Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 871: A 42-year-old smoker has developed an acute anterior wall myocardial infarction. Which of the following coronary arteries is most likely to show obstruction?

A. Left anterior descending artery (Correct Answer)
B. Left posterior descending artery
C. Right coronary artery
D. Circumflex artery

Explanation: ### Explanation **Correct Option: A. Left Anterior Descending Artery (LAD)** The **Left Anterior Descending (LAD)** artery is the primary blood supply to the anterior wall of the left ventricle and the anterior two-thirds of the interventricular septum. In clinical practice, the LAD is the most commonly occluded vessel in myocardial infarction (MI). Obstruction of this artery leads to an **Anterior Wall MI**, typically characterized by ST-segment elevation in leads **V1 to V4** on an ECG [1]. **Incorrect Options:** * **B. Left Posterior Descending Artery (PDA):** This artery supplies the posterior and inferior walls of the heart [2]. Occlusion results in an Inferior or Posterior MI. * **C. Right Coronary Artery (RCA):** In 85% of individuals (right-dominant circulation), the RCA gives rise to the PDA. Obstruction usually leads to an **Inferior Wall MI** (leads II, III, aVF) and may involve the Right Ventricle. * **D. Circumflex Artery (LCx):** The LCx supplies the lateral wall of the left ventricle. Obstruction leads to a **Lateral Wall MI**, seen in leads I, aVL, V5, and V6 [3]. **High-Yield Clinical Pearls for NEET-PG:** * **"The Widow Maker":** The LAD is often referred to by this name due to the high mortality associated with its occlusion. * **ECG Correlation:** * Anterior Wall: V1–V4 (LAD) [1] * Septal: V1–V2 (LAD) * Lateral Wall: I, aVL, V5, V6 (LCx) * Inferior Wall: II, III, aVF (RCA > LCx) * **Most Common Site of MI:** LAD (40–50%) > RCA (30–40%) > LCx (15–20%). * **Papillary Muscle Rupture:** While the anterolateral papillary muscle has dual supply (LAD/LCx), the **posteromedial** papillary muscle is supplied solely by the PDA (usually RCA), making it more susceptible to rupture post-MI.

Question 872: Which of the following is a characteristic ECG change seen in hypokalemia?

A. Tall T wave
B. Short QRS interval
C. Depressed ST segment (Correct Answer)
D. Absent P wave

Explanation: ### Explanation **Hypokalemia** (serum potassium <3.5 mEq/L) affects the repolarization phase of the cardiac action potential [1]. As potassium levels drop, the resting membrane potential becomes more negative, and the duration of the action potential increases. **Why Option C is Correct:** In hypokalemia, the ECG typically shows a progressive sequence of changes: 1. **ST-segment depression** and T-wave flattening/inversion. 2. **Prominent U waves** (the most characteristic finding), often seen best in precordial leads V2–V4. 3. Apparent **prolongation of the QU interval** (often mistaken for a long QT interval) [1]. The ST depression occurs due to altered ventricular repolarization gradients caused by low extracellular potassium. **Analysis of Incorrect Options:** * **A. Tall T wave:** This is a hallmark of **Hyperkalemia** (specifically "tall, tented T waves"). In hypokalemia, T waves become flat or inverted [1]. * **B. Short QRS interval:** Hypokalemia actually causes **widening of the QRS complex** in severe cases, not shortening. * **D. Absent P wave:** This is seen in severe **Hyperkalemia** (due to atrial paralysis) or Atrial Fibrillation [1]. In hypokalemia, P waves may actually become slightly peaked or prominent. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of Hypo":** Hypokalemia = **Hypo** (flat) T waves + **Hypo** (depressed) ST segment + Prominent **U** waves. * **Arrhythmia Risk:** Hypokalemia predisposes patients to **Digoxin toxicity** and can trigger Torsades de Pointes. * **Management:** Always check Magnesium levels; refractory hypokalemia cannot be corrected until **hypomagnesemia** [2] is treated.

Question 873: Which of the following increases susceptibility to coronary artery disease?

