Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1151: Antibiotic prophylaxis for infective endocarditis is indicated in which of the following conditions?

A. Isolated secundum atrial septal defect (ASD)
B. Mitral valve prolapse without regurgitation
C. Prior coronary artery bypass graft
D. Coarctation of the aorta (Correct Answer)

Explanation: ### Explanation The current guidelines for **Infective Endocarditis (IE) prophylaxis** (AHA/ESC) have become significantly more restrictive, limiting antibiotic use to only those patients at the **highest risk** of adverse outcomes from IE [1]. **Why Coarctation of the Aorta is Correct:** Under the updated guidelines, IE prophylaxis is indicated for **Cyanotic Congenital Heart Disease (CHD)** that has not been repaired, or repaired CHD with residual shunts or valvular regurgitation at the site of a prosthetic device. **Coarctation of the aorta** is classified as a high-risk structural cardiac condition because it creates high-velocity turbulent flow, which predisposes the endothelium to bacterial seeding. While some modern guidelines have moved away from routine prophylaxis for simple acyanotic lesions, in the context of NEET-PG and standard clinical teaching, it remains the only "high-risk" structural lesion among the choices provided. **Why the Other Options are Incorrect:** * **A. Isolated Secundum ASD:** This is a low-pressure shunt with minimal turbulence; it does not require prophylaxis. * **B. Mitral Valve Prolapse (MVP) without regurgitation:** MVP, even with regurgitation, is no longer an indication for prophylaxis unless it is part of a formal valve replacement. * **C. Prior CABG:** Coronary artery bypass grafts are vascular procedures, not valvular or structural intracardiac repairs, and do not carry an increased risk for IE [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Indications for Prophylaxis:** 1. Prosthetic heart valves (including TAVI). 2. Prior history of IE. 3. Unrepaired cyanotic CHD. 4. Repaired CHD with prosthetic material (first 6 months). 5. Cardiac transplant recipients with valve regurgitation [1]. * **Procedures requiring prophylaxis:** Only **dental procedures** involving manipulation of gingival tissue or periapical region of teeth [1]. * **Drug of Choice:** **Amoxicillin** (2g orally 30-60 mins before). If allergic, use **Clindamycin** (600mg) or Azithromycin (500mg).

Question 1152: Rescue PCI is indicated for which of the following conditions?

A. Persistent chest pain with ST elevation more than 60 minutes after thrombolysis
B. Persistent chest pain with ST elevation more than 30 minutes after thrombolysis
C. Persistent chest pain with ST elevation more than 90 minutes after thrombolysis (Correct Answer)
D. Persistent chest pain with ST elevation more than 120 minutes after thrombolysis

Explanation: **Explanation:** **Rescue PCI** (Percutaneous Coronary Intervention) is defined as urgent PCI performed in a patient who has failed pharmacological reperfusion (thrombolysis). The primary criterion for determining "failed thrombolysis" is the failure of ST-segment elevation to resolve by at least **50% within 60 to 90 minutes** of the administration of the fibrinolytic agent [1]. In clinical practice and for NEET-PG purposes, the **90-minute mark** is the gold standard threshold. If a patient continues to experience persistent chest pain and lacks ST-segment resolution at 90 minutes, it indicates that the infarct-related artery remains occluded, necessitating immediate mechanical intervention to salvage the myocardium. **Analysis of Options:** * **Option A (60 mins):** While ST resolution is monitored starting at 60 minutes, 90 minutes is the definitive cutoff to confirm fibrinolytic failure before escalating to Rescue PCI. * **Option B (30 mins):** This is too early to assess the efficacy of thrombolytic drugs, as the peak effect often takes longer. * **Option D (120 mins):** Waiting 120 minutes unnecessarily delays reperfusion ("Time is Muscle"), increasing the risk of myocardial necrosis and heart failure. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pharmacoinvasive Strategy:** This refers to routine PCI performed 3–24 hours after *successful* thrombolysis. 2. **Best Indicator of Reperfusion:** The most reliable clinical sign of successful reperfusion is the **resolution of ST-segment elevation** (>50%) [1]. 3. **Reperfusion Arrhythmia:** Accelerated Idioventricular Rhythm (AIVR) is the most common arrhythmia seen after successful reperfusion and usually does not require treatment. 4. **Door-to-Needle Time:** Should be <30 minutes (for thrombolysis). 5. **Door-to-Balloon Time:** Should be <90 minutes (for Primary PCI) [1].

