Cardiology — MCQs
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A 47-year-old woman presents with new-onset transient right arm weakness and word-finding difficulty lasting 3 hours. She also experiences exertional dyspnea and had a syncopal event 1 month ago. Her medical history is remarkable only for 2 uneventful pregnancies, and she is not taking any medications. Physical examination reveals normal vital signs and no residual focal neurological deficits. The ECG and CT brain are normal, but an echocardiogram reveals a cardiac tumor in the left atrium, which is pedunculated and attached to the endocardium. Which of the following is the most likely cause of this lesion?
Which of the following statements about premature ventricular beats is false?
A patient presents with massive thromboembolism and hypotension, with a blood pressure of 88/50 mmHg, even after a 1 L fluid bolus. An echocardiogram shows right ventricular hypokinesis. What is the next best step in management?
A patient with an 8 cm x 8 cm abscess in the right lobe of the liver was treated with multiple aspirations and systemic amebicide. A cavity remains in the right lobe, which is now empty. A seven-day course of luminal amebicides has been completed. What is the recommended follow-up plan?
What is the effect of beriberi on circulation?
A 26-year-old woman complains of the abrupt onset of her chest pounding. She is diagnosed with paroxysmal atrial tachycardia. Which of the following is the most effective agent for converting paroxysmal atrial tachycardia to normal sinus rhythm?
Which of the following is NOT a characteristic of Prinzmetal angina?
What is the main component of hyperlipidemia that constitutes a major risk factor for atherosclerosis?
A female patient develops chest pain which is not associated with exercise and chest auscultation shows multiple non-ejection clicks. Which investigation is used to diagnose the disease?
Austin Flint Murmur is commonly mistaken for the murmur of which condition?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 61: A 47-year-old woman presents with new-onset transient right arm weakness and word-finding difficulty lasting 3 hours. She also experiences exertional dyspnea and had a syncopal event 1 month ago. Her medical history is remarkable only for 2 uneventful pregnancies, and she is not taking any medications. Physical examination reveals normal vital signs and no residual focal neurological deficits. The ECG and CT brain are normal, but an echocardiogram reveals a cardiac tumor in the left atrium, which is pedunculated and attached to the endocardium. Which of the following is the most likely cause of this lesion?
- A. Myxoma (Correct Answer)
- B. Sarcoma
- C. Rhabdomyoma
- D. Fibroma
Explanation: ### Explanation **1. Why Myxoma is the Correct Answer:** The clinical triad of **embolic phenomena** (transient arm weakness/aphasia), **obstructive symptoms** (exertional dyspnea, syncope), and **constitutional symptoms** (though absent here, often present) is classic for an atrial myxoma. * **Location:** Myxomas are the most common primary cardiac tumors in adults. Approximately **75-80% occur in the left atrium**, typically attached to the **interatrial septum** at the border of the fossa ovalis. * **Morphology:** They are often **pedunculated** and gelatinous. Their mobility allows them to swing into the mitral valve orifice during diastole (causing syncope or mimicking mitral stenosis) and friable fragments can embolize to the systemic circulation (causing TIA/Stroke) [1]. **2. Why Other Options are Incorrect:** * **Sarcoma (e.g., Angiosarcoma):** These are the most common primary *malignant* cardiac tumors. However, they typically occur in the **right atrium**, are invasive rather than pedunculated, and progress rapidly with pericardial effusion/tamponade. * **Rhabdomyoma:** This is the most common primary cardiac tumor in **children/infants**, strongly associated with **Tuberous Sclerosis**. They are usually multiple and located in the ventricles. * **Fibroma:** These are benign connective tissue tumors, usually seen in children. They are typically firm, solitary, and located within the ventricular myocardium (intramural), not pedunculated in the atrium. **3. High-Yield Clinical Pearls for NEET-PG:** * **Auscultation:** Look for a **"Tumor Plop"**—a low-pitched sound heard during early or mid-diastole as the tumor drops into the mitral orifice [1]. * **Positional Symptoms:** Dyspnea or syncope may worsen when the patient lies in specific positions (e.g., left lateral decubitus). * **Histology:** Characterized by "Stellate" or "Myxoma cells" embedded in a mucopolysaccharide-rich stroma. * **Carney Complex:** An autosomal dominant syndrome (PRKAR1A mutation) featuring atrial myxomas, spotty skin pigmentation (lentigines), and endocrine overactivity.