A. Type V hyperlipoproteinemia
B. Von Willebrand's disease
C. Nephrotic syndrome (Correct Answer)
D. Systemic lupus erythematosus

Explanation: ### Explanation **Correct Option: C. Nephrotic Syndrome** Nephrotic syndrome is a potent risk factor for premature coronary artery disease (CAD). The underlying mechanism is **severe dyslipidemia** caused by the liver's compensatory increase in lipoprotein synthesis (including VLDL and LDL) in response to low oncotic pressure from hypoalbuminemia. Additionally, there is a loss of antithrombin III and proteins C and S in the urine, creating a **hypercoagulable state**. This combination of high LDL levels and pro-thrombotic tendency significantly accelerates atherosclerosis. **Analysis of Incorrect Options:** * **A. Type V Hyperlipoproteinemia:** This involves elevated VLDL and chylomicrons. While it significantly increases the risk of **acute pancreatitis**, it is not as strongly associated with CAD as Type IIa, IIb, or III hyperlipoproteinemias. * **B. Von Willebrand's Disease:** This is a bleeding disorder characterized by a deficiency or dysfunction of vWF. Because vWF is essential for platelet adhesion, its deficiency may actually have a paradoxical **protective effect** against arterial thrombosis and atherosclerosis. * **D. Systemic Lupus Erythematosus (SLE):** While SLE is associated with accelerated atherosclerosis (often due to chronic inflammation and steroid use), **Nephrotic Syndrome** (which can be a manifestation of SLE as Lupus Nephritis) is considered a more direct metabolic driver of CAD in the context of standard medical examinations. **High-Yield Pearls for NEET-PG:** * **Friedrickson Classification:** Type IIa (High LDL) and Type IIb (High LDL + VLDL) are the most strongly associated with CAD [1]. * **Nephrotic Syndrome Triad for CAD:** Hyperlipidemia + Hypercoagulability + Hypertension [2]. * **Protective Factors:** High levels of HDL (High-Density Lipoprotein) and regular physical activity are the primary factors that decrease CAD susceptibility [1].

Question 874: When the P-R interval in a bipolar limb lead electrocardiograph prolongs beyond 0.20 seconds, what condition does the patient have?

A. Third degree complete block
B. Second degree Type 2 block
C. First degree complete block (Correct Answer)
D. Second degree incomplete block

Explanation: The **P-R interval** represents the time taken for electrical impulses to travel from the SA node, through the atria, and across the AV node to the ventricles [2]. In a healthy adult, the normal P-R interval ranges from **0.12 to 0.20 seconds** (3 to 5 small squares). **1. Why First-degree Heart Block is correct:** First-degree heart block is defined by a **fixed prolongation of the P-R interval >0.20 seconds**, where every P wave is followed by a QRS complex (1:1 conduction) [1]. The term "complete" in the option refers to the fact that the delay is consistent and every beat is conducted, though it is more commonly referred to simply as "First-degree AV block." **2. Why the other options are incorrect:** * **Second-degree Type 2 (Mobitz II):** Characterized by intermittent, sudden "dropped" QRS complexes without prior P-R prolongation [1]. The P-R interval remains constant before the dropped beat. * **Third-degree (Complete) Block:** There is a total dissociation between atria and ventricles (P waves and QRS complexes occur independently). The P-R interval is variable and inconsistent. * **Second-degree Incomplete Block:** This is a broad category including Mobitz I (Wenckebach), where the P-R interval progressively lengthens until a QRS is dropped [1]. **High-Yield NEET-PG Pearls:** * **Location of Delay:** In First-degree block, the delay most commonly occurs within the **AV node**. * **Clinical Significance:** Usually asymptomatic and requires no treatment unless drug-induced (e.g., Beta-blockers, Digoxin, Calcium Channel Blockers). * **ECG Tip:** 1 small square = 0.04s; 1 large square = 0.20s. If the P-R interval is longer than one large square, it is a First-degree block.

Question 875: Which of the following is NOT a feature of ventricular tachycardia?

