Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 321: Fixed and wide splitting of the second heart sound is characteristic of which of the following conditions?

A. Ventricular Septal Defect (VSD)
B. Atrial Septal Defect (ASD) (Correct Answer)
C. Patent Ductus Arteriosus (PDA)
D. Tetralogy of Fallot

Explanation: ### Explanation **Correct Option: B. Atrial Septal Defect (ASD)** The second heart sound (S2) consists of two components: A2 (Aortic) and P2 (Pulmonary). In a normal heart, inspiration increases venous return to the right heart, delaying P2 and causing a "physiological split." In **Atrial Septal Defect (ASD)**, the splitting is: 1. **Wide:** Due to a chronic volume overload of the right ventricle (RV), it takes longer for the RV to eject its blood, leading to a delayed P2 [1]. 2. **Fixed:** This is the hallmark. In ASD, the respiratory variations in venous return are balanced by the left-to-right shunt across the defect [1]. During inspiration, the shunt decreases as systemic venous return increases; during expiration, the shunt increases. This keeps the RV stroke volume constant throughout the respiratory cycle, resulting in a split that does not change with breathing. **Analysis of Incorrect Options:** * **A. Ventricular Septal Defect (VSD):** Typically presents with a **pansystolic murmur** [2]. While it may cause a wide split S2 (due to early A2 or delayed P2), the split is **not fixed** and varies with respiration. * **C. Patent Ductus Arteriosus (PDA):** Characterized by a **continuous machinery murmur** [4]. It often results in a "paradoxical split" if the shunt is large enough to delay A2. * **D. Tetralogy of Fallot:** Characterized by a **single S2** because the pulmonary component (P2) is often inaudible due to severe pulmonary stenosis and the anterior displacement of the aorta [3]. **High-Yield NEET-PG Pearls:** * **Fixed Wide Split S2:** Pathognomonic for ASD (specifically Secundum type) [1]. * **Paradoxical Splitting (P2 before A2):** Seen in Left Bundle Branch Block (LBBB) and severe Aortic Stenosis. * **Wide Variable Splitting:** Seen in Right Bundle Branch Block (RBBB) and Pulmonary Stenosis. * The murmur in ASD is actually a **midsystolic flow murmur** over the pulmonary area (due to increased flow across the valve), not the shunt itself.

Question 322: Which of the following is not typically heard in a patient with mitral stenosis?

A. Loud S1
B. Opening snap
C. Mid-diastolic murmur
D. S3 (Correct Answer)

Explanation: In Mitral Stenosis (MS), the mitral valve orifice is narrowed, creating a pressure gradient between the left atrium and left ventricle. [1] **Why S3 is NOT heard in Mitral Stenosis:** The **third heart sound (S3)** is a ventricular filling sound caused by a rapid rush of blood into a compliant, dilated left ventricle (LV). In significant mitral stenosis, the narrowed valve acts as a physical barrier, **preventing rapid ventricular filling**. [3, 5] Therefore, the LV remains "underfilled" and non-dilated. The presence of an S3 effectively rules out significant MS and instead suggests conditions like Mitral Regurgitation or Heart Failure. [4] **Explanation of Incorrect Options:** * **Loud S1:** In early-to-moderate MS, the mitral leaflets are wide apart at the end of diastole due to high atrial pressure. When the ventricle contracts, the leaflets slam shut over a greater distance, creating a loud S1. [1] (Note: S1 becomes soft if the valve is heavily calcified). * **Opening Snap (OS):** This high-pitched sound occurs due to the sudden tensing of the chordae tendineae and stenotic valve leaflets as they "snap" open under high atrial pressure. [1, 2] * **Mid-diastolic Murmur:** This is the hallmark of MS. It is a low-pitched "rumble" heard at the apex, caused by turbulent flow across the narrowed valve. [1, 3] **High-Yield NEET-PG Pearls:** * **Severity Marker:** The shorter the **A2-OS interval**, the more severe the MS (indicating higher left atrial pressure). [2] * **Graham Steell Murmur:** An early diastolic murmur of pulmonary regurgitation heard in MS due to secondary pulmonary hypertension. * **Ortner’s Syndrome:** Hoarseness of voice in MS due to an enlarged left atrium compressing the left recurrent laryngeal nerve.

