Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 701: What is the most common cause of acute right ventricular failure?

A. Massive pulmonary embolism (Correct Answer)
B. Tricuspid stenosis
C. Pulmonary stenosis
D. Tricuspid regurgitation

Explanation: Explanation: 1. Why Massive Pulmonary Embolism (PE) is the Correct Answer: Acute right ventricular (RV) failure occurs when there is a sudden, significant increase in RV afterload [1]. In Massive Pulmonary Embolism, a large thrombus obstructs the pulmonary arterial bed (usually >50% obstruction). This leads to a precipitous rise in pulmonary vascular resistance. Because the right ventricle is a thin-walled, low-pressure pump designed for high compliance rather than high pressure, it cannot compensate for this sudden "afterload mismatch." This results in RV dilation, wall tension increase, and eventual failure (cor pulmonale) [1]. Thrombolysis is indicated in patients presenting with acute massive PE accompanied by cardiogenic shock [1]. 2. Why the Other Options are Incorrect: * B. Tricuspid Stenosis: This is a chronic valvular condition. It limits flow into the RV rather than causing RV failure; instead, it leads to right atrial enlargement and systemic venous congestion. * C. Pulmonary Stenosis: While this increases RV afterload, it is typically a congenital or chronic condition. The RV undergoes compensatory hypertrophy over years. It does not cause acute failure unless it is exceptionally severe and sudden in presentation, which is rare compared to PE. * D. Tricuspid Regurgitation: This is usually a consequence of RV failure and dilation (functional TR) rather than the primary acute cause. Chronic primary TR leads to RV volume overload, which the ventricle tolerates for a long period before failing. 3. High-Yield Clinical Pearls for NEET-PG: * McConnell’s Sign: A highly specific echocardiographic finding in acute PE—akinesia of the RV free wall with sparing of the apex. * S1Q3T3 Pattern: The classic (though not most common) ECG finding in PE indicating acute right heart strain [1]. * Most Common Cause of Chronic RV Failure: Left-sided heart failure (due to secondary pulmonary hypertension). * Gold Standard Investigation: CT Pulmonary Angiography (CTPA) is the investigation of choice for diagnosing PE.

Question 702: A 50-year-old man presents to the emergency room with several hours of progressively increasing chest pain that no longer responds to sublingual nitroglycerin. This type of angina is thought to be due to which of the following conditions?

A. Atherosclerosis alone
B. Coronary artery embolism
C. Coronary artery spasm
D. Thrombosis with or without underlying atherosclerosis (Correct Answer)

Explanation: The clinical presentation describes **Unstable Angina (UA)**, characterized by chest pain that is increasing in frequency/severity (crescendo angina) and is no longer relieved by rest or nitroglycerin [2]. **1. Why Option D is Correct:** The primary pathophysiology of Unstable Angina and Non-ST Elevation Myocardial Infarction (NSTEMI) is the **rupture or erosion of an unstable atherosclerotic plaque**. This leads to platelet aggregation and the formation of a **non-occlusive (subtotal) thrombus** [1]. Unlike stable angina, where the lumen is simply narrowed by a fixed plaque, the acute change in UA is driven by this dynamic thrombotic process, which significantly reduces coronary blood flow. **2. Why Other Options are Incorrect:** * **Option A (Atherosclerosis alone):** This is the hallmark of **Stable Angina**. It involves a fixed, calcified plaque that causes pain only during increased myocardial oxygen demand (exertion) and is typically relieved by rest or nitroglycerin [3]. * **Option B (Coronary artery embolism):** While a cause of MI, it is rare. It is usually associated with infective endocarditis, prosthetic valves, or atrial fibrillation. * **Option C (Coronary artery spasm):** This refers to **Prinzmetal (Variant) Angina**. While it causes pain at rest, it typically shows transient ST-segment elevation on ECG and responds promptly to nitroglycerin or calcium channel blockers. **Clinical Pearls for NEET-PG:** * **Acute Coronary Syndrome (ACS)** includes Unstable Angina, NSTEMI, and STEMI [2]. * **UA vs. NSTEMI:** Both present similarly, but NSTEMI has elevated cardiac biomarkers (Troponins), indicating myocardial necrosis, whereas UA does not [2]. * **Braunwald Classification** is used to grade the severity of Unstable Angina. * **Management:** Immediate treatment involves "MONA" (Morphine, Oxygen, Nitrates, Aspirin) and antiplatelet/anticoagulant therapy.

