Cardiology Practice Questions

Q: A patient with heart failure developed recurrent sustained monomorphic ventricular tachycardia. What is/are the appropriate treatment(s)?

Implantable Cardioverter-Defibrillator. **Explanation:** The primary goal in managing a patient with heart failure (HF) and recurrent sustained monomorphic ventricular tachycardia (VT) is the prevention of **Sudden Cardiac Death (SCD)**. **Why ICD is the Correct Answer:** According to current guidelines (ACC/AHA/ESC), an **Implantable Cardioverter-Defibrillator (ICD)** is the treatment of choice for **secondary prevention** of SCD in patients who have experienced sustained VT, especially in the setting of structural heart disease like heart failure [1]. While drugs may reduce the frequency of episodes, only the ICD has been proven to significantly improve survival by providing immediate internal cardioversion/defibrillation during life-threatening arrhythmias [1]. **Analysis of Incorrect Options:** * **A & B (Encainide and Flecainide):** These are Class 1C antiarrhythmics. The landmark **CAST (Cardiac Arrhythmia Suppression Trial)** proved that these drugs actually *increase* mortality in patients with prior myocardial infarction or structural heart disease due to their potent **pro-arrhythmic effects**. They are strictly contraindicated in heart failure. * **D (Beta-blockers):** While beta-blockers are a cornerstone of heart failure therapy and help reduce the burden of VT, they are generally insufficient as a standalone treatment for *recurrent sustained* VT [1]. They are used as adjunctive therapy alongside an ICD. **High-Yield Clinical Pearls for NEET-PG:** * **Amiodarone** is the preferred antiarrhythmic drug for VT in heart failure patients if an ICD is not feasible or to reduce frequent ICD shocks, as it is "neutral" regarding mortality. * **Class 1C drugs** (Flecainide, Propafenone) are for "Normal Hearts" only. * **Primary Prevention:** ICD is also indicated in HF patients with an Ejection Fraction (EF) ≤ 35% and NYHA Class II/III symptoms despite optimal medical therapy [1].

Q: In a patient with mitral stenosis, disappearance of Loud S1 is associated with all except?

Mild mitral stenosis. Explanation: In **Mitral Stenosis (MS)**, a **Loud S1** (tapping S1) is a hallmark finding [1]. It occurs because the thickened but mobile mitral leaflets are wide apart at the end of diastole and shut abruptly with high pressure. The disappearance of this loud S1 indicates that the valve is either too rigid to snap shut or that other physiological factors are interfering with its closure. **Why "Mild Mitral Stenosis" is the correct answer:** In **Mild MS**, the valve leaflets remain mobile and the pressure gradient is sufficient to snap them shut forcefully, resulting in a **Loud S1**. As MS progresses to a "tight" or "severe" stage with significant calcification, the S1 becomes soft or muffled [2]. Therefore, mild MS is associated with the *presence* of a loud S1, not its disappearance. **Analysis of Incorrect Options:** * **A. Calcified Valve:** When the mitral valve becomes heavily calcified and immobile, it can no longer "snap" shut. This leads to a soft or absent S1 and is also associated with the disappearance of the Opening Snap (OS) [2]. * **B. Aortic Regurgitation (AR):** Co-existing AR (specifically the Austin Flint phenomenon) or the rapid rise in left ventricular pressure can cause the mitral valve to close prematurely or less forcefully, softening the S1. * **C. Heart Block:** In First-degree Heart Block (prolonged PR interval), the mitral leaflets have more time to float back toward a closed position before ventricular systole begins. Consequently, they close from a shorter distance, resulting in a soft S1. **Clinical Pearls for NEET-PG:** * **Loud S1 + Opening Snap:** Indicates a mobile, non-calcified mitral valve [1]. * **Soft S1 in MS:** Suggests a rigid, calcified valve or severe subvalvular thickening [2]. * **The "Rule of S1":** S1 is loud in MS, short PR interval, and hyperdynamic states (tachycardia). S1 is soft in MR, long PR interval (1st-degree block), and severe/calcified MS.

Q: All of the following are features of Mobitz type I block except?