Question 1153: Which of the following can detect the volume of infarcted area in acute myocardial infarction?

A. Echocardiogram
B. Electrocardiogram
C. Levels of Creatine Phosphokinase-MB (CPK-MB)
D. Thallium scan (Correct Answer)

Explanation: The correct answer is **Thallium scan (Thallium-201)**. Thallium-201 is a potassium analogue that is actively taken up by viable myocardial cells via the Na+/K+ ATPase pump. In the setting of an acute myocardial infarction (AMI), necrotic or infarcted tissue lacks blood flow and viable cell membranes, resulting in a "cold spot" (perfusion defect) on the scan [1]. The size and intensity of this defect are directly proportional to the **volume of the infarcted area**, making it a highly sensitive tool for quantifying the extent of myocardial damage. **Why other options are incorrect:** * **Echocardiogram:** While excellent for detecting regional wall motion abnormalities (RWMA) and estimating the Ejection Fraction (EF), it cannot definitively distinguish between acutely infarcted, stunned, or hibernating myocardium [2]. * **Electrocardiogram (ECG):** An ECG identifies the location (e.g., anterior vs. inferior) and the age of the infarct (ST-elevation vs. Q-waves), but it is a poor indicator of the actual volumetric size of the necrosis [4], [5]. * **CPK-MB Levels:** These enzymes indicate the *presence* and *timing* of myocardial injury. While the peak level roughly correlates with infarct size, it is influenced by reperfusion (washout phenomenon) and is less precise for volume measurement than nuclear imaging. **High-Yield Clinical Pearls for NEET-PG:** * **Thallium-201 vs. Technetium-99m Sestamibi:** Thallium is better for viability (redistribution), while Sestamibi is preferred for anatomical imaging due to better energy resolution. * **"Hot Spot" Imaging:** While Thallium shows "cold spots," **Technetium-99m Pyrophosphate** binds to calcium in necrotic cells, creating a "hot spot" (specifically used for infarct aging) [1]. * **Gold Standard:** Cardiac MRI (Delayed Gadolinium Enhancement) is currently the gold standard for quantifying infarct size [3], but among the given options, Thallium scan is the classic choice.

Question 1154: Which enzyme is most specific for myocardial infarction?

A. Creatine phosphokinase-MM (CPK-MM)
B. Creatine phosphokinase-MB (CPK-MB) (Correct Answer)
C. Creatine phosphokinase-BB (CPK-BB)
D. Lactate dehydrogenase (LDH)

Explanation: The diagnosis of Myocardial Infarction (MI) relies on detecting biomarkers released from necrotic cardiac myocytes. Among the options provided, **Creatine phosphokinase-MB (CPK-MB)** is the most specific enzyme for cardiac tissue [2]. 1. **Why CPK-MB is correct:** Creatine kinase exists as three isoenzymes. While CPK-MM is found in skeletal muscle and CPK-BB in the brain, **CPK-MB** is primarily localized in the myocardium (comprising about 15-30% of total CK in the heart). It rises within 4–6 hours of an infarct, peaks at 24 hours, and returns to baseline within 48–72 hours. Its rapid clearance makes it the "gold standard" for detecting **re-infarction**. 2. **Why other options are incorrect:** * **CPK-MM (Option A):** This is the predominant isoenzyme in skeletal muscle. Elevations occur in trauma, intramuscular injections, or strenuous exercise, making it non-specific for the heart. * **CPK-BB (Option B):** Found mainly in the brain and gastrointestinal tract; it is rarely elevated in the blood and has no role in MI diagnosis. * **LDH (Option D):** Lactate dehydrogenase is found in many tissues (liver, RBCs, muscle). While LDH-1 was historically used for late diagnosis, it lacks specificity and has been replaced by more modern markers [2]. **High-Yield NEET-PG Pearls:** * **Most Specific Marker overall:** **Cardiac Troponins (I and T)** are more specific and sensitive than CPK-MB and are the current preferred diagnostic markers [1]. * **Earliest Marker:** **Myoglobin** rises first (within 1–2 hours) but lacks specificity. * **Marker for Re-infarction:** **CPK-MB** is the answer of choice because Troponins remain elevated for up to 7–14 days, masking a second event.

