Cardiology Practice Questions

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: 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: 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.

Q: Which one of the following drugs should be avoided in Wolff-Parkinson-White (WPW) Syndrome?

Digoxin. In **Wolff-Parkinson-White (WPW) Syndrome**, patients possess an accessory pathway (Bundle of Kent) that bypasses the AV node. The primary danger in WPW is the development of Atrial Fibrillation (AF), where rapid impulses can travel down the accessory pathway, leading to Ventricular Fibrillation and sudden cardiac death [1]. **Why Digoxin is Avoided (The Correct Answer):** Digoxin (along with Calcium Channel Blockers like Verapamil and Beta-blockers) primarily acts by slowing conduction through the **AV node** [2]. By blocking the physiological "gatekeeper," Digoxin paradoxically enhances conduction through the **accessory pathway**. This decreases the refractory period of the bypass tract, allowing more rapid impulses to reach the ventricles, potentially triggering fatal arrhythmias. **Analysis of Other Options:** * **Procainamide:** This is often the drug of choice for stable WPW with tachycardia. It works by increasing the refractory period of both the atrium and the **accessory pathway**, thereby slowing the rapid conduction. * **Amiodarone:** This is a Class III antiarrhythmic that increases the refractory period of all cardiac tissues, including the accessory pathway. It is generally considered safe in WPW. * **Adenosine:** While Adenosine blocks the AV node (similar to Digoxin), its ultra-short half-life makes it the drug of choice for terminating **Orthodromic** AVRT. However, it is avoided in WPW patients presenting with AF. In the context of this question, Digoxin is the classic "absolute" avoidance due to its prolonged effect. **High-Yield Clinical Pearls for NEET-PG:** * **The "ABCD" of drugs to avoid in WPW with AF:** **A**denosine (in AF), **B**eta-blockers, **C**alcium channel blockers (Verapamil/Diltiazem), and **D**igoxin. * **Treatment of Choice (Hemodynamically Unstable):** DC Cardioversion. * **Definitive Treatment:** Radiofrequency Catheter Ablation of the accessory pathway.

Q: Which of the following is NOT true regarding hypertrophic obstructive cardiomyopathy?

Systolic dysfunction. Hypertrophic Obstructive Cardiomyopathy (HOCM) is primarily a disease of **diastolic dysfunction**, not systolic dysfunction. **1. Why "Systolic Dysfunction" is the correct answer (The False Statement):** In HOCM, the ventricular walls are thickened, leading to a hyperdynamic state. The **Ejection Fraction (EF) is typically normal or even supranormal** (>70%). Systolic function remains preserved until the very end-stages of the disease ("burnt-out" phase). Therefore, stating that HOCM is characterized by systolic dysfunction is clinically incorrect. **2. Analysis of Incorrect Options:** * **Concentric Hypertrophy:** While HOCM is classically known for *asymmetric* septal hypertrophy, the overall pathology involves significant thickening of the ventricular walls (concentric-like remodeling) without chamber dilation, making this a characteristic feature. * **Diastolic Dysfunction:** This is the hallmark of HOCM. The thickened, stiff myocardium cannot relax properly during diastole, leading to impaired filling and elevated left ventricular end-diastolic pressure (LVEDP). * **Double Apical Impulse:** This is a classic clinical sign. The first impulse is due to a forceful atrial contraction (S4) against a stiff ventricle (palpable S4), and the second is the actual ventricular apex beat. In some cases, a "triple ripple" may be felt. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant (most common mutation: **Beta-myosin heavy chain** or Myosin-binding protein C) [1]. * **Murmur Dynamics:** The systolic murmur of HOCM **increases** with Valsalva and standing (decreased preload) and **decreases** with squatting or handgrip (increased preload/afterload). * **Histology:** Characterized by **myocyte disarray** and interstitial fibrosis [1]. * **Drug of Choice:** Beta-blockers (to increase diastolic filling time). Avoid Nitrates and Diuretics as they worsen the outflow obstruction.

Q: Ebstein anomaly is associated with all the following except?

