Cardiology Practice Questions

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 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: 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: In a clinical context, the most common toxin causing Dilated Cardiomyopathy is:

Alcohol. ***Alcohol*** - Chronic excessive **alcohol consumption** is a well-established and prevalent cause of **dilated cardiomyopathy (DCM)**, leading to alcoholic cardiomyopathy [1]. - Alcohol and its metabolite, **acetaldehyde**, have direct toxic effects on **myocardial cells**, impairing contractility and leading to ventricular dilation [1]. *Chemotherapeutic agents* - Certain **chemotherapeutic agents**, such as **anthracyclines** (e.g., doxorubicin), can cause dose-dependent cardiotoxicity leading to DCM. - While significant, their incidence of causing DCM is less common in the general population compared to alcohol abuse. *Heavy metal* - **Heavy metal toxicity**, particularly from **lead**, **mercury**, or **cobalt**, can contribute to cardiomyopathy. - This is a less common cause of DCM in clinical practice compared to alcohol, often seen in specific industrial exposures or poisoning. *Occupational exposure* - **Occupational exposures** to certain chemicals or toxins can rarely cause DCM, but this category is broad and less frequently implicated than alcohol. - Specific toxins would need to be identified; without that, it's not the most common clinical cause.

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

aVL. 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.

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

Bizarre QRS complexes. ### 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.

Q: The most common reentrant tachycardia associated with WPW syndrome is

Orthodromic atrioventricular reentry. ***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.

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.

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

Pressure in the aorta is the same as in the left ventricle. ***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 1

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 2

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 3

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 4

In a clinical context, the most common toxin causing Dilated Cardiomyopathy is:

Accepted Answer

Alcohol

Answer

Chemotherapeutic agents

Answer

Heavy metal

Answer

Occupational exposure

Question 5

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 6

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

Accepted Answer

aVL

Answer

I

Answer

II

Answer

III

Question 7

Which of the following ECG features are characteristic of ventricular tachycardia?

Accepted Answer

Bizarre QRS complexes

Answer

Presence of AV dissociation [fusion beats]

Answer

Prolonged duration of QRS complexes

Answer

P pulmonale

Question 8

The most common reentrant tachycardia associated with WPW syndrome is

Accepted Answer

Orthodromic atrioventricular reentry

Answer

Antidromic atrioventricular reentry

Answer

Rapidly conducting atrial fibrillation

Answer

None of the options

Question 9

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

Question 10

Which of the following is NOT a feature of aortic stenosis?

Accepted Answer

Pressure in the aorta is the same as in the left ventricle

Answer

Presence of pulsus tardus

Answer

Presence of ejection systolic murmur

Answer

Congestive heart failure

Cardiology — MCQs

Cardiology — MCQs

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