Cardiology Practice Questions

Q: ECG features of Athlete's Heart include all of the following except:

Shortened QT Interval. **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.

Q: What causes Torsades de pointes?

Prolonged QT interval. **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].

Q: What is the most common arrhythmia observed after reperfusion syndrome?

Accelerated Idioventricular Rhythm (AIVR). ### 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.

Q: 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?

Admit and start heparin.. ### 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).

Q: 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?

High normal blood pressure. ### 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 180 and/or DBP >120 mmHg. It is an "Emergency" if there is end-organ damage and an "Urgency" if there is not.

Q: Which of the following conditions is characterized by a continuous murmur?

Systemic arteriovenous fistula. **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.

Q: Elevated JVP is seen in which of the following conditions?

Corpulmonale. **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.

Q: Wenckebach's phenomenon is seen in which type of heart block?

Second-degree heart block type I. **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 1

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?

Accepted Answer

Constrictive Pericarditis

Answer

Cardiac Tamponade

Answer

Restrictive Cardiomyopathy

Answer

Right Ventricular Myocardial Infarction

Question 2

ECG features of Athlete's Heart include all of the following except:

Accepted Answer

Shortened QT Interval

Answer

High QRS Voltage

Answer

Early repolarization

Answer

Tall peaked T waves

Question 3

What causes Torsades de pointes?

Accepted Answer

Prolonged QT interval

Answer

Wide QRS complex

Answer

Short QRS complex

Answer

Short QT interval

Question 4

What is the most common arrhythmia observed after reperfusion syndrome?

Accepted Answer

Accelerated Idioventricular Rhythm (AIVR)

Answer

Ventricular Tachycardia (VT)

Answer

Ventricular Fibrillation

Answer

Paroxysmal Supraventricular Tachycardia (PSVT)

Question 5

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?

Accepted Answer

Admit and start heparin.

Answer

Admit and start thrombolysis.

Answer

Admit and observe for rising cardiac biomarkers.

Answer

Increase the dose of long-acting nitrates and manage as an outpatient.

Question 6

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?

Accepted Answer

High normal blood pressure

Answer

Normotensive

Answer

Stage 1 hypertension

Answer

Stage 2 hypertension

Question 7

Which of the following conditions is characterized by a continuous murmur?

Accepted Answer

Systemic arteriovenous fistula

Answer

Aortic stenosis combined with aortic regurgitation

Answer

Patent ductus arteriosus with reversal of shunt

Answer

All of the above

Question 8

Elevated JVP is seen in which of the following conditions?

Accepted Answer

Corpulmonale

Answer

Pneumonia

Answer

ARDS

Answer

Pleural effusion

Question 9

Wenckebach's phenomenon is seen in which type of heart block?

Accepted Answer

Second-degree heart block type I

Answer

First-degree heart block

Answer

Second-degree heart block type II

Answer

Third-degree heart block

Question 10

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?

Accepted Answer

Significant pericardial effusion on echocardiography

Answer

Pericardial friction rub

Answer

Mobitz Type II block

Answer

Lower limb vein thrombosis

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?