Cardiology Practice Questions

Q: Which of the following is NOT true about Hypertrophic Obstructive Cardiomyopathy?

Beta agonists are useful.. **Explanation:** Hypertrophic Obstructive Cardiomyopathy (HOCM) is characterized by a hyperdynamic left ventricle and dynamic outflow obstruction. The correct answer is **A** because **Beta-agonists are contraindicated**, not useful, in HOCM. **1. Why Option A is the correct answer (False statement):** Beta-agonists (like Dobutamine or Isoproterenom) increase myocardial contractility (inotropy) and heart rate (chronotropy). In HOCM, increased contractility worsens the narrowing of the outflow tract, while increased heart rate reduces diastolic filling time. This exacerbates the dynamic obstruction and decreases cardiac output. Conversely, **Beta-blockers** are the first-line treatment as they slow the heart rate and reduce contractility, allowing for better ventricular filling. **2. Analysis of other options:** * **Option B:** Asymmetrical Septal Hypertrophy (ASH) is the hallmark of HOCM, where the interventricular septum is significantly thicker than the posterior wall (Ratio >1.3:1). * **Option C:** Obstruction is "dynamic" because it varies with loading conditions. It is caused by the thickened septum and the **Systolic Anterior Motion (SAM)** of the mitral valve. * **Option D:** A double apical impulse (or "triple" in some cases) occurs due to a forceful atrial contraction against a stiff ventricle (S4) followed by the sustained ventricular apex beat. **Clinical Pearls for NEET-PG:** * **Murmur Dynamics:** The systolic murmur of HOCM **increases** with maneuvers that decrease preload (Valsalva, standing) and **decreases** with maneuvers that increase preload or afterload (Squatting, Handgrip). * **Drug of Choice:** Beta-blockers (Propranolol/Atenolol). Verapamil is an alternative. * **Avoid:** Nitrates, Diuretics, and Digitalis (these worsen the obstruction). * **Genetic Basis:** Most commonly due to mutations in the **Beta-myosin heavy chain** or Myosin-binding protein C [1].

Q: The most common cause of tricuspid regurgitation is secondary to:

Dilatation of the right ventricle. Tricuspid Regurgitation (TR) is classified into two types: **Primary (Organic)** and **Secondary (Functional)**. **Why Option B is correct:** The most common cause of TR is **Secondary (Functional) TR**, accounting for over 80% of cases [1]. It occurs not due to a primary valve defect, but because of **dilatation of the right ventricle (RV)** and the tricuspid annulus [1]. This is typically a consequence of pulmonary hypertension (secondary to left-sided heart disease), RV infarction, or cardiomyopathy [1]. The enlargement of the RV causes tethering of the valve leaflets, preventing proper coaptation. **Why other options are incorrect:** * **Option A (Rheumatic Heart Disease):** While a common cause of *primary* TR in developing countries, it rarely occurs in isolation and is almost always associated with mitral or aortic valve involvement [1]. * **Option C (Coronary Artery Disease):** While CAD can cause mitral regurgitation (via papillary muscle dysfunction), it is an uncommon cause of TR unless it leads to significant RV infarction or chronic left-sided heart failure. * **Option D (Endocarditis):** IV drug abuse is the most common cause of *isolated primary* TR, but it is far less frequent than functional TR caused by RV dilatation. **High-Yield Clinical Pearls for NEET-PG:** * **Physical Exam:** Look for a holosystolic murmur at the left lower sternal border that increases with inspiration (**Carvallo’s sign**) [1]. * **Jugular Venous Pulse (JVP):** Characterized by a prominent **'v' wave** and a steep 'y' descent [1]. * **Pulsatile Liver:** Severe TR often presents with a tender, pulsatile liver (congestive hepatomegaly) [1].

Q: An early systolic murmur may be caused by all of the following, EXCEPT:

Aortic stenosis. **Explanation:** The key to answering this question lies in distinguishing between the timing of systolic murmurs. **Aortic Stenosis (AS)** typically produces a **mid-systolic (ejection systolic) murmur** [2]. The murmur begins after the first heart sound (S1), following the period of isovolumetric contraction, peaks in mid-systole as flow velocity across the valve reaches its maximum, and ends before the second heart sound (S2) [1]. Therefore, it is not an early systolic murmur. **Analysis of Options:** * **Small Ventricular Septal Defect (VSD):** In a small VSD (Maladie de Roger), the high pressure gradient between the left and right ventricles exists primarily in early systole. As the muscular septum contracts, the defect may be physically closed or narrowed, causing the murmur to cease before S2. * **Papillary Muscle Dysfunction:** This often leads to acute or transient mitral regurgitation. Because the papillary muscles fail to tension the leaflets early in systole, the regurgitation (and thus the murmur) occurs predominantly in the early-to-mid systolic phase. * **Tricuspid Regurgitation (TR):** While TR is often holosystolic, it can present as an early systolic murmur, particularly in cases of acute TR or when right ventricular pressures are not significantly elevated. **NEET-PG High-Yield Pearls:** * **AS Murmur:** Classically described as "crescendo-decrescendo." The later the peak of the murmur, the more severe the stenosis. * **Innocent Murmurs:** These are almost always mid-systolic; a holosystolic or diastolic murmur is never physiological [2]. * **Handgrip Exercise:** Increases afterload, which decreases the intensity of an AS murmur but increases the intensity of MR and VSD murmurs.

