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: 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 1463: 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 1464: 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 1465: 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 1466: 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 1467: Which of the following is not a contraindication for percutaneous balloon mitral valvotomy?

A. Severe mitral regurgitation
B. Commissural calcification
C. Left atrial thrombus
D. Presence of pulmonary hypertension (Correct Answer)

Explanation: Presence of pulmonary hypertension - The presence of **pulmonary hypertension** is typically an indication, not a contraindication, for percutaneous balloon mitral valvotomy, as reducing mitral stenosis can alleviate pulmonary pressures. [1] - Alleviating the **mitral valve obstruction** can improve forward flow and reduce back pressure on the pulmonary circulation. *Left atrial thrombus* - A **left atrial thrombus** is a contraindication as it poses a significant risk of systemic embolism during the procedure. [1] - Imaging, typically transesophageal echocardiography, is performed to rule out thrombosis before the procedure. *Severe mitral regurgitation* - **Severe mitral regurgitation** is a contraindication because the procedure aims to open the mitral valve, which could worsen an already problematic regurgitation. - In such cases, **surgical repair** or replacement is usually a more appropriate intervention. *Commissural calcification* - **Significant commissural calcification** is a contraindication as it hinders successful balloon inflation and increases the risk of complications such as leaflet tearing or inadequate valve opening. - The presence of calcification often indicates a less pliable valve that is unlikely to respond well to balloon dilatation.

Question 1468: HOCM is common in which age group?

A. 10 - 30 years
B. 20 - 40 years (Correct Answer)
C. 30 - 50 years
D. 40 - 60 years

Explanation: ***20 - 40 years*** - **Hypertrophic obstructive cardiomyopathy (HOCM)** is most commonly diagnosed in young to middle-aged adults, often presenting with symptoms during this age range [1]. - While it is a genetic condition present from birth, symptoms and diagnosis frequently occur in individuals who are **20 to 40 years old** [1]. *10 - 30 years* - While HOCM can manifest in adolescence, the peak incidence and symptomatic presentation typically extend into the 30s, making this range too narrow. - Many individuals in this group might be diagnosed during routine screenings or due to family history, but active symptom presentation often continues beyond 30 [1]. *30 - 50 years* - This age group is partially correct, but the onset often begins earlier, in the 20s. - Significant clinical manifestations and diagnoses are often made before the age of 30, making the 20-40 range more accurate for typical presentation. *40 - 60 years* - Although HOCM can persist and cause problems in older age, initial diagnoses and symptom onset are less common in this age group compared to younger adults [1]. - Patients diagnosed in this range often represent later presentations or milder forms that become symptomatic with aging [1].

Question 1469: Which of the following is NOT a feature of aortic stenosis?

A. Presence of pulsus tardus
B. Presence of ejection systolic murmur
C. Pressure in the aorta is the same as in the left ventricle (Correct Answer)
D. Congestive heart failure

Explanation: ***Pressure in the aorta is the same as in the left ventricle*** - In **aortic stenosis**, there is a significant pressure gradient across the aortic valve during systole [2], meaning the **left ventricular pressure** is much higher than the **aortic pressure** to overcome the narrowed opening. - If the pressures were the same, it would indicate an unimpeded flow, suggesting the absence of significant stenosis. *Presence of ejection systolic murmur* - An **ejection systolic murmur** is a classic auscultatory finding in aortic stenosis, resulting from turbulent blood flow across the narrowed valve during systole [2]. [1] - This murmur is typically heard best at the **right upper sternal border** and radiates to the carotid arteries [2]. *Presence of pulsus tardus* - **Pulsus tardus** (or pulsus parvus et tardus) refers to a pulse that is weak (parvus) and delayed (tardus), which is characteristic of significant aortic stenosis [2]. - This occurs because the left ventricle ejects blood slowly and with reduced peak velocity into the aorta due to the **obstruction** at the valve. *Congestive heart failure* - **Congestive heart failure (CHF)** is a common complication of severe aortic stenosis. - The increased afterload on the left ventricle leads to **left ventricular hypertrophy** and eventual dysfunction, causing symptoms such as dyspnea, fatigue, and edema [1].

Question 1470: 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.

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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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