Cardiology Practice Questions

Q: Which of the following is NOT seen in association with reverse splitting of S2?

Complete heart block. **Explanation:** The second heart sound (S2) consists of two components: **A2 (Aortic)** and **P2 (Pulmonary)**. In a normal physiological state, A2 precedes P2. **Reverse (Paradoxical) splitting** occurs when there is a significant delay in the closure of the aortic valve, causing A2 to occur *after* P2. **Why Complete Heart Block (CHB) is the correct answer:** In Complete Heart Block, the atria and ventricles beat independently (AV dissociation) [1], [3]. While it can cause a "variable intensity" of S1 (Bruit de Canon), it does not inherently cause a consistent delay in left ventricular ejection that would lead to reverse splitting of S2. Therefore, it is not typically associated with this finding. **Analysis of Incorrect Options (Causes of Reverse Splitting):** * **LBBB (Option A):** This is the most common cause. Delayed electrical activation of the left ventricle leads to delayed mechanical contraction and late closure of the aortic valve. * **Systolic Hypertension (Option C):** High systemic pressure creates increased resistance to left ventricular ejection, prolonging the ejection time and delaying A2. * **Aortic Stenosis (Option D):** The narrowed valve orifice causes prolonged left ventricular ejection time to force blood through the obstruction, delaying A2 [4]. **NEET-PG High-Yield Pearls:** 1. **Paradoxical Split:** The split narrows during inspiration and widens during expiration (the opposite of physiological splitting). 2. **Wide Fixed Split:** Classically seen in **Atrial Septal Defect (ASD)** [2]. 3. **Wide Variable Split:** Seen in **RBBB** or Pulmonary Stenosis (where P2 is delayed). 4. **Soft/Absent A2:** A classic sign of severe calcific Aortic Stenosis [4].

Q: What is the most common cause of mitral valve disease?

Rheumatic fever. **Explanation:** **Rheumatic Heart Disease (RHD)**, resulting from **Rheumatic Fever**, remains the most common cause of acquired mitral valve disease worldwide, particularly in developing countries like India [1]. It is the leading cause of **Mitral Stenosis (MS)** and a frequent cause of Mitral Regurgitation (MR). The underlying mechanism involves an autoimmune response (molecular mimicry) following a Group A Streptococcal infection, leading to chronic inflammation, commissural fusion, and "fish-mouth" deformity of the valve. **Analysis of Incorrect Options:** * **Infective Endocarditis (A):** While it can cause acute, severe mitral regurgitation due to leaflet destruction or chordae rupture [2], it is less common than RHD and typically presents as an acute febrile illness rather than chronic valvular disease. * **Myxoma (B):** Atrial myxomas are the most common primary cardiac tumors. While they can physically obstruct the mitral orifice (mimicking mitral stenosis), they are rare clinical entities compared to the prevalence of RHD. * **Tuberculosis (C):** TB primarily affects the pericardium (causing constrictive pericarditis). It does not directly involve the endocardium or heart valves. **High-Yield Clinical Pearls for NEET-PG:** * **Mitral Stenosis:** RHD is the cause in nearly **99%** of cases of MS. * **Auscultation:** Look for a loud S1, an Opening Snap (OS), and a mid-diastolic rumbling murmur [3]. * **Mitral Regurgitation:** In developed nations, **Mitral Valve Prolapse (MVP/Myxomatous degeneration)** has overtaken RHD as the most common cause of isolated MR. * **Aschoff Bodies:** These are the pathognomonic histological features of acute rheumatic carditis.

Q: Which one of the following findings is NOT associated with left-sided heart failure?

Hepatojugular reflux. ### Explanation **1. Why Hepatojugular Reflux (HJR) is the Correct Answer:** Hepatojugular reflux is a clinical sign of **Right-Sided Heart Failure (RHF)**. It occurs when manual pressure over the liver increases venous return to a failing right ventricle that cannot compensate, leading to a sustained rise in the Jugular Venous Pressure (JVP). While chronic left-sided heart failure (LHF) can eventually lead to RHF (the most common cause), HJR specifically reflects right ventricular dysfunction or systemic venous congestion, not isolated LHF [2]. **2. Analysis of Incorrect Options (Findings associated with LHF):** * **Pulmonary Edema (Option A):** In LHF, the left ventricle fails to pump blood forward, causing increased pressure in the left atrium and pulmonary veins. This hydrostatic pressure forces fluid into the alveoli, leading to pulmonary edema [1]. * **Paroxysmal Nocturnal Dyspnea (Option C):** This is a classic symptom of LHF. When a patient lies flat, interstitial fluid from the lower extremities is redistributed into the central circulation. A failing left ventricle cannot handle this increased preload, resulting in acute pulmonary congestion at night [2]. * **Prerenal Azotemia (Option D):** LHF causes a "forward failure" state with decreased cardiac output. This leads to reduced renal perfusion, triggering an increase in Blood Urea Nitrogen (BUN) and Creatinine, known as prerenal azotemia [3]. **3. Clinical Pearls for NEET-PG:** * **Most common cause of RHF:** Left-sided heart failure [2]. * **Earliest symptom of LHF:** Exertional dyspnea [2]. * **Specific sign of LHF:** Pulsus alternans (alternating strong and weak peripheral pulses). * **HJR Technique:** Apply firm pressure over the RUQ for 10–30 seconds; a positive result is a sustained rise in JVP >3 cm. It is highly suggestive of an elevated Pulmonary Capillary Wedge Pressure (PCWP).