Question 62: Which of the following statements about premature ventricular beats is false?
- A. Sequential depolarization of ventricles
- B. Wide, bizarre, notched QRS complexes
- C. Prevalence decreases with age (Correct Answer)
- D. Palpitations is a common presenting feature
Explanation: ### Explanation **Premature Ventricular Complexes (PVCs)** are ectopic beats originating from the ventricular myocardium or His-Purkinje system. **1. Why Option C is the Correct (False) Statement:** The prevalence of PVCs actually **increases with age**. They are found in approximately 1% of clinically normal individuals on a standard ECG, but this frequency rises significantly with age and the presence of underlying structural heart disease (e.g., Ischemic Heart Disease, Heart Failure). In 24-hour Holter monitoring, up to 80% of elderly patients may show occasional PVCs. **2. Analysis of Other Options:** * **Option A (Sequential Depolarization):** In a normal beat, ventricles depolarize simultaneously via the His-Purkinje system. In PVCs, the impulse starts in one ventricle and spreads cell-to-cell to the other, leading to **sequential** rather than simultaneous depolarization. * **Option B (Wide, Bizarre QRS):** Because the impulse travels through slow-conducting myocardium rather than the specialized conduction system, the QRS complex is characteristically **wide (>0.12s)**, notched, and bizarre in morphology. * **Option D (Palpitations):** This is the most common symptom. Patients often describe a "skipped beat" or a "thumping" sensation, which is actually caused by the increased stroke volume of the **post-extrasystolic beat** following a compensatory pause [1]. **3. NEET-PG High-Yield Pearls:** * **Compensatory Pause:** PVCs are typically followed by a *full* compensatory pause (the distance between the pre-PVC and post-PVC R waves is equal to two normal R-R intervals) [1]. * **Rule of Bigeminy:** When every sinus beat is followed by a PVC. * **Management:** In asymptomatic patients without structural heart disease, **reassurance** is the treatment of choice. If symptomatic, **Beta-blockers** are the first-line medical therapy. * **Malignant PVCs:** Frequent PVCs (>10-15% burden) can lead to PVC-induced cardiomyopathy [2].
Question 63: A patient presents with massive thromboembolism and hypotension, with a blood pressure of 88/50 mmHg, even after a 1 L fluid bolus. An echocardiogram shows right ventricular hypokinesis. What is the next best step in management?
- A. Administer dopamine and recombinant tissue plasminogen activator, 100 mg IV. (Correct Answer)
- B. Continue IV fluids at 500 mL/hr for a total of 4 L of fluid resuscitation.
- C. Refer for inferior vena cava filter placement and continue current management.
- D. Refer for surgical embolectomy.
Explanation: ### Explanation The patient presents with **Massive Pulmonary Embolism (PE)**, defined by the presence of sustained hypotension (systolic BP < 90 mmHg or a drop of ≥ 40 mmHg from baseline) and evidence of right ventricular (RV) dysfunction. **1. Why Option A is Correct:** In massive PE, the primary cause of death is acute right heart failure. The management priority is twofold: **hemodynamic support** and **rapid thrombolysis** [2]. * **Thrombolysis (rtPA):** Recombinant tissue plasminogen activator (100 mg IV over 2 hours) is indicated to rapidly dissolve the clot, reduce pulmonary artery pressure, and improve RV function [2]. * **Vasopressors (Dopamine/Norepinephrine):** These are essential to maintain systemic blood pressure and ensure adequate coronary perfusion to the strained right ventricle while waiting for the thrombolytic to work. **2. Why the Other Options are Incorrect:** * **Option B:** While initial fluid boluses (500–1000 mL) are helpful, aggressive fluid resuscitation (>1.5–2 L) can be harmful. Excessive volume causes RV overdistension, which shifts the interventricular septum to the left, further reducing left ventricular filling and worsening hypotension. * **Option C:** IVC filters prevent future emboli but do not treat the current life-threatening obstruction. They are indicated only if anticoagulation is contraindicated or has failed. * **Option D:** Surgical embolectomy is a "rescue" therapy reserved for patients where thrombolysis is strictly contraindicated or has failed [2]. **Clinical Pearls for NEET-PG:** * **Submassive PE:** Characterized by RV dysfunction (on Echo or elevated Troponin/BNP) but with **normal** blood pressure [2]. Management is usually anticoagulation (LMWH), though "rescue thrombolysis" may be considered. * **Gold Standard Diagnosis:** CT Pulmonary Angiography (CTPA) [1]. * **ECG Findings:** Most common is sinus tachycardia; most specific is the **S1Q3T3** pattern (sign of acute cor pulmonale) [3]. * **Drug of Choice:** For hemodynamically stable PE, LMWH or Fondaparinux is preferred over UFH. For unstable PE (Massive), UFH is preferred due to its short half-life if surgery is needed.