A. AV dissociation
B. Capture or fusion beats
C. Good response to carotid sinus massage (Correct Answer)
D. A history of myocardial infarction

Explanation: **Explanation:** Ventricular Tachycardia (VT) is a life-threatening arrhythmia originating from the ventricles, often occurring in the setting of structural heart disease. **Why Option C is correct:** Carotid sinus massage (CSM) increases vagal tone, which primarily affects the SA and AV nodes. While CSM can slow or terminate Supraventricular Tachycardias (SVT) involving the AV node (like AVNRT), it has **no effect on Ventricular Tachycardia**. A lack of response to vagal maneuvers is a hallmark feature that helps differentiate VT from SVT with aberrancy. **Analysis of Incorrect Options:** * **A. AV Dissociation:** This is a pathognomonic feature of VT. It occurs when the atria and ventricles beat independently (P waves are "buried" or dissociated from QRS complexes). * **B. Capture or Fusion Beats:** These are highly specific for VT. A **fusion beat** occurs when a supraventricular impulse and a ventricular impulse "collide" to form a hybrid QRS. A **capture beat** occurs when a supraventricular impulse "captures" the ventricle briefly, producing a normal-looking QRS amidst the wide-complex tachycardia. * **D. History of Myocardial Infarction:** This is the strongest clinical predictor of VT. In a patient with a prior MI presenting with wide-complex tachycardia, there is a >90% probability that the rhythm is VT. **NEET-PG High-Yield Pearls:** * **Brugada’s Criteria:** Used to differentiate VT from SVT with aberrancy (e.g., absence of RS complex in precordial leads). * **Northwest Axis:** A QRS axis between -90° and 180° ("extreme axis deviation") strongly suggests VT. * **Treatment:** Hemodynamically unstable VT requires immediate **synchronized DC cardioversion**. Stable VT is typically treated with **Amiodarone** (drug of choice) or Lidocaine.

Question 876: All of the following auscultatory findings are heard in chronic mitral stenosis except?

A. Mid-diastolic murmur
B. Third heart sound (Correct Answer)
C. Opening snap
D. Loud S1

Explanation: In Mitral Stenosis (MS), the presence of a **Third Heart Sound (S3)** is an "exclusionary finding." An S3 occurs during the phase of rapid ventricular filling; in MS, the narrowed mitral orifice restricts this rapid flow, preventing the sudden deceleration of blood against the ventricular wall required to produce the sound [4]. If an S3 is heard in a patient with suspected MS, it strongly suggests associated **Mitral Regurgitation (MR)** [4] or heart failure, rather than isolated MS. **Explanation of Options:** * **Loud S1:** In MS, the mitral valve leaflets remain wide apart at the end of diastole due to the pressure gradient [2]. The sudden, forceful closure of these leaflets by ventricular systole produces a loud, "tapping" S1 [2]. (Note: S1 becomes soft if the valve is heavily calcified). * **Opening Snap (OS):** This high-pitched sound occurs due to the sudden tensing of the chordae and stenotic leaflets when the valve opens [1]. A short **S2-OS interval** indicates more severe MS [1]. * **Mid-diastolic Murmur (MDM):** This is the hallmark of MS, caused by turbulent flow across the narrowed valve. It is low-pitched (rumbling) and best heard at the apex with the bell in the left lateral decubitus position [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Graham Steell Murmur:** A pulmonary regurgitation murmur heard in severe MS due to pulmonary hypertension. * **Severity Markers:** The severity of MS is best indicated by the **duration** of the MDM and the **shortness** of the S2-OS interval [1]. * **Presystolic Accentuation:** The murmur gets louder just before S1 due to atrial contraction; this disappears if the patient develops **Atrial Fibrillation** [2].

Question 877: Which of the following conditions is NOT associated with long and peaked 'a' waves in the jugular venous pulse waveform?