Question 1155: Which of the following conditions is characterized by the absence of P waves on an electrocardiogram?

A. Atrial fibrillation (Correct Answer)
B. Atrial asystole
C. Ventricular fibrillation
D. Ventricular tachycardia

Explanation: **Explanation:** The hallmark of **Atrial Fibrillation (AF)** is the replacement of organized atrial activity (P waves) with rapid, chaotic, and irregular **fibrillatory (f) waves**. This occurs due to multiple re-entrant wavelets firing simultaneously in the atria, most commonly originating from the pulmonary veins [1]. Because the AV node is bombarded by these irregular impulses, the ventricular response is "irregularly irregular," which is the classic diagnostic triad for AF on an ECG: absence of P waves, presence of f-waves, and irregular R-R intervals [1]. **Analysis of Incorrect Options:** * **Atrial Asystole:** This refers to the total absence of atrial electrical and mechanical activity (atrial standstill). While P waves are absent, there are also no fibrillatory waves, and the rhythm is usually a slow junctional or ventricular escape rhythm, unlike the rapid/irregular nature of AF [2]. * **Ventricular Fibrillation (VF):** This is a terminal rhythm characterized by a complete lack of identifiable P, QRS, or T waves. The ECG shows a chaotic, undulating baseline. It is a pulseless rhythm requiring immediate defibrillation. * **Ventricular Tachycardia (VT):** This is characterized by wide QRS complexes. While P waves are often "hidden" or dissociated (AV dissociation), they are technically present but obscured by the rapid ventricular rate. **High-Yield NEET-PG Pearls:** * **Most common cause of AF:** Long-standing Hypertension (globally) and Mitral Stenosis (in developing countries). * **ECG finding:** "Irregularly irregular" rhythm. * **Treatment of choice:** Hemodynamically unstable patients require **synchronized DC cardioversion**. Stable patients are managed with rate control (Beta-blockers/CCBs) and anticoagulation (based on CHADS₂-VASc score). * **Ashman Phenomenon:** A long R-R interval followed by a short R-R interval resulting in an aberrantly conducted wide QRS complex, often seen in AF.

Question 1156: All of the following murmurs may be heard in patients with aortic regurgitation except?

A. High-pitched decrescendo diastolic murmur.
B. Soft, low-pitched mid-diastolic rumbling murmur.
C. Mid-systolic ejection flow murmur.
D. Pansystolic murmur. (Correct Answer)

Explanation: **Explanation:** In Aortic Regurgitation (AR), the primary hemodynamic abnormality is the backflow of blood from the aorta into the left ventricle (LV) during diastole. **1. Why Pansystolic Murmur is the Correct Answer:** A **pansystolic (holosystolic) murmur** is characteristic of regurgitation between chambers with a significant pressure gradient throughout the entire systole, such as **Mitral Regurgitation (MR)** [3], **Tricuspid Regurgitation (TR)**, or **Ventricular Septal Defect (VSD)**. In AR, the pathology occurs during diastole; therefore, a pansystolic murmur is not a feature of isolated aortic regurgitation. **2. Analysis of Other Options:** * **High-pitched decrescendo diastolic murmur (Option A):** This is the **classical murmur of AR** [1]. It is heard best at the left sternal border (3rd/4th intercostal space) with the patient leaning forward in expiration. It represents the high-pressure regurgitant flow from the aorta to the LV [2]. * **Soft, low-pitched mid-diastolic rumbling murmur (Option B):** This is known as the **Austin Flint murmur**. It occurs because the regurgitant jet from the aorta strikes the anterior leaflet of the mitral valve, causing it to partially close and creating "functional" mitral stenosis [1]. * **Mid-systolic ejection flow murmur (Option C):** In chronic AR, the LV stroke volume is significantly increased (due to the added regurgitant volume). This high-volume flow across the aortic valve during systole creates a functional flow murmur [1], even in the absence of true aortic stenosis. **Clinical Pearls for NEET-PG:** * **Duroziez’s sign:** Systolic and diastolic bruits heard over the femoral artery. * **De Musset’s sign:** Head nodding in sync with the heartbeat. * **Corrigan’s Pulse:** "Water-hammer" or collapsing pulse. * **Hill’s Sign:** Popliteal systolic BP > Brachial systolic BP by >20 mmHg (most sensitive clinical sign for severity).

