Cardiology Practice Questions

Q: Bacterial endocarditis is rarely seen in which of the following cardiac conditions?

Secundum Atrial Septal Defect (ASD). The susceptibility to **Infective Endocarditis (IE)** is primarily determined by the presence of high-velocity turbulent blood flow. Turbulence causes endothelial damage, leading to the deposition of fibrin and platelets (non-bacterial thrombotic endocarditis), which serves as a nidus for bacterial colonization during bacteremia. **Why Secundum ASD is the Correct Answer:** In a Secundum Atrial Septal Defect, the pressure gradient between the left and right atrium is **minimal**. Consequently, the shunt is characterized by **low-velocity, non-turbulent flow**. This lack of significant turbulence means the endocardium remains intact, making the risk of IE extremely low [1]. Therefore, antibiotic prophylaxis is generally not recommended for isolated ASDs. **Analysis of Incorrect Options:** * **VSD (Option A):** Small to medium VSDs involve a high-pressure gradient between the ventricles, creating high-velocity jets that damage the right ventricular endocardium [1]. * **PDA (Option B):** The high pressure difference between the aorta and the pulmonary artery creates significant turbulence at the pulmonary end of the ductus. * **MVP (Option C):** Mitral regurgitation associated with MVP creates turbulent flow back into the atrium, increasing IE risk, especially if the leaflets are thickened. **NEET-PG High-Yield Pearls:** * **Highest Risk Conditions:** Prosthetic heart valves, previous IE, and cyanotic congenital heart disease (e.g., Tetralogy of Fallot). * **Lowest Risk Conditions:** Secundum ASD, s/p 6 months of successful repair of VSD/PDA/ASD, and physiological/innocent murmurs. * **Common Site:** In VSD, the vegetation usually forms on the **right ventricular side** of the defect (the "jet strike" area).

Q: Comment on the ECG finding shown below?

Epsilon wave. ***Epsilon wave*** - A **small deflection** after the QRS complex that represents **delayed activation** of parts of the right ventricle, pathognomonic for **arrhythmogenic right ventricular cardiomyopathy (ARVC)**. - ARVC involves **fibro-fatty replacement** of right ventricular myocardium, commonly affects **young athletes**, and carries high risk of **sudden cardiac death**. *Delta wave* - Represents **pre-excitation** via an **accessory pathway** in **Wolff-Parkinson-White syndrome**, appearing as a **slurred upstroke** of the QRS complex. - Associated with **short PR interval** and **wide QRS complex**, not the small post-QRS deflection seen in epsilon waves. *Prominent U wave* - A **positive deflection** after the T wave, commonly seen in **hypokalemia**, **bradycardia**, or **quinidine toxicity**. - Appears as a **separate wave** following the T wave, distinct from the small post-QRS epsilon wave pattern. *Deep Q wave* - Represents **myocardial necrosis** in **myocardial infarction**, appearing as **deep negative deflections** at the beginning of the QRS complex. - Indicates **full-thickness myocardial damage** and is unrelated to the conduction abnormalities seen in ARVC.

Q: A 55-year-old female presents with Levine sign, hiccups, and vomiting episodes. On examination, HR=50/min with BP =100/60 mm Hg with elevated JVP. ECG technician is yet to arrive. Which coronary artery is likely to be involved?

RCA. ### Explanation The clinical presentation points toward an **Inferior Wall Myocardial Infarction (IWMI)** with Right Ventricular (RV) involvement. **1. Why RCA is the correct answer:** * **Levine Sign:** Indicates ischemic chest pain. * **Hiccups and Vomiting:** These are classic "autonomic symptoms" often associated with inferior wall MI due to irritation of the **vagus nerve** (Bezold-Jarisch reflex) and diaphragmatic irritation [2]. * **Bradycardia (HR=50/min):** The **Right Coronary Artery (RCA)** supplies the SA node (in 60% of people) and the AV node (in 90%). Ischemia to the RCA frequently leads to sinus bradycardia or AV blocks [2]. * **Elevated JVP + Hypotension:** This triad (with clear lungs) suggests **Right Ventricular Infarction**, which occurs in nearly 40% of RCA-related inferior MIs [2]. **2. Why other options are incorrect:** * **LAD (Left Anterior Descending):** Usually causes Anterior Wall MI. This typically presents with tachycardia (due to sympathetic activation) and signs of left heart failure (pulmonary edema), not bradycardia or elevated JVP. * **LCX (Left Circumflex):** Supplies the lateral wall. While it can occasionally supply the inferior wall (in left-dominant circulation), the combination of bradycardia and RV involvement is much more characteristic of the RCA [1]. * **Left Main:** Occlusion usually leads to massive anterolateral infarction, cardiogenic shock, and high mortality; it does not typically present with isolated inferior/RV symptoms. **Clinical Pearls for NEET-PG:** * **Bezold-Jarisch Reflex:** Triad of bradycardia, hypotension, and apnea triggered by inferior wall ischemia [3]. * **RV Infarction Management:** Avoid nitrates, diuretics, and morphine (they decrease preload). The treatment of choice is **IV fluids** to maintain right-sided filling pressures. * **ECG Clue:** ST-elevation in Lead III > Lead II strongly suggests RCA over LCX.