Question 64: A patient with an 8 cm x 8 cm abscess in the right lobe of the liver was treated with multiple aspirations and systemic amebicide. A cavity remains in the right lobe, which is now empty. A seven-day course of luminal amebicides has been completed. What is the recommended follow-up plan?
- A. Stool examination only
- B. Ultrasound (USG) weekly for 1 month, followed by monthly USG until 1 year (Correct Answer)
- C. Ultrasound (USG) weekly for 3 months, followed by CT scan at 3 months
- D. Ultrasound (USG) or CT scan monthly, and stool examination weekly
Explanation: ### Explanation **Concept:** The management of an Amoebic Liver Abscess (ALA) involves both clinical and radiological monitoring [1]. Even after successful treatment with systemic amebicides (like Metronidazole) and aspiration, the radiological resolution of the abscess cavity lags significantly behind clinical improvement [2]. A large cavity (like the 8 cm x 8 cm one described) can take anywhere from **6 months to 2 years** to disappear completely on imaging. **Why Option B is Correct:** The standard protocol for follow-up involves serial Ultrasound (USG) to ensure the cavity is shrinking and to rule out secondary infection or recurrence [3]. The recommended frequency is **weekly for the first month**, followed by **monthly assessments** until the cavity is no longer visible (which can take up to a year). This ensures that the "empty" space is healing by fibrosis rather than refilling. **Why Other Options are Incorrect:** * **Option A:** Stool examination is used to confirm the eradication of the intestinal phase (using luminal amebicides), but it cannot monitor the healing of a hepatic parenchymal lesion [1]. * **Option C:** A CT scan is unnecessary for routine follow-up of a known, responding ALA [3]. USG is the preferred, cost-effective, and radiation-free modality for serial monitoring. * **Option D:** Weekly stool examinations are clinically unnecessary once a full course of luminal amebicides (e.g., Diloxanide furoate or Paromomycin) is completed. **NEET-PG High-Yield Pearls:** * **Most common site:** Right lobe (due to the bulk of the liver and portal blood flow distribution). * **Anchovy sauce pus:** Characteristic appearance of ALA aspirate (sterile, odorless, reddish-brown) [1]. * **Treatment of choice:** Metronidazole (systemic) followed by a luminal amebicide (to prevent relapse from the gut). * **Indications for Aspiration:** Large size (>5-10 cm), failure to respond to medical therapy within 48-72 hours, or risk of rupture (especially in the left lobe) [2].
Question 65: What is the effect of beriberi on circulation?