Question 323: Positive Hepatojugular Reflux is found in all of the following conditions, except?

A. Tricuspid Regurgitation
B. Precapillary Pulmonary Hypertension
C. Right Ventricular Infarction
D. Decreased Afterload (Correct Answer)

Explanation: **Explanation:** The **Hepatojugular Reflux (HJR)**, or more accurately the abdominojugular reflux, is a clinical sign elicited by applying firm pressure over the upper abdomen for 10–30 seconds. A positive result is defined as a sustained rise in Jugular Venous Pressure (JVP) of >3 cm that persists for at least 15 seconds. **Why "Decreased Afterload" is the correct answer:** A positive HJR indicates that the **Right Ventricle (RV) is unable to accommodate increased venous return** (the "preload bolus" pushed from the hepatic sinusoids). **Decreased afterload** (e.g., systemic vasodilation) generally improves cardiac output and reduces the workload on the heart; it does not cause venous congestion or RV failure. Therefore, it would not lead to a positive HJR. **Analysis of Incorrect Options:** * **Tricuspid Regurgitation:** The RV is already volume-overloaded. Added venous return from abdominal compression further increases the pressure, which is transmitted back to the JVP. * **Precapillary Pulmonary Hypertension:** High pulmonary artery pressure increases the **afterload** of the RV. This leads to RV dysfunction [1] and an inability to pump out the extra blood volume during the HJR maneuver. * **Right Ventricular Infarction:** A damaged, non-compliant RV [1] cannot expand or pump effectively to handle the increased venous return, leading to a sustained rise in JVP. **High-Yield NEET-PG Pearls:** * **Most Common Cause:** The most common cause of a positive HJR is **Right Heart Failure** secondary to elevated Pulmonary Capillary Wedge Pressure (Left Heart Failure). * **Constrictive Pericarditis:** HJR is typically **positive** in constrictive pericarditis but **negative** in cardiac tamponade (where the venous return is restricted from entering the heart). * **Clinical Utility:** It is a highly specific sign for identifying a wedge pressure >15 mmHg and helps differentiate hepatic enlargement due to congestion (positive HJR) from primary liver disease (negative HJR).

Question 324: All of the following are considered minor criteria for infective endocarditis EXCEPT?

A. Evidence of endocardial involvement documented by echocardiography (Correct Answer)
B. Janeway lesions
C. Embolic disease
D. Osler's nodes

Explanation: This question tests your knowledge of the **Modified Duke Criteria**, which is the gold standard for diagnosing Infective Endocarditis (IE) [1]. ### **Explanation of the Correct Answer** **Option A (Evidence of endocardial involvement)** is a **Major Criterion**, not a minor one [1]. According to the Modified Duke Criteria, major criteria include: 1. **Positive Blood Cultures:** Typical organisms from two separate cultures [1]. 2. **Evidence of Endocardial Involvement:** Positive echocardiogram showing a vegetation, abscess, or new valvular regurgitation [1]. Since the question asks for the exception among minor criteria, Option A is the correct choice. ### **Analysis of Incorrect Options (Minor Criteria)** The following are all classified as **Minor Criteria**: * **Option B (Janeway lesions):** These are painless, erythematous macules on palms/soles representing **vascular phenomena** (embolic) [1]. * **Option C (Embolic disease):** Includes arterial emboli, mycotic aneurysms, and intracranial hemorrhages [1]. These are also **vascular phenomena**. * **Option D (Osler's nodes):** These are painful, pea-sized nodules on fingers/toes representing **immunological phenomena** [1]. Other immunological signs include Roth spots and Glomerulonephritis. ### **NEET-PG High-Yield Pearls** * **Diagnosis of IE:** Requires 2 Major OR 1 Major + 3 Minor OR 5 Minor criteria [1]. * **Janeway vs. Osler:** Remember **"Janeway is Just a spot (painless)"** and **"Osler is Ouch (painful)."** * **Most Common Valve:** Mitral valve is most commonly involved overall; however, the **Tricuspid valve** is most common in IV drug users. * **Most Common Organism:** *Staphylococcus aureus* is now the most common cause of acute IE globally [2].

