Cardiology Practice Questions

Q: Congenital long QT syndrome has a tendency to develop which of the following conditions?

Ventricular tachycardia. **Congenital Long QT Syndrome (LQTS)** is a genetic channelopathy characterized by a prolongation of the QT interval on an ECG, reflecting delayed ventricular repolarization [1]. This delay is primarily due to mutations in cardiac ion channels (most commonly K+ or Na+). **Why Ventricular Tachycardia is correct:** The fundamental pathophysiology involves **Early After-Depolarizations (EADs)**. When repolarization is prolonged, calcium channels can recover from inactivation and trigger a premature action potential [2]. If these EADs reach a threshold, they trigger a specific type of polymorphic ventricular tachycardia known as **Torsades de Pointes (TdP)** [1]. TdP can either spontaneously revert to sinus rhythm or degenerate into ventricular fibrillation, leading to syncope or sudden cardiac death [2]. **Why incorrect options are wrong:** * **A & B (Sinus Bradycardia/Tachycardia):** While some forms of LQTS (like LQT1) are triggered by sympathetic activity (tachycardia), the sinus node rhythm itself is not the primary pathology. The life-threatening complication is ventricular, not sinus-driven. * **C (Supraventricular Tachycardia):** SVTs originate above the Bundle of His. LQTS specifically affects the ventricular myocardium's repolarization phase; therefore, the resulting arrhythmias are ventricular in origin. **High-Yield Clinical Pearls for NEET-PG:** * **Romano-Ward Syndrome:** Autosomal Dominant (AD), pure cardiac involvement (most common). * **Jervell and Lange-Nielsen Syndrome:** Autosomal Recessive (AR), associated with **sensorineural deafness**. * **Triggers:** LQT1 (Exercise/Swimming), LQT2 (Auditory stimuli/Emotion), LQT3 (Sleep/Rest). * **Management:** Beta-blockers (Propranolol/Nadolol) are the mainstay; ICD for high-risk patients. Avoid QT-prolonging drugs (e.g., Macrolides, Ondansetron, Class IA/III antiarrhythmics).

Q: A 50-year-old patient complains of dizziness and palpitations. What does the ECG show?

Bradycardia-tachycardia syndrome. ***Bradycardia-tachycardia syndrome*** - Demonstrates **alternating periods** of bradycardia and tachycardia on ECG, characteristic of **sick sinus syndrome** in older patients. - Symptoms of **dizziness and palpitations** correlate with the fluctuating heart rates, requiring **pacemaker therapy** for management. *Mobitz I block* - Shows **progressive PR interval prolongation** followed by a dropped QRS complex in a **Wenckebach pattern**. - Typically **asymptomatic** and does not cause the alternating bradycardia-tachycardia pattern seen in this patient. *Mobitz II block* - Characterized by **sudden dropped QRS complexes** without prior PR interval prolongation, with **constant PR intervals**. - Usually presents with **consistent bradycardia** rather than alternating heart rate patterns with palpitations. *Complete heart block* - Shows **complete AV dissociation** with independent atrial and ventricular rhythms, resulting in **severe bradycardia**. - Presents with **persistent slow heart rate** and does not explain the palpitations from tachycardic episodes.

Q: What are the causes of constrictive pericarditis?

All of the above. **Explanation:** Constrictive pericarditis (CP) is the end-stage result of chronic inflammation of the pericardium, leading to a thickened, fibrotic, and often calcified pericardial sac [1]. This rigid shell restricts diastolic filling of the heart. * **Tuberculosis (Option A):** Globally, and specifically in India, TB remains the **most common cause** of constrictive pericarditis [1]. It typically presents with significant pericardial thickening and "eggshell" calcification on a chest X-ray [1]. * **Systemic Lupus Erythematosus (Option B):** Connective tissue disorders (SLE, Rheumatoid Arthritis, Scleroderma) cause chronic serositis [2]. While SLE more commonly causes acute pericarditis or effusion, chronic inflammation can progress to constriction. * **Histoplasmosis (Option C):** Fungal infections, particularly Histoplasmosis and Coccidioidomycosis, are recognized granulomatous causes of pericardial inflammation that can lead to chronic fibrosis and constriction. Since all three conditions are established etiologies, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause (Developed countries):** Idiopathic or viral, followed by post-cardiac surgery and radiation therapy. 2. **Most common cause (Developing countries/India):** Tuberculosis. 3. **Kussmaul’s Sign:** A paradoxical rise in JVP during inspiration (highly characteristic of CP). 4. **Pericardial Knock:** A high-pitched sound heard in early diastole due to the sudden cessation of ventricular filling. 5. **Imaging Gold Standard:** Cardiac MRI or CT (to measure pericardial thickness; >4mm is suggestive). 6. **Treatment of choice:** Surgical pericardiectomy ("Pericardial stripping").

Q: Which of the following is true regarding neurocardiogenic syncope?

