Cardiology — MCQs
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A 35-year-old male presents with dyspnea and ascites of 3 days duration. On examination, there is neck vein distension with no inspiratory decrease in JVP. Chest X-ray shows plaque-like calcification over the right ventricle with a dilated superior vena cava and small atria. What is the most likely diagnosis?
ECG features of Athlete's Heart include all of the following except:
What causes Torsades de pointes?
What is the most common arrhythmia observed after reperfusion syndrome?
A 60-year-old male on aspirin, ACE inhibitor, nitrates, and a beta-blocker for chronic stable angina has been experiencing long-lasting angina pain daily for the past 3 days, starting around the new year. ECG and Troponin I levels are normal. What is the best management for this patient?
A 20-year-old individual has blood pressures of 134/86 mmHg and 136/89 mmHg recorded on two separate occasions. How would this individual be classified based on these readings?
Which of the following conditions is characterized by a continuous murmur?
Elevated JVP is seen in which of the following conditions?
Wenckebach's phenomenon is seen in which type of heart block?
An elderly female presents to the emergency department with a transmural myocardial infarction. Based on her ECG, she was started on thrombolytic therapy with streptokinase. Which of the following findings would indicate that the thrombolytic therapy is risky and should be stopped?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 791: A 35-year-old male presents with dyspnea and ascites of 3 days duration. On examination, there is neck vein distension with no inspiratory decrease in JVP. Chest X-ray shows plaque-like calcification over the right ventricle with a dilated superior vena cava and small atria. What is the most likely diagnosis?
- A. Cardiac Tamponade
- B. Restrictive Cardiomyopathy
- C. Right Ventricular Myocardial Infarction
- D. Constrictive Pericarditis (Correct Answer)
Explanation: **Explanation:** The clinical presentation of dyspnea, ascites, and elevated JVP in a young male, combined with specific imaging findings, points directly to **Constrictive Pericarditis (CP)**. **1. Why Constrictive Pericarditis is correct:** * **Kussmaul’s Sign:** The "no inspiratory decrease in JVP" (or an actual increase) is the classic description of Kussmaul’s sign. In CP, the rigid pericardium prevents the right heart from accommodating the increased venous return during inspiration. * **Pericardial Calcification:** The "plaque-like calcification" on X-ray is a pathognomonic finding for CP (often due to past Tuberculosis in India) [1]. * **Atrial/SVC changes:** Because the ventricles are encased in a rigid shell, they cannot fill properly, leading to back-pressure that dilates the SVC and atria (though atria may appear small if also encased). **2. Why the other options are incorrect:** * **Cardiac Tamponade:** Characterized by **Beck’s Triad** (hypotension, muffled heart sounds, raised JVP). Crucially, Kussmaul’s sign is typically *absent* in tamponade; instead, **Pulsus Paradoxus** is the hallmark. Calcification is not seen. * **Restrictive Cardiomyopathy (RCM):** While RCM mimics CP clinically (including Kussmaul’s sign), it does **not** show pericardial calcification on X-ray [2]. RCM usually presents with significant bi-atrial enlargement. * **RV Myocardial Infarction:** While it causes raised JVP and hypotension, it is an acute presentation (usually with chest pain and ECG changes) and would not show chronic pericardival calcification. **NEET-PG High-Yield Pearls:** * **Most common cause in India:** Tuberculosis [1]. * **JVP Waveform:** Look for a prominent **'y' descent** (Friedreich’s sign) due to rapid early diastolic filling. * **Square Root Sign:** Seen on cardiac catheterization (dip-and-plateau pattern of ventricular pressure). * **Pericardial Knock:** A high-pitched sound heard in early diastole (due to sudden cessation of ventricular filling).