Question 325: A pansystolic murmur is present in all of the following cardiac conditions, EXCEPT:

A. Mitral regurgitation
B. Mitral stenosis (Correct Answer)
C. Ventricular septal defect
D. Tricuspid regurgitation

Explanation: **Explanation:** A **pansystolic (holosystolic) murmur** occurs when there is a pressure gradient between two chambers throughout the entire duration of systole (from $S_1$ to $S_2$) [1]. **Why Mitral Stenosis is the Correct Answer:** Mitral Stenosis (MS) is a **diastolic murmur**, not a systolic one [2]. It occurs when the mitral valve fails to open fully during ventricular filling. It is characterized by an opening snap followed by a **mid-diastolic rumbling murmur** with presystolic accentuation [3]. Since it occurs during diastole, it cannot be pansystolic. **Analysis of Incorrect Options:** * **Mitral Regurgitation (MR):** High pressure in the left ventricle (LV) compared to the left atrium (LA) throughout systole causes blood to leak backward, creating a high-pitched pansystolic murmur loudest at the apex [4]. * **Tricuspid Regurgitation (TR):** Similar to MR, the pressure gradient between the right ventricle and right atrium persists throughout systole. It is loudest at the left lower sternal border and typically increases with inspiration (**Carvallo’s sign**). * **Ventricular Septal Defect (VSD):** The left-to-right shunt persists as long as LV pressure exceeds RV pressure during systole, resulting in a harsh pansystolic murmur, usually loudest at Erb’s point. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pansystolic Murmurs mnemonic:** "MTV" (Mitral regurgitation, Tricuspid regurgitation, VSD). 2. **Dynamic Auscultation:** MR/VSD murmurs increase with handgrip (increased afterload), while TR increases with inspiration. 3. **Exception:** A very small VSD (Maladie de Roger) produces a very loud murmur, whereas a large VSD may have a softer murmur due to equilibrated pressures. 4. **Mitral Stenosis:** Always look for "Loud $S_1$" and "Opening Snap" in the clinical stem [3].

Question 326: Quincke's sign in aortic regurgitation refers to which of the following?

A. Pulsation of the uvula in time with the heartbeat
B. Prominent retinal artery pulsation
C. Capillary nail bed pulsation (Correct Answer)
D. Pulsating liver in time with the heartbeat

Explanation: **Explanation:** **Aortic Regurgitation (AR)** is characterized by a high stroke volume and a rapid fall in arterial pressure during diastole, leading to a **wide pulse pressure** [1]. This "hyperdynamic circulation" results in numerous peripheral signs, of which **Quincke’s sign** is a classic manifestation. * **Correct Answer (C):** Quincke’s sign refers to **capillary pulsations** visible in the nail beds. It is elicited by applying gentle pressure to the tip of the fingernail; the nail bed alternates between flushing (systole) and blanching (diastole). This occurs due to the transmission of large pressure waves into the microvasculature. **Analysis of Incorrect Options:** * **Option A (Müller’s sign):** This refers to systolic pulsations of the **uvula**. * **Option B (Becker’s sign):** This refers to visible pulsations of the **retinal arteries** or arterioles upon ophthalmoscopic examination. * **Option D (Rosenbach’s sign):** This refers to systolic pulsations of the **liver**. (Note: A pulsating liver is also a hallmark of Tricuspid Regurgitation). **High-Yield Clinical Pearls for NEET-PG:** * **De Musset’s sign:** Rhythmic head nodding in time with the heartbeat [1]. * **Corrigan’s pulse:** "Water-hammer" pulse characterized by a rapid upstroke and collapse [1], [2]. * **Traube’s sign:** "Pistol shot" sounds heard over the femoral arteries. * **Duroziez’s sign:** A systolic and diastolic murmur heard over the femoral artery when compressed by the stethoscope. * **Hill’s sign:** Popliteal systolic BP exceeding brachial systolic BP by >20 mmHg (the most sensitive sign for AR severity).

Question 327: The Framingham Risk Score is used to determine which of the following?