Constant PR interval. **Explanation:** Mobitz Type I (Wenckebach) is a second-degree AV block characterized by a progressive delay in conduction at the AV node [1]. **Why Option A is the Correct Answer:** In Mobitz Type I, the hallmark feature is a **progressive prolongation of the PR interval** in successive beats until a P-wave is completely blocked (dropped QRS) [1]. Therefore, a **constant PR interval** is not a feature of Mobitz Type I; rather, it is characteristic of Mobitz Type II or First-degree AV block [1]. **Analysis of Other Options:** * **B. Normal QRS morphology:** Since the block occurs within the AV node (proximal to the Bundle of His), the ventricular conduction remains normal [1]. Thus, the QRS complex is typically narrow (<0.12s). * **C. Regular atrial rhythm:** The SA node fires normally, resulting in a constant P-P interval [1]. The "irregularity" of the pulse is purely due to the intermittent failure of AV conduction. * **D. Atrial rate equals ventricular rate:** This is the **incorrect** statement in the context of the question's logic (though the question asks for "except"). In any second-degree block, there are more P waves than QRS complexes (e.g., 3:2 or 4:3 conduction), meaning the **atrial rate is faster than the ventricular rate.** *(Note: In standard medical exams, if multiple options seem incorrect, the most defining physiological mismatch—like the PR interval behavior—is the intended answer.)* **High-Yield Clinical Pearls for NEET-PG:** * **Site of Block:** Usually the AV Node [1]. * **Vagal Tone:** Increased vagal tone (e.g., in athletes or during sleep) can cause Mobitz I [1]. It often improves with atropine or exercise. * **Prognosis:** Generally benign and rarely progresses to complete heart block [1]. * **Wenckebach Phenomenon:** Characterized by "group beating" and a progressive shortening of the R-R interval before the dropped beat.

Q: What ECG change is seen in hypocalcemia?

QT prolongation. ### Explanation **Correct Option: A. QT prolongation** **Mechanism:** The QT interval on an ECG represents the total duration of ventricular depolarization and repolarization. In **hypocalcemia**, the low extracellular calcium levels lead to a **prolongation of Phase 2 (the plateau phase)** of the cardiac action potential. During this phase, the inward movement of calcium through L-type calcium channels is slowed, delaying the onset of repolarization. On the ECG, this specifically manifests as a **prolonged ST segment**, which results in an overall **prolongation of the QT interval**. **Analysis of Incorrect Options:** * **B & C (PR Interval changes):** The PR interval reflects AV nodal conduction [3]. While hyperkalemia or certain drugs (like Beta-blockers) can prolong the PR interval [1], and conditions like WPW syndrome shorten it [3], calcium levels do not primarily affect the PR interval. * **D (QT Shortening):** This is the classic ECG finding in **hypercalcemia**. High calcium levels shorten the plateau phase (Phase 2) and accelerate repolarization, leading to a shortened ST segment and QT interval. **High-Yield Clinical Pearls for NEET-PG:** * **Hypocalcemia:** Prolonged QT interval (specifically due to a long ST segment). T-waves usually remain normal. * **Hypercalcemia:** Shortened QT interval; may also see "Osborn waves" (though more common in hypothermia). * **Hypokalemia:** Flattened T-waves, **U-waves**, and ST-depression. * **Hyperkalemia:** Tall **tented T-waves**, widened QRS, and loss of P-waves (Sine wave pattern in severe cases) [1]. * **Clinical Correlation:** A prolonged QT interval in hypocalcemia can predispose patients to *Torsades de Pointes* [2], although this is less common than in hypomagnesemia or hypokalemia.

Q: An elderly female presented to the emergency room in an unconscious state. She has a history of similar episodes in the past few months. An ECG was performed, and the resulting graph is provided. Which of the following is the most probable cause?