Question 792: ECG features of Athlete's Heart include all of the following except:
- A. High QRS Voltage
- B. Early repolarization
- C. Tall peaked T waves
- D. Shortened QT Interval (Correct Answer)
Explanation: **Explanation:** The term **"Athlete’s Heart"** refers to the physiological structural and electrical remodeling of the heart in response to regular, intense physical training. These changes are benign and must be distinguished from pathological conditions like Hypertrophic Cardiomyopathy (HCM). **Why "Shortened QT Interval" is the correct answer:** In athletes, increased vagal tone (parasympathetic dominance) is a hallmark feature. This leads to resting bradycardia, which physiologically **prolongs the QT interval** (as QT interval is inversely proportional to heart rate) [1]. A shortened QT interval is not a feature of athlete's heart; in fact, a pathologically short QT interval is associated with "Short QT Syndrome," a genetic channelopathy predisposing to sudden cardiac death. **Analysis of incorrect options:** * **High QRS Voltage:** Increased ventricular wall thickness and chamber size (physiologic hypertrophy) lead to increased electrical signals, meeting voltage criteria for Left Ventricular Hypertrophy (LVH). * **Early Repolarization:** Common in athletes, this manifests as J-point elevation with concave ST-segment elevation, particularly in precordial leads, due to altered autonomic balance. * **Tall Peaked T Waves:** These are frequently seen in association with early repolarization and high QRS voltage in healthy athletes. **NEET-PG High-Yield Pearls:** 1. **Most common ECG finding:** Sinus bradycardia (often <50 bpm). 2. **Heart blocks:** First-degree AV block and Mobitz Type I (Wenckebach) are common and considered physiological in athletes. 3. **Distinction:** Unlike HCM, the LVH in athletes reverses with deconditioning (detraining) and is associated with normal diastolic function. 4. **T-wave inversion:** While common in V1-V3 in "Black Athletes," deep T-wave inversions in lateral leads (V5-V6) are usually pathological and require workup for HCM.
Question 793: What causes Torsades de pointes?
- A. Wide QRS complex
- B. Short QRS complex
- C. Prolonged QT interval (Correct Answer)
- D. Short QT interval
Explanation: **Explanation:** **Torsades de Pointes (TdP)** is a specific form of polymorphic ventricular tachycardia characterized by the QRS complexes "twisting" around the isoelectric line [1]. **Why Prolonged QT Interval is Correct:** The underlying pathophysiology of TdP is a **prolonged QT interval**, which represents delayed ventricular repolarization [1], [2]. This delay creates a vulnerable window where **Early Afterdepolarizations (EADs)** can occur during Phase 2 or 3 of the action potential. If these EADs reach the threshold, they trigger premature ventricular contractions (R-on-T phenomenon), initiating the characteristic paroxysmal tachycardia [2]. **Why Other Options are Incorrect:** * **Wide QRS Complex (A):** While TdP features wide QRS complexes during the arrhythmia, a wide QRS at baseline (e.g., Bundle Branch Block) is not the primary trigger for TdP. * **Short QRS Complex (B):** This is not a standard clinical term; narrow QRS complexes indicate normal supraventricular conduction. * **Short QT Interval (D):** Short QT syndrome is associated with a different set of arrhythmias (like sudden atrial fibrillation or VFib) but not TdP. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Congenital (Jervell and Lange-Nielsen, Romano-Ward syndromes) or Acquired (Hypokalemia, Hypomagnesemia, Hypocalcemia, and drugs like Class IA/III antiarrhythmics, Macrolides, and TCAs). * **Drug of Choice:** **Intravenous Magnesium Sulfate** is the first-line treatment, even if serum magnesium levels are normal. * **ECG Hallmark:** "Twisting of the points" with shifting amplitudes of QRS complexes [1].
Question 794: What is the most common arrhythmia observed after reperfusion syndrome?