A. Tricuspid atresia
B. Ebstein's anomaly
C. Hyperkalemia (Correct Answer)
D. Right atrial enlargement

Explanation: **Explanation:** The **'a' wave** in the jugular venous pulse (JVP) corresponds to **right atrial contraction**. It occurs just before the first heart sound (S1) and the carotid upstroke. A "giant" or "peaked" 'a' wave occurs whenever the right atrium must contract against increased resistance. **Why Hyperkalemia is the correct answer:** Hyperkalemia is an electrolyte abnormality that affects cardiac conduction and repolarization. On an **Electrocardiogram (ECG)**, it characteristically causes **"tall, peaked T waves,"** which result from altered repolarization as plasma levels rise [1]. However, it has no direct mechanical effect on the right atrial pressure or the JVP waveform. Therefore, it is not associated with peaked 'a' waves. **Analysis of Incorrect Options:** * **Tricuspid Atresia:** Since the tricuspid valve is absent, the right atrium contracts against a blind pouch or a restrictive interatrial septum, leading to significantly elevated right atrial pressures and giant 'a' waves. * **Ebstein’s Anomaly:** This involves the downward displacement of tricuspid valve leaflets. The resulting "atrialized" right ventricle and tricuspid regurgitation/stenosis dynamics often lead to prominent 'a' waves due to decreased right ventricular compliance. * **Right Atrial Enlargement:** Any condition causing RA hypertrophy (like Pulmonary Stenosis or Pulmonary Hypertension) results in forceful atrial contraction to fill a stiff right ventricle, producing peaked 'a' waves. **NEET-PG High-Yield Pearls:** * **Giant 'a' waves:** Seen in Tricuspid Stenosis, Pulmonary Stenosis, and Right Heart Failure. * **Cannon 'a' waves:** Occur when the atrium contracts against a **closed** tricuspid valve (e.g., Complete Heart Block, Ventricular Tachycardia). * **Absent 'a' waves:** Pathognomonic for **Atrial Fibrillation** (no coordinated atrial contraction). * **Giant 'v' waves:** Characteristic of **Tricuspid Regurgitation**.

Question 878: A patient with VSD develops pulmonary hypertension. What is the characteristic feature?

A. Ejection systolic murmur in the pulmonary area
B. Cyanosis (Correct Answer)
C. Inverted 'T' wave in ECG
D. Clubbing

Explanation: When a patient with a large Ventricular Septal Defect (VSD) develops severe pulmonary hypertension, it leads to **Eisengmenger Syndrome**. This occurs because the chronic left-to-right shunt causes structural remodeling of the pulmonary vasculature, increasing pulmonary vascular resistance (PVR). Once PVR exceeds systemic vascular resistance, the shunt **reverses** (becomes right-to-left) [1]. Deoxygenated blood enters the systemic circulation, leading to **differential cyanosis** and clubbing [1]. **Analysis of Options:** * **Cyanosis (Correct):** This is the hallmark of shunt reversal (Eisengerization). It signifies that the pulmonary pressures have reached systemic levels, making the VSD "silent" or "balanced." * **Ejection systolic murmur (Incorrect):** While a pulmonary flow murmur may exist, the characteristic **pansystolic murmur** of the VSD actually **disappears** as the pressure gradient between the ventricles equalizes. * **Inverted T-wave (Incorrect):** While ECG changes like Right Ventricular Hypertrophy (RVH) and Right Axis Deviation are common, T-wave inversion is non-specific and not the "characteristic" clinical feature of the transition to Eisenmenger syndrome. * **Clubbing (Incorrect):** While clubbing occurs in Eisenmenger syndrome, it is a *sequela* of chronic hypoxia. In the context of NEET-PG questions regarding the "development" of pulmonary hypertension in VSD, **cyanosis** is the primary clinical sign of the shunt reversal. **High-Yield Clinical Pearls:** 1. **The "Silent" VSD:** As pulmonary hypertension worsens, the loud pansystolic murmur of a small VSD softens and eventually vanishes. 2. **Physical Exam:** Look for a palpable P2, a loud/accentuated S2, and a Graham-Steell murmur (pulmonary regurgitation). 3. **Contraindication:** Once Eisenmenger syndrome is established, surgical closure of the VSD is **strictly contraindicated** as the defect now acts as a pressure-release valve for the right heart [2].

Question 879: Antibiotic prophylaxis is indicated in which of the following conditions?

