Cardiology — MCQs

A 58-year-old man with no prior cardiac history presents with retrosternal chest pain starting at rest and lasting 30 minutes. The pain radiates to the left arm and is associated with diaphoresis and dyspnea. His blood pressure is 150/90 mm Hg, pulse 100/min, the heart sounds are normal, and the lungs are clear to auscultation. Which of the following is the next most appropriate investigation?

Q130Easy

Which valve is most commonly affected in Rheumatic Heart Disease?

Cardiology Indian Medical PG Practice Questions and MCQs

Question 121: Which organism most commonly leads to infective endocarditis?

A. Staphylococcus aureus (Correct Answer)
B. Klebsiella
C. Streptococcus pneumoniae
D. Neisseria meningitidis

Explanation: ### Explanation **Correct Answer: A. Staphylococcus aureus** **1. Why Staphylococcus aureus is correct:** In recent decades, the epidemiology of Infective Endocarditis (IE) has shifted. *Staphylococcus aureus* is now the **most common cause of IE worldwide**, particularly in developed nations and urban centers [1]. This shift is attributed to the rise in healthcare-associated infections, intravenous drug use (IVDU), and the increasing use of prosthetic valves and indwelling cardiac devices. *S. aureus* is highly virulent, capable of infecting previously healthy (native) valves, and often leads to acute, fulminant disease with rapid valvular destruction [1]. In any patient with staphylococcal bacteraemia, especially injection drug-users, the possibility of endocarditis must be considered [2]. **2. Why the other options are incorrect:** * **B. Klebsiella:** Gram-negative bacilli like *Klebsiella* are rare causes of IE. When they do occur, they are typically part of the HACEK group or associated with specific healthcare exposures, but they are never the leading cause. * **C. Streptococcus pneumoniae:** While a classic cause of "Austrian Syndrome" (triad of pneumonia, meningitis, and endocarditis), it is now an infrequent cause of IE due to the widespread use of antibiotics and vaccines [1]. * **D. Neisseria meningitidis:** This organism primarily causes meningitis and sepsis (meningococcemia). It is an extremely rare cause of endocarditis. **3. Clinical Pearls for NEET-PG:** * **Most common cause overall:** *Staphylococcus aureus* [1]. * **Most common cause in Subacute IE/Native Valve (Community-acquired):** *Viridans group Streptococci* (historically #1, now #2 globally) [1]. * **Most common cause in IVDU:** *Staphylococcus aureus* (often affecting the Tricuspid valve) [2]. * **Early Prosthetic Valve IE (<1 year):** *Staphylococcus epidermidis* (Coagulase-negative Staph) [2]. * **IE associated with Colon Cancer:** *Streptococcus gallolyticus* (formerly *S. bovis*) [1]. * **Culture-negative IE:** Most commonly due to prior antibiotic use; otherwise, consider *Coxiella burnetii* or *Bartonella* [3].

Question 122: 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 [2]. **S2 (Second Heart Sound)** marks the end of ventricular systole and the beginning of diastole [2]. Therefore, sounds occurring shortly after S2 are **diastolic sounds**, while sounds occurring shortly after S1 (and before S2) are **systolic sounds** [3]. **Why Ejection Click is the Correct Answer:** An **Ejection Click** occurs in early systole, shortly after the **S1** heart sound [1]. It is caused by the abrupt opening of the semilunar valves (Aortic or Pulmonary) or the sudden distension of the great vessels. Since it occurs during the ejection phase of systole, it cannot occur after S2 [1]. **Analysis of Incorrect Options (Diastolic Sounds):** * **Opening Snap:** Occurs in early diastole due to the forceful opening of a stenosed 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 low-pitched sound heard in early-to-mid diastole, caused by an **Atrial Myxoma** "plopping" into the atrioventricular orifice. **High-Yield 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. **S3 vs. Pericardial Knock:** Both occur in early diastole, but the Pericardial Knock occurs earlier and is higher pitched than a physiological or pathological S3. 3. **Non-Ejection Click:** Mid-systolic clicks are classically associated with **Mitral Valve Prolapse (MVP)** [1]. 4. **Ejection Click Exception:** An Aortic ejection click is typically heard best at the apex and does not vary with respiration, whereas a Pulmonary ejection click decreases in intensity during inspiration.

Question 123: All of the following may be seen in a patient with cardiac tamponade, except?