Q: Congenital long QT syndrome can lead to which of the following?

Polymorphic ventricular tachycardia. **Explanation:** **Congenital Long QT Syndrome (LQTS)** is a channelopathy caused by mutations in cardiac ion channels (most commonly K+ or Na+), leading to delayed ventricular repolarization [3]. This delay is reflected as a prolonged QT interval on an ECG. **Why the correct answer is right:** The hallmark complication of LQTS is **Torsades de Pointes (TdP)**, a specific form of **polymorphic ventricular tachycardia** [1]. The prolonged repolarization phase makes the myocardium vulnerable to "early after-depolarizations" (EADs). If these EADs reach a threshold, they trigger a run of rapid, irregular QRS complexes that appear to "twist" around the isoelectric line. This can lead to syncope, seizures, or degenerate into ventricular fibrillation and sudden cardiac death [1], [2]. **Why the incorrect options are wrong:** * **A. Complete heart block:** This is a conduction failure between the atria and ventricles (AV node pathology), not a repolarization abnormality. * **C. Acute myocardial infarction:** This is caused by coronary artery occlusion and ischemia, whereas LQTS is a primary electrical/genetic disorder. * **D. Recurrent supraventricular tachycardia (SVT):** SVTs originate above the Bundle of His. LQTS specifically affects ventricular repolarization, leading to ventricular, not supraventricular, arrhythmias. **High-Yield Clinical Pearls for NEET-PG:** * **Romano-Ward Syndrome:** Autosomal dominant, pure cardiac involvement (most common). * **Jervell and Lange-Nielsen Syndrome:** Autosomal recessive, associated with **sensorineural deafness**. * **Triggers:** TdP in LQTS is often triggered by sympathetic stimulation (exercise, sudden noise, or emotional stress) [1]. * **Management:** Beta-blockers (Propranolol/Nadolol) are the first-line treatment; ICDs are used for high-risk patients [1].

Q: Which condition is most likely associated with the given ECG tracing?

Renal failure. ***Renal failure*** - **Hyperkalemia** from impaired potassium excretion leads to characteristic ECG changes including **peaked T waves**, **widened QRS complexes**, and potential **sine wave** pattern. - Progressive ECG changes occur as potassium levels rise: **peaked T waves** → **PR prolongation** → **QRS widening** → **sine wave** → **asystole**. *Conn's syndrome* - Causes **hypokalemia** due to excess mineralocorticoid activity, leading to **flattened T waves** and **U waves**, not peaked T waves. - Associated with **hypertension** and **metabolic alkalosis**, but ECG changes are opposite to those seen in hyperkalemia. *Multiple myeloma* - Primarily causes **hypercalcemia** which produces **shortened QT intervals** on ECG, not the peaked T waves of hyperkalemia. - May also cause **renal dysfunction** as a secondary effect, but the primary electrolyte abnormality is elevated calcium. *SIADH* - Results in **hyponatremia** which typically does not produce specific characteristic ECG changes like peaked T waves. - May cause **nonspecific ST-T wave changes** in severe cases, but hyperkalemic ECG patterns are not associated with low sodium levels.

Q: What is the most common valvular lesion seen with carcinoid syndrome?

Tricuspid insufficiency and pulmonic stenosis. ### Explanation **Underlying Medical Concept** Carcinoid heart disease occurs in approximately 50% of patients with systemic carcinoid syndrome (usually from metastatic neuroendocrine tumors). The pathology is driven by high circulating levels of **serotonin (5-HT)**, which causes plaque-like fibrous endocardial thickening. These plaques predominantly affect the **right side of the heart**. The serotonin causes the tricuspid valve leaflets to become thickened, shortened, and retracted, leading to **Tricuspid Insufficiency (Regurgitation)** [1]. Simultaneously, the pulmonic valve cusps become scarred and immobile, leading to **Pulmonic Stenosis**. **Analysis of Options** * **Option B (Correct):** Serotonin-induced fibrosis typically results in a "fixed" open tricuspid valve (Insufficiency) and a narrowed pulmonic orifice (Stenosis). [1] * **Option A:** While pulmonic stenosis is correct, the tricuspid valve is more commonly incompetent (regurgitant) than stenotic. * **Options C & D:** Left-sided lesions (Mitral/Aortic) are **rare** because the lungs contain **monoamine oxidase (MAO)**, which inactivates serotonin before it reaches the left heart. Left-sided involvement only occurs in the presence of a right-to-left shunt (e.g., PFO) or primary bronchial carcinoids. **NEET-PG High-Yield Pearls** * **Biochemical Marker:** 24-hour urinary **5-HIAA** (metabolite of serotonin) is used for diagnosis. * **Location:** Right-sided lesions are the hallmark. [1] * **Pathognomonic Feature:** Glistening white "carcinoid plaques" on the endocardial surface. * **Management:** Somatostatin analogues (Octreotide) help control symptoms, but definitive treatment for severe valve disease is surgical replacement.