2:1 block. ***2:1 block*** - **2:1 AV block** (second-degree AV block, Mobitz type II) causes **Stokes-Adams attacks** - recurrent syncopal episodes due to sudden bradycardia and reduced cardiac output. - ECG shows **every second P wave blocked** from conducting to the ventricles, resulting in a 2:1 P:QRS ratio, commonly causing symptomatic bradycardia in elderly patients. *Paroxysmal Supraventricular Tachycardia (PSVT)* - PSVT typically presents with **narrow QRS complex tachycardia** (150-250 bpm) and rarely causes unconsciousness unless associated with underlying heart disease. - Episodes are usually **self-limiting** and patients remain conscious, experiencing palpitations and chest discomfort rather than syncope. *Atrial flutter* - Characterized by **sawtooth pattern** of flutter waves and typically maintains a ventricular rate of 150 bpm with 2:1 conduction, but patients usually remain conscious. - While it can cause hemodynamic compromise, **syncope is uncommon** unless there's severe underlying cardiac dysfunction. *Ventricular bigeminy* - Shows **alternating normal beats and premature ventricular contractions (PVCs)**, creating a coupled rhythm pattern on ECG. - Generally **well-tolerated hemodynamically** and rarely causes syncope unless PVCs are frequent enough to significantly reduce cardiac output.

Q: A 63-year-old woman with a history of aortic stenosis and left ventricular hypertrophy experienced cardiac arrest and died. Which of the following predisposes to sudden cardiac death?

Hypokalemia. ### Explanation **Correct Option: B. Hypokalemia** In patients with **Aortic Stenosis (AS)** and **Left Ventricular Hypertrophy (LVH)**, the myocardium is highly susceptible to electrical instability. Hypokalemia lowers the resting membrane potential and prolongs ventricular repolarization (QT prolongation), which significantly increases the risk of life-threatening ventricular arrhythmias (VT/VF) and sudden cardiac death (SCD). In the context of LVH, the thickened muscle already has altered conduction properties, making electrolyte imbalances particularly lethal. **Analysis of Incorrect Options:** * **A. Split first heart sound:** A split S1 is a common physiological finding (closure of mitral then tricuspid valves) and does not predispose to SCD. In AS, the more relevant finding is a **reversed (paradoxical) splitting of S2**. * **C. Soft murmur at the left sternal border that varies with inspiration:** This describes a physiological or mild tricuspid regurgitation murmur. Murmurs that increase with inspiration are right-sided and generally benign in the context of SCD risk. * **D. Failure of the CVP to rise (Negative Hepato-jugular Reflux):** A positive HJR (rise in CVP >3 cm H2O) indicates fluid overload or right heart failure. A negative HJR is a normal finding and does not correlate with an increased risk of sudden death. **High-Yield Clinical Pearls for NEET-PG:** * **AS Triad (SAD):** Syncope, Angina, and Dyspnea. Once symptoms appear, the risk of SCD increases dramatically. * **ECG in Hypokalemia:** Look for flattened T-waves, prominent **U-waves**, and ST-segment depression. * **Critical AS:** Defined by a valve area ** 40 mmHg**. * **Avoid in AS:** Vasodilators (like ACE inhibitors or Nitrates) should be used with extreme caution as they can cause a catastrophic drop in preload/afterload, leading to syncope or arrest.

Q: Brugada syndrome is characterized by what ECG finding?

ST elevation. Explanation: Brugada Syndrome is an autosomal dominant genetic disorder caused by a mutation in the SCN5A gene, which encodes the cardiac sodium channel. This leads to a defect in the inward sodium current, primarily affecting the right ventricular outflow tract (RVOT). Why ST elevation is correct: The hallmark ECG finding in Brugada Syndrome is coved-type ST-segment elevation (≥2 mm) followed by a negative T-wave in the right precordial leads (V1–V3). This is known as the Type 1 Brugada pattern. It is often described as having a "shark fin" or "saddle-back" appearance. These changes occur due to an imbalance between inward and outward currents during the early repolarization phase of the action potential. Why other options are incorrect: * Prolonged PR interval: Associated with first-degree AV block or conditions like hyperkalemia and Lyme disease [3], but not the diagnostic hallmark of Brugada. * Prolonged QT interval: Characteristic of Long QT Syndrome (LQTS), which predisposes to Torsades de Pointes [2]. Brugada typically has a normal QT interval. * Tall T waves: Usually seen in hyperkalemia (peaked T waves) [3] or the hyperacute phase of myocardial infarction [1]. High-Yield Clinical Pearls for NEET-PG: * Demographics: Most common in young males of Southeast Asian descent. * Clinical Presentation: Sudden cardiac death (SCD) due to polymorphic ventricular tachycardia or ventricular fibrillation, often occurring during sleep or while at rest. * Triggers: Fever, alcohol, and certain drugs (e.g., sodium channel blockers) can unmask the ECG pattern. * Management: The only proven effective treatment for symptomatic patients or those at high risk is an Implantable Cardioverter Defibrillator (ICD).

