Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1461: A patient presents with chest pain and an ECG showing ST-segment elevation. After treatment, the ECG shows resolution of ST-segment changes, but the patient continues to have chest pain. What is the most likely diagnosis?

A. Acute myocardial infarction
B. Myocarditis
C. Pericarditis
D. Takotsubo cardiomyopathy (Correct Answer)

Explanation: ***Takotsubo cardiomyopathy*** - Characterized by **transient ventricular dysfunction** (often apical ballooning) mimicking a heart attack, usually triggered by severe emotional or physical stress. - **Resolution of ST-segment elevation** but persistent chest pain after initial presentation, especially if coronary angiography is normal, strongly suggests this diagnosis. *Acute myocardial infarction* - While initially presenting with **ST-segment elevation** and chest pain, resolution of ST-segment changes without corresponding clinical improvement or complete resolution of symptoms would be unusual without reperfusion, and persistent pain might indicate ongoing ischemia or complications [1], [2]. - The key difference here is the **spontaneous resolution of ST elevation** while pain persists, and the absence of clear coronary artery occlusion in Takotsubo. *Myocarditis* - **Myocarditis** can cause chest pain and ECG abnormalities, including ST-segment elevation, but the specific pattern of resolution of ST changes with persistent pain and the typical trigger of emotional stress are less characteristic. - Diagnosis often involves **cardiac MRI** showing inflammation and is not characterized by the quick resolution of acute ECG changes seen here. *Pericarditis* - Pericarditis typically presents with **pleuritic chest pain** that is relieved by leaning forward, and diffused ST-segment elevation (often PR depression) followed by T-wave inversions. - The **resolution of ST-segment changes** mentioned, especially in the context of an initial ST elevation that might mimic an MI, does not fit the typical evolutionary ECG changes of pericarditis.

Question 1462: Downhill esophageal varices develop as a result of obstruction of which vein?

A. Portal vein
B. Hepatic vein
C. Superior vena cava (Correct Answer)
D. Inferior vena cava

Explanation: ***Superior vena cava*** - Downhill esophageal varices are caused by obstruction of the **superior vena cava (SVC)**, leading to increased pressure in the venous drainage of the upper esophagus. - The collateral circulation needed to bypass the SVC obstruction involves veins that drain into the **azygos system**, which then communicates with the esophageal veins. *Portal vein* - Obstruction of the **portal vein** or portal hypertension typically leads to **uphill esophageal varices**, affecting the lower esophagus [1]. - These varices are part of the collateral circulation formed to decompress the portal system, often seen in conditions like **cirrhosis** [1]. *Hepatic vein* - Obstruction of the **hepatic veins** (e.g., Budd-Chiari syndrome) causes blood to back up into the liver, leading to **portal hypertension** and potentially uphill esophageal varices. - This condition primarily affects the liver and causes a distinct clinical picture of ascites, hepatomegaly, and abdominal pain, not directly downhill varices. *Inferior vena cava* - Obstruction of the **inferior vena cava (IVC)** primarily affects venous return from the lower body and the liver (if above the hepatic veins). - While it can indirectly affect portal pressure if liver drainage is compromised, it is not the direct cause of esophageal varices, especially not the downhill type, which involves the superior venous drainage.

Question 1463: Which of the following is not seen in patent ductus arteriosus?

A. Left atrial hypertrophy
B. Left ventricular enlargement
C. Continuous murmur
D. Attenuated S1 (Correct Answer)

Explanation: ***Attenuated S1*** - A **patent ductus arteriosus (PDA)** typically presents with a loud **S1 sound** due to increased blood flow through the mitral and tricuspid valves. - An attenuated, or soft, S1 would suggest impaired ventricular filling or reduced ventricular contractility, which is not characteristic of PDA. *Left atrial hypertrophy* - In a PDA, blood shunts from the aorta to the pulmonary artery, leading to **increased pulmonary blood flow** and **pulmonary venous return to the left atrium** [1]. - This chronic volume overload causes **left atrial dilation** and subsequent hypertrophy as it works harder to pump excess blood into the left ventricle. *Left ventricular enlargement* - The increased pulmonary venous return from the PDA results in **volume overload** of the left ventricle [1]. - The left ventricle has to pump a larger volume of blood, leading to **left ventricular dilation** and hypertrophy over time [1]. *Continuous murmur* - The classic physical finding in PDA is a **continuous "machinery-like" murmur**, best heard at the upper left sternal border [1]. - This murmur is continuous because blood flows from the higher-pressure aorta into the lower-pressure pulmonary artery throughout both systole and diastole [1].

Question 1464: Which of the following features is NOT a characteristic of tetralogy of Fallot?

