Cardiology Practice Questions

Q: A patient develops Mitral Regurgitation following myocardial infarction. The likely cause for this complication is

Rupture of chorda tendinae. **Explanation:** Acute Mitral Regurgitation (MR) following a Myocardial Infarction (MI) is a critical mechanical complication. The correct answer is **Rupture of chordae tendineae** (or more commonly, the **papillary muscle** to which they attach) [1]. **Why Option B is Correct:** During an MI, the blood supply to the papillary muscles is compromised. The **posteromedial papillary muscle** is most vulnerable because it has a single blood supply (usually the Right Coronary Artery), whereas the anterolateral muscle has dual supply. Ischemia leads to necrosis and subsequent rupture of the papillary muscle or its chordae tendineae. This results in a "flail leaflet," causing acute, severe MR and rapid-onset pulmonary edema [1]. **Why Other Options are Incorrect:** * **Option A:** Heart valves are endocardial structures and do not "infarct" directly; they dysfunction due to damage to the supporting apparatus (muscles/chordae). * **Option C:** While ventricular dilatation (remodeling) can cause "functional MR" by stretching the mitral annulus, this is typically a **chronic** process rather than an acute post-MI complication [1]. * **Option D:** Atrial fibrillation can occur post-MI and may worsen MR due to loss of atrial kick and annular dilation, but it is not the primary structural cause of post-MI MR [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Timing:** Papillary muscle rupture typically occurs **2 to 7 days** post-MI. * **Clinical Sign:** A new-onset, harsh **pansystolic murmur** at the apex radiating to the axilla [1]. * **Diagnosis:** Transthoracic or Transesophageal Echocardiography is the gold standard. * **Management:** This is a surgical emergency. Stabilize with afterload reducers (Nitroprusside) or an Intra-aortic Balloon Pump (IABP) before definitive surgery.

Q: Cardiac tamponade causes pulsus:

Paradoxus. ### Explanation **Correct Answer: C. Paradoxus** **Mechanism of Pulsus Paradoxus in Cardiac Tamponade:** Pulsus paradoxus is defined as an exaggerated drop in systolic blood pressure (>10 mmHg) during inspiration. In cardiac tamponade, the heart is compressed by fluid within a non-compliant pericardial sac [1]. During inspiration, increased venous return to the right ventricle (RV) causes the RV to expand. Due to the fixed space, the RV pushes the interventricular septum toward the left ventricle (LV). This "ventricular interdependence" reduces LV filling and stroke volume, leading to a significant drop in systemic blood pressure. **Analysis of Incorrect Options:** * **A. Pulsus Alternans:** Characterized by alternating strong and weak beats with a regular rhythm. It is a hallmark of **severe Left Ventricular Failure (LVF)**. * **B. Pulsus Bigemini:** A rhythm where a normal beat is followed by a premature ventricular contraction (PVC). It is commonly seen in **Digoxin toxicity**. * **C. Pulsus Parvus (et Tardus):** Refers to a pulse that is small in amplitude and late/slow to rise. This is the classic finding in **Aortic Stenosis**. **NEET-PG High-Yield Pearls:** * **Beck’s Triad (Tamponade):** Hypotension, Jugular Venous Distension (JVD), and Muffled heart sounds. * **ECG Finding:** Electrical Alternans (alternating QRS amplitude due to the heart "swinging" in fluid) [1]. * **JVP Finding:** Prominent ‘x’ descent with an **absent or diminished ‘y’ descent** (distinguishes it from Constrictive Pericarditis, where ‘y’ is prominent). * **Reverse Pulsus Paradoxus:** Seen in Hypertrophic Obstructive Cardiomyopathy (HOCM) and patients on positive pressure ventilation.

Q: Which cardiac marker remains diagnostic 10 days after a myocardial infarction?

Troponin. **Explanation:** The diagnosis of myocardial infarction (MI) relies heavily on the temporal profile of cardiac biomarkers. **Troponin (specifically Troponin T and I)** is the correct answer because it remains elevated in the serum for a prolonged period following myocardial necrosis [2]. * **Troponin T** can remain elevated for up to **10–14 days**, while **Troponin I** stays elevated for **7–10 days**. This extended window makes Troponin the most useful marker for "late diagnosis" in patients who present several days after the onset of chest pain. **Analysis of Incorrect Options:** * **CPK-MB:** This marker rises within 4–6 hours but returns to baseline within **48–72 hours**. Its short half-life makes it the gold standard for detecting **re-infarction**, but it is useless for diagnosis 10 days post-MI. * **LDH (Lactate Dehydrogenase):** While LDH stays elevated longer than CPK-MB (up to 7–10 days), it has been largely replaced by Troponins due to a lack of cardiac specificity [1]. However, even LDH levels typically normalize or significantly decline by day 10. * **Myoglobin:** This is the **earliest marker** to rise (1–3 hours) but is highly non-specific and returns to baseline within **24 hours**. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Marker:** Myoglobin. * **Most Specific Marker:** Troponin I. * **Marker for Re-infarction:** CPK-MB. * **Troponin T vs. I:** Troponin T is more likely to be falsely elevated in patients with chronic kidney disease (CKD). * **The "Window Period":** If a patient presents at 96 hours, CPK-MB will be normal, but Troponin will still be diagnostic [2].