Question 703: Which of the following is the treatment of choice for Atrial fibrillation in patients with WPW syndrome who are hemodynamically unstable?

A. Procainamide
B. Digoxin
C. DC Cardioversion (Correct Answer)
D. Radio-frequency ablation of the bypass tract

Explanation: ### Explanation **1. Why DC Cardioversion is the Correct Answer:** In any patient with a tachyarrhythmia (including AF with WPW) who is **hemodynamically unstable** (hypotension, altered mental status, chest pain, or acute heart failure), the immediate treatment of choice is **Synchronized DC Cardioversion**. In WPW syndrome, AF is particularly dangerous because the accessory pathway (Bundle of Kent) has a short refractory period, allowing rapid conduction to the ventricles. This can lead to extremely high ventricular rates, potentially degenerating into Ventricular Fibrillation (VF) and cardiac arrest. **2. Analysis of Incorrect Options:** * **Procainamide (Option A):** This is the drug of choice for **hemodynamically stable** patients with pre-excited AF. It slows conduction through the accessory pathway. * **Digoxin (Option B):** This is **strictly contraindicated** [2]. AV nodal blocking agents (ABCD: Atenolol/Beta-blockers, Blockers of Calcium/Verapamil, Clonidine, Digoxin) paradoxically enhance conduction through the accessory pathway, increasing the risk of VF [2]. * **Radio-frequency Ablation (Option D):** This is the **definitive/long-term treatment** for WPW syndrome to prevent recurrences [1], but it is not the initial management in an acute, unstable emergency. **3. Clinical Pearls for NEET-PG:** * **The "FBI" Rule:** AF in WPW presents as a rhythm that is **F**ast, **B**road (QRS), and **I**rregular. * **Contraindicated Drugs:** Avoid "ABCD" (Adenosine, Beta-blockers, Calcium channel blockers, Digoxin) in pre-excited AF. * **Definitive Treatment:** RFA of the accessory tract is the gold standard for long-term cure [1]. * **Emergency Rule:** Stability dictates management. Unstable = Shock; Stable = Medicate (Procainamide/Ibutilide).

Question 704: All of the following findings during an exercise tolerance test are associated with left coronary artery disease except?

A. Early onset of ST depression
B. Persistence of ST segment changes late into the recovery phase
C. Failure to increase systolic blood pressure by at least 20 mm Hg (Correct Answer)
D. ST segment elevation in aVR

Explanation: The goal of an exercise tolerance test (ETT) is to identify markers of high-risk coronary artery disease (CAD), specifically Left Main (LM) or multivessel disease. [1] **Why Option C is the correct answer:** While an inadequate blood pressure response is a marker of significant ischemia, the specific criterion for high-risk CAD is a **drop in systolic blood pressure (SBP) below baseline** or a failure of SBP to rise **above 120 mmHg**. [1] A failure to increase SBP by 20 mmHg is a non-specific finding and does not carry the same prognostic weight for Left Main disease as a frank drop in pressure (exertional hypotension), which reflects global left ventricular dysfunction. **Analysis of Incorrect Options:** * **Option A (Early onset):** ST depression occurring in Stage I of the Bruce protocol (within the first 3 minutes) is a classic indicator of severe, extensive ischemia (LM or 3-vessel disease). * **Option B (Persistence into recovery):** If ST-segment changes take more than 5–6 minutes to return to baseline during the recovery phase, it correlates strongly with multivessel disease and a poor prognosis. * **Option D (ST elevation in aVR):** This is a high-yield EKG marker. ST elevation in lead aVR (especially ≥1 mm) during exercise, accompanied by diffuse ST depression in other leads, is highly predictive of **Left Main Coronary Artery (LMCA)** stenosis or proximal Left Anterior Descending (LAD) occlusion. **Clinical Pearls for NEET-PG:** * **High-risk ETT criteria:** ST depression >2 mm, downsloping ST segment, onset at low workloads (<6 METS), and exertional hypotension. [1] * **Absolute Contraindication to ETT:** Acute MI (within 2 days), unstable angina, symptomatic severe aortic stenosis, and acute myocarditis. * **Duke Treadmill Score:** Used for prognosis; it incorporates exercise time, ST deviation, and the presence of angina.