A. Right ventricular hypertrophy
B. Pulmonary stenosis
C. Atrial septal defect (Correct Answer)
D. Ventricular septal defect

Explanation: ***Atrial septal defect*** - While other **cardiac anomalies** can coexist with Tetralogy of Fallot, an **atrial septal defect (ASD)** is not one of its four defining characteristics. - The classic description of Tetralogy of Fallot includes **pulmonary stenosis**, **right ventricular hypertrophy**, **overriding aorta**, and a **ventricular septal defect.** [1] *Ventricular septal defect* - A **large ventricular septal defect (VSD)** is one of the four essential components of Tetralogy of Fallot, allowing for unoxygenated blood to mix with oxygenated blood. [1] - The size of the **VSD** is typically large and unrestrictive, leading to pressure equalization between the ventricles. [1] *Right ventricular hypertrophy* - **Right ventricular hypertrophy** develops as a compensatory mechanism due to the increased resistance from the **pulmonary stenosis**, making the right ventricle work harder to pump blood. [1] - It is a direct consequence of the elevated pressure in the right ventricle, necessary to overcome the obstruction to pulmonary blood flow. *Pulmonary stenosis* - **Pulmonary stenosis**, or the narrowing of the pulmonary outflow tract, is a critical component that determines the severity of cyanosis in Tetralogy of Fallot. [1] - The degree of **right ventricular outflow tract obstruction** significantly impacts the amount of blood shunted across the VSD and into the aorta.

Question 1465: The most common reentrant tachycardia associated with WPW syndrome is

A. Orthodromic atrioventricular reentry (Correct Answer)
B. Antidromic atrioventricular reentry
C. Rapidly conducting atrial fibrillation
D. None of the options

Explanation: ***Orthodromic atrioventricular reentry*** - This is the **most common type** of reentrant tachycardia in **WPW syndrome**, accounting for approximately 90-95% of cases [2]. - Involves **conduction down the AV node-His-Purkinje system** and **retrograde up the accessory pathway**, resulting in a narrow QRS tachycardia [2]. *Antidromic atrioventricular reentry* - This form of reentrant tachycardia is **less common**, involving conduction **down the accessory pathway** and retrograde up the AV node. - It presents with a **wide QRS complex tachycardia**, mimicking VT, due to ventricular pre-excitation [1]. *Rapidly conducting atrial fibrillation* - While **atrial fibrillation** can occur in WPW syndrome and conduct rapidly across the accessory pathway, it is an **arrhythmia, not a reentrant tachycardia itself** [2]. - Rapid conduction via the accessory pathway during AF can lead to **ventricular fibrillation**, which is life-threatening, but it is not the most common reentrant mechanism [2]. *None of the options* - This option is incorrect as **orthodromic atrioventricular reentry** is indeed the most common reentrant tachycardia in WPW syndrome.

Question 1466: Which of the following ECG features are characteristic of ventricular tachycardia?

A. Bizarre QRS complexes (Correct Answer)
B. Presence of AV dissociation [fusion beats]
C. Prolonged duration of QRS complexes
D. P pulmonale

Explanation: ### Original Explanation ***Bizarre QRS complexes*** - In **ventricular tachycardia (VT)**, the electrical impulse originates from the ventricles, bypassing the normal conduction system [1]. - This leads to **aberrant ventricular activation**, resulting in **wide** and **unusual-looking QRS complexes** [1]. *Presence of AV dissociation [fusion beats]* - While **AV dissociation** can be present in VT, it is **not a universal characteristic** and is often seen in other wide complex tachycardias as well [1]. - **Fusion beats** are a specific type of AV dissociation where a ventricular and supraventricular impulse simultaneously activate the ventricles, which reinforces the diagnosis of VT; however, bizarre QRS complexes are a more direct visual indicator of ventricular origin [1]. *Prolonged duration of QRS complexes* - A prolonged QRS duration (typically **>0.12 seconds**) is characteristic of **wide complex tachycardias**, including VT [1]. - However, the term "bizarre" goes beyond simple prolongation to describe the **unusual morphology and irregular shapes** that are highly suggestive of a ventricular origin [1]. *P pulmonale* - **P pulmonale** refers to a **tall, peaked P wave** in leads II, III, and aVF, indicative of **right atrial enlargement**. - This finding is associated with conditions like **pulmonary hypertension** or **pulmonary embolism** and has no direct relevance to the diagnosis of ventricular tachycardia.

Question 1467: In patients with inferior wall myocardial infarction, reciprocal changes in ECG are typically observed in which of the following leads?