Question 1

A patient with heart failure developed recurrent sustained monomorphic ventricular tachycardia. What is/are the appropriate treatment(s)?

Accepted Answer

Implantable Cardioverter-Defibrillator

Answer

Encainide

Answer

Flecainide

Answer

Beta-blockers

Question 2

In a patient with mitral stenosis, disappearance of Loud S1 is associated with all except?

Accepted Answer

Mild mitral stenosis

Answer

Calcified valve

Answer

Aortic regurgitation

Answer

Heart block

Question 3

All of the following are features of Mobitz type I block except?

Accepted Answer

Constant PR interval

Answer

Normal QRS morphology

Answer

Regular atrial rhythm

Answer

Atrial rate equals ventricular rate

Question 4

What ECG change is seen in hypocalcemia?

Accepted Answer

QT prolongation

Answer

Prolonged PR interval

Answer

Shortened PR interval

Answer

QT Shortening

Question 5

Amyloidosis of the heart presents with which of the following?

Accepted Answer

Arrhythmia

Answer

AV block

Answer

High voltage complexes

Answer

Aortic stenosis

Question 6

An elderly female presented to the emergency room in an unconscious state. She has a history of similar episodes in the past few months. An ECG was performed, and the resulting graph is provided. Which of the following is the most probable cause?

Accepted Answer

2:1 block

Answer

Paroxysmal Supraventricular Tachycardia (PSVT)

Answer

Atrial flutter

Answer

Ventricular bigeminy

Question 7

A 78-year-old woman presents with an acute anterior wall myocardial infarction, accompanied by hypotension and pulmonary congestion. Her blood pressure is 90/70 mm Hg, pulse is 110/min, JVP is at 8 cm, and heart sounds are normal. The lungs exhibit bibasilar crackles, and her extremities are cool and diaphoretic. What would central hemodynamic monitoring most likely reveal in this patient?

Accepted Answer

Increased right atrial pressure (RAP), decreased cardiac output (CO), and increased systemic vascular resistance (SVR).

Answer

Decreased right atrial pressure (RAP), low cardiac output (CO), and increased systemic vascular resistance (SVR).

Answer

Increased right atrial pressure (RAP), decreased cardiac output (CO), and decreased systemic vascular resistance (SVR).

Answer

Decreased right atrial pressure (RAP), increased cardiac output (CO), and decreased systemic vascular resistance (SVR).

Question 8

A 63-year-old woman with a history of aortic stenosis and left ventricular hypertrophy experienced cardiac arrest and died. Which of the following predisposes to sudden cardiac death?

Accepted Answer

Hypokalemia

Answer

Split first heart sound

Answer

Soft murmur at the left sternal border that varies with inspiration

Answer

Failure of the central venous pressure to rise more than 1 cm H2O with 30 seconds of pressure on the liver (hepato-jugular reflux)

Question 9

Brugada syndrome is characterized by what ECG finding?

Accepted Answer

ST elevation

Answer

Prolonged PR interval

Answer

Prolonged QT interval

Answer

Tall T waves

Question 10

A 70-year-old man with hypertension presents with severe chest pain and diaphoresis. On examination, he has bounding pulses with wide pulse pressure. A diastolic murmur is heard along the right sternal border. Which of the following is the possible etiology?

Accepted Answer

Aortic dissection

Answer

STEMI with papillary muscle dysfunction

Answer

Myocarditis with functional regurgitation

Answer

Flash pulmonary edema

Cardiology — MCQs

Cardiology — MCQs

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