A. Severity of Congestive Heart Failure (CHF)
B. Diagnosis of Congestive Heart Failure (CHF)
C. Cardiovascular mortality risk due to atherosclerosis (Correct Answer)
D. Need for stenting in chronic stable angina

Explanation: **Explanation:** The **Framingham Risk Score (FRS)** is a validated clinical tool used to estimate an individual's **10-year risk of developing coronary heart disease (CHD)** or experiencing major cardiovascular events (mortality/morbidity) due to atherosclerosis [1]. It integrates multiple risk factors—age, gender, total cholesterol, HDL cholesterol, smoking status, and systolic blood pressure—to categorize patients into low, intermediate, or high-risk groups [1]. This helps clinicians decide on the intensity of primary prevention strategies, such as statin therapy [2]. **Analysis of Options:** * **Option A & B:** These are incorrect. The Framingham Risk Score is for **primary prevention of atherosclerosis**. For the **diagnosis** of Congestive Heart Failure (CHF), clinicians use the **Framingham Criteria** (Major and Minor criteria like PND, JVP elevation, and S3 gallop). For the **severity** of CHF, the **NYHA Classification** (Functional) or **ACC/AHA Stages** (Structural) are used. * **Option D:** The need for stenting in chronic stable angina is determined by symptomatic burden, response to medical therapy, and objective evidence of ischemia (e.g., Stress Test or FFR), not by a 10-year risk calculator [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Framingham Criteria for CHF:** Remember that 2 major OR 1 major + 2 minor criteria are required for diagnosis. * **QRISK3 & ASCVD Risk Estimator:** These are newer alternatives to the Framingham score used in modern guidelines (NICE and AHA/ACC respectively). * **Diabetes Mellitus:** In many risk models, DM is considered a **"Coronary Artery Disease Risk Equivalent,"** automatically placing the patient in a high-risk category.

Question 328: A patient with mitral stenosis has developed pulmonary artery hypertension. Which of the following auscultatory findings may be heard?

A. Early diastolic, crescendo murmur
B. Mid-systolic, crescendo-decrescendo murmur
C. Pan-systolic murmur (Correct Answer)
D. Mid-diastolic, rumbling murmur

Explanation: The correct answer is **Pan-systolic murmur**. **1. Why it is correct:** In patients with long-standing Mitral Stenosis (MS), the chronic increase in left atrial pressure leads to reactive **Pulmonary Artery Hypertension (PAH)** [1]. This increased pressure in the pulmonary circuit causes the right ventricle (RV) to enlarge and fail, leading to **Functional Tricuspid Regurgitation (TR)** due to the stretching of the tricuspid annulus. Tricuspid Regurgitation characteristically produces a **pan-systolic (holosystolic) murmur**, best heard at the left lower sternal border, which typically increases in intensity during inspiration (**Carvallo’s sign**). **2. Why the other options are incorrect:** * **Option A (Early diastolic, crescendo murmur):** This is incorrect. While PAH can cause an early diastolic murmur (Graham Steell murmur) due to functional pulmonary regurgitation, it is **decrescendo** in nature, not crescendo. * **Option B (Mid-systolic, crescendo-decrescendo murmur):** This is typical of Aortic Stenosis or Flow murmurs. While PAH may cause a brief pulmonary ejection click/murmur, the pan-systolic murmur of TR is a more definitive finding of secondary RV involvement. * **Option D (Mid-diastolic, rumbling murmur):** This is the classic murmur of **Mitral Stenosis** itself [1]. While present in this patient, the question specifically asks for findings associated with the *development of PAH*. **Clinical Pearls for NEET-PG:** * **Graham Steell Murmur:** A high-pitched, blowing, decrescendo early diastolic murmur heard in the pulmonary area due to functional PR in severe PAH. * **Signs of PAH in MS:** Loud P2 (palpable as Dressler’s sign), Right Ventricular Heave, and the murmur of TR [1]. * **Carvallo’s Sign:** Helps differentiate TR (increases with inspiration) from MR (does not increase with inspiration).

Question 329: All of the following features can differentiate between ventricular tachycardia and supraventricular tachycardia EXCEPT?

