Cardiology Practice Questions

Q: A 50-year-old man had an attack of myocardial infarction and developed ventricular ectopics and a low ejection fraction. Which of the following antiarrhythmic drugs should be given?

Beta-blocker. ### Explanation **Correct Answer: C. Beta-blocker** The management of post-myocardial infarction (MI) arrhythmias focuses on reducing mortality and preventing sudden cardiac death (SCD). **Why Beta-blockers are the drug of choice:** In patients with a history of MI and a low ejection fraction (EF), **Beta-blockers** (e.g., Metoprolol, Carvedilol) are the first-line therapy [1]. They reduce myocardial oxygen demand, decrease sympathetic overactivity, and prevent ventricular remodeling [2]. Most importantly, they are the only class of drugs in this list proven to **reduce mortality** and the risk of arrhythmic death in patients with coronary artery disease and heart failure [1, 2]. **Why other options are incorrect:** * **Flecainide (Class IC):** The landmark **CAST (Cardiac Arrhythmia Suppression Trial)** study proved that Class IC agents increase mortality in post-MI patients due to their pro-arrhythmic effects in scarred myocardium [3]. They are strictly contraindicated in structural heart disease. * **Mexiletine (Class IB):** While it can suppress ventricular ectopics, it has not shown a mortality benefit and is generally reserved as an adjunct therapy for refractory cases. * **Radio-frequency ablation:** This is typically indicated for symptomatic, drug-refractory ventricular tachycardia or specific focal ectopics, but it is not the initial medical management for post-MI ventricular ectopics. **High-Yield Clinical Pearls for NEET-PG:** * **CAST Trial Key Takeaway:** Never use Class IC antiarrhythmics (Flecainide, Propafenone) in patients with prior MI or CAD [3]. * **Low EF + Post-MI:** The most effective intervention to prevent SCD is an **ICD (Implantable Cardioverter Defibrillator)** if the EF remains ≤35% despite optimal medical therapy. * **Amiodarone:** It is "neutral" regarding mortality in post-MI patients; it suppresses arrhythmias but does not improve survival like Beta-blockers do.

Q: A 28-year-old woman presents with symptoms of chest pain that changes with positioning, is worse when lying down, and relieved when sitting up. She also reports increasing dyspnea and edema. On examination, her blood pressure is 85/60 mm Hg with a positive pulsus paradoxus, a low-volume pulse at 110/min, and distant heart sounds. The JVP is at 7 cm with a negative Kussmaul's sign. ECG shows low voltages, and CXR reveals a large cardiac silhouette. What is the most likely diagnosis for a patient presenting with shortness of breath and peripheral edema with these findings?

Cardiac tamponade. The clinical presentation is a classic description of **Cardiac Tamponade**, characterized by the accumulation of fluid in the pericardial space leading to increased intrapericardial pressure and impaired cardiac filling [1]. **Why Cardiac Tamponade is correct:** The patient exhibits **Beck’s Triad**: hypotension (85/60 mm Hg), distant/muffled heart sounds, and elevated JVP. The positional chest pain suggests underlying pericarditis [3]. Key diagnostic features mentioned include: * **Pulsus Paradoxus:** A drop in systolic BP >10 mmHg during inspiration (hallmark of tamponade). * **Negative Kussmaul’s Sign:** In tamponade, the JVP typically falls during inspiration (unlike constrictive pericarditis). * **ECG/CXR:** Low voltage complexes and a "water-bottle" heart silhouette are characteristic [1]. **Why other options are incorrect:** * **Constrictive Pericarditis:** While it shares features like elevated JVP and edema, it is characterized by a **positive Kussmaul’s sign** (paradoxical rise in JVP on inspiration) and a pericardial knock, rather than muffled heart sounds [4]. * **Restrictive Cardiomyopathy:** Presents with heart failure symptoms and a positive Kussmaul’s sign, but usually lacks the acute hypotension and the specific CXR/ECG findings of large pericardial effusion. * **RVMI:** While it causes hypotension and raised JVP, it typically presents with clear lung fields and specific ST-segment elevations in right-sided leads (V4R), not muffled heart sounds or low voltage ECG [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Beck’s Triad:** Hypotension, Muffled Heart Sounds, Raised JVP. * **Pulsus Paradoxus:** Also seen in severe asthma, COPD, and tension pneumothorax. * **JVP Waveform:** In tamponade, there is a **prominent 'x' descent** but an **absent/diminished 'y' descent** (due to restricted diastolic filling). * **Treatment of Choice:** Immediate **Pericardiocentesis**.

Q: What is not true of the "a" wave of venous pulsations in the neck?