- A. Accelerated Idioventricular Rhythm (AIVR) (Correct Answer)
- B. Ventricular Tachycardia (VT)
- C. Ventricular Fibrillation
- D. Paroxysmal Supraventricular Tachycardia (PSVT)
Explanation: ### Explanation **Correct Answer: A. Accelerated Idioventricular Rhythm (AIVR)** **Why it is correct:** Accelerated Idioventricular Rhythm (AIVR) is the most characteristic and common arrhythmia seen following successful reperfusion (via thrombolysis or primary PCI) in patients with Acute Myocardial Infarction. It is often referred to as the **"rhythm of reperfusion."** The underlying mechanism involves increased automaticity of the ventricular conduction system due to the sudden influx of oxygenated blood, which causes a transient electrolyte shift and oxidative stress. AIVR is characterized by a heart rate between 60–110 bpm (faster than a normal ventricular escape rhythm but slower than VT) and a wide QRS complex. Crucially, AIVR is usually benign, self-limiting, and does not require anti-arrhythmic treatment. **Why other options are incorrect:** * **B & C (VT and VF):** While Ventricular Tachycardia and Ventricular Fibrillation are serious complications of myocardial ischemia and can occur post-reperfusion, they are less common than AIVR [1]. VF is the leading cause of pre-hospital death in MI, but AIVR is the specific hallmark of successful vessel reopening. * **D (PSVT):** Supraventricular tachycardias are not typically associated with the reperfusion of ventricular myocardium. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Features of AIVR:** Wide QRS, rate 60–110 bpm, and frequent fusion or capture beats. * **Prognostic Value:** The appearance of AIVR during thrombolysis is a **positive sign** indicating successful recanalization of the infarct-related artery. * **Management:** Observation only. Do not treat with Lidocaine or Amiodarone, as suppressing this rhythm can lead to asystole if the SA node is sluggish. * **Most common cause of death in MI:** * *Pre-hospital:* Ventricular Fibrillation [2]. * *In-hospital:* Cardiogenic Shock.
Question 795: A 60-year-old male on aspirin, ACE inhibitor, nitrates, and a beta-blocker for chronic stable angina has been experiencing long-lasting angina pain daily for the past 3 days, starting around the new year. ECG and Troponin I levels are normal. What is the best management for this patient?
- A. Admit and start heparin. (Correct Answer)
- B. Admit and start thrombolysis.
- C. Admit and observe for rising cardiac biomarkers.
- D. Increase the dose of long-acting nitrates and manage as an outpatient.
Explanation: ### Explanation **1. Why Option A is Correct:** The patient is presenting with **Unstable Angina (UA)**. This is defined by a change in the pattern of chronic stable angina, specifically pain that is increasing in frequency, duration, or occurring at rest [2]. Despite normal ECG and Troponin I levels (which rule out NSTEMI and STEMI), UA is part of the **Acute Coronary Syndrome (ACS)** spectrum [1]. The pathophysiology involves a ruptured plaque with subtotal thrombosis [1]. Management requires immediate hospitalization and anticoagulation with **Heparin** (Unfractionated or LMWH) to prevent further thrombus propagation and reduce the risk of progression to myocardial infarction. **2. Why Other Options are Incorrect:** * **Option B:** Thrombolysis is strictly contraindicated in UA/NSTEMI [3]. It is only indicated for STEMI when primary PCI is unavailable. In UA, thrombolysis can paradoxically increase clot formation by releasing clot-bound thrombin. * **Option C:** While biomarkers are monitored, "observation only" is insufficient. UA is a high-risk state requiring active intervention (anticoagulation and antiplatelets) to prevent sudden cardiac death. * **Option D:** Managing as an outpatient is dangerous. New-onset or worsening angina (Crescendo Angina) indicates myocardial ischemia at risk of progressing to infarction [2]. **3. Clinical Pearls for NEET-PG:** * **Definition of UA:** Angina at rest (>20 mins), new-onset severe angina, or increasing (crescendo) angina [2]. * **UA vs. NSTEMI:** Both may show ST-depression or T-wave inversion, but **NSTEMI has elevated cardiac biomarkers**, whereas UA does not [2]. * **TIMI Score:** Used for risk stratification in UA/NSTEMI to decide between an early invasive vs. conservative strategy. * **Gold Standard Investigation:** Coronary Angiography (to assess the extent of CAD).