Question 705: A patient with short PR interval and Delta waves on ECG presents with Atrial Fibrillation and rapid ventricular rate. He is hemodynamically stable. All of the following agents may be used in the management, except?

A. Verapamil (Correct Answer)
B. Procainamide
C. Ibutilide
D. Amiodarone

Explanation: **Explanation:** The patient presents with **Wolff-Parkinson-White (WPW) syndrome** (indicated by short PR interval and delta waves) complicated by **Atrial Fibrillation (AF)**. In WPW, an accessory pathway (Bundle of Kent) exists alongside the AV node [1]. **Why Verapamil is the Correct Answer (Contraindicated):** Verapamil is a non-dihydropyridine Calcium Channel Blocker (CCB) that selectively blocks the **AV node**. In WPW with AF, blocking the AV node forces all atrial impulses to travel exclusively through the accessory pathway. Unlike the AV node, the accessory pathway lacks "decremental conduction" (it does not slow down rapid impulses). This can lead to a 1:1 conduction of atrial impulses to the ventricles, resulting in **Ventricular Fibrillation (VF)** and sudden cardiac death. Other agents to avoid include Beta-blockers, Digoxin, and Adenosine (ABCD: Adenosine, Beta-blockers, CCBs, Digoxin). **Analysis of Other Options:** * **Procainamide (Option B):** The drug of choice for hemodynamically stable WPW with AF. It increases the refractory period of the accessory pathway, slowing the heart rate. * **Ibutilide (Option C):** A Class III antiarrhythmic that can be used for chemical cardioversion in stable patients as it slows conduction in the accessory pathway. * **Amiodarone (Option D):** Though its use is controversial in some guidelines due to its minor AV-blocking effects, it is generally considered an option in stable patients as it affects both the AV node and the accessory pathway. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hemodynamically Unstable WPW + AF:** Immediate **DC Cardioversion** is the treatment of choice. 2. **Definitive Treatment:** Radiofrequency Ablation (RFA) of the accessory pathway. 3. **ECG Hallmark:** Delta wave (slurred upstroke of QRS) representing pre-excitation [1]. 4. **Avoid "ABCD"** in WPW with AF: **A**denosine, **B**eta-blockers, **C**alcium channel blockers, **D**igoxin.

Question 706: McConnell's sign in echocardiography is seen in which condition?

A. Myocardial Infarction (MI)
B. Pulmonary Embolism (PE) (Correct Answer)
C. Sarcoidosis
D. Hypertrophic Obstructive Cardiomyopathy (HOCM)

Explanation: **Explanation:** **McConnell’s sign** is a highly specific echocardiographic finding for **Acute Pulmonary Embolism (PE)**. It is characterized by **akinesia (lack of movement) of the right ventricular (RV) free wall with sparing of the apex**, which remains hyperdynamic. 1. **Why it occurs in PE:** In acute PE, a sudden increase in pulmonary artery pressure causes acute RV pressure overload [1]. The RV free wall, being thin, fails to contract against this high resistance (akinesia). However, the RV apex is tethered to the hyperdynamic left ventricle, causing it to appear to contract normally or even vigorously. This "apical sparing" distinguishes PE from other causes of RV dysfunction. 2. **Analysis of Incorrect Options:** * **Myocardial Infarction (MI):** While an RV infarct causes RV wall motion abnormalities, it typically involves the entire wall (including the apex) and does not show the specific apical sparing seen in McConnell’s sign [2]. * **Sarcoidosis:** Cardiac sarcoidosis typically presents with restrictive cardiomyopathy, arrhythmias, or localized wall thinning/aneurysms, but not this specific RV pattern. * **HOCM:** This is characterized by asymmetrical septal hypertrophy and systolic anterior motion (SAM) of the mitral valve, affecting the left ventricle rather than the right. **High-Yield Clinical Pearls for NEET-PG:** * **Specificity:** McConnell’s sign has a high specificity (approx. 94%) but low sensitivity for PE. * **Other Echo findings in PE:** * **60/60 sign:** Pulmonary artery acceleration time <60ms + midsystolic notch. * **D-shaped Left Ventricle:** Due to the interventricular septum shifting toward the LV during diastole (RV pressure overload). * **TAPSE:** Tricuspid Annular Plane Systolic Excursion is often reduced (<16mm) in PE, indicating RV dysfunction.