Q: Which of the following is NOT true regarding murmurs heard in hypertrophic obstructive cardiomyopathy?

Systolic murmur increases with hand grip. In Hypertrophic Obstructive Cardiomyopathy (HOCM), the murmur is primarily caused by dynamic Left Ventricular Outflow Tract (LVOT) obstruction. The intensity of the murmur depends on the **Left Ventricular (LV) volume**: anything that decreases LV volume (decreased preload or afterload) increases the obstruction and the murmur, while anything that increases LV volume (increased preload or afterload) decreases the murmur. **Explanation of Options:** * **Option C (Correct):** Handgrip exercise increases **afterload** (systemic vascular resistance) [1]. Increased afterload pushes back against the LV, increasing the ventricular volume and "forcing" the outflow tract open [1]. This **decreases** the intensity of the HOCM murmur [2]. Therefore, the statement that it increases is false. * **Option A:** Squatting increases both **preload** (venous return) and **afterload**. This increases LV volume, which reduces the obstruction and **decreases** the murmur [2]. * **Option B:** The Valsalva maneuver (strain phase) decreases venous return (**preload**). This reduces LV volume, allowing the hypertrophied septum and mitral valve to appose more easily, thereby **increasing** the murmur. * **Option D:** Beta-blockers are negative inotropes. They decrease the force of contraction and increase diastolic filling time, which reduces the dynamic obstruction and **decreases** the murmur. **High-Yield Clinical Pearls for NEET-PG:** 1. **The "Rule of Two":** HOCM and Mitral Valve Prolapse (MVP) are the only two murmurs that **increase** with Valsalva and standing (decreased preload). 2. **Dynamic Nature:** Unlike Valvular Aortic Stenosis (which decreases with Valsalva) [3], the HOCM murmur changes significantly with bedside maneuvers. 3. **Handgrip Differentiation:** Handgrip increases the murmur of Mitral Regurgitation and VSD but decreases the murmur of HOCM and Aortic Stenosis.

Q: What is the most common cause of sudden cardiac death?

Ventricular fibrillation. ### Explanation **1. Why Ventricular Fibrillation (VF) is Correct:** Sudden Cardiac Death (SCD) is most commonly triggered by a lethal cardiac arrhythmia. Among these, **Ventricular Fibrillation (VF)** is the most frequent terminal rhythm, accounting for approximately 75–80% of cases [2]. In VF, the ventricles quiver rapidly and irregularly instead of pumping blood [1], leading to an immediate loss of cardiac output, circulatory collapse, and death within minutes if not defibrillated [3]. The most common underlying structural cause leading to VF is **Coronary Artery Disease (CAD)**, particularly acute myocardial ischemia or scarring from a previous infarct. **2. Why the Other Options are Incorrect:** * **Atrial Fibrillation (AF):** While AF is the most common sustained arrhythmia, it involves the atria. It increases the risk of stroke (embolic events) and heart failure but is rarely a direct cause of sudden death as the AV node protects the ventricles from the rapid atrial rate. * **PSVT:** These are typically narrow-complex tachycardias (like AVNRT). While they cause palpitations, dizziness, or syncope, they are almost never life-threatening in patients with normal heart structures. * **A-V Block:** While complete heart block (3rd degree) can cause asystole or severe bradycardia leading to death, it is a much less common cause of SCD compared to tachyarrhythmias like VF. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common underlying pathology for SCD:** Coronary Artery Disease (CAD). * **Most common cause of SCD in young athletes (<35 years):** Hypertrophic Cardiomyopathy (HCM). * **The "Golden Hour":** Survival rates for VF decrease by 7–10% for every minute that passes without defibrillation [2]. * **Primary Prevention:** In patients with low Ejection Fraction (<35%), an Implantable Cardioverter Defibrillator (ICD) is the treatment of choice to prevent SCD.