A. Raised JVP
B. Hypotension with narrowed pulse pressure
C. Muffled heart sounds
D. Atrial flutter (Correct Answer)

Explanation: **Explanation:** Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, leading to increased intrapericardial pressure that exceeds intracardiac pressure. This results in impaired diastolic filling of the heart chambers [1]. **Why Atrial Flutter is the correct answer:** Atrial flutter is not a characteristic feature of cardiac tamponade. The classic ECG finding in tamponade is **Electrical Alternans** (alternating QRS amplitude due to the heart "swinging" in the fluid) and sinus tachycardia [1]. Atrial arrhythmias are uncommon because the high intrapericardial pressure tends to compress the thin-walled atria, often preventing the development of organized macro-reentrant circuits like flutter. **Analysis of Incorrect Options:** * **A. Raised JVP:** This is a hallmark of tamponade. Due to impaired right ventricular filling, venous return is backed up, leading to jugular venous distension. Notably, the **'y' descent is absent** or blunted in the JVP waveform because the high intrapericardial pressure prevents rapid ventricular filling. * **B. Hypotension with narrowed pulse pressure:** As stroke volume falls due to decreased diastolic filling, systolic blood pressure drops. The body compensates with peripheral vasoconstriction, which maintains diastolic pressure, resulting in a narrow pulse pressure. * **C. Muffled heart sounds:** The accumulation of pericardial fluid acts as an insulator, dampening the transmission of sound from the heart to the chest wall. **High-Yield Clinical Pearls for NEET-PG:** 1. **Beck’s Triad:** Hypotension, Raised JVP, and Muffled heart sounds (classic for acute tamponade). 2. **Pulsus Paradoxus:** An exaggerated drop in systolic BP (>10 mmHg) during inspiration. 3. **Echocardiography:** The gold standard for diagnosis; look for **early diastolic collapse of the Right Ventricle** and late diastolic collapse of the Right Atrium [1]. 4. **Management:** Immediate **pericardiocentesis** is the treatment of choice [1].

Question 124: Troponin-T is preferable to CPK-MB in the diagnosis of acute myocardial infarction in all of the following situations except?

A. Bedside diagnosis of myocardial infarction
B. After coronary artery bypass grafting
C. Reinfarction after 4 days (Correct Answer)
D. Small infarct

Explanation: **Explanation:** The diagnosis of Acute Myocardial Infarction (AMI) relies on the kinetics of cardiac biomarkers. The choice between Troponin-T (cTnT) and CK-MB depends on their respective "washout" periods and sensitivity. **1. Why "Reinfarction after 4 days" is the correct answer:** Troponin-T levels remain elevated in the blood for **10–14 days** after an initial MI. If a patient suffers a second infarct (reinfarction) on day 4, the Troponin levels will already be high from the first event, making it difficult to distinguish a new rise. In contrast, **CK-MB returns to baseline within 48–72 hours**. Therefore, if CK-MB rises again after day 3, it is a specific indicator of a new, acute reinfarction. **2. Analysis of Incorrect Options:** * **Bedside diagnosis (A):** Rapid bedside Troponin assays (Point-of-Care Testing) are highly sensitive and specific, making them superior to CK-MB for quick triage in the ER. * **After CABG (B):** Troponins are more cardio-specific [1]. While CK-MB can be elevated due to skeletal muscle trauma during surgery, Troponins provide a more accurate assessment of actual myocardial injury during the procedure [1]. * **Small Infarct (D):** Troponins are significantly more sensitive than CK-MB. They can detect "micro-infarctions" (e.g., in NSTEMI) that might not cause a rise in CK-MB levels. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Marker:** Myoglobin (rises in 1–2 hours), but it is non-specific [2]. * **Most Specific Marker:** Cardiac Troponin I (cTnI). * **Marker for Reinfarction:** CK-MB (due to short half-life). * **Troponin Kinetics:** Rises in 3–4 hours, peaks at 18–24 hours, stays elevated for 10–14 days. * **False Positive Troponin:** Can occur in Chronic Kidney Disease (CKD), Pulmonary Embolism, and Sepsis.

Question 125: A 65-year-old man with a long history of hypertension presents to the emergency department with tearing chest pain that radiates to the back. An electrocardiogram is normal, as are cardiac enzymes. A chest radiograph demonstrates widening of the mediastinum. What is the most likely diagnosis?

