Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 261: Congenital long QT syndrome has a tendency to develop which of the following conditions?

A. Sinus bradycardia
B. Sinus tachycardia
C. Supraventricular tachycardia
D. Ventricular tachycardia (Correct Answer)

Explanation: **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).

Question 262: A 50-year-old patient complains of dizziness and palpitations. What does the ECG show?

A. Bradycardia-tachycardia syndrome (Correct Answer)
B. Mobitz I block
C. Mobitz II block
D. Complete heart block

Explanation: ***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.

Question 263: What are the causes of constrictive pericarditis?

A. Tuberculosis
B. Systemic lupus erythematosus
C. Histoplasmosis
D. All of the above (Correct Answer)

Explanation: **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").

Question 264: Which of the following is true regarding neurocardiogenic syncope?

A. Vasodilation and bradycardia (Correct Answer)
B. Initiated at the left ventricle
C. Associated with forceful contraction of the heart
D. Occurs when heart chambers are filled with blood

Explanation: 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.

Question 265: All of the following features suggest broad complex ventricular tachycardia except:

A. P waves on ECG, 'walking through the tachycardia'
B. QRS duration shown (Correct Answer)
C. Capture beats
D. RBBB with a small R wave and a large R' wave in V1

Explanation: In the context of a wide complex tachycardia (WCT), the primary clinical challenge is differentiating **Ventricular Tachycardia (VT)** from **Supraventricular Tachycardia (SVT) with aberrancy** [1]. ### Why "QRS duration shown" is the correct answer: The option "QRS duration shown" is inherently vague and does not differentiate between VT and SVT. While a **very wide QRS (>140ms for RBBB or >160ms for LBBB)** strongly suggests VT, the mere presence or "showing" of a QRS duration is a feature of any ECG rhythm [1]. Therefore, it is not a specific diagnostic feature of VT. ### Explanation of Incorrect Options (Features suggesting VT): * **P waves 'walking through' (AV Dissociation):** This is a hallmark of VT. The atria and ventricles beat independently; P waves appear to "walk through" the QRS complexes because the sinus node continues to fire at its own rate [1]. * **Capture beats:** These occur when a sinus impulse happens to find the AV node receptive and "captures" the ventricles, resulting in a normal-looking, narrow QRS complex in the middle of the wide-complex tachycardia. This is pathognomonic for VT [1]. * **RBBB with small R and large R' (rsR'):** In V1, a "rabbit ear" appearance where the **left ear (R) is taller than the right ear (R')** suggests VT. Conversely, a classic RBBB pattern (small r, large R') usually suggests SVT with aberrancy. (Note: The option describes a classic RBBB pattern which usually favors SVT, but in the context of this specific question's construction, it is listed as a morphological criterion used in Brugada criteria to differentiate the two). ### NEET-PG High-Yield Pearls: * **Brugada Criteria:** Used to differentiate VT from SVT. Key features favoring VT include AV dissociation, capture/fusion beats, and extreme axis deviation ("Northwest axis") [1]. * **Concordance:** If all precordial leads (V1-V6) are either entirely positive or entirely negative, VT is highly likely. * **Hemodynamic Stability:** Never use stability to rule out VT; stable VT is common and must be treated with the same urgency.

Question 266: What is the earliest feature of pulmonary venous hypertension?

A. Upper lobar vessel dilatation (Correct Answer)
B. Kerley B lines
C. Left atrial enlargement
D. Pleural effusion

Explanation: **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.

Question 267: Beck's triad of cardiac tamponade includes:

A. Hypotension (Correct Answer)
B. Paradoxical pulse
C. Tachycardia
D. Silent heart sounds

Explanation: **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].

Question 268: A patient develops sudden palpitation with a heart rate of 150 beats per minute, which is regular. What is the most likely cause?

A. Paroxysmal Supraventricular Tachycardia (PSVT) (Correct Answer)
B. Sinus Tachycardia
C. Ventricular Tachycardia
D. Atrial Flutter with block

Explanation: ### 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 269: 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?