A. QRS duration < 0.14 seconds
B. Ventricular rate > 160/min (Correct Answer)
C. Variable first heart sound
D. Relieved by carotid sinus massage

Explanation: This question tests the ability to distinguish between **Ventricular Tachycardia (VT)** and **Supraventricular Tachycardia (SVT)** with aberrancy, a common clinical dilemma in cardiology. [1] ### **Explanation of the Correct Answer** **Option B (Ventricular rate > 160/min)** is the correct answer because the heart rate itself is **not** a reliable differentiator. Both VT and SVT can present with rates ranging from 140 to 250 beats per minute. [1] There is significant overlap in heart rates between the two conditions, making this feature non-diagnostic. [2] ### **Analysis of Incorrect Options** * **A. QRS duration < 0.14 seconds:** A QRS duration **> 0.14s** (in RBBB pattern) or **> 0.16s** (in LBBB pattern) strongly favors VT. [1] Conversely, a narrower QRS (though still > 0.12s) is more common in SVT with aberrancy. * **C. Variable first heart sound (S1):** This occurs in VT due to **Atrioventricular (AV) dissociation**. [1] Since the atria and ventricles contract independently, the position of the mitral valve leaflets varies at the onset of systole, leading to a changing intensity of S1. In SVT, the relationship is fixed, and S1 is constant. * **D. Relieved by carotid sinus massage:** Vagal maneuvers like carotid sinus massage can terminate or slow down SVT (especially AVNRT/AVRT) by increasing AV nodal refractory periods. However, they typically have **no effect on VT**. ### **Clinical Pearls for NEET-PG** * **AV Dissociation:** The presence of **Capture beats** or **Fusion beats** is pathognomonic (100% specific) for VT. [1] * **Brugada Criteria:** Used to differentiate VT from SVT; the most important initial step is looking for the absence of RS complexes in all precordial leads (V1-V6). * **Hemodynamic Stability:** Never use stability to differentiate; VT can often present in a conscious, stable patient. * **Rule of Thumb:** In a patient with a history of ischemic heart disease or prior MI, a wide-complex tachycardia should be treated as **VT until proven otherwise**.

Question 330: What is the drug of choice for Paroxysmal Supraventricular Tachycardia?

A. Digitalis
B. Adenosine (Correct Answer)
C. Adrenaline
D. Verapamil

Explanation: **Explanation:** **Paroxysmal Supraventricular Tachycardia (PSVT)**, most commonly caused by AV Nodal Reentrant Tachycardia (AVNRT), involves a reentry circuit within the AV node [1]. **Why Adenosine is the Drug of Choice:** Adenosine is the first-line pharmacological treatment for stable PSVT [1]. It acts by binding to **A1 receptors** in the AV node, leading to the activation of potassium channels and inhibition of calcium current. This results in a transient, potent **AV nodal conduction block**, which effectively "breaks" the reentry circuit and restores sinus rhythm [1]. Its ultra-short half-life (<10 seconds) allows for rapid action and quick clearance, making it both effective and safe for acute termination. **Analysis of Incorrect Options:** * **Digitalis (Digoxin):** While it slows AV conduction, its onset of action is too slow (hours) for the acute termination of PSVT [1]. It is primarily used for rate control in chronic atrial fibrillation. * **Adrenaline (Epinephrine):** This is a sympathomimetic drug that increases heart rate and conduction velocity. It would worsen tachycardia and is contraindicated in PSVT. * **Verapamil:** A non-dihydropyridine Calcium Channel Blocker. It was previously the drug of choice but is now a **second-line agent**. It has a longer half-life and carries a higher risk of prolonged hypotension compared to Adenosine. **High-Yield Clinical Pearls for NEET-PG:** * **Initial Step:** Vagal maneuvers (e.g., Carotid sinus massage or Valsalva) should be attempted before drugs. * **Administration:** Adenosine must be given as a **rapid IV bolus** (6mg, then 12mg) followed by a saline flush due to its short half-life. * **Contraindications:** Avoid Adenosine in patients with **Asthma** (can cause bronchospasm) and 2nd/3rd-degree heart block [1]. * **Side Effects:** Patients often experience a transient, distressing feeling of "impending doom," chest pain, or flushing. * **Unstable Patients:** If the patient is hemodynamically unstable (hypotension, altered mentation), the treatment of choice is **Synchronized DC Cardioversion**.

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Cardiology — MCQs

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