A. I
B. aVL (Correct Answer)
C. II
D. III

Explanation: aVL - In an **inferior wall MI**, the inferior leads (II, III, aVF) show **ST elevation**, while the **anterior-inferior leads**, particularly **aVL**, often show **reciprocal ST depression** [1]. - This reciprocal change indicates **ischemia** in an area opposite to the primary infarction, reflecting the electrical opposition of the injured myocardial regions [3]. *I* - Lead I is a **lateral lead** and typically does not show significant reciprocal changes in inferior wall myocardial infarction. - While it may sometimes show minor changes, **aVL** is more characteristic for reciprocal changes in this context due to its superior orientation. *II* - Lead II is an **inferior lead** and would show primary signs of an **inferior wall MI**, such as **ST elevation**, not reciprocal changes [2]. - Reciprocal changes are seen in leads electrically opposite to the area of infarction. *III* - Lead III is also an **inferior lead** and would display primary **ST elevation** during an inferior wall MI [2]. - It does not show reciprocal changes as it is directly involved in sensing the electrical activity of the infarcted inferior wall.

Question 1468: Ejection click of pulmonary stenosis is better heard in

A. Patient bending forward
B. Patient lying in left lateral position
C. Expiration
D. Inspiration (Correct Answer)

Explanation: Inspiration - The **pulmonic ejection click** is associated with the opening of a **domed pulmonary valve** during systole [1]. - During **inspiration**, increased right ventricular filling causes more blood to be ejected, leading to earlier and louder opening of the stenotic pulmonary valve, making the click more prominent. Expiration - During **expiration**, venous return to the right side of the heart is reduced, decreasing right ventricular volume and making the pulmonic ejection click less noticeable or even absent. - This respiratory variation helps distinguish a pulmonic ejection click from an aortic ejection click, which does not vary with respiration [1]. Patient bending forward - **Bending forward** is a maneuver primarily used to accentuate **aortic regurgitation** murmurs, not to optimize the hearing of a pulmonic ejection click. - This position brings the heart closer to the chest wall, enhancing sounds originating from the left side of the heart. Patient lying in left lateral position - The **left lateral position** is commonly used to accentuate **mitral valve** sounds, such as the opening snap of mitral stenosis or the murmur of mitral regurgitation [1]. - This position does not specifically improve the audibility of a pulmonic ejection click.

Question 1469: Which of the following statements is true about Prinzmetal's angina?

A. Occurs due to atherosclerotic obstruction of coronary arteries
B. It typically occurs during exercise
C. May present at rest (Correct Answer)
D. Beta-blockers are the first-line treatment for Prinzmetal's angina.

Explanation: ***May present at rest*** - Prinzmetal's angina, also known as **variant angina**, is characterized by episodes of chest pain that typically occur at **rest**, often in the early morning hours, which is a key distinguishing feature from stable angina. - This presentation at rest is due to transient **coronary artery spasm**, reducing blood flow to the myocardium. *Occurs due to atherosclerotic obstruction of coronary arteries* - While patients with Prinzmetal's angina may have some underlying atherosclerosis, the direct cause of the anginal episodes is **coronary artery spasm**, not fixed atherosclerotic obstruction. - **Stable angina** and **unstable angina** are primarily caused by atherosclerotic narrowing. *It typically occurs during exercise* - **Stable angina**, not Prinzmetal's angina, is the type of angina that typically occurs during **physical exertion** or emotional stress. - Prinzmetal's angina is notable for its occurrence at rest, often without clear precipitating factors, distinguishing it from exertional angina. *Beta-blockers are the first-line treatment for Prinzmetal's angina.* - **Calcium channel blockers** (e.g., diltiazem, verapamil, nifedipine) and **nitrates** are the first-line treatments for Prinzmetal's angina because they help relax the coronary arteries and prevent spasm. - **Beta-blockers** are generally avoided or used with caution in Prinzmetal's angina as they can potentially worsen coronary artery spasm.

Question 1470: Prolonged QT interval is seen in all of the following except

A. Hypokalemia
B. Hypocalcemia
C. Hypernatremia (Correct Answer)
D. Use of macrolide antibiotics

Explanation: ***Hypernatremia*** - **Hypernatremia** does not typically cause a prolonged QT interval; instead, it tends to cause **shortening of the QT interval** due to its effect on cardiomyocyte repolarization. - The primary cardiac effects of hypernatremia involve alterations in **myocardial contractility** and **arrhythmia risk**, but not QT prolongation. *Hypokalemia* - **Hypokalemia** leads to changes in myocardial repolarization, causing **QT prolongation** which increases the risk of **Torsades de Pointes** [1], [2]. - This occurs because low potassium levels affect the outward potassium currents, extending the action potential duration. *Hypocalcemia* - **Hypocalcemia** prolongs the **QT interval** by extending the ST segment duration without significantly affecting the T wave morphology directly. - Reduced extracellular calcium levels interfere with the voltage-gated calcium channels, impacting the plateau phase of the cardiac action potential. *Use of macrolide antibiotics* - Many **macrolide antibiotics**, such as **azithromycin** and **erythromycin**, are known to inhibit cardiac potassium channels (specifically **IKr current**), thereby prolonging the QT interval [2]. - This effect can lead to a significant risk of **ventricular arrhythmias**, including **Torsades de Pointes** [2], [3].

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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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Cardiology — MCQs

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