Question 1157: Which of the following is NOT a manifestation of acute aortic dissection?

A. Pericardial effusion
B. Aortic regurgitation
C. Mitral regurgitation (Correct Answer)
D. Acute myocardial infarction

Explanation: **Explanation:** Acute aortic dissection (AAD) typically involves a tear in the aortic intima, allowing blood to enter the media and create a false lumen [1]. The manifestations of AAD are usually related to the **retrograde extension** of this dissection or the compression of adjacent structures. **Why Mitral Regurgitation (MR) is the correct answer:** Mitral regurgitation is **not** a typical manifestation of aortic dissection. The mitral valve is anatomically separated from the aortic root by the intervalvular fibrosa. Aortic dissection primarily affects the aortic valve and the structures proximal to the aortic root. MR would only occur as a secondary complication of global left ventricular dysfunction (e.g., following a massive MI), but it is not a direct mechanical consequence of the dissection itself [3]. **Why the other options are incorrect:** * **Aortic Regurgitation (AR):** This is a classic manifestation of Type A dissection. It occurs due to the circumferential dilatation of the aortic root, which prevents the valve leaflets from coapting, or the dissection flap prolapsing through the valve [2]. * **Pericardial Effusion/Tamponade:** This occurs if the dissection ruptures through the adventitia into the pericardial space. It is the most common cause of death in Type A aortic dissection. * **Acute Myocardial Infarction (AMI):** This occurs in 1–2% of cases when the dissection flap extends into the coronary ostia (most commonly the **Right Coronary Artery**, leading to inferior wall MI). **Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** CT Angiography (stable patients) or Transesophageal Echocardiogram (unstable patients). * **Stanford Classification:** Type A involves the ascending aorta (Surgical emergency); Type B involves only the descending aorta (Medical management) [1]. * **Blood Pressure:** Look for a significant BP differential (>20 mmHg) between the arms. * **Chest X-ray:** Classically shows a widened mediastinum.

Question 1158: Which of the following statements is FALSE about Takotsubo Cardiomyopathy?

A. It is due to major catecholamine discharge.
B. It involves left ventricular contractile dysfunction.
C. It presents with acute chest pain.
D. Echocardiographic findings never revert back to normal. (Correct Answer)

Explanation: **Takotsubo Cardiomyopathy**, also known as "Broken Heart Syndrome" or "Stress-induced Cardiomyopathy," is a transient cardiac syndrome that mimics an acute coronary syndrome (ACS) [1]. **Why Option D is the Correct (False) Statement:** The hallmark of Takotsubo Cardiomyopathy is its **reversibility**. Unlike a typical myocardial infarction where necrosis leads to permanent scarring, the regional wall motion abnormalities (RWMA) in Takotsubo usually **resolve completely within 1–4 weeks**. Therefore, echocardiographic findings do revert to normal as the myocardium recovers from "stunning." **Analysis of Other Options:** * **Option A (True):** The pathophysiology is driven by a **massive surge in catecholamines** (epinephrine/norepinephrine) triggered by intense emotional or physical stress. This leads to microvascular dysfunction or direct myocyte toxicity [3]. * **Option B (True):** It involves transient **LV contractile dysfunction**, typically manifesting as "apical ballooning" where the apex is akinetic/hypokinetic while the base remains hypercontractile [2]. * **Option C (True):** Patients most commonly present with **acute retrosternal chest pain** and dyspnea, often accompanied by ST-segment elevation on ECG and elevated cardiac biomarkers, making it indistinguishable from an MI at presentation [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** Most common in **post-menopausal women** following a stressful trigger. * **Echocardiography:** Classic finding is **Apical Ballooning** (resembling a Japanese octopus trap, or "Takotsubo"). * **Coronary Angiography:** Crucial for diagnosis; it typically shows **absence of obstructive coronary artery disease** or acute plaque rupture. * **Prognosis:** Generally excellent with supportive care, though complications like heart failure or arrhythmias can occur in the acute phase [1].

Question 1159: Which test is not useful in a patient with a history of syncopal attack?