A. Angina pectoris
B. Infective endocarditis (Correct Answer)
C. Pulmonary embolism
D. Before all minor surgical procedures

Explanation: **Explanation:** The primary goal of antibiotic prophylaxis in cardiology is to prevent **Infective Endocarditis (IE)** in high-risk patients undergoing procedures that may cause transient bacteremia [1]. According to current AHA/ESC guidelines, prophylaxis is indicated for patients with specific high-risk cardiac conditions (e.g., prosthetic valves, previous IE, or certain congenital heart diseases) before high-risk dental procedures involving gingival manipulation [2]. **Analysis of Options:** * **Infective Endocarditis (Correct):** This is the only condition listed where antibiotic prophylaxis is a standard clinical protocol to prevent the colonization of damaged endocardium or prosthetic material by bacteria (commonly *Viridans group streptococci*). * **Angina Pectoris:** This is an ischemic condition caused by coronary artery disease. It is not an infectious process, and there is no risk of endocardial infection associated with it. * **Pulmonary Embolism:** This is a thrombotic or embolic vascular event. Antibiotics play no role in its management or prevention. * **Before all minor surgical procedures:** Prophylaxis is **not** recommended for all minor surgeries. It is specifically reserved for dental procedures involving the manipulation of gingival tissue or the periapical region of teeth. It is no longer recommended for routine GI or GU procedures unless an active infection is present [2]. **High-Yield Pearls for NEET-PG:** * **Drug of Choice:** Oral **Amoxicillin** (2g) given 30–60 minutes before the procedure. * **If Penicillin allergic:** Use Clindamycin (600mg), Cephalexin, or Azithromycin. * **High-risk conditions requiring prophylaxis:** 1. Prosthetic heart valves (including TAVI) [2]. 2. Prior history of Infective Endocarditis. 3. Cyanotic Congenital Heart Disease (unrepaired). 4. Repaired CHD with prosthetic material (first 6 months). 5. Cardiac transplant recipients who develop valvulopathy.

Question 880: A 62-year-old man with carcinoma of the lung presented to the emergency department with respiratory distress. ECG showed electrical alternans. What is the most likely diagnosis?

A. Pneumothorax
B. Pleural effusion
C. Cardiac tamponade (Correct Answer)
D. Constrictive pericarditis

Explanation: ### Explanation **Correct Answer: C. Cardiac Tamponade** The clinical presentation of respiratory distress in a patient with lung cancer, combined with the classic ECG finding of **electrical alternans**, is pathognomonic for **cardiac tamponade** [1]. * **Mechanism:** In cardiac tamponade, a large pericardial effusion causes the heart to "swing" back and forth within the fluid-filled pericardial sac [1]. This physical movement changes the heart's axis relative to the ECG electrodes with every beat, resulting in beat-to-beat variations in the amplitude of the QRS complexes (and sometimes P and T waves). * **Clinical Context:** Malignancy (especially lung and breast cancer) is a leading cause of pericardial effusion progressing to tamponade [1]. **Analysis of Incorrect Options:** * **A. Pneumothorax:** While it causes respiratory distress and can shift the mediastinum, it does not cause electrical alternans. ECG might show decreased QRS voltage or axis deviation, but not beat-to-beat variation. * **B. Pleural Effusion:** Large effusions cause respiratory distress and "dullness on percussion," but they do not affect the heart's electrical axis in a swinging motion. * **D. Constrictive Pericarditis:** This involves a rigid, scarred pericardium. While it shares some clinical features with tamponade (like JVD), the heart is "fixed" rather than "swinging," so electrical alternans is absent. **NEET-PG High-Yield Pearls:** 1. **Beck’s Triad:** Hypotension, Jugular Venous Distension (JVD), and Muffled heart sounds (classic for acute tamponade). 2. **Pulsus Paradoxus:** An inspiratory drop in systolic BP >10 mmHg; a hallmark clinical sign. 3. **ECG Findings:** Low voltage QRS complexes + Electrical alternans [1]. 4. **Chest X-ray:** "Water-bottle" or "Flask-shaped" heart (seen in large chronic effusions) [1]. 5. **Management:** Immediate **Pericardiocentesis** is the treatment of choice.

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Cardiomyopathies

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Congenital Heart Disease in Adults

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Cardiology — MCQs

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