- A. Hyperdynamic circulation (Correct Answer)
- B. Hypovolemic shock
- C. Bradycardia
- D. Pulsus paradoxus
Explanation: Wet Beriberi, caused by a severe deficiency of Thiamine (Vitamin B1), leads to a classic state of high-output heart failure characterized by hyperdynamic circulation [1]. The underlying pathophysiology involves systemic peripheral vasodilation (decreased systemic vascular resistance) due to the accumulation of pyruvate and lactate, which act as local vasodilators. This results in an increased venous return to the heart, leading to an increased stroke volume and cardiac output [1]. Clinically, this manifests as a wide pulse pressure, bounding pulses [2], and warm extremities. Analysis of Incorrect Options: * B. Hypovolemic shock: Beriberi causes fluid retention and volume overload (edema) due to heart failure, the opposite of hypovolemia. * C. Bradycardia: Hyperdynamic states typically present with tachycardia to maintain the high cardiac output [1]. * D. Pulsus paradoxus: This is a sign of cardiac tamponade [3] or severe asthma/COPD, not high-output failure. High-Yield NEET-PG Pearls: * Dry Beriberi: Presents as symmetrical peripheral neuropathy (sensory and motor). * Wet Beriberi: Presents with high-output heart failure and edema. * Shoshin Beriberi: A fulminant, acute form of wet beriberi leading to rapid cardiovascular collapse and lactic acidosis. * Treatment: Immediate IV Thiamine. Always administer thiamine before glucose in malnourished patients to prevent precipitating Wernicke-Korsakoff syndrome.
Question 66: A 26-year-old woman complains of the abrupt onset of her chest pounding. She is diagnosed with paroxysmal atrial tachycardia. Which of the following is the most effective agent for converting paroxysmal atrial tachycardia to normal sinus rhythm?
- A. Digoxin
- B. Lidocaine
- C. Atropine
- D. Adenosine (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Adenosine** **Mechanism and Rationale:** Paroxysmal Supraventricular Tachycardia (PSVT), often referred to in clinical scenarios as paroxysmal atrial tachycardia, most commonly involves a re-entry circuit involving the Atrioventricular (AV) node (e.g., AVNRT) [1], [3]. **Adenosine** is the drug of choice for the acute termination of stable PSVT [2]. It works by binding to **A1 receptors** in the AV node, causing an increase in potassium efflux and inhibition of calcium influx. This results in transient hyperpolarization and a **profound slowing of AV nodal conduction**, effectively "breaking" the re-entry circuit and allowing the SA node to regain control. It has an ultra-short half-life (<10 seconds), making it ideal for rapid conversion. **Why Other Options are Incorrect:** * **A. Digoxin:** While it slows AV conduction, its onset of action is too slow (hours) for the acute conversion of paroxysmal tachyarrhythmias [2]. * **B. Lidocaine:** This is a Class IB antiarrhythmic that acts on sodium channels in the ventricles. It is used for ventricular arrhythmias (like VT) and has no efficacy in supraventricular tachycardias [2]. * **C. Atropine:** This is an anticholinergic used to *increase* the heart rate in symptomatic bradycardia; it would worsen tachycardia. **High-Yield Clinical Pearls for NEET-PG:** * **Administration:** Adenosine must be given as a **rapid IV bolus** followed by a saline flush due to its short half-life. * **Side Effects:** Patients often experience a transient, distressing feeling of "impending doom," chest pain, or flushing. * **Contraindications:** Avoid in patients with **Asthma** (can cause bronchospasm) and high-grade heart blocks [2]. * **Drug Interactions:** The dose should be **decreased** in patients on Dipyridamole or Carbamazepine and **increased** in patients consuming high amounts of Theophylline or Caffeine (adenosine receptor antagonists) [2].
Question 67: Which of the following is NOT a characteristic of Prinzmetal angina?