A. Electrophysiological testing
B. Tilt table testing
C. PET Scan (Correct Answer)
D. Holter monitoring

Explanation: **Explanation:** The primary goal in evaluating syncope is to distinguish between cardiac, orthostatic, and neurally mediated causes [1]. **Why PET Scan is the Correct Answer:** A **PET (Positron Emission Tomography) scan** is a functional imaging modality used primarily for assessing myocardial viability, detecting malignancy, or evaluating brain metabolism in dementia/epilepsy. It has **no established role** in the routine diagnostic workup of syncope, as it does not provide information on cardiac rhythm, valvular function, or autonomic reflexes—the three pillars of syncope evaluation. **Why the other options are incorrect:** * **Tilt Table Testing (HUTT):** This is the gold standard for diagnosing **Vasovagal Syncope** (neurally mediated) and orthostatic hypotension [2]. It provokes a bradycardic or hypotensive response in susceptible individuals. * **Holter Monitoring:** This is essential for detecting **transient arrhythmias** (e.g., Sick Sinus Syndrome, AV blocks, or VT) that may not be captured on a standard 12-lead ECG [3]. * **Electrophysiological (EP) Testing:** This invasive procedure is indicated in patients with structural heart disease or unexplained syncope where an arrhythmic cause is highly suspected but unproven by non-invasive means. **Clinical Pearls for NEET-PG:** * **Most common cause of syncope:** Vasovagal (Neurocardiogenic). * **Most common cardiac cause:** Arrhythmias. * **Initial investigation of choice:** A detailed history, physical exam (including orthostatic vitals), and a **12-lead ECG** [3]. * **San Francisco Syncope Rule (CHESS):** High-risk criteria include **C**HF, **H**ematocrit <30%, **E**CG abnormalities, **S**hortness of breath, and **S**ystolic BP <90 mmHg.

Question 1160: A 63-year-old man presents with a triad of angina, syncope, and congestive heart failure. Which of the following valvular heart lesions can be suspected?

A. Mitral stenosis
B. Tricuspid regurgitation
C. Aortic stenosis (Correct Answer)
D. Aortic regurgitation

Explanation: ### Explanation The correct answer is **Aortic Stenosis (AS)**. The classic clinical triad of **Angina, Syncope, and Dyspnea (Heart Failure)**—often remembered by the mnemonic **"ASH"** or **"SAD"**—is the hallmark presentation of symptomatic severe Calcific Aortic Stenosis [2]. * **Pathophysiology:** In AS, the narrowed valve orifice creates a significant pressure gradient, leading to **Left Ventricular Hypertrophy (LVH)** to maintain cardiac output [1]. * **Angina:** Occurs due to increased myocardial oxygen demand (from LVH) and decreased supply (compression of coronary arteries) [5]. * **Syncope:** Usually exertional, caused by the inability of the heart to increase cardiac output across the fixed obstruction during exercise, leading to cerebral hypoperfusion [2]. * **Heart Failure:** Develops as the ventricle eventually fails due to chronic pressure overload [1]. #### Why other options are incorrect: * **Mitral Stenosis:** Typically presents with dyspnea, hemoptysis, and atrial fibrillation. The classic triad is not associated with this lesion. * **Tricuspid Regurgitation:** Usually presents with signs of right-sided heart failure (raised JVP, hepatomegaly, edema) rather than angina or syncope. * **Aortic Regurgitation:** Presents with features of volume overload and a wide pulse pressure (e.g., Water-hammer pulse) [4]. While it can cause heart failure and angina, the specific triad of "Angina-Syncope-HF" is classically diagnostic of Stenosis. #### High-Yield Clinical Pearls for NEET-PG: 1. **Murmur:** Aortic Stenosis presents as a **harsh crescendo-decrescendo systolic murmur** radiating to the carotids [2]. 2. **Pulse:** Characterized by **Pulsus Parvus et Tardus** (slow-rising, low-amplitude pulse) [2]. 3. **Prognosis:** Once symptoms appear, survival drops significantly: Angina (~5 years), Syncope (~3 years), Heart Failure (~2 years). 4. **Indication for Surgery:** The onset of any of these three symptoms is a definitive indication for **Aortic Valve Replacement (AVR)** [3].

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Cardiology — MCQs

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