Cardiology — MCQs
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Which condition is associated with the ECG pattern known as pseudo P pulmonale?
Downhill esophageal varices develop as a result of obstruction of which vein?
Which of the following features is NOT a characteristic of tetralogy of Fallot?
Which of the following is not seen in patent ductus arteriosus?
Prolonged QT interval is seen in all of the following except
Which of the following statements is true about Prinzmetal's angina?
Which of the following is NOT a clinical sign of widened pulse pressure seen in patients with aortic regurgitation?
Episode of stable angina pectoris typically lasts for
Which of the following is not a contraindication for percutaneous balloon mitral valvotomy?
The most common reentrant tachycardia associated with WPW syndrome is
Cardiology Indian Medical PG Practice Questions and MCQs
Question 1461: Which condition is associated with the ECG pattern known as pseudo P pulmonale?
- A. Hyponatremia
- B. Hypocalcemia
- C. Hypokalemia
- D. Hypercalcemia (Correct Answer)
Explanation: ***Hypercalcemia*** - **Hypercalcemia** can cause a characteristic ECG pattern known as pseudo P pulmonale due to its effects on **myocardial repolarization**. - This condition leads to a **shortened QT interval** which causes the T wave to merge with the P wave, giving the appearance of a tall, peaked P wave. *Hypokalemia* - **Hypokalemia** typically presents with **flattened T waves**, prominent U waves, and ST-segment depression on an ECG [1]. - It can prolong repolarization, which is the opposite effect observed with pseudo P pulmonale [1]. *Hyponatremia* - **Hyponatremia** has a less defined direct effect on ECG patterns compared to other electrolyte imbalances. - Severe hyponatremia may lead to **QRS widening** or **bradycardia**, but not pseudo P pulmonale [1]. *Hypocalcemia* - **Hypocalcemia** characteristically causes **prolongation of the QT interval** on an ECG due to delayed ventricular repolarization [2]. - This is distinct from the shortened QT seen in hypercalcemia that contributes to pseudo P pulmonale.
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 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: 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 1465: 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].
Question 1466: 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 1467: Which of the following is NOT a clinical sign of widened pulse pressure seen in patients with aortic regurgitation?
- A. Corrigan's pulse
- B. Quincke's sign
- C. Pulsus paradoxus (Correct Answer)
- D. De Musset's sign
Explanation: ***Pulsus paradoxus*** - **Pulsus paradoxus** is an abnormally large decrease in **systolic blood pressure and pulse wave amplitude** during inspiration, which is typically associated with **cardiac tamponade** or severe respiratory conditions like **asthma** or **COPD**, not specifically widened pulse pressure in aortic regurgitation. - While it reflects pulse examination, it reflects impaired ventricular filling due to extrinsic compression or lung overinflation, not primarily the consequence of increased stroke volume and rapid diastolic runoff as seen in aortic regurgitation. *Corrigan's pulse* - **Corrigan's pulse** is a **bounding and forceful pulse** that rapidly collapses, often described as a **water-hammer pulse**, which is a classic sign of **aortic regurgitation** due to a high stroke volume and rapid fall in diastolic pressure [1]. - This sign directly reflects the **widened pulse pressure**, where a large systolic ejection causes a strong pulse, followed by a sudden decrease in peripheral pressure [1]. *Quincke's sign* - **Quincke's sign** refers to visible **capillary pulsations** in the nail beds, which are blanching and flushing of the capillaries when gentle pressure is applied to the fingernail, typically indicative of **aortic regurgitation**. - This phenomenon occurs because of the **capillary vasodilation** and the significant **systolic-diastolic pressure difference** transmitted to the peripheral circulation. *De Musset's sign* - **De Musset's sign** is a rhythmic **head nodding with each heartbeat**, which is an uncommon but specific sign of **severe aortic regurgitation** [1]. - This physical manifestation results from the **large stroke volume** and **widened pulse pressure** leading to significant movement of the head and neck vessels with each cardiac contraction [1].
Question 1468: Episode of stable angina pectoris typically lasts for
- A. Less than 1 min
- B. 2 - 5 mins (Correct Answer)
- C. 5 - 10 mins
- D. > 10 mins
Explanation: ***2 - 5 mins*** - Episodes of **stable angina pectoris** are typically brief, lasting between 2 and 5 minutes [1]. - The chest discomfort is usually relieved by **rest** or sublingual **nitroglycerin** [1]. *Less than 1 min* - Anginal episodes usually last longer than 1 minute; very brief chest pain is often not typical for angina. - This duration might suggest a different etiology, potentially **musculoskeletal pain** or **esophageal spasm**. *5 - 10 mins* - While a single episode can sometimes last up to 10 minutes, this duration is at the upper limit for typical stable angina. - If pain persists for this long or longer, it raises suspicion for **unstable angina** or **myocardial infarction** [1]. *> 10 mins* - Chest pain lasting longer than 10 minutes is usually concerning for **unstable angina** or an **acute myocardial infarction** [1]. - It requires urgent medical evaluation to rule out more serious cardiac events.
Question 1469: 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 1470: 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.
Practice by Chapter
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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