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

Myocardial infarction. **Explanation:** **Why Myocardial Infarction (MI) is the correct answer:** Sudden Cardiac Death (SCD) is most frequently caused by lethal ventricular arrhythmias, specifically **Ventricular Fibrillation (VF)** [1]. The most common underlying substrate for these arrhythmias is **Coronary Artery Disease (CAD)**. Acute myocardial infarction or acute myocardial ischemia triggers an electrical instability in the myocardium, leading to disorganized electrical activity (VF) and immediate circulatory collapse [2]. Statistically, CAD/MI accounts for approximately 70-80% of all sudden cardiac deaths in the adult population. **Analysis of Incorrect Options:** * **B. Aortic Stenosis:** While severe aortic stenosis is a known cause of SCD (due to exertional syncope or arrhythmias), it is far less common than ischemic heart disease. * **C. Dilated Cardiomyopathy (DCM):** DCM is a significant cause of arrhythmic death, particularly in younger patients or those with low ejection fractions, but it ranks second to CAD in overall prevalence. * **D. Electrolyte Abnormalities:** Hypokalemia and hypomagnesemia can predispose a patient to arrhythmias (like Torsades de Pointes), but they are usually "triggers" or exacerbating factors rather than the primary structural cause of death in the general population [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of SCD overall:** Coronary Artery Disease (MI) [2]. * **Most common cause of SCD in young athletes (<35 years):** Hypertrophic Cardiomyopathy (HCM) in the US; Arrhythmogenic Right Ventricular Dysplasia (ARVD) in some European regions. * **Most common arrhythmia in the first hour of MI:** Ventricular Fibrillation [3]. * **Timeframe:** SCD is defined as death occurring within 1 hour of the onset of symptoms (witnessed) or within 24 hours of being seen alive and stable (unwitnessed).

Q: Which of the following biomarkers has been shown to correlate best with pulmonary vascular resistance in patients with heart failure?

Endothelin-1 (ET-1). ### Explanation **Correct Answer: C. Endothelin-1 (ET-1)** **Why Endothelin-1 is correct:** Endothelin-1 (ET-1) is a potent endogenous vasoconstrictor produced by vascular endothelial cells [1]. In patients with heart failure (HF), ET-1 levels are significantly elevated due to neurohormonal activation. Unlike natriuretic peptides, which primarily reflect ventricular stretch and volume status, **ET-1 levels correlate most strongly with pulmonary vascular resistance (PVR)** and pulmonary artery wedge pressure. ET-1 contributes to the pathophysiology of HF by causing systemic and pulmonary vasoconstriction, promoting myocardial hypertrophy, and inducing vascular remodeling. It is considered a strong independent predictor of mortality and the severity of pulmonary hypertension in HF patients. **Why other options are incorrect:** * **A & B (BNP and ANP):** While BNP and ANP are gold-standard biomarkers for diagnosing heart failure and assessing ventricular wall stress (volume/pressure overload), they correlate better with **filling pressures** (like LVEDP) rather than specific vascular resistance [2, 3]. They are "vasodilatory" peptides, acting in opposition to the effects of ET-1 [3]. * **D (Endothelin-2):** ET-2 is an isomer of endothelin, but it is primarily produced in the kidneys and intestine [1]. It does not play a significant role in the cardiovascular hemodynamics of heart failure compared to ET-1. **High-Yield Clinical Pearls for NEET-PG:** * **ET-1** is the most potent vasoconstrictor known (10x more potent than Angiotensin II) [1]. * **Bosentan** is a dual endothelin receptor antagonist (ET-A and ET-B) used in Pulmonary Arterial Hypertension (PAH). * **BNP** has a high **Negative Predictive Value (NPV)**; if BNP is normal, heart failure is highly unlikely [2]. * **Neprilysin inhibitors** (e.g., Sacubitril) work by preventing the breakdown of ANP/BNP, thereby promoting vasodilation and natriuresis.

Q: In a patient with a history of recurrent syncope, a Holter recording shows a QT interval of 680 msec. Which disease is suspected in this patient?

Long QT syndrome. **Explanation:** **1. Why Long QT Syndrome (LQTS) is correct:** The hallmark of LQTS is the prolongation of the QT interval on the ECG, representing delayed ventricular repolarization [1]. The normal QTc (corrected QT) is typically 500 msec is considered high risk). This delay predisposes patients to **Torsades de Pointes (TdP)**, a polymorphic ventricular tachycardia that can lead to recurrent syncope or sudden cardiac death [1], [2]. **2. Why other options are incorrect:** * **Brugada Syndrome:** Characterized by a pseudo-right bundle branch block (RBBB) and ST-segment elevation in leads V1-V3 (Coved type). It does not involve QT prolongation. * **Arrhythmogenic RV Dysplasia (ARVD):** Involves fibro-fatty replacement of the right ventricular myocardium. Key ECG findings include the **Epsilon wave** (small notch at the end of the QRS) and T-wave inversions in V1-V3. * **Lev’s Disease:** An acquired form of complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system (sclerosis of the cardiac skeleton), typically seen in the elderly. **3. High-Yield Clinical Pearls for NEET-PG:** * **Congenital LQTS Types:** * **Romano-Ward Syndrome:** Autosomal Dominant (Pure cardiac phenotype). * **Jervell and Lange-Nielsen Syndrome:** Autosomal Recessive (Associated with **sensorineural deafness**). * **Triggers:** LQT1 is often triggered by exercise/swimming; LQT2 by auditory stimuli (alarm clocks); LQT3 occurs during sleep. * **Management:** Beta-blockers (Propranolol/Nadolol) are the first-line treatment; ICD is indicated for high-risk patients. Avoid QT-prolonging drugs (e.g., Macrolides, Ondansetron, Class IA/III antiarrhythmics).