Vasodilation and bradycardia. Explanation: Neurocardiogenic syncope (Vasovagal syncope) is the most common cause of fainting. It is mediated by the **Bezold-Jarisch reflex**, a cardio-inhibitory reflex [1]. **1. Why Option A is correct:** The pathophysiology involves a sudden surge in sympathetic activity followed by a paradoxical, overwhelming parasympathetic (vagal) response [1]. This leads to two primary effects: * **Vasodilation:** Due to sympathetic withdrawal (vasodepressor response), leading to hypotension [1]. * **Bradycardia:** Due to increased vagal tone (cardio-inhibitory response) [1]. The combination of low blood pressure and low heart rate results in cerebral hypoperfusion and loss of consciousness [1][2]. **2. Why other options are incorrect:** * **Option B & C:** The reflex is initiated in the **inferoposterior wall of the left ventricle**. It is triggered by **vigorous/forceful contractions** of a relatively **underfilled (empty) ventricle** (e.g., due to prolonged standing or dehydration) [1]. This stimulates mechanoreceptors (C-fibers) that falsely signal the brain that the heart is overloaded, triggering the reflex. * **Option D:** The reflex occurs when the heart chambers are **depleted of blood** (low preload), not filled [1]. **Clinical Pearls for NEET-PG:** * **Triggers:** Prolonged standing, emotional stress, pain, or sight of blood [1][2]. * **Prodrome:** Characterized by nausea, pallor, diaphoresis (sweating), and blurred vision [2]. * **Diagnosis:** Primarily clinical; **Head-up Tilt Table Test (HUTT)** is the gold standard for confirmation. * **Management:** Reassurance, increasing fluid/salt intake, and physical counter-pressure maneuvers (e.g., leg crossing, handgrip). Midodrine can be used in refractory cases.

Q: What is the earliest feature of pulmonary venous hypertension?

Upper lobar vessel dilatation. **Explanation:** Pulmonary venous hypertension (PVH) occurs when the left heart fails to pump blood efficiently, leading to increased pressure in the pulmonary veins. This process follows a predictable radiological sequence on a chest X-ray: **1. Why "Upper lobar vessel dilatation" is correct:** This is the earliest sign of PVH (Grade 1). Normally, in an upright position, gravity causes the lower lobe vessels to be larger than the upper lobe vessels. When pulmonary venous pressure rises (12–18 mmHg), it triggers reactive vasoconstriction in the lower lobes. Blood is then shunted to the upper lobes, causing the upper lobe vessels to dilate. This phenomenon is known as **Cephalization** or **Antler Sign**. **2. Why the other options are incorrect:** * **Kerley B lines:** These represent interstitial edema (Grade 2) and occur when pressures reach 18–25 mmHg. They are horizontal lines at the lung bases representing thickened interlobular septa. They appear *after* cephalization. * **Left atrial enlargement:** While often present in chronic conditions like mitral stenosis, it is a structural cause/consequence rather than a specific radiological feature of the pulmonary vasculature sequence. * **Pleural effusion:** This represents a more advanced stage of heart failure (Grade 3/Alveolar edema) where fluid spills into the pleural space. **Clinical Pearls for NEET-PG:** * **Staging of PVH on CXR:** * **Grade 1 (12-18 mmHg):** Cephalization (Upper lobe diversion). * **Grade 2 (18-25 mmHg):** Interstitial edema (Kerley B lines, peribronchial cuffing). * **Grade 3 (>25 mmHg):** Alveolar edema (Bat-wing appearance, Pleural effusion). * **PCWP Correlation:** Pulmonary Capillary Wedge Pressure (PCWP) is the gold standard for measuring these pressures clinically.

Q: Beck's triad of cardiac tamponade includes:

Hypotension. **Explanation:** Beck’s triad is a classic clinical sign of **acute cardiac tamponade**, first described by Claude Beck in 1935 [1]. It represents the physiological consequences of increased intrapericardial pressure, which restricts diastolic filling of the heart. The triad consists of: 1. **Hypotension:** Due to decreased stroke volume and cardiac output [2]. 2. **Jugular Venous Distension (JVD):** Resulting from impaired venous return to the right atrium. 3. **Muffled (Distant) Heart Sounds:** Caused by the insulating effect of the pericardial fluid between the heart and the chest wall. **Analysis of Options:** * **A. Hypotension (Correct):** This is a core component of the triad. As intrapericardial pressure rises, it exceeds right-sided filling pressures, leading to a drop in cardiac output and systemic blood pressure. * **B. Paradoxical Pulse:** While Pulsus Paradoxus (a drop in systolic BP >10 mmHg during inspiration) is a hallmark finding in tamponade, it is **not** part of Beck’s triad. * **C. Tachycardia:** This is the earliest compensatory mechanism in tamponade to maintain cardiac output, but it is not a component of the triad. * **D. Silent heart sounds:** While heart sounds are "muffled" or "distant," they are rarely completely "silent." The specific terminology used in the triad is muffled heart sounds. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Findings:** Look for low voltage QRS complexes and **Electrical Alternans** (pathognomonic) [1]. * **Chest X-ray:** Shows a "Water-bottle" or "Money-bag" shaped heart (usually in chronic/large effusions) [1]. * **Echocardiography:** The gold standard for diagnosis; shows **early diastolic collapse of the Right Ventricle** and late diastolic collapse of the Right Atrium [1]. * **Management:** Immediate **Pericardiocentesis** is the treatment of choice [1].