A. Arteriovenous fistula
B. Atherosclerotic aneurysm
C. Syphilitic aneurysm
D. Dissecting aneurysm (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Dissecting aneurysm (Aortic Dissection)** The clinical presentation is classic for **Aortic Dissection**. The hallmark features include: 1. **Clinical History:** Long-standing hypertension is the most significant risk factor [1]. 2. **Pain Profile:** Sudden onset of "tearing" or "ripping" chest pain radiating to the interscapular region (back) [1]. 3. **Imaging:** A widened mediastinum on chest X-ray is the classic initial radiographic finding (seen in ~80% of cases). 4. **Differential Diagnosis:** Normal ECG and cardiac enzymes help rule out Acute Myocardial Infarction, which is the primary mimic [4]. **Why other options are incorrect:** * **A. Arteriovenous fistula:** This involves an abnormal communication between an artery and a vein. It typically presents with a continuous bruit or thrill and signs of high-output heart failure, not acute tearing chest pain. * **B. Atherosclerotic aneurysm:** While atherosclerosis causes true aneurysms (e.g., Abdominal Aortic Aneurysm), these are often asymptomatic until they rupture [2]. They do not typically present with the acute "tearing" sensation characteristic of an intimal flap dissection. * **C. Syphilitic aneurysm:** A late complication of tertiary syphilis (endarteritis obliterans of vasa vorum), it primarily involves the **ascending aorta** and leads to a "tree-bark" appearance. It usually presents as a chronic saccular aneurysm or aortic regurgitation rather than acute dissection. **NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** CT Angiography (CTA) is the investigation of choice in hemodynamically stable patients [1]. Transesophageal Echocardiogram (TEE) is preferred if the patient is unstable [3]. * **Classification:** * **Stanford Type A:** Involves ascending aorta (Surgical emergency) [1]. * **Stanford Type B:** Involves descending aorta only (Medical management with Beta-blockers like Labetalol to reduce dP/dt) [1]. * **Physical Exam:** Look for pulse deficit (asymmetric pulses) or a new murmur of aortic regurgitation.

Question 126: What energy level is appropriate for defibrillation of ventricular fibrillation?

A. 120 J
B. 250 J (Correct Answer)
C. 300 J
D. 400 J

Explanation: The management of Ventricular Fibrillation (VF) and pulseless Ventricular Tachycardia (pVT) relies on immediate high-energy unsynchronized shocks (defibrillation) [1]. **Why 250 J is the correct answer:** In the context of traditional **Monophasic Defibrillators**, the standard protocol follows a "step-up" approach if the initial shock fails. While the first shock is typically 200 J, the second shock is administered at **250 J** (or 300 J depending on the specific guideline version), and the third at 360 J. In many classic medical examinations like NEET-PG, 250 J is recognized as the appropriate intermediate energy level for escalating therapy in monophasic waveforms. **Analysis of Incorrect Options:** * **A. 120 J:** This is the starting dose for **Biphasic Defibrillators** (range 120–200 J). For monophasic devices, 120 J is insufficient for VF. * **C. 300 J:** While 300 J is used as the second or third shock in some monophasic protocols, 250 J is the more classically tested "next step" after an initial 200 J failure in older standardized curricula. * **D. 400 J:** This exceeds the standard maximum recommended energy level. The maximum dose for adult defibrillation is typically capped at **360 J** to prevent myocardial damage. **Clinical Pearls for NEET-PG:** * **Biphasic vs. Monophasic:** Biphasic is now the gold standard as it requires less energy (120–200 J) and causes less post-shock myocardial dysfunction. * **Synchronized vs. Unsynchronized:** Use **Unsynchronized** shocks (Defibrillation) for VF/Pulseless VT [1]. Use **Synchronized Cardioversion** for unstable SVT, Atrial Fibrillation, or VT with a pulse. * **Pediatric Dose:** Initial dose is **2 J/kg**, second dose is **4 J/kg**, and subsequent doses $\geq$ 4 J/kg (max 10 J/kg or adult dose).

Question 127: Renal artery stenosis may occur in all of the following conditions except?