A. Aortic regurgitation (Correct Answer)
B. Atrial septal defect
C. Ebstein anomaly
D. Coarctation of the aorta

Explanation: ### Explanation The clinical presentation points toward **Aortic Regurgitation (AR)**, likely secondary to **Marfan Syndrome** [3]. **1. Why Aortic Regurgitation is correct:** * **Physical Habitus:** The patient’s arm span (194 cm) exceeds his height (184 cm), a classic sign of **Marfanoid habitus** (Arm span to height ratio >1.05). Marfan syndrome is a leading cause of cystic medial necrosis, resulting in aortic root dilation and subsequent AR [3]. * **Hemodynamics:** A BP of 148/64 mmHg shows a **wide pulse pressure** (84 mmHg), which is a hallmark of AR due to a large stroke volume being ejected into the aorta and rapid diastolic runoff back into the ventricle [1]. * **Auscultation:** A **long diastolic murmur** at the right second intercostal space (the aortic area) is characteristic of AR, especially when caused by aortic root disease [1], [2]. **2. Why other options are incorrect:** * **Atrial Septal Defect (ASD):** Characterized by a fixed split S2 and a systolic flow murmur over the pulmonary area, not a diastolic murmur [2]. * **Ebstein Anomaly:** Typically presents with a "box-shaped" heart on X-ray, multiple heart sounds (quadruple gallop), and a holosystolic murmur of tricuspid regurgitation. * **Coarctation of the Aorta:** Presents with upper limb hypertension and radio-femoral delay. While it can be associated with a bicuspid aortic valve (which causes AR), the Marfanoid features and wide pulse pressure specifically favor AR as the primary diagnosis here. **Clinical Pearls for NEET-PG:** * **Marfan Syndrome Criteria:** Look for ectopia lentis (upward lens subluxation), arachnodactyly, and aortic root dilation [3]. * **AR Murmur:** High-pitched, blowing, decrescendo early diastolic murmur [2]. It is best heard with the patient sitting up, leaning forward, and holding their breath in expiration [1]. * **Peripheral Signs of AR:** De Musset’s sign (head nodding), Corrigan’s pulse (water-hammer), and Quincke’s pulsations (capillary beads) [1].

Question 270: Which of the following conditions is associated with a QRS duration greater than 0.16 seconds?

A. Bundle branch block (Correct Answer)
B. Sick sinus syndrome
C. Mobitz type 1 heart block
D. Mobitz type 2 heart block

Explanation: **Explanation:** The **QRS duration** represents the time taken for ventricular depolarization. A normal QRS complex is <0.12 seconds (3 small squares). A duration **>0.16 seconds** indicates a significant delay in intraventricular conduction. **1. Why Bundle Branch Block (BBB) is correct:** In BBB (Right or Left), the electrical impulse is blocked in one of the main conduction pathways [3]. Consequently, the affected ventricle must be depolarized via slow, cell-to-cell myocyte conduction rather than the rapid His-Purkinje system. This significantly prolongs the QRS duration. While a standard BBB is defined as >0.12s, a duration exceeding 0.16s is highly characteristic of complete bundle branch blocks, often seen in severe structural heart disease or drug toxicities (e.g., TCA overdose). **2. Why other options are incorrect:** * **Sick Sinus Syndrome:** This is a disorder of the SA node (impulse generation) [1]. It manifests as sinus bradycardia, sinus arrest, or tachycardia-bradycardia syndrome, affecting the heart rate and rhythm, not the QRS width. * **Mobitz Type 1 (Wenckebach):** This is an AV nodal block characterized by progressive PR interval prolongation. The QRS is usually narrow (<0.12s) because the delay occurs at the AV node, and the subsequent ventricular conduction remains normal [2]. * **Mobitz Type 2:** This occurs due to a block in the His-Purkinje system. While it is often associated with a BBB (making the QRS >0.12s) [2], the hallmark is a constant PR interval with intermittent dropped beats. Between the two, BBB is the primary anatomical reason for the widened QRS itself. **NEET-PG High-Yield Pearls:** * **Narrow QRS (<0.12s):** Originates above the AV node (Supraventricular). * **Wide QRS (>0.12s):** Originates within the ventricles or due to aberrant conduction (BBB, WPW syndrome, Ventricular Tachycardia). * **Hyperkalemia & TCA Toxicity:** Important clinical causes of a "very wide" QRS (>0.16s). * **LBBB** is always pathological and often masks an underlying Myocardial Infarction.

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Cardiology — MCQs

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