Q: A 36-year-old man presents with the sensation of a racing heart. His blood pressure is 110/70, respiratory rate 14/min, and O2 saturation 98%. ECG is shown. Carotid massage and Valsalva maneuver do not improve the heart rate. Which of the following is the initial therapy of choice?

Adenosine 6-mg rapid IV bolus. ***Adenosine 6-mg rapid IV bolus*** - **Adenosine** is the **first-line pharmacologic treatment** for supraventricular tachycardia (SVT) after failed vagal maneuvers due to its rapid onset and short half-life. - It works by blocking **AV node conduction** temporarily, breaking the re-entrant circuit in **AVNRT** or **AVRT** within seconds of administration. *Verapamil 2.5 to 5 mg IV over 1 to 2 minutes* - While **verapamil** is effective for SVT, it has a **longer half-life** and slower onset compared to adenosine, making it a second-line option. - Risk of **hypotension** and **negative inotropic effects** make it less preferred as initial therapy in hemodynamically stable patients. *Diltiazem 0.25-mg/kg IV over 2 minutes* - **Diltiazem** is another **calcium channel blocker** that can terminate SVT but has slower onset than adenosine. - Like verapamil, it carries risk of **hypotension** and **bradycardia**, making it less ideal as first-line treatment. *Digoxin 0.5 mg IV slowly* - **Digoxin** has a very **slow onset** (hours) and is not appropriate for acute SVT termination. - Its mechanism involves **vagal stimulation** and **AV node depression**, but the delayed effect makes it unsuitable for emergency SVT management.

Q: A 68-year-old male admitted to the ICU for acute exacerbation of COPD develops sudden onset of palpitations. The ECG shows irregular rhythm with varying P wave morphology and varying PR intervals. What is the most likely diagnosis?

Multifocal atrial tachycardia. ### Explanation **Multifocal Atrial Tachycardia (MAT)** is the correct diagnosis based on the classic triad of clinical and ECG findings presented: 1. **Clinical Context:** MAT is most commonly associated with severe underlying pulmonary disease, particularly **Acute Exacerbation of COPD**. It is often triggered by hypoxia, hypercapnia, or the use of theophylline/beta-agonists. 2. **ECG Criteria:** The diagnosis requires: * An irregular rhythm (irregularly irregular). * At least **three distinct P-wave morphologies** in the same lead. * Varying PR and PP intervals. * Atrial rate typically >100 bpm. #### Analysis of Incorrect Options: * **A. Atrial Fibrillation:** While also "regularly irregular," AF is characterized by the **absence of discernible P waves** (replaced by fibrillatory waves) [1]. This patient has distinct, albeit varying, P waves. * **B. Ventricular Tachycardia:** This presents as a wide-complex, regular tachycardia. The presence of P waves and an irregular rhythm makes this diagnosis unlikely. * **C. Acute Myocardial Infarction:** While MI can trigger arrhythmias, it typically presents with ST-segment and T-wave changes rather than the specific P-wave morphology variations described. #### NEET-PG High-Yield Pearls: * **Treatment Priority:** The primary treatment for MAT is **treating the underlying cause** (e.g., correcting hypoxia/COPD exacerbation). * **Pharmacotherapy:** If rate control is needed, **Verapamil (Calcium Channel Blocker)** is the drug of choice. * **Contraindication:** **Beta-blockers are generally avoided** in these patients due to the risk of worsening bronchospasm in the setting of COPD. * **Wandering Atrial Pacemaker (WAP):** If the heart rate is <100 bpm with the same P-wave criteria, the diagnosis is WAP.

Q: Which of the following statements regarding a patient with atrial fibrillation is false?