Q: A patient develops sudden palpitation with a heart rate of 150 beats per minute, which is regular. What is the most likely cause?

Paroxysmal Supraventricular Tachycardia (PSVT). ### Explanation **1. Why PSVT is the Correct Answer:** The clinical presentation of **sudden onset** palpitations [2] with a **regular** heart rate of exactly **150 bpm** is a classic "textbook" description of Paroxysmal Supraventricular Tachycardia (PSVT), most commonly AVNRT [1]. In PSVT, the heart rate typically ranges between 150–250 bpm [1]. The "paroxysmal" nature refers to the abrupt start and termination [2], which distinguishes it from physiological tachycardias. **2. Analysis of Incorrect Options:** * **Sinus Tachycardia:** While regular, it usually has an identifiable underlying cause (fever, exercise, anxiety) and the rate typically fluctuates. It does not start "suddenly" but rather builds up gradually. * **Ventricular Tachycardia (VT):** While regular, VT usually presents in patients with structural heart disease (e.g., old MI) and often causes hemodynamic instability [3]. While 150 bpm is possible, PSVT is a more common cause of sudden palpitations in a stable patient. * **Atrial Flutter with block:** Atrial flutter typically has an atrial rate of 300 bpm. With a common **2:1 conduction block**, the ventricular rate is indeed exactly 150 bpm. However, PSVT is statistically the more "classic" answer for sudden-onset regular palpitations in exam scenarios unless "saw-tooth waves" are mentioned. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice (Acute):** Adenosine (6mg → 12mg → 12mg rapid IV push). It works by slowing conduction through the AV node. * **Vagal Maneuvers:** Carotid sinus massage or Valsalva maneuver are the first-line non-pharmacological treatments. * **Definitive Treatment:** Radiofrequency Ablation (RFA) of the slow pathway. * **ECG Finding:** Narrow QRS complex tachycardia with absent or retrograde P-waves [1].

Question 1

Congenital long QT syndrome has a tendency to develop which of the following conditions?

Accepted Answer

Ventricular tachycardia

Answer

Sinus bradycardia

Answer

Sinus tachycardia

Answer

Supraventricular tachycardia

Question 2

A 50-year-old patient complains of dizziness and palpitations. What does the ECG show?

Accepted Answer

Bradycardia-tachycardia syndrome

Answer

Mobitz I block

Answer

Mobitz II block

Answer

Complete heart block

Question 3

What are the causes of constrictive pericarditis?

Accepted Answer

All of the above

Answer

Tuberculosis

Answer

Systemic lupus erythematosus

Answer

Histoplasmosis

Question 4

Which of the following is true regarding neurocardiogenic syncope?

Accepted Answer

Vasodilation and bradycardia

Answer

Initiated at the left ventricle

Answer

Associated with forceful contraction of the heart

Answer

Occurs when heart chambers are filled with blood

Question 5

All of the following features suggest broad complex ventricular tachycardia except:

Accepted Answer

QRS duration shown

Answer

P waves on ECG, 'walking through the tachycardia'

Answer

Capture beats

Answer

RBBB with a small R wave and a large R' wave in V1

Question 6

What is the earliest feature of pulmonary venous hypertension?

Accepted Answer

Upper lobar vessel dilatation

Answer

Kerley B lines

Answer

Left atrial enlargement

Answer

Pleural effusion

Question 7

Beck's triad of cardiac tamponade includes:

Accepted Answer

Hypotension

Answer

Paradoxical pulse

Answer

Tachycardia

Answer

Silent heart sounds

Question 8

A patient develops sudden palpitation with a heart rate of 150 beats per minute, which is regular. What is the most likely cause?

Accepted Answer

Paroxysmal Supraventricular Tachycardia (PSVT)

Answer

Sinus Tachycardia

Answer

Ventricular Tachycardia

Answer

Atrial Flutter with block

Question 9

A 35-year-old athlete with a height of 184 cm, arm span of 194 cm, pulse rate of 64/min, and BP of 148/64 mm Hg presents with a long diastolic murmur heard over the right second intercostal space on routine chest auscultation. What is the probable diagnosis?

Accepted Answer

Aortic regurgitation

Answer

Atrial septal defect

Answer

Ebstein anomaly

Answer

Coarctation of the aorta

Question 10

Which of the following conditions is associated with a QRS duration greater than 0.16 seconds?

Accepted Answer

Bundle branch block

Answer

Sick sinus syndrome

Answer

Mobitz type 1 heart block

Answer

Mobitz type 2 heart block

Cardiology — MCQs

Cardiology — MCQs

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