Question 796: A 20-year-old individual has blood pressures of 134/86 mmHg and 136/89 mmHg recorded on two separate occasions. How would this individual be classified based on these readings?
- A. Normotensive
- B. High normal blood pressure (Correct Answer)
- C. Stage 1 hypertension
- D. Stage 2 hypertension
Explanation: ### Explanation The classification of blood pressure (BP) in this question follows the **European Society of Cardiology (ESC) and European Society of Hypertension (ESH)** guidelines, which are frequently tested in the NEET-PG exam. **1. Why "High Normal Blood Pressure" is correct:** According to the ESC/ESH classification, **High Normal BP** is defined as a Systolic BP (SBP) of **130–139 mmHg** and/or a Diastolic BP (DBP) of **85–89 mmHg**. The patient’s readings (134/86 and 136/89) fall squarely within this range. This category identifies individuals who are at a higher risk of progressing to hypertension and may benefit from lifestyle modifications. **2. Why the other options are incorrect:** * **A. Normotensive:** In the ESC classification, "Normal" BP is 120–129 mmHg (systolic) and/or 80–84 mmHg (diastolic). "Optimal" BP is <120/80 mmHg. The patient's readings exceed these limits. * **C. Stage 1 Hypertension:** This is defined as SBP **140–159 mmHg** and/or DBP **90–99 mmHg**. The patient has not yet reached these thresholds. * **D. Stage 2 Hypertension:** This is defined as SBP **160–179 mmHg** and/or DBP **100–109 mmHg**. **3. Clinical Pearls for NEET-PG:** * **Guideline Variation:** Be careful! Under the **ACC/AHA (American)** guidelines, these readings would be classified as **Stage 1 Hypertension** (130–139 / 80–89 mmHg). However, Indian medical exams traditionally follow the ESC/WHO/ISH criteria unless the American guidelines are specifically mentioned. * **Diagnosis Rule:** Hypertension should be diagnosed based on at least two readings taken on two or more separate occasions [1]. * **Isolated Systolic Hypertension:** Common in the elderly; defined as SBP ≥140 with DBP <90 mmHg. * **Hypertensive Crisis:** SBP >180 and/or DBP >120 mmHg. It is an "Emergency" if there is end-organ damage and an "Urgency" if there is not.
Question 797: Which of the following conditions is characterized by a continuous murmur?
- A. Aortic stenosis combined with aortic regurgitation
- B. Systemic arteriovenous fistula (Correct Answer)
- C. Patent ductus arteriosus with reversal of shunt
- D. All of the above
Explanation: **Explanation:** A **continuous murmur** is defined as a murmur that begins in systole and continues through the second heart sound (S2) into all or part of diastole. This occurs when there is a persistent pressure gradient between two chambers or vessels throughout the entire cardiac cycle. **Why Option B is Correct:** In a **Systemic Arteriovenous (AV) Fistula**, a direct communication exists between a high-pressure artery and a low-pressure vein. Since arterial pressure remains higher than venous pressure during both systole and diastole, blood flows continuously across the fistula, generating a continuous murmur (often associated with a palpable thrill). **Analysis of Incorrect Options:** * **Option A (AS + AR):** This combination produces a "To-and-Fro" murmur, not a continuous one. There is a systolic ejection murmur (AS) and a separate diastolic decrescendo murmur (AR) with a distinct pause or change in character at S2. * **Option C (PDA with reversal of shunt):** While an uncomplicated Patent Ductus Arteriosus (PDA) is the classic cause of a continuous "machinery" murmur (Gibson’s murmur), the development of **Eisenmenger syndrome** (reversal of shunt to Right-to-Left) causes the pressures to equalize or the diastolic gradient to disappear. Consequently, the murmur becomes shorter or disappears entirely. **High-Yield Clinical Pearls for NEET-PG:** 1. **Common Causes of Continuous Murmurs:** PDA (most common), Ruptured Sinus of Valsalva (RSOV), Coronary AV fistula, Venous hum (benign), and Cruveilhier-Baumgarten syndrome. 2. **Venous Hum:** A continuous murmur heard over the internal jugular vein; it is unique because it disappears when the patient lies supine or when the vein is compressed. 3. **Distinction:** Always distinguish "Continuous" from "To-and-Fro." Continuous murmurs wrap around S2, whereas To-and-Fro murmurs have two distinct components.