Q: All of the following statements about chronic constrictive pericarditis are true except?

The commonest cause in India is 'Idiopathic'.. **Explanation:** The correct answer is **Option A**. In the context of India, **Tuberculosis** remains the most common cause of chronic constrictive pericarditis (CCP) [1]. While "Idiopathic" or post-viral causes are the leading etiology in developed nations, the high prevalence of TB in the Indian subcontinent makes it the primary driver of pericardial thickening and calcification [1]. **Analysis of other options:** * **Option B (Kussmaul’s Sign):** This is a classic finding in CCP. It refers to the paradoxical rise (or lack of fall) in Jugular Venous Pressure (JVP) during inspiration because the rigid pericardium prevents the right ventricle from expanding to accommodate increased venous return. * **Option C (Ascites vs. Edema):** In CCP, **Ascites precox** is often seen. Due to chronic high systemic venous pressure and hepatic congestion, ascites develops early and is often more prominent than peripheral edema. * **Option D (RV End-Diastolic Pressure):** In CCP, there is "equalization of diastolic pressures" in all four cardiac chambers. The rigid shell limits ventricular filling, leading to an elevation and plateauing of the RVEDP, LVEDP, and mean atrial pressures. **NEET-PG High-Yield Pearls:** * **Square Root Sign:** Also known as the "Dip and Plateau" pattern seen on pressure tracings of the ventricles. * **Pericardial Knock:** A high-pitched sound heard in early diastole due to the sudden cessation of ventricular filling. * **Chest X-ray:** May show pericardial calcification (best seen in lateral view). * **Treatment:** The definitive treatment is **Surgical Pericardiectomy** [1].

Question 1

A patient develops Mitral Regurgitation following myocardial infarction. The likely cause for this complication is

Accepted Answer

Rupture of chorda tendinae

Answer

Infarction involving the valve

Answer

Dilatation of the ventricle

Answer

Atrial fibrillation

Question 2

Cardiac tamponade causes pulsus:

Accepted Answer

Paradoxus

Answer

Alternans

Answer

Bigemini

Answer

Parvus

Question 3

Ebstein anomaly of the tricuspid valve consists of?

Accepted Answer

Downward displacement of an abnormal tricuspid valve into the right ventricle

Answer

Upward displacement of an abnormal tricuspid valve into the right atrium

Answer

Upward displacement of an abnormal tricuspid valve into the right ventricle

Answer

Downward displacement of an abnormal tricuspid valve into the right atrium

Question 4

Which cardiac marker remains diagnostic 10 days after a myocardial infarction?

Accepted Answer

Troponin

Answer

CPK-MB

Answer

LDH

Answer

Myoglobin

Question 5

Which of the following is seen in a patient with tricuspid incompetence?

Accepted Answer

Hepatic pulsation

Answer

A wave in JVP

Answer

Mid diastolic murmur

Answer

Normal cardiac output

Question 6

What is the most common cause of sudden arrhythmic death?

Accepted Answer

Myocardial infarction

Answer

Aortic stenosis

Answer

Dilated cardiomyopathy

Answer

Electrolyte abnormalities

Question 7

Which of the following is NOT a cause of elevated jugular venous pressure with hypotension?

Accepted Answer

Second-degree atrioventricular block

Answer

Cardiac tamponade

Answer

Right ventricular myocardial infarction

Answer

Heart failure

Question 8

Which of the following biomarkers has been shown to correlate best with pulmonary vascular resistance in patients with heart failure?

Accepted Answer

Endothelin-1 (ET-1)

Answer

Brain Natriuretic Peptide (BNP)

Answer

Atrial Natriuretic Peptide (ANP)

Answer

Endothelin-2 (ET-2)

Question 9

In a patient with a history of recurrent syncope, a Holter recording shows a QT interval of 680 msec. Which disease is suspected in this patient?

Accepted Answer

Long QT syndrome

Answer

Brugada syndrome

Answer

Arrhythmogenic RV dysplasia

Answer

Lev's disease

Question 10

All of the following statements about chronic constrictive pericarditis are true except?

Accepted Answer

The commonest cause in India is 'Idiopathic'.

Answer

Kussmaul's sign is present.

Answer

Ascites is not in proportion to edema.

Answer

Right ventricular end-diastolic pressure is raised.

Cardiology — MCQs

Cardiology — MCQs

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