Ventricular septal defect (VSD). **Explanation:** Ebstein anomaly is a congenital heart defect characterized by the **downward displacement of the tricuspid valve leaflets** (septal and posterior) into the right ventricle. This results in "atrialization" of the right ventricle, leading to a massive right atrium and severe tricuspid regurgitation. **Why Ventricular Septal Defect (VSD) is the correct answer:** While Ebstein anomaly is frequently associated with inter-atrial communications, it is **rarely associated with a Ventricular Septal Defect (VSD)**. The primary structural pathology involves the tricuspid valve and the right-sided chambers, not the ventricular septum. **Analysis of other options:** * **Patent Foramen Ovale (PFO) / ASD:** These are found in over 80-90% of cases. The high pressure in the right atrium causes a right-to-left shunt across the PFO/ASD, leading to cyanosis. * **Massive heart on CXR:** Due to the extreme dilation of the right atrium, the chest X-ray typically shows a **"box-shaped" or "balloon-shaped" heart** with a very high cardiothoracic ratio. * **Tall, broad P waves:** Known as **"Himalayan P waves,"** these occur due to massive right atrial enlargement. They are a classic ECG finding in Ebstein anomaly. **High-Yield Clinical Pearls for NEET-PG:** 1. **Maternal Risk Factor:** Strongly associated with maternal **Lithium** intake during the first trimester. 2. **ECG Findings:** Himalayan P waves, right bundle branch block (RBBB), and a high incidence of **Wolff-Parkinson-White (WPW) syndrome** (Type B). 3. **Auscultation:** Characterized by a "multi-click" or "sail sound" (loud T1) and a quadruple gallop rhythm. 4. **Cyanosis:** Occurs due to the right-to-left shunt at the atrial level, despite it being an obstructive-like right-sided lesion.

Q: A 22-year-old woman with no past medical history is found to have a systolic ejection murmur on routine physical examination. She has no symptoms and feels well. The murmur is heard along the right and left sternal borders and it decreases with handgrip exercises. For the patient with a systolic murmur, what is the most likely diagnosis?

Hypertrophic obstructive cardiomyopathy (HOCM). ### Explanation The correct diagnosis is **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. **1. Why HOCM is correct:** The murmur in HOCM is a **systolic ejection murmur** caused by dynamic left ventricular outflow tract (LVOT) obstruction [1]. The key to this question lies in the response to the **handgrip exercise**. * **Handgrip** increases afterload (systemic vascular resistance). * Increased afterload increases the volume of blood in the left ventricle, which pushes the interventricular septum away from the mitral valve. * This reduces the LVOT obstruction, thereby **decreasing the intensity** of the HOCM murmur [1]. * (Note: HOCM and Mitral Valve Prolapse are the only two murmurs that typically *decrease* with increased afterload/preload maneuvers like squatting or handgrip). **2. Why the other options are incorrect:** * **Aortic Stenosis (AS):** While AS also presents with a systolic ejection murmur, handgrip increases afterload, which typically **increases or maintains** the pressure gradient across the valve, and it does not significantly soften the murmur like it does in HOCM [1]. * **Mitral Regurgitation (MR) & Tricuspid Regurgitation (TR):** These are **holosystolic** (pansystolic) murmurs, not ejection murmurs. Furthermore, handgrip increases the intensity of MR due to increased backpressure from the aorta [2]. **3. NEET-PG High-Yield Pearls:** * **HOCM Murmur Dynamics:** * *Increases with:* Valsalva, Standing (decreased preload/ventricular volume). * *Decreases with:* Squatting, Handgrip, Passive leg raise (increased preload/afterload). * **Genetic Basis:** Most commonly due to mutations in **Beta-myosin heavy chain** or Myosin-binding protein C. * **ECG Finding:** Look for "dagger-like" Q waves in lateral leads (I, aVL, V5-V6). * **Sudden Cardiac Death:** HOCM is the most common cause of SCD in young athletes.

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

What causes Torsades de pointes?

Accepted Answer

Prolonged QT interval

Answer

Wide QRS complex

Answer

Short QRS complex

Answer

Short QT interval

Question 3

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 4

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 5

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 6

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

Question 7

Which one of the following drugs should be avoided in Wolff-Parkinson-White (WPW) Syndrome?

Accepted Answer

Digoxin

Answer

Adenosine

Answer

Procainamide

Answer

Amiodarone

Question 8

Which of the following is NOT true regarding hypertrophic obstructive cardiomyopathy?

Accepted Answer

Systolic dysfunction

Answer

Concentric hypertrophy

Answer

Diastolic dysfunction

Answer

Double apical impulse

Question 9

Ebstein anomaly is associated with all the following except?

Accepted Answer

Ventricular septal defect (VSD)

Answer

Patent foramen ovale

Answer

Massive heart on chest X-ray

Answer

Tall, broad P wave

Question 10

A 22-year-old woman with no past medical history is found to have a systolic ejection murmur on routine physical examination. She has no symptoms and feels well. The murmur is heard along the right and left sternal borders and it decreases with handgrip exercises. For the patient with a systolic murmur, what is the most likely diagnosis?

Accepted Answer

Hypertrophic obstructive cardiomyopathy (HOCM)

Answer

Aortic stenosis

Answer

Mitral regurgitation (chronic)

Answer

Tricuspid regurgitation

Cardiology — MCQs

Cardiology — MCQs

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