Brain imaging is not done. ### Explanation In the clinical management of a patient presenting with **Atrial Fibrillation (AF)**, the primary goals are hemodynamic stabilization, rate/リズム control, and thromboembolic risk assessment. **1. Why "Brain imaging is not done" is the correct (False) statement:** Atrial fibrillation is the leading cause of cardioembolic strokes. While not every stable AF patient requires immediate neuroimaging, it is **routinely indicated** if there is any suspicion of a Transient Ischemic Attack (TIA) or acute stroke [1]. Furthermore, in the context of initiating anticoagulation, a baseline CT/MRI may be necessary to rule out intracranial hemorrhage [1]. Therefore, stating that brain imaging is "not done" is clinically incorrect. **2. Analysis of other options:** * **Troponin I is sent:** This is a standard part of the initial workup. AF can be triggered by an acute myocardial infarction (MI), or conversely, the rapid ventricular rate in AF can cause "demand ischemia," leading to elevated Troponin levels. * **Echocardiogram is done:** This is a **mandatory** investigation [2]. A Transthoracic Echo (TTE) assesses chamber size, valvular morphology (e.g., Mitral Stenosis), and left ventricular function. A Transesophageal Echo (TEE) is the gold standard to rule out a left atrial appendage (LAA) thrombus before cardioversion [1]. **Clinical Pearls for NEET-PG:** * **CHADS₂-VASc Score:** Used to determine the need for long-term anticoagulation in non-valvular AF. * **Holiday Heart Syndrome:** AF triggered by excessive alcohol consumption. * **Treatment of Choice:** For hemodynamically unstable AF, the immediate treatment is **Synchronized DC Cardioversion**. * **Ashman Phenomenon:** A long R-R interval followed by a short R-R interval resulting in an aberrantly conducted QRS complex (usually RBBB morphology).

Question 1

Tako-tsubo cardiomyopathy is a type of:

Accepted Answer

Dilated cardiomyopathy

Answer

Restrictive cardiomyopathy

Answer

Hypertrophic cardiomyopathy

Answer

Toxic cardiomyopathy

Question 2

Which of the following is NOT true about Hypertrophic Obstructive Cardiomyopathy?

Accepted Answer

Beta agonists are useful.

Answer

Asymmetrical hypertrophy of the septum.

Answer

Dynamic left ventricular outflow obstruction.

Answer

Double apical impulse.

Question 3

The most common cause of tricuspid regurgitation is secondary to:

Accepted Answer

Dilatation of the right ventricle

Answer

Rheumatic heart disease

Answer

Coronary artery disease

Answer

Endocarditis due to intravenous drug abuse

Question 4

An early systolic murmur may be caused by all of the following, EXCEPT:

Accepted Answer

Aortic stenosis

Answer

Small ventricular septal defect

Answer

Papillary muscle dysfunction

Answer

Tricuspid regurgitation

Question 5

A 36-year-old man presents with the sensation of a racing heart. His blood pressure is 110/70, respiratory rate 14/min, and O2 saturation 98%. ECG is shown. Carotid massage and Valsalva maneuver do not improve the heart rate. Which of the following is the initial therapy of choice?

Accepted Answer

Adenosine 6-mg rapid IV bolus

Answer

Verapamil 2.5 to 5 mg IV over 1 to 2 minutes

Answer

Diltiazem 0.25-mg/kg IV over 2 minutes

Answer

Digoxin 0.5 mg IV slowly

Question 6

A 68-year-old male admitted to the ICU for acute exacerbation of COPD develops sudden onset of palpitations. The ECG shows irregular rhythm with varying P wave morphology and varying PR intervals. What is the most likely diagnosis?

Accepted Answer

Multifocal atrial tachycardia

Answer

Atrial fibrillation

Answer

Ventricular tachycardia

Answer

Acute myocardial infarction

Question 7

A 16-year-old girl presents with chest pain and respiratory distress. On physical examination, she is short of breath, wheezing, and gasping for air. Cardiac auscultation reveals a prominent pansystolic murmur and a prominent third heart sound. Chest X-ray shows marked enlargement of the heart. The patient expired despite intensive supportive measures. Microscopic examination of the myocardium at autopsy discloses aggregates of mononuclear cells arranged around centrally located deposits of eosinophilic collagen. What is the appropriate diagnosis?

Accepted Answer

Rheumatic heart disease

Answer

Acute bacterial endocarditis

Answer

Subacute bacterial endocarditis

Answer

Viral myocarditis

Question 8

Which of the following statements regarding a patient with atrial fibrillation is false?

Accepted Answer

Brain imaging is not done

Answer

Troponin I is sent

Answer

Echocardiogram is done

Answer

All of the above

Question 9

Reasons for preference of internal jugular vein over external jugular vein for measurement of JVP include all except?

Accepted Answer

Increased sympathetic activity in IJV

Answer

IJV is in direct continuation with the right atrium

Answer

EJV passes through more facial planes

Answer

Prominent valves at the proximal portion of EJV

Question 10

A 60-year-old patient presents with recurrent TIA episodes. Echocardiography shows the candle flame sign. What is the probable etiology?

Accepted Answer

Rheumatic fever during youth

Answer

Senile calcification of the heart valve

Answer

Long-standing undiagnosed hypertension

Answer

Undiagnosed congenital condition

Cardiology — MCQs

Cardiology — MCQs

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