypertension:** This leads to right heart failure and passive hepatic congestion (congestive hepatomegaly), but without significant TR, there is no systolic retrograde flow to cause active pulsations. **NEET-PG High-Yield Pearls:** * **JVP Finding:** TR is classically associated with a **prominent 'v' wave** and a steep 'y' descent in the Jugular Venous Pulse [2]. * **Murmur:** TR presents as a pansystolic murmur at the left lower sternal border that **increases with inspiration** (Carvallo’s sign) [2]. * **Clinical Triad of Severe TR:** Pulsatile liver, prominent 'v' waves in JVP, and a pansystolic murmur [2]. * **Other causes of pulsatile liver:** Constrictive pericarditis and Tricuspid Stenosis (though these typically cause *presystolic* pulsations due to a prominent 'a' wave) [2].

Question 369: Which of the following is not a clinical sign associated with mitral stenosis?

A. Malar flush
B. Atrial fibrillation
C. Pan-systolic murmur which radiates to axilla (Correct Answer)
D. Tapping, undisplaced apex beat

Explanation: **Explanation:** The correct answer is **C. Pan-systolic murmur which radiates to axilla**. This murmur is the hallmark of **Mitral Regurgitation (MR)**, not Mitral Stenosis (MS) [2]. In MR, blood flows back from the high-pressure left ventricle into the low-pressure left atrium during systole, creating a high-pitched blowing murmur [2]. **Analysis of Options:** * **Malar Flush (Option A):** This is a classic sign of severe MS. It presents as plum-colored patches over the cheeks due to low cardiac output and systemic vasoconstriction leading to facial capillary congestion [1]. * **Atrial Fibrillation (Option B):** MS causes significant left atrial (LA) enlargement and pressure overload. This stretches the atrial fibers, leading to electrical remodeling and a very high incidence of AFib [1]. * **Tapping, Undisplaced Apex Beat (Option D):** In MS, the apex beat is "tapping" in character, which is actually a palpable loud first heart sound (S1) [1]. It remains **undisplaced** because MS is a pressure-loading lesion for the LA; the left ventricle remains normal-sized or even small. A displaced apex indicates ventricular enlargement (e.g., MR or AR). **NEET-PG High-Yield Pearls for Mitral Stenosis:** * **Auscultation:** Characterized by a loud S1, an **Opening Snap (OS)**, and a **mid-diastolic rumbling murmur** heard best at the apex in the left lateral position [1], [3]. * **Severity Marker:** The shorter the **A2-OS interval**, the more severe the stenosis (reflecting higher LA pressure) [3]. * **Graham Steell Murmur:** An early diastolic decrescendo murmur of pulmonary regurgitation seen in MS patients with secondary pulmonary hypertension [1]. * **Most common cause:** Rheumatic Heart Disease.

Question 370: What is the most common cause of recurrent syncope?

A. Carotid sinus hypersensitivity
B. Carotid artery stenosis
C. Embolus
D. Neurocardiogenic (Correct Answer)

Explanation: **Explanation:** **Neurocardiogenic syncope**, also known as vasovagal syncope or "the common faint," is the most frequent cause of syncope across all age groups, accounting for nearly 50% of cases [1]. It is a type of reflex syncope mediated by a sudden failure of the autonomic nervous system to maintain blood pressure, leading to transient cerebral hypoperfusion [2]. The pathophysiology typically involves the **Bezold-Jarisch reflex**, where vigorous ventricular contraction in a volume-depleted heart triggers mechanoreceptors, leading to paradoxical bradycardia (parasympathetic) and peripheral vasodilation (sympathetic withdrawal) [1]. **Analysis of Incorrect Options:** * **Carotid sinus hypersensitivity (A):** While a form of reflex syncope, it is much less common than neurocardiogenic syncope and typically occurs in elderly males during activities like shaving or wearing tight collars [1]. * **Carotid artery stenosis (B):** This is a common misconception. Carotid stenosis causes focal neurological deficits (Stroke/TIA) rather than global cerebral hypoperfusion (syncope). * **Embolus (C):** Pulmonary embolism can cause syncope, but it is usually an acute, life-threatening event rather than a cause of "recurrent" syncope. **High-Yield Clinical Pearls for NEET-PG:** * **Prodrome:** Neurocardiogenic syncope is classically preceded by a prodrome of nausea, pallor, diaphoresis, and "tunnel vision" [2]. * **Gold Standard Test:** The **Head-up Tilt Table Test (HUTT)** is used to confirm the diagnosis in recurrent or high-risk cases. * **Management:** Reassurance, physical counter-pressure maneuvers (leg crossing, handgrip), and increased fluid/salt intake are first-line treatments. Midodrine or Fludrocortisone may be used in refractory cases.

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Cardiology — MCQs

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