Question 707: A 60-year-old marathon runner complains of episodes of dizziness. On auscultation, an ejection systolic murmur is heard. What is the most likely clinical diagnosis?

A. Hypertension with Atrial fibrillation
B. Left Ventricular Hypertrophy with Valvular Aortic Stenosis (Correct Answer)
C. Right Ventricular Hypertrophy with Valvular Pulmonic Stenosis
D. Brugada Syndrome

Explanation: The clinical presentation of a **60-year-old** patient with **dizziness (syncope/near-syncope)** and an **ejection systolic murmur (ESM)** is a classic description of **Aortic Stenosis (AS)**. [1] **1. Why Option B is Correct:** Valvular Aortic Stenosis creates an obstruction to the left ventricular outflow tract. This results in a harsh ESM heard best at the right second intercostal space, radiating to the carotids. [1] To overcome this pressure gradient, the left ventricle undergoes compensatory concentric **Left Ventricular Hypertrophy (LVH)**. Dizziness or syncope occurs because the fixed cardiac output cannot meet the systemic demand during exertion (or in this case, a marathon runner's activity). [2] **2. Why Incorrect Options are Wrong:** * **Option A:** Hypertension usually presents with an S4 or a loud A2, not a classic ESM. While AFib can coexist, it does not explain the murmur or the exertional dizziness as specifically as AS. * **Option C:** Pulmonic Stenosis also causes an ESM, but it is heard best at the left upper sternal border and is associated with RVH. It is much rarer in a 60-year-old and typically presents with right-sided heart failure symptoms rather than exertional syncope. * **Option D:** Brugada Syndrome is a channelopathy causing sudden cardiac death due to ventricular arrhythmias. It presents with specific ECG changes (coved ST elevation in V1-V3) but **no heart murmur**. **Clinical Pearls for NEET-PG:** * **Classic Triad of AS (SAD):** **S**yncope, **A**ngina, and **D**yspnea. * **Physical Signs:** *Pulsus parvus et tardus* (slow-rising, low-volume pulse) and a paradoxical split of S2. [1] * **Most Common Cause:** In patients >65, it is senile calcific AS; in younger patients, it is often a Bicuspid Aortic Valve. [2] * **Murmur Intensity:** The later the peak of the ESM, the more severe the stenosis.

Question 708: Pulsus bisfriens is seen in all except?

A. Mitral valve prolapse (Correct Answer)
B. Aortic stenosis with aortic regurgitation
C. Severe aortic regurgitation
D. Hypertrophic obstructive cardiomyopathy (HOCM)

Explanation: **Explanation:** **Pulsus Bisferiens** (from the Latin *bis* for twice and *ferire* for beat) is a physical finding where the arterial pulse has two strong systolic peaks separated by a mid-systolic dip. It is typically found in conditions where there is a rapid ejection of a large stroke volume into the aorta. **Why Mitral Valve Prolapse (MVP) is the correct answer:** MVP is characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole [1]. While it may be associated with mitral regurgitation, it does **not** produce the rapid, high-volume ejection required to create a double-systolic peak in the peripheral pulse. Therefore, it is not a cause of pulsus bisferiens. **Analysis of incorrect options:** * **Aortic Stenosis with Aortic Regurgitation (AS + AR):** This is the classic cause. The AR increases stroke volume (causing the first peak), while the AS creates a high-velocity jet, followed by a mid-systolic dip and a second peak (tidal wave). * **Severe Aortic Regurgitation:** The massive stroke volume and rapid ejection can create two distinct systolic waves, especially in a hyperdynamic state [2]. * **HOCM:** In HOCM, there is a "Venturi effect" causing mid-systolic obstruction [1]. This results in an initial rapid ejection (percussion wave), a sudden drop due to obstruction, and a subsequent rise (tidal wave) as ejection continues. **Clinical Pearls for NEET-PG:** * **Pulsus Bisferiens vs. Dicrotic Pulse:** Bisferiens has two peaks in **systole**, whereas a dicrotic pulse has one peak in systole and one in **diastole** (seen in low cardiac output states like severe heart failure). * **HOCM Pulse:** Often described as "spike and dome" or "triple ripple" (if a palpable S4 is present). * **Best site to palpate:** Pulsus bisferiens is best appreciated in the **brachial or femoral arteries** rather than the carotid.

