Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1531: Which one of the following is not an early complication of acute myocardial infarction?

A. Pericarditis
B. Papillary muscle dysfunction
C. Ventricular septal defect
D. Dressler's syndrome (Correct Answer)

Explanation: ***Dressler's syndrome*** - **Dressler's syndrome** (post-myocardial infarction syndrome) is a **late complication** of acute myocardial infarction, typically occurring weeks to months after the event. - It is an **immune-mediated pericarditis**, characterized by chest pain, fever, and pericardial effusion, but is not seen immediately following an MI. *Papillary muscle dysfunction* - **Papillary muscle dysfunction** or rupture can occur as an **early complication** due to ischemia and necrosis of the muscle, leading to **mitral regurgitation** [1]. - This usually manifests within hours to days of the infarct, especially in **inferior MIs** affecting the posterior papillary muscle. *Ventricular septal defect* - A **ventricular septal defect (VSD)** is an **early mechanical complication** resulting from necrosis and rupture of the interventricular septum. - It typically presents within the **first week** after an MI, causing a new **holosystolic murmur** and signs of heart failure. *Pericarditis* - **Early pericarditis** (within a few days of MI) results from inflammation overlying the necrotic myocardial tissue [1]. - It presents with **pleuritic chest pain** that improves with leaning forward and a **pericardial friction rub**, and is distinct from Dressler's syndrome.

Question 1532: Which of the following is not typically used for secondary prevention of myocardial infarction?

A. Aspirin
B. Statins
C. Beta blockers
D. Warfarin (Correct Answer)

Explanation: ***Warfarin*** - While Warfarin is an **anticoagulant**, its primary role is in preventing *thromboembolism* in conditions like **atrial fibrillation** [1] or **mechanical heart valves**, not routinely for general **secondary prevention of MI** unless specific indications exist. - Unlike the other options, it doesn't directly address the underlying plaque rupture or reduce the workload of the heart in the typical post-MI patient. *Aspirin* - **Aspirin** is a cornerstone of secondary prevention after MI due to its **antiplatelet** effects, which help prevent future clot formation [2]. - It reduces the risk of recurrent MI, stroke, and cardiovascular death by inhibiting **platelet aggregation** [2]. *Statins* - **Statins** are crucial for secondary prevention as they aggressively lower **LDL cholesterol** levels, stabilizing existing plaques and preventing further plaque progression. - They have pleiotropic effects beyond lipid lowering, including **anti-inflammatory** and **endothelial function improvement**. *Beta blockers* - **Beta blockers** reduce myocardial oxygen demand by decreasing heart rate and contractility, which helps prevent recurrent ischemic events and improves survival post-MI [3]. - They are particularly beneficial in patients with **left ventricular dysfunction** or **hypertension** following an MI [1].

Question 1533: In the context of chest pain evaluation, which is the best way to differentiate between stable angina and NSTEMI?

A. ECG
B. Cardiac-biomarker (Correct Answer)
C. Trans thoracic Echocardiography
D. Multi uptake gated Acquisition scan

Explanation: **Cardiac-biomarker** - **Cardiac biomarkers**, particularly **troponin**, are crucial for differentiating between **unstable angina** and **NSTEMI** [1], [2]. In NSTEMI, there is evidence of **myocardial necrosis**, leading to elevated cardiac troponins [2]. - **Stable angina** and **unstable angina** do not involve myocardial necrosis, so troponin levels remain within the normal range [1]. *ECG* - While an **ECG** is essential in the initial assessment of chest pain, it may show **non-specific changes** in both **unstable angina** and **NSTEMI**, such as T-wave inversions or ST-segment depression [2]. - The definitive distinction of **NSTEMI** often relies on **sequential biomarker measurements**, as ECG changes alone may not be sufficient for diagnosis or differentiation from unstable angina [2]. *Trans thoracic Echocardiography* - **Echocardiography** can show **regional wall motion abnormalities** that might suggest ischemia, but these findings are not specific enough to differentiate between **stable angina** and **NSTEMI** immediately. - It is more useful for assessing **ventricular function**, identifying **valvular disease**, or detecting other causes of chest pain, rather than acute differentiation of coronary syndromes. *Multi uptake gated Acquisition scan* - A **MUGA scan** assesses **left ventricular ejection fraction** and wall motion, primarily used in evaluating global cardiac function and monitoring cardiotoxicity from chemotherapy. - It is **not a first-line diagnostic tool** for differentiating between acute coronary syndromes like **stable angina** and **NSTEMI** because it does not directly detect acute myocardial injury.

Question 1534: In a patient with heart disease, which condition is most commonly associated with left atrial enlargement?