A. Atherosclerosis
B. Fibromuscular dysplasia
C. Takayasu's arteritis
D. Polyarteritis nodosa (Correct Answer)

Explanation: **Explanation:** The correct answer is **Polyarteritis nodosa (PAN)**. The underlying medical concept involves the **size and location of the vessels** affected. Renal artery stenosis (RAS) involves the narrowing of the main renal artery or its primary branches. * **Why Polyarteritis nodosa is the exception:** PAN is a systemic necrotizing vasculitis that typically affects **medium and small-sized muscular arteries**. In the kidneys, it involves the **interlobar and arcuate arteries** (intra-renal vessels), rather than the main renal artery. Instead of stenosis, PAN is characterized by the formation of **microaneurysms** (appearing as a "string of pearls" on angiography), which can rupture or lead to infarction, but not classic renal artery stenosis. **Analysis of other options:** * **Atherosclerosis:** The most common cause of RAS (approx. 90%), typically involving the **proximal third/ostium** of the renal artery in elderly patients. * **Fibromuscular Dysplasia (FMD):** The second most common cause, typically seen in **young females**. It involves the **distal two-thirds** of the renal artery, showing a "string of beads" appearance. * **Takayasu’s Arteritis:** A large-vessel vasculitis ("pulseless disease") that commonly involves the aorta and its major branches, including the **ostium of the renal arteries**, leading to stenosis and renovascular hypertension. **High-Yield Clinical Pearls for NEET-PG:** 1. **Gold Standard Investigation:** Renal Angiography is the definitive test for diagnosing RAS. 2. **Clinical Clue:** Suspect RAS if a patient develops acute renal failure after starting **ACE inhibitors** (due to loss of efferent arteriolar vasoconstriction). 3. **Bruit:** A systolic-diastolic epigastric bruit is highly suggestive of RAS. 4. **PAN Association:** PAN is strongly associated with **Hepatitis B** (HBsAg positivity) and characteristically **spares the lungs**.

Question 128: Which of the following represents the earliest ECG changes in a patient with Hypokalemia?

A. Pseudo-P-Pulmonale
B. Flattening of T wave (Correct Answer)
C. Development of U wave
D. Fusion of TU waves

Explanation: **Explanation:** In hypokalemia, the resting membrane potential of cardiac myocytes becomes more negative, leading to delayed repolarization. The ECG changes follow a progressive, sequential pattern as serum potassium levels drop [1]. **Why "Flattening of T wave" is correct:** The **earliest** recognizable ECG change in hypokalemia is the **decrease in T-wave amplitude (flattening)**. As potassium levels fall below 3.0 mEq/L, the T-wave becomes progressively lower in voltage. This occurs before the prominent appearance of U waves or ST-segment depression. **Analysis of Incorrect Options:** * **C. Development of U wave:** While highly characteristic of hypokalemia, prominent U waves typically appear *after* the T-wave has started to flatten. The U wave is best seen in precordial leads (V2-V4). * **D. Fusion of TU waves:** This occurs in more severe hypokalemia. As the T-wave flattens and the U-wave grows, they eventually merge, often leading to a "pseudo-prolonged QT interval" (actually a QU interval). * **A. Pseudo-P-Pulmonale:** This refers to an increase in P-wave amplitude and duration. While it can occur in hypokalemia, it is a later finding compared to T-wave changes [1]. **High-Yield NEET-PG Pearls:** * **Sequence of Changes:** T-wave flattening → ST depression → Prominent U waves → TU fusion (QU prolongation). * **The "QU" Interval:** In hypokalemia, the QT interval appears prolonged, but it is actually the **QU interval** due to T and U wave fusion. * **Arrhythmias:** Hypokalemia predisposes patients to Digoxin toxicity and can trigger *Torsades de Pointes* due to the prolonged repolarization phase [1]. * **Differential:** Remember that **Hyperkalemia** presents with the opposite early change: Tall, peaked "tented" T-waves [1].

Question 129: A 58-year-old man with no prior cardiac history presents with retrosternal chest pain starting at rest and lasting 30 minutes. The pain radiates to the left arm and is associated with diaphoresis and dyspnea. His blood pressure is 150/90 mm Hg, pulse 100/min, the heart sounds are normal, and the lungs are clear to auscultation. Which of the following is the next most appropriate investigation?