Occurs just after the carotid artery pulse. The Jugular Venous Pulse (JVP) reflects pressure changes in the right atrium. Understanding its timing relative to the cardiac cycle is crucial for NEET-PG. ### Why Option C is Correct (The False Statement) The **'a' wave** represents **atrial contraction** [1]. In the cardiac cycle, atrial contraction occurs at the end of diastole, just before the closure of the AV valves [1]. Therefore, the 'a' wave occurs **just before** the first heart sound (S1) and **before** the carotid artery pulse [2]. The carotid pulse corresponds to ventricular systole (specifically the 'c' wave of the JVP). ### Explanation of Other Options * **Option A (Tricuspid Stenosis):** In TS, the right atrium must contract against a narrowed orifice, leading to increased resistance and **giant 'a' waves**. * **Option B (Atrial Fibrillation):** Since the 'a' wave is produced by coordinated atrial contraction, it is characteristically **absent/abolished** in AF, where the atria only quiver. * **Option D (Complete Heart Block):** When the atria contract against a closed tricuspid valve (which happens when the P wave falls between QRS and T waves during AV dissociation), it produces intermittent, very large waves known as **Cannon 'a' waves**. ### High-Yield Clinical Pearls * **'a' wave:** Atrial contraction (absent in AF; giant in TS, PS, and Pulmonary HTN). * **'c' wave:** Carotid impact/Tricuspid bulging during ventricular contraction [2]. * **'x' descent:** Atrial relaxation. * **'v' wave:** Venous filling against a closed tricuspid valve (giant in Tricuspid Regurgitation). * **'y' descent:** Emptying of the atrium into the ventricle (rapid/steep in Constrictive Pericarditis - *Friedreich's sign*).

Q: What is the investigation of choice to assess cardiotoxicity of anthracycline drugs?

Echocardiogram. **Explanation:** **Anthracycline-induced cardiotoxicity** (caused by drugs like Doxorubicin and Daunorubicin) typically manifests as dose-dependent, irreversible dilated cardiomyopathy. **1. Why Echocardiography is the Correct Choice:** Transthoracic Echocardiography (TTE) is the **investigation of choice** because it is non-invasive, widely available, and allows for the serial monitoring of the **Left Ventricular Ejection Fraction (LVEF)** [1]. A decline in LVEF is the primary marker used to diagnose cardiotoxicity and guide the discontinuation of chemotherapy. Modern guidelines also emphasize **Global Longitudinal Strain (GLS)** via speckle-tracking echocardiography as a more sensitive tool to detect subclinical toxicity before the LVEF actually drops [1]. **2. Why Other Options are Incorrect:** * **Myocardial Biopsy:** While this is the *most definitive* (gold standard) method to detect early histological changes (like vacuolization), it is invasive and carries risks, making it impractical for routine screening. * **ECG:** Though it may show non-specific ST-T wave changes or arrhythmias, it lacks the sensitivity and specificity to quantify ventricular function or predict heart failure [2]. * **CT Angiography:** This is used to visualize coronary anatomy and is not the standard modality for functional assessment of chemotherapy-induced muscle damage [3]. **Clinical Pearls for NEET-PG:** * **MUGA Scan:** Historically considered the most accurate/reproducible for LVEF, but Echocardiography is preferred today due to lack of radiation. * **Dexrazoxane:** An iron-chelating agent used to *prevent* anthracycline-induced cardiomyopathy. * **Cumulative Dose:** Risk increases significantly once Doxorubicin exceeds **450–550 mg/m²**. * **Biomarkers:** Elevated **Troponin I** levels during chemotherapy can also predict a higher risk of subsequent cardiotoxicity.

Q: What is the most common cause of dilated cardiomyopathy?