A. Mitral stenosis (Correct Answer)
B. Tricuspid regurgitation
C. AR
D. None of the options

Explanation: ***Mitral stenosis*** - **Mitral stenosis** leads to an obstruction of blood flow from the **left atrium to the left ventricle**, causing pressure buildup in the left atrium [1]. - This increased pressure over time results in **left atrial enlargement** as the chamber struggles to push blood through the narrowed valve [1]. *Tricuspid regurgitation* - **Tricuspid regurgitation** involves the backflow of blood from the **right ventricle to the right atrium**. - This condition primarily affects the **right side of the heart**, leading to **right atrial enlargement**, not left. *AR* - **Aortic regurgitation (AR)** is the backflow of blood from the **aorta into the left ventricle**. - While AR can cause **left ventricular enlargement** and eventually lead to left atrial dilation, it is not the most common direct cause of *primary* left atrial enlargement compared to mitral stenosis [2]. *None of the options* - **Mitral stenosis** is a well-established cause of significant left atrial enlargement due to the direct pressure overload it imposes on the left atrium [1].

Question 1535: Torsades de pointes is seen in all except

A. Hyponatremia (Correct Answer)
B. Hypomagnesemia
C. Hypokalemia
D. Hypocalcemia

Explanation: ***Hyponatremia*** - **Hyponatremia** (low sodium levels) primarily affects neuronal function and can lead to neurological symptoms like seizures and altered mental status [1]. - It does not directly cause **QT prolongation** or **Torsades de Pointes (TdP)**, which are typically associated with electrolyte imbalances affecting cardiac repolarization. *Hypocalcemia* - **Hypocalcemia** (low calcium levels) can prolong the **QT interval** on an electrocardiogram. - Prolongation of the QT interval increases the risk of developing **Torsades de Pointes**, a life-threatening polymorphic ventricular tachycardia [2]. *Hypomagnesemia* - **Hypomagnesemia** (low magnesium levels) is a common cause and aggravator of **Torsades de Pointes**. - Magnesium plays a crucial role in cardiac ion channel function, and its deficiency can lead to significant **QT prolongation** and ventricular arrhythmias. *Hypokalemia* - **Hypokalemia** (low potassium levels) can prolong the **QT interval** and increase the risk of developing ventricular arrhythmias, including **Torsades de Pointes** [1]. - Potassium channels are essential for cardiac repolarization, and their dysfunction due to low potassium can destabilize myocardial electrical activity [1].

Question 1536: Absent P Wave is seen on an ECG in:

A. Cor Pulmonale
B. Mitral Stenosis
C. Chronic Obstructive Pulmonary Disease (COPD)
D. Atrial Fibrillation (AF) (Correct Answer)

Explanation: ***Atrial Fibrillation (AF)*** - In **atrial fibrillation**, the atria beat chaotically and irregularly, leading to the absence of coordinated **atrial depolarization**, thus no distinct P wave is seen [1]. - The ECG characteristically shows an **irregularly irregular rhythm** with narrow QRS complexes and no discernible P waves. *Cor Pulmonale* - Cor pulmonale involves right ventricular hypertrophy and dilation due to lung disease, which can cause peaked **P waves (P pulmonale)** in leads II, III, aVF, indicating right atrial enlargement. - It does not typically lead to the absence of P waves but rather changes in their morphology. *Mitral Stenosis* - **Mitral stenosis** can cause left atrial enlargement, which typically manifests as a broad, notched **P wave (P mitrale)**, especially in lead II, and a prominent negative phase in V1. - P waves are present but altered in appearance due to the increased atrial pressure and volume. *Chronic Obstructive Pulmonary Disease (COPD)* - Patients with **COPD** often show signs of right atrial enlargement, similar to cor pulmonale, resulting in **P pulmonale** on the ECG due to increased pulmonary pressures. - While other ECG changes like low voltage and right axis deviation may be present, the P wave is generally present, though often peaked.

Question 1537: Which of the following is associated with WPW syndrome?

A. Ebstein anomaly (Correct Answer)
B. TOF
C. VSD
D. TAPVC

Explanation: ***Ebstein anomaly*** - **Ebstein anomaly** is a congenital heart defect characterized by apical displacement of the septal and posterior leaflets of the tricuspid valve, which is strongly associated with **Wolff-Parkinson-White (WPW) syndrome.** - WPW syndrome, involving an **accessory pathway** that bypasses the AV node [1], is found in 5-25% of patients with Ebstein anomaly, predisposing them to re-entrant tachycardias [3]. *TOF* - **Tetralogy of Fallot (TOF)** is a complex cyanotic congenital heart defect that includes four main features: VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy [2]. - There is no direct or strong association between TOF and WPW syndrome. *VSD* - A **Ventricular Septal Defect (VSD)** is a common congenital heart defect where there is an opening in the interventricular septum, allowing blood to flow between the ventricles [4]. - While VSDs can occur with other cardiac anomalies, there is no specific or frequent association with WPW syndrome. *TAPVC* - **Total Anomalous Pulmonary Venous Connection (TAPVC)** is a rare congenital heart defect where all four pulmonary veins connect to the systemic venous circulation instead of the left atrium. - This condition does not have a recognized association with WPW syndrome.

Question 1538: Under which condition are steroids administered in rheumatic fever?