Q: The Bundle of Kent is associated with which of the following conditions?

Wolff-Parkinson-White syndrome. **Wolff-Parkinson-White (WPW) syndrome** is the correct answer because it is characterized by the presence of an accessory pathway known as the **Bundle of Kent** [1]. In a normal heart, the AV node is the only electrical bridge between the atria and ventricles. In WPW, the Bundle of Kent bypasses the AV node, leading to **pre-excitation** of the ventricles [2]. This results in the classic ECG triad: 1. **Short PR interval** ( 0.12s) [1]. **Analysis of Incorrect Options:** * **Sick Sinus Syndrome:** Refers to SA node dysfunction leading to alternating bradycardia and tachycardia (Tachy-Brady syndrome); it does not involve accessory pathways. * **Lown-Ganong-Levine (LGL) Syndrome:** Associated with the **James fibers** (intranodal accessory pathway). It presents with a short PR interval but a **normal QRS** (no delta wave) [1]. * **Stokes-Adams Syndrome:** Refers to sudden syncope caused by a complete heart block or severe arrhythmia leading to decreased cardiac output. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Contraindication:** Avoid **ABCD** (Atropine/Adenosine, Beta-blockers, Calcium channel blockers, Digoxin) in WPW with Atrial Fibrillation, as they block the AV node and may force conduction through the Bundle of Kent, risking Ventricular Fibrillation [2]. * **Treatment of Choice:** Radiofrequency ablation of the accessory pathway. * **Association:** WPW syndrome is sometimes associated with **Ebstein’s anomaly**.

Question 1

Which of the following is NOT seen in association with reverse splitting of S2?

Accepted Answer

Complete heart block

Answer

Left bundle branch block (LBBB)

Answer

Systolic hypertension

Answer

Aortic stenosis

Question 2

A patient with angina, exertional syncope, and left ventricular hypertrophy is diagnosed with aortic stenosis. What is the predicted lifespan of this patient?

Accepted Answer

3 years

Answer

1 year

Answer

2 years

Answer

4 years

Question 3

What is the most common cause of mitral valve disease?

Accepted Answer

Rheumatic fever

Answer

Infective endocarditis

Answer

Myxoma

Answer

Tuberculosis

Question 4

Unequal pulses in upper and lower extremities (i.e., radio-femoral delay) is/are seen in which of the following conditions?

Accepted Answer

Post-ductal coarctation of the aorta

Answer

Aortic dissection

Answer

Supra-valvular aortic stenosis

Answer

Sub-valvular aortic stenosis

Question 5

A 70-year-old male patient presented to the emergency department with pain in the epigastrium and difficulty in breathing for 6 hours. On examination, his heart rate was 56 beats per minute and the blood pressure was 106/60 mm Hg. Chest examination was normal. The patient has been taking omeprazole for gastroesophageal reflux disease for the last 6 months. What should be the initial investigation?

Accepted Answer

An ECG

Answer

An upper GI endoscopy

Answer

Urgent ultrasound of the abdomen

Answer

An x-ray chest

Question 6

Which one of the following findings is NOT associated with left-sided heart failure?

Accepted Answer

Hepatojugular reflux

Answer

Pulmonary edema

Answer

Paroxysmal nocturnal dyspnea

Answer

Prerenal azotemia

Question 7

Which of the following is NOT true regarding murmurs heard in hypertrophic obstructive cardiomyopathy?

Accepted Answer

Systolic murmur increases with hand grip

Answer

Systolic murmur decreases on squatting

Answer

Systolic murmur increases on Valsalva maneuver

Answer

Systolic murmur decreases on taking a beta-blocker

Question 8

Water hammer pulse is typically seen in which condition?

Accepted Answer

Aortic regurgitation

Answer

Aortic stenosis

Answer

Aortic stenosis and aortic regurgitation

Answer

Mitral regurgitation

Question 9

What is the most common cause of sudden cardiac death?

Accepted Answer

Ventricular fibrillation

Answer

Atrial fibrillation

Answer

Paroxysmal supraventricular tachycardia (PSVT)

Answer

Atrioventricular (A-V) block

Question 10

The Bundle of Kent is associated with which of the following conditions?

Accepted Answer

Wolff-Parkinson-White syndrome

Answer

Sick sinus syndrome

Answer

Long-Ganong-Levine syndrome

Answer

Stokes-Adams syndrome

Cardiology — MCQs

Cardiology — MCQs

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