Alcohol. **Explanation:** **Dilated Cardiomyopathy (DCM)** is characterized by ventricular dilation and impaired systolic function [1]. While the majority of cases are classified as "idiopathic," **Alcohol** is recognized as the most common identifiable (non-idiopathic) cause of secondary dilated cardiomyopathy [1]. 1. **Why Alcohol is Correct:** Chronic ethanol consumption has a direct toxic effect on the myocardium and its metabolites (like acetaldehyde). It interferes with mitochondrial function, calcium handling, and protein synthesis. It is dose-dependent; however, unlike many other causes, alcoholic cardiomyopathy is potentially reversible if the patient practices total abstinence in the early stages [1]. 2. **Analysis of Incorrect Options:** * **Viral Infection:** While viral myocarditis (e.g., Coxsackie B, Adenovirus) is a frequent precursor to DCM, it is statistically less common than chronic alcohol-induced damage in the general adult population. * **Pregnancy:** Peripartum cardiomyopathy is a specific, rare form of DCM occurring in the last month of pregnancy or the first five months postpartum. It is not the "most common" cause. * **Metabolic Disease:** Conditions like thiamine deficiency (Wet Beriberi) or thyroid dysfunction can cause DCM, but these represent a much smaller percentage of cases compared to toxins like alcohol. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of DCM overall:** Idiopathic (often has a genetic basis, e.g., *TTN* gene mutation encoding Titin) [1]. * **Most common identifiable cause:** Alcohol [1]. * **Reversibility:** Alcoholic DCM is one of the few reversible forms of heart failure with lifestyle modification [1]. * **Drug-induced DCM:** Doxorubicin (Anthracyclines) is a classic board-favorite cause of irreversible, dose-dependent DCM. * **Echo Finding:** "Global hypokinesia" with a reduced ejection fraction (EF <40%).

Question 1

Which of the following is the first-line vasopressor in the management of cardiogenic shock?

Accepted Answer

Norepinephrine

Answer

Epinephrine

Answer

Dopamine

Answer

Dobutamine

Question 2

A 50-year-old man had an attack of myocardial infarction and developed ventricular ectopics and a low ejection fraction. Which of the following antiarrhythmic drugs should be given?

Accepted Answer

Beta-blocker

Answer

Flecainide

Answer

Mexiletine

Answer

Radio-frequency ablation technique

Question 3

A 28-year-old woman presents with symptoms of chest pain that changes with positioning, is worse when lying down, and relieved when sitting up. She also reports increasing dyspnea and edema. On examination, her blood pressure is 85/60 mm Hg with a positive pulsus paradoxus, a low-volume pulse at 110/min, and distant heart sounds. The JVP is at 7 cm with a negative Kussmaul's sign. ECG shows low voltages, and CXR reveals a large cardiac silhouette. What is the most likely diagnosis for a patient presenting with shortness of breath and peripheral edema with these findings?

Accepted Answer

Cardiac tamponade

Answer

Constrictive pericarditis

Answer

Restrictive cardiomyopathy

Answer

Right ventricle myocardial infarction (RVMI)

Question 4

What is not true of the "a" wave of venous pulsations in the neck?

Accepted Answer

Occurs just after the carotid artery pulse

Answer

Exaggerated in tricuspid stenosis

Answer

Abolished in atrial fibrillation

Answer

Exaggerated in complete heart block when the P wave falls between the QRS and T waves

Question 5

Presence of a pansystolic murmur of Mitral Regurgitation with left axis deviation in a patient with an Atrial Septal Defect suggests what?

Accepted Answer

Ostium primum with floppy mitral valve

Answer

Transposition of the Great Arteries (TGA)

Answer

Ostium secundum with floppy mitral valve

Answer

Pulmonary Hypertension

Question 6

A 20-year-old college basketball player presents with chest pain and palpitations during practice. He denies dyspnea, tachypnea, family history of cardiac disease, and social history of alcohol or drug use. Cardiac auscultation is unremarkable, and ECG shows frequent premature ventricular contractions (PVCs). What is the most appropriate next step in evaluation and/or management?

Accepted Answer

Obtain urine drug screen

Answer

Arrange treadmill stress test

Answer

Obtain Doppler ultrasound of deep veins of lower legs

Answer

Institute cardio-selective beta-blocker therapy

Question 7

What is the investigation of choice to assess cardiotoxicity of anthracycline drugs?

Accepted Answer

Echocardiogram

Answer

Myocardial biopsy

Answer

ECG

Answer

CT angiography

Question 8

What is the most common cause of dilated cardiomyopathy?

Accepted Answer

Alcohol

Answer

Viral infection

Answer

Pregnancy

Answer

Metabolic disease

Question 9

A 32-year-old asymptomatic woman has a rapidly rising, forceful pulse that collapses quickly. Which of the following is the most likely diagnosis?

Accepted Answer

aortic regurgitation

Answer

mitral stenosis

Answer

mitral regurgitation

Answer

aortic stenosis

Question 10

A 55-year-old hypertensive patient presents with a standing blood pressure of 190/105 mmHg and a sitting blood pressure of 180/100 mmHg. The patient also exhibits an irregularly irregular rhythm, a double apical impulse, and bilateral basal crepitations, with no audible murmurs. The heart rate is not determinable. What is the likely underlying cause?

Accepted Answer

Left ventricular hypertrophy

Answer

Left atrial myoma

Answer

Mitral regurgitation

Answer

Cor pulmonale

Cardiology — MCQs

Cardiology — MCQs

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