A. CT scan - chest
B. Chest X-ray (CXR)
C. Cardiac troponin
D. Electrocardiogram (ECG) (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer (D) is Right:** The patient presents with classic symptoms of **Acute Coronary Syndrome (ACS)**: retrosternal chest pain at rest, radiation to the left arm, diaphoresis, and dyspnea [1], [5]. In any patient with suspected ACS, the **Electrocardiogram (ECG)** is the most critical initial investigation. According to AHA/ESC guidelines, an ECG should be performed and interpreted within **10 minutes** of presentation. It is the primary tool used to triage patients into ST-Elevation Myocardial Infarction (STEMI) or Non-ST Elevation ACS (NSTE-ACS), which dictates immediate management (e.g., urgent reperfusion vs. stabilization) [2], [4]. **2. Why the Other Options are Wrong:** * **Cardiac Troponin (C):** While essential for diagnosing NSTEMI, troponins take 3–6 hours to rise significantly [3]. Waiting for lab results delays the diagnosis of a STEMI, which can be identified immediately on an ECG. * **Chest X-ray (B):** CXR is useful to rule out differential diagnoses like pneumonia or pneumothorax, but it is not the priority when an MI is suspected. It should be performed after the ECG. * **CT Scan - Chest (A):** This is indicated if aortic dissection or pulmonary embolism is strongly suspected. However, given the classic presentation of ACS, an ECG must always come first to rule out cardiac ischemia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Door-to-ECG time:** Goal is <10 minutes. * **Gold Standard for STEMI:** Primary Percutaneous Coronary Intervention (PCI) within 90 minutes of medical contact. * **Silent MI:** Common in elderly, females, and diabetics; often presents with "anginal equivalents" like dyspnea or epigastric pain [5]. * **ECG Evolution:** Hyperacute T-waves → ST elevation → Q waves → T-wave inversion [4].

Question 130: Which valve is most commonly affected in Rheumatic Heart Disease?

A. Mitral (Correct Answer)
B. Tricuspid
C. Aortic
D. Pulmonary

Explanation: In Rheumatic Heart Disease (RHD), the **Mitral valve** is the most frequently affected valve (involved in approximately 95% of cases) [1]. The underlying mechanism involves molecular mimicry, where antibodies against Group A Streptococcal M-protein cross-react with endocardial structures. The mitral valve is most susceptible due to the high hemodynamic stress and pressure gradients it handles during ventricular systole, leading to valvulitis, chordae thickening, and eventually, the classic "fish-mouth" or "button-hole" stenosis. All patients with mitral stenosis, particularly those with atrial fibrillation, are at risk from left atrial thrombosis and systemic thromboembolism [1]. **2. Analysis of Incorrect Options:** * **Aortic Valve (Option C):** This is the **second most common** valve involved. It is rarely affected in isolation and is usually seen in combination with mitral valve disease. Isolated aortic involvement is more common in males. * **Tricuspid Valve (Option B):** This is the **third most common** valve affected. It is almost never involved alone and typically presents as tricuspid regurgitation secondary to mitral valve pathology and pulmonary hypertension [1]. * **Pulmonary Valve (Option D):** This is the **least commonly** affected valve in RHD. Involvement is extremely rare and usually clinically insignificant. **3. NEET-PG High-Yield Pearls:** * **Order of Frequency:** Mitral > Aortic > Tricuspid > Pulmonary (**M > A > T > P**). * **Most Common Lesion:** Mitral Regurgitation (MR) is the most common early finding in acute rheumatic carditis, while Mitral Stenosis (MS) is the hallmark of chronic RHD [1]. * **Pathognomonic Feature:** **Aschoff bodies** (granulomatous lesions) in the myocardium are diagnostic of acute rheumatic fever. * **McCallum’s Patch:** A corrugated area of endocardial thickening usually found in the posterior wall of the left atrium, caused by regurgitant jets in MR.

Practice by Chapter

Coronary Artery Disease and Angina

Practice Questions

Acute Coronary Syndromes

Practice Questions

Heart Failure

Practice Questions

Cardiac Arrhythmias

Practice Questions

Valvular Heart Diseases

Practice Questions

Cardiomyopathies

Practice Questions

Pericardial Diseases

Practice Questions

Congenital Heart Disease in Adults

Practice Questions

Hypertension and Hypertensive Emergencies

Practice Questions

Pulmonary Hypertension

Practice Questions

Non-invasive Cardiac Diagnostics

Practice Questions

Preventive Cardiology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?