A. Presence of carditis (Correct Answer)
B. Presence of subcutaneous nodules
C. Presence of multiple symptoms
D. Presence of chorea

Explanation: **Presence of carditis** - **Carditis** is the most serious manifestation of **rheumatic fever**, as it can lead to permanent **rheumatic heart disease** [1]. - **Corticosteroids** are administered to reduce the inflammation of the heart in cases of moderate to severe carditis, preventing or minimizing long-term damage [1]. *Presence of subcutaneous nodules* - **Subcutaneous nodules** are a minor manifestation of **rheumatic fever** and do not typically require steroid administration. - They are generally **painless** and resolve spontaneously, and their presence alone does not indicate the need for such aggressive anti-inflammatory treatment. *Presence of multiple symptoms* - The presence of **multiple minor symptoms** or asymptomatic major symptoms (other than **carditis**) does not warrant steroid use. - Steroid administration is reserved for situations with high potential for **morbidity** or **mortality**, such as severe **cardiac inflammation** [1]. *Presence of chorea* - **Sydenham's chorea** is a neurological manifestation of **rheumatic fever** and is usually managed with **antidopaminergic drugs** (e.g., haloperidol) or sedatives. - While it can be distressing, **corticosteroids** are generally not indicated for chorea unless there is co-existing **carditis** [1].

Question 1539: Graham Steell murmur is associated with which of the following conditions?

A. Pulmonary Regurgitation (PR) (Correct Answer)
B. Tricuspid Regurgitation (TR)
C. Tricuspid Stenosis (TS)
D. Pulmonary Stenosis (PS)

Explanation: ***Pulmonary Regurgitation (PR)*** - The **Graham Steell murmur** is a high-pitched, decrescendo early diastolic murmur heard best at the left sternal border associated with **pulmonary hypertension**. [1] - It results from dilation of the pulmonary artery due to **elevated pulmonary pressures**, leading to functional pulmonary valve regurgitation. [1] *Tricuspid Regurgitation (TR)* - TR typically presents as a **holosystolic murmur** best heard at the left lower sternal border, often increasing with inspiration (Carvallo's sign). - It is caused by improper coaptation of the tricuspid valve leaflets, often due to **right ventricular dilation**. *Tricuspid Stenosis (TS)* - TS is characterized by a **diastolic rumble** heard best at the lower left sternal border, often with an opening snap. [2] - It is relatively rare and often associated with **rheumatic heart disease**. *Pulmonary Stenosis (PS)* - PS typically produces a **systolic ejection murmur** heard at the upper left sternal border, often radiating to the back. - It is caused by **obstruction to blood flow** from the right ventricle to the pulmonary artery.

Question 1540: What is the most likely cause of fluid overload in a patient presenting with shortness of breath?

A. Nephritic syndrome
B. Cardiac failure (Correct Answer)
C. TB
D. Portal hypertension

Explanation: ***Cardiac failure*** - **Cardiac failure** leads to reduced cardiac output, causing blood to back up in the **pulmonary and systemic circulation**, resulting in fluid accumulation in the lungs (pulmonary edema), which manifests as **shortness of breath** [1]. - The heart's inability to pump efficiently results in increased hydrostatic pressure in capillaries, pushing fluid into interstitial spaces and pleural effusions, exacerbating respiratory distress [1]. *Nephritic syndrome* - **Nephritic syndrome** is characterized by inflammation of the glomeruli, leading to **hematuria, proteinuria, and hypertension**. While it can cause fluid retention due to impaired kidney function, it primarily presents with acute renal injury and less direct, rapid onset pulmonary edema compared to cardiac failure. - The fluid accumulation in **nephritic syndrome** is more generalized (edema) rather than acutely focused on pulmonary congestion leading to shortness of breath, as seen in heart failure. *TB* - **Tuberculosis (TB)** primarily affects the lungs, causing **inflammation, granuloma formation, and tissue destruction**, but usually does not directly cause acute fluid overload and pulmonary edema leading to shortness of breath in the manner that heart failure does. - While **TB** can cause pleural effusions, it is not typically associated with widespread fluid overload and acute pulmonary congestion as a primary mechanism of shortness of breath. *Portal hypertension* - **Portal hypertension** is an increase in blood pressure within the **portal venous system**, usually due to liver cirrhosis. This primarily leads to fluid accumulation in the **abdominal cavity (ascites)** and sometimes peripheral edema. - While significant ascites can indirectly limit diaphragmatic movement and cause some breathlessness, it does not directly cause the acute **pulmonary edema** and fluid overload that are hallmarks of cardiac failure presenting with severe shortness of breath.

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Coronary Artery Disease and Angina

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Acute Coronary Syndromes

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Heart Failure

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Cardiac Arrhythmias

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Valvular Heart Diseases

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Cardiomyopathies

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Pericardial Diseases

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Congenital Heart Disease in Adults

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Hypertension and Hypertensive Emergencies

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Pulmonary Hypertension

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Non-invasive Cardiac Diagnostics

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Preventive Cardiology

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Cardiology — MCQs

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