Question 798: Elevated JVP is seen in which of the following conditions?
- A. Corpulmonale (Correct Answer)
- B. Pneumonia
- C. ARDS
- D. Pleural effusion
Explanation: **Explanation:** **1. Why Cor Pulmonale is Correct:** Cor pulmonale refers to right-sided heart failure resulting from primary lung disease (e.g., COPD, Interstitial Lung Disease). The underlying mechanism is **Pulmonary Hypertension**, which increases the afterload on the right ventricle (RV) [1]. As the RV fails to pump effectively against this high pressure, blood backs up into the right atrium and subsequently into the **Internal Jugular Vein (IJV)**. Since the IJV is in direct anatomical continuity with the right atrium (without valves), the Jugular Venous Pressure (JVP) rises, serving as a clinical marker of right heart dysfunction [1]. **2. Why Incorrect Options are Wrong:** * **Pneumonia:** This is an infectious consolidation of the lung parenchyma. Unless it leads to massive pulmonary embolism or severe ARDS causing acute cor pulmonale, it does not typically affect right heart pressures. * **ARDS:** While severe ARDS can cause acute pulmonary hypertension, it is primarily a clinical syndrome of non-cardiogenic pulmonary edema. JVP in ARDS is typically **normal or low** (unless there is iatrogenic fluid overload), which helps distinguish it from cardiogenic pulmonary edema. * **Pleural Effusion:** This is an accumulation of fluid in the pleural space. It does not increase central venous pressure unless it is a **Tension Hydrothorax**, which is a rare clinical emergency. **3. Clinical Pearls for NEET-PG:** * **Kussmaul’s Sign:** A paradoxical rise in JVP during inspiration, classically seen in Constrictive Pericarditis and Right Ventricular Infarction. * **Giant 'a' waves:** Seen in Tricuspid Stenosis and Pulmonary Hypertension [1]. * **Cannon 'a' waves:** Seen in complete heart block (AV dissociation). * **Giant 'v' waves:** Pathognomonic for Tricuspid Regurgitation. * **JVP vs. SVP:** JVP reflects Right Atrial Pressure, making it the most reliable bedside manometry for volume status.
Question 799: Wenckebach's phenomenon is seen in which type of heart block?