- A. Pain at rest and ST elevation during the attack (Correct Answer)
- B. ST elevation during the attack
- C. Pain at rest and a normal ECG without pain
- D. Pain at rest and represents transmural ischemia
Explanation: Prinzmetal angina (also known as variant angina) is caused by focal coronary artery vasospasm rather than atherosclerotic narrowing. This spasm leads to transient, total occlusion of a coronary artery, resulting in **transmural ischemia**. **Why Option A is the "Correct" Answer (The Exception):** In the context of this specific question format, Option A is likely intended as the "incorrect" statement because it describes the *classic* presentation of Prinzmetal angina. However, in many NEET-PG style questions, if the options are poorly phrased or overlapping, the key is to identify the statement that does not fit the "NOT" criteria. *Note: If this is a "Which is NOT" question and Option A is marked correct, it implies a technical error in the question's phrasing, as A, B, C, and D are all actually true characteristics of the disease.* **Analysis of Characteristics:** * **Option B & D:** During an acute spasm, there is **ST-segment elevation** (not depression) because the ischemia is **transmural** (involving the full thickness of the wall). This distinguishes it from stable angina, which is subendocardial. * **Option C:** A hallmark of Prinzmetal angina is that chest pain typically occurs **at rest** (often in the early morning) and the **ECG returns to normal** once the spasm resolves. **High-Yield Clinical Pearls for NEET-PG:** * **Triggers:** Smoking is a major risk factor; cocaine or triptans can precipitate attacks. * **Diagnosis:** Gold standard is coronary angiography with provocative testing (e.g., **Ergonovine or Acetylcholine**). * **Treatment:** **Calcium Channel Blockers (CCBs)** and Nitrates are first-line. [1] * **Contraindication:** **Beta-blockers** are strictly contraindicated as they can lead to unopposed alpha-adrenergic stimulation, worsening the vasospasm.
Question 68: What is the main component of hyperlipidemia that constitutes a major risk factor for atherosclerosis?
- A. High density lipoprotein (HDL) cholesterol
- B. Intermediate density lipoprotein (IDL) cholesterol
- C. Low density lipoprotein (LDL) cholesterol (Correct Answer)
- D. Very low density lipoprotein (VLDL) cholesterol
Explanation: The correct answer is **C. Low density lipoprotein (LDL) cholesterol.** **Why LDL is the Correct Answer:** LDL cholesterol is considered the primary pro-atherogenic lipoprotein [1]. It contains the highest percentage of cholesterol and is small enough to penetrate the arterial intima. Once in the subendothelial space, LDL undergoes **oxidation**, leading to its uptake by macrophages via scavenger receptors. This process transforms macrophages into **foam cells**, which form the "fatty streak"—the earliest visible lesion of atherosclerosis [3]. High levels of LDL are directly and linearly correlated with the risk of Coronary Artery Disease (CAD) [1]. **Analysis of Incorrect Options:** * **A. HDL Cholesterol:** Known as "good cholesterol," HDL is **cardioprotective**. It facilitates reverse cholesterol transport, carrying cholesterol away from peripheral tissues and arteries back to the liver for excretion [1]. * **B. IDL Cholesterol:** IDL is a transient intermediate formed during the conversion of VLDL to LDL. While it is pro-atherogenic, it is not the "main" component measured or targeted in clinical practice compared to LDL [1]. * **D. VLDL Cholesterol:** VLDL primarily transports endogenous triglycerides. While elevated VLDL (hypertriglyceridemia) is a risk factor, it is less potent than LDL in initiating the atherosclerotic plaque [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Friedewald Formula:** LDL = Total Cholesterol – HDL – (Triglycerides/5). (Note: This is invalid if TG >400 mg/dL). * **Apolipoprotein B (ApoB):** This is the primary structural protein found on all potentially atherogenic particles (LDL, VLDL, IDL) [1]. It is often considered a more accurate predictor of risk than LDL-C alone. * **Statins:** The first-line treatment for hyperlipidemia, acting via HMG-CoA reductase inhibition to primarily lower LDL levels [2]. * **Target LDL:** For patients with very high cardiovascular risk (e.g., recent ACS), the current goal is often <55 mg/dL.
Question 69: A female patient develops chest pain which is not associated with exercise and chest auscultation shows multiple non-ejection clicks. Which investigation is used to diagnose the disease?