Q: Wolff-Parkinson-White (WPW) syndrome is characterized by which of the following electrocardiographic findings?

Delta wave. **Explanation:** **Wolff-Parkinson-White (WPW) Syndrome** is a pre-excitation syndrome caused by the presence of an accessory pathway (the **Bundle of Kent**) that bypasses the AV node [1]. This allows electrical impulses to reach the ventricles earlier than usual. 1. **Why "Delta wave" is correct:** In WPW, the impulse travels through the accessory pathway faster than the slow-conducting AV node. This results in premature ventricular depolarization, which manifests on an ECG as a slurred upstroke of the QRS complex, known as a **Delta wave** [1]. Because of this pre-excitation, the **PR interval is shortened (<0.12s)** and the **QRS complex is widened** [1], [2]. 2. **Why other options are incorrect:** * **Prolonged PR interval:** This is characteristic of First-degree AV block. In WPW, the PR interval is characteristically *shortened* because the AV nodal delay is bypassed [1]. * **U wave:** This is a small wave following the T wave, most commonly associated with **hypokalemia**, hypercalcemia, or thyrotoxicosis. * **Heart block:** This refers to a delay or interruption in conduction (e.g., AV block), whereas WPW is a state of "accelerated" conduction. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Short PR interval ( 120ms) [1]. * **Associated Arrhythmia:** Most commonly associated with AV Reentrant Tachycardia (AVRT) [2]. * **Drug Contraindication:** Avoid **ABCD** drugs (Adenosine, Beta-blockers, Calcium channel blockers, Digoxin) in WPW with Atrial Fibrillation, as they block the AV node and may favor conduction through the accessory pathway, leading to Ventricular Fibrillation [2]. * **Definitive Treatment:** Radiofrequency ablation of the accessory pathway.

Question 1

Bacterial endocarditis is rarely seen in which of the following cardiac conditions?

Accepted Answer

Secundum Atrial Septal Defect (ASD)

Answer

Ventricular Septal Defect (VSD)

Answer

Patent Ductus Arteriosus (PDA)

Answer

Mitral Valve Prolapse (MVP)

Question 2

Comment on the ECG finding shown below?

Accepted Answer

Epsilon wave

Answer

Delta wave

Answer

Prominent U wave

Answer

Deep Q wave

Question 3

A 55-year-old female presents with Levine sign, hiccups, and vomiting episodes. On examination, HR=50/min with BP =100/60 mm Hg with elevated JVP. ECG technician is yet to arrive. Which coronary artery is likely to be involved?

Accepted Answer

RCA

Answer

LAD

Answer

LCX

Answer

Left main coronary artery

Question 4

Congenital long QT syndrome can lead to which of the following?

Accepted Answer

Polymorphic ventricular tachycardia

Answer

Complete heart block

Answer

Acute myocardial infarction

Answer

Recurrent supraventricular tachycardia

Question 5

Which condition is most likely associated with the given ECG tracing?

Accepted Answer

Renal failure

Answer

Conn's syndrome

Answer

Multiple myeloma

Answer

SIADH

Question 6

What is the most common valvular lesion seen with carcinoid syndrome?

Accepted Answer

Tricuspid insufficiency and pulmonic stenosis

Answer

Tricuspid stenosis and pulmonic stenosis

Answer

Mitral stenosis and aortic stenosis

Answer

Mitral insufficiency and aortic stenosis

Question 7

Wolff-Parkinson-White (WPW) syndrome is characterized by which of the following electrocardiographic findings?

Accepted Answer

Delta wave

Answer

Prolonged PR interval

Answer

U wave

Answer

Heart block

Question 8

Which one of the following is of most serious prognostic significance in a patient of essential hypertension?

Accepted Answer

Papilledema and progressive renal failure

Answer

Diastolic blood pressure greater than 130 mmHg

Answer

Transient ischemic attacks

Answer

Left ventricular hypertrophy

Question 9

Increased AV nodal blockade leads to termination of tachycardia in all except?

Accepted Answer

Atrial flutter

Answer

Atrial tachycardia

Answer

AVN

Answer

Orthodromic AV re-entry

Question 10

A 48-year-old, previously healthy woman reports having suddenly lost consciousness four times in the past 6 months. In three instances, she was unconscious for only a few minutes. After the fourth episode 1 month ago, she was unconscious for 6 hours and had weakness in her right arm and difficulty speaking. On physical examination, she is afebrile, and her blood pressure is normal. No murmurs are auscultated. She has good carotid pulses with no bruits. Which of the following cardiac lesions is most likely to be present in this woman?

Accepted Answer

Left atrial myxoma

Answer

Bicuspid aortic valve

Answer

Coronary artery thrombosis

Answer

Mitral valve stenosis

Cardiology — MCQs

Cardiology — MCQs

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