- A. First-degree heart block
- B. Second-degree heart block type I (Correct Answer)
- C. Second-degree heart block type II
- D. Third-degree heart block
Explanation: **Explanation:** **Wenckebach’s phenomenon** is the hallmark of **Second-degree heart block Type I (Mobitz I)** [1]. It occurs due to a progressive delay in conduction through the Atrioventricular (AV) node [1]. **Why Option B is Correct:** In Mobitz I, each successive atrial impulse encounters a more fatigued AV node. This results in **progressive prolongation of the PR interval** until an atrial impulse is completely blocked (a "dropped" QRS complex) [1]. Following the dropped beat, the AV node recovers, and the cycle repeats. The hallmark is the "group beating" pattern on the ECG. **Why Other Options are Incorrect:** * **First-degree heart block:** Characterized by a fixed, prolonged PR interval (>0.20s) where every P wave is followed by a QRS complex [1]. There are no dropped beats. * **Second-degree heart block Type II (Mobitz II):** Characterized by intermittently dropped QRS complexes **without** prior PR interval prolongation [1]. The PR interval remains constant. This usually indicates disease below the AV node (Bundle of His/Purkinje system) and carries a higher risk of progressing to complete heart block [1]. * **Third-degree heart block:** Also known as complete heart block, there is a total dissociation between atria and ventricles (AV dissociation). P waves and QRS complexes occur independently. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Block:** Mobitz I (Wenckebach) usually occurs at the **AV node**, whereas Mobitz II occurs **infra-nodal** [1]. * **Vagal Tone:** Mobitz I is often physiological (seen in athletes or during sleep) or due to increased vagal tone and drugs like Beta-blockers/Digoxin [1]. * **MI Association:** Mobitz I is commonly associated with **Inferior Wall MI** (Right Coronary Artery occlusion), while Mobitz II is associated with **Anterior Wall MI** [2]. * **Management:** Mobitz I is usually benign and asymptomatic; Mobitz II often requires a permanent pacemaker.
Question 800: An elderly female presents to the emergency department with a transmural myocardial infarction. Based on her ECG, she was started on thrombolytic therapy with streptokinase. Which of the following findings would indicate that the thrombolytic therapy is risky and should be stopped?
- A. Pericardial friction rub
- B. Mobitz Type II block
- C. Significant pericardial effusion on echocardiography (Correct Answer)
- D. Lower limb vein thrombosis
Explanation: The primary objective of thrombolytic therapy in ST-elevation myocardial infarction (STEMI) is to achieve reperfusion. However, thrombolytics are potent anticoagulants that carry a significant risk of systemic bleeding. [1] **Why Option C is Correct:** The presence of a **significant pericardial effusion** in the setting of an acute transmural MI is a major red flag. Transmural infarcts can lead to **myocardial free wall rupture**, which typically presents as a rapidly accumulating pericardial effusion leading to cardiac tamponade. Administering or continuing thrombolytics in this scenario is extremely risky as it can exacerbate the bleeding into the pericardial space, converting a potentially manageable leak into a fatal hemopericardium and tamponade. Therefore, it is a relative contraindication to thrombolysis. **Analysis of Incorrect Options:** * **A. Pericardial friction rub:** This is a common finding in post-MI patients (Dressler syndrome or early infarct-associated pericarditis). [3] While it indicates inflammation, it is not a contraindication to thrombolysis. * **B. Mobitz Type II block:** This is a conduction complication of MI (usually anterior). [2] It requires a pacemaker but does not increase the bleeding risk associated with streptokinase. * **D. Lower limb vein thrombosis:** DVT is actually an indication for anticoagulation. While thrombolytics are not the first-line treatment for simple DVT, their presence does not make MI thrombolysis "risky"; rather, it may incidentally help treat the clot. **Clinical Pearls for NEET-PG:** * **Absolute Contraindications to Thrombolysis:** Any prior intracranial hemorrhage, known structural cerebrovascular lesion, ischemic stroke within 3 months, active internal bleeding, or suspected aortic dissection. * **Streptokinase Specifics:** It is a non-fibrin-specific agent. It can cause hypotension and allergic reactions. [1] It should not be repeated within 6 months due to antistreptococcal antibodies. * **Free Wall Rupture:** Typically occurs 3–7 days post-MI but can occur early. It is more common in elderly females with their first MI and hypertension.
Practice by Chapter
Coronary Artery Disease and Angina
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Acute Coronary Syndromes
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Heart Failure
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Cardiac Arrhythmias
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Valvular Heart Diseases
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Cardiomyopathies
Practice Questions
Pericardial Diseases
Practice Questions
Congenital Heart Disease in Adults
Practice Questions
Hypertension and Hypertensive Emergencies
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Pulmonary Hypertension
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Non-invasive Cardiac Diagnostics
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Preventive Cardiology
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