- A. Echocardiography (Correct Answer)
- B. Pyrophosphate scan
- C. Thallium 201 scan
- D. ECG
Explanation: The clinical presentation of atypical chest pain (not associated with exercise) combined with **multiple non-ejection clicks** on auscultation is a classic hallmark of **Mitral Valve Prolapse (MVP)**, also known as Barlow’s Syndrome. **1. Why Echocardiography is the Correct Answer:** Echocardiography is the **gold standard** and definitive investigation for diagnosing MVP. It allows for the visualization of the mitral valve leaflets displacing into the left atrium (usually >2 mm) during systole. It also assesses the severity of associated mitral regurgitation and the thickness of the leaflets (myxomatous degeneration). **2. Analysis of Incorrect Options:** * **Pyrophosphate Scan (Technetium-99m PYP):** This is a nuclear imaging test used primarily to detect **Transthyretin Amyloid Cardiomyopathy (ATTR)** or to identify areas of recent myocardial infarction. It has no role in diagnosing valvular prolapse. * **Thallium 201 Scan:** This is a myocardial perfusion scan used to evaluate **Ischemic Heart Disease (IHD)** and myocardial viability. While the patient has chest pain, the specific finding of "non-ejection clicks" points to a structural valvular issue rather than coronary artery disease. [2], [3] * **ECG:** While an ECG might show non-specific ST-T wave changes or arrhythmias in MVP patients, it is **not diagnostic**. It cannot visualize the mechanical displacement of the valve. [1] **Clinical Pearls for NEET-PG:** * **Auscultation:** The classic finding is a **mid-systolic click** followed by a late systolic murmur. Multiple clicks suggest complex redundant tissue. * **Dynamic Auscultation:** The click and murmur move **earlier** in systole (closer to S1) with maneuvers that decrease preload (e.g., **Standing, Valsalva**). They move **later** (closer to S2) with maneuvers that increase preload or afterload (e.g., **Squatting, Handgrip**). * **Association:** MVP is frequently associated with connective tissue disorders like **Marfan Syndrome** and Ehlers-Danlos Syndrome.
Question 70: Austin Flint Murmur is commonly mistaken for the murmur of which condition?
- A. Mitral regurgitation
- B. Pulmonary regurgitation
- C. Tricuspid stenosis
- D. Mitral stenosis (Correct Answer)
Explanation: ### Explanation **1. Why Mitral Stenosis is the correct answer:** The **Austin Flint murmur** is a low-pitched, mid-diastolic rumbling murmur heard at the apex in patients with **severe chronic Aortic Regurgitation (AR)**. It occurs because the regurgitant jet from the aorta strikes the anterior leaflet of the mitral valve, causing it to partially close (functional narrowing) and vibrate [2]. This creates a "functional" mitral stenosis. Because both the Austin Flint murmur and true **Mitral Stenosis (MS)** are mid-diastolic rumbles heard best at the apex, they are frequently confused [3]. **2. Why other options are incorrect:** * **Mitral Regurgitation (A):** This is a pansystolic murmur radiating to the axilla, whereas Austin Flint is diastolic [1]. * **Pulmonary Regurgitation (B):** This causes an early diastolic murmur (Graham Steell murmur) heard at the left upper sternal border, not a mid-diastolic rumble at the apex. * **Tricuspid Stenosis (C):** While this is a mid-diastolic rumble, it is heard best at the left lower sternal border and increases with inspiration (Carvallo’s sign), unlike the Austin Flint murmur [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Differentiation:** To distinguish Austin Flint from true MS, look for the **Opening Snap (OS)** and **Loud S1**. These are present in MS but **absent** in Austin Flint [4]. * **Amyl Nitrite Test:** Inhalation of amyl nitrite decreases peripheral resistance, increasing the Austin Flint murmur (due to increased AR) but decreasing the murmur of true MS. * **Eponyms to remember:** * *Graham Steell Murmur:* Pulmonary regurgitation secondary to pulmonary hypertension. * *Carey Coombs Murmur:* Mid-diastolic murmur in acute Rheumatic Fever (due to mitral valvulitis).
Practice by Chapter
Coronary Artery Disease and Angina
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Acute Coronary Syndromes
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Heart Failure
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Cardiac Arrhythmias
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Valvular Heart Diseases
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Cardiomyopathies
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Pericardial Diseases
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Congenital Heart Disease in Adults
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Hypertension and Hypertensive Emergencies
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Pulmonary Hypertension
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Non-invasive Cardiac Diagnostics
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Preventive Cardiology
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