Cardiology Practice Questions

Q: At what time frame does peripartum cardiomyopathy typically occur?

Within 5 months of delivery. ***Within 5 months of delivery*** - **Peripartum cardiomyopathy** is defined as the development of heart failure with **left ventricular systolic dysfunction** occurring during the **last month of pregnancy or within five months after delivery**. - The postpartum component extends up to **5 months (approximately 20 weeks)** after delivery, making this the most complete answer among the given options. - This timeframe is essential for differentiating **peripartum cardiomyopathy** from other forms of cardiomyopathy. *Within 6 weeks of delivery* - While this represents the traditional postpartum period and many cases do present within 6 weeks, the diagnostic definition of **peripartum cardiomyopathy** extends further to **5 months postpartum**. - This narrower timeframe would miss cases presenting between 6 weeks and 5 months, thus not encompassing the full diagnostic criteria. *Within 24 months of delivery* - This timeframe significantly exceeds the established diagnostic window for **peripartum cardiomyopathy**. - Heart failure presenting beyond 5 months postpartum would likely be classified as **dilated cardiomyopathy** or another form of cardiomyopathy with different underlying causes. *Within 7 days of delivery* - This is too narrow a window and represents only the immediate postpartum period. - While some cases can present acutely in the first week, the diagnostic definition allows for onset up to **5 months postpartum**, and limiting it to 7 days would miss the majority of cases.

Q: What is a potential cause of cardiogenic shock other than myocardial infarction (MI)?

Acute mitral regurgitation. ***Acute mitral regurgitation*** - **Acute mitral regurgitation** is a severe form of valvular heart disease where the mitral valve fails to close properly, leading to a sudden backflow of blood into the left atrium during systole. [1] - This significantly reduces **forward cardiac output** and increases left atrial pressure, which can rapidly lead to pulmonary edema and cardiogenic shock, even in the absence of MI. [1] *Ventricular septal rupture* - While a **ventricular septal rupture** can cause cardiogenic shock, it is typically a **complication of myocardial infarction**, meaning it would fall under MI as the underlying cause. [2] - This condition involves a hole in the septum separating the ventricles, leading to a shunt and increased workload on the right ventricle, causing cardiogenic shock. *Isolated right ventricular shock* - **Isolated right ventricular shock** is often caused by conditions like a **massive pulmonary embolism** or a right ventricular infarction. [2] - While it can lead to shock, it is distinct from general cardiogenic shock which often implies left ventricular dysfunction or severe myocardial compromise, and the question asks for a cause *other than* MI, which can cause right ventricular shock. *None of the options* - This option is incorrect because **acute mitral regurgitation** is a distinct and significant cause of cardiogenic shock, independent of MI. [1]

Q: 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?

Takotsubo cardiomyopathy. ***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.

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

Atrial septal defect. ***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.

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

Superior vena cava. ***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.

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

Attenuated S1. ***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].

Q: Which of the following is NOT a clinical sign of widened pulse pressure seen in patients with aortic regurgitation?

Pulsus paradoxus. ***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].

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

Hypernatremia. ***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].

Q: Episode of stable angina pectoris typically lasts for

2 - 5 mins. ***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.

Q: Which of the following is not a contraindication for percutaneous balloon mitral valvotomy?

Presence of pulmonary hypertension. 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 1

At what time frame does peripartum cardiomyopathy typically occur?

Accepted Answer

Within 5 months of delivery

Answer

Within 6 weeks of delivery

Answer

Within 24 months of delivery

Answer

Within 7 days of delivery

Question 2

What is a potential cause of cardiogenic shock other than myocardial infarction (MI)?

Accepted Answer

Acute mitral regurgitation

Answer

Ventricular septal rupture

Answer

Isolated right ventricular shock

Answer

None of the options

Question 3

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?

Accepted Answer

Takotsubo cardiomyopathy

Answer

Acute myocardial infarction

Answer

Myocarditis

Answer

Pericarditis

Question 4

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

Accepted Answer

Atrial septal defect

Answer

Right ventricular hypertrophy

Answer

Pulmonary stenosis

Answer

Ventricular septal defect

Question 5

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

Accepted Answer

Superior vena cava

Answer

Portal vein

Answer

Hepatic vein

Answer

Inferior vena cava

Question 6

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

Accepted Answer

Attenuated S1

Answer

Left atrial hypertrophy

Answer

Left ventricular enlargement

Answer

Continuous murmur

Question 7

Which of the following is NOT a clinical sign of widened pulse pressure seen in patients with aortic regurgitation?

Accepted Answer

Pulsus paradoxus

Answer

Corrigan's pulse

Answer

Quincke's sign

Answer

De Musset's sign

Question 8

Prolonged QT interval is seen in all of the following except

Accepted Answer

Hypernatremia

Answer

Hypokalemia

Answer

Hypocalcemia

Answer

Use of macrolide antibiotics

Question 9

Episode of stable angina pectoris typically lasts for

Accepted Answer

2 - 5 mins

Answer

Less than 1 min

Answer

5 - 10 mins

Answer

> 10 mins

Question 10

Which of the following is not a contraindication for percutaneous balloon mitral valvotomy?

Accepted Answer

Presence of pulmonary hypertension

Answer

Severe mitral regurgitation

Answer

Commissural calcification

Answer

Left atrial thrombus

Cardiology — MCQs

Cardiology — MCQs

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