Question 709: Which one of the following does not cause pulsus paradoxus?

A. Severe aortic regurgitation (Correct Answer)
B. Cardiac tamponade
C. Constrictive pericarditis
D. Acute severe bronchial asthma

Explanation: **Explanation** **Pulsus paradoxus** is defined as an exaggerated fall in systolic blood pressure (>10 mmHg) during inspiration. Under normal physiological conditions, inspiration increases venous return to the right heart, causing the interventricular septum to bulge slightly into the left ventricle (LV), minimally reducing LV stroke volume. **Why Severe Aortic Regurgitation (AR) is the Correct Answer:** In severe AR, the left ventricle is chronically volume-overloaded and dilated [3]. This high-pressure, high-volume state in the LV prevents the interventricular septum from shifting toward the left side during inspiration. Furthermore, the regurgitant flow from the aorta into the LV maintains LV filling even when pulmonary venous return decreases. Therefore, the inspiratory drop in blood pressure is abolished. In fact, AR is often associated with a "wide pulse pressure" [1] rather than pulsus paradoxus. **Analysis of Incorrect Options:** * **Cardiac Tamponade:** This is the classic cause. The heart is encased in a fixed volume of fluid; increased right-heart filling during inspiration forces the septum to bulge significantly into the LV (ventricular interdependence), severely reducing stroke volume [2]. * **Constrictive Pericarditis:** Similar to tamponade, the rigid pericardium limits total cardiac volume, leading to exaggerated septal shift during inspiration. * **Acute Severe Bronchial Asthma:** Large negative intrathoracic pressures during inspiration increase the afterload on the LV and increase venous return to the RV, both of which contribute to a significant drop in systolic BP. **High-Yield Clinical Pearls for NEET-PG:** * **Reverse Pulsus Paradoxus:** Seen in Hypertrophic Obstructive Cardiomyopathy (HOCM) and intermittent mandatory ventilation. * **Kussmaul’s Sign:** Paradoxical rise in JVP on inspiration; seen in Constrictive Pericarditis but **not** typically in Cardiac Tamponade [2]. * **Pulsus Alternans:** Alternating strong and weak beats; a hallmark of severe Left Ventricular Systolic Failure.

Question 710: Rheumatic activity involves which valves?

A. Aortic & tricuspid
B. Aortic & pulmonary
C. Mitral & tricuspid
D. Mitral & aortic (Correct Answer)

Explanation: **Explanation:** Rheumatic Heart Disease (RHD) is a sequela of Rheumatic Fever caused by an autoimmune response to Group A Streptococcal pharyngitis [1]. The disease primarily affects the endocardium, leading to valvulitis. **Why Mitral & Aortic are correct:** The frequency of valvular involvement in RHD is directly proportional to the hemodynamic stress (pressure) experienced by the valve. The **Mitral valve** is the most commonly affected (found in nearly all cases), followed by the **Aortic valve** [1]. This is because the left-sided heart chambers operate under significantly higher pressures than the right-sided chambers, leading to greater mechanical trauma and subsequent inflammatory scarring. **Analysis of Incorrect Options:** * **A & B (Aortic, Tricuspid, and Pulmonary):** The Pulmonary valve is the least commonly affected valve in RHD. Isolated pulmonary involvement is extremely rare and usually only occurs in the context of severe multivalvular disease. * **C (Mitral & Tricuspid):** While the Tricuspid valve can be involved, it is almost never affected in isolation. It is typically involved only after the mitral and aortic valves have already sustained significant damage. **High-Yield Clinical Pearls for NEET-PG:** * **Order of Frequency:** Mitral > Aortic > Tricuspid > Pulmonary (M > A > T > P). * **Most Common Lesion:** Mitral Regurgitation (MR) is the most common finding in *acute* rheumatic carditis [1]; Mitral Stenosis (MS) is the classic hallmark of *chronic* RHD. * **Pathognomonic Feature:** **Aschoff bodies** (granulomatous inflammation) in the myocardium. * **McCallum’s Patch:** An area of endocardial thickening in the left atrium caused by regurgitant jets in MR.

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Cardiomyopathies

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Pericardial Diseases

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Congenital Heart Disease in Adults

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Cardiology — MCQs

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