Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1001: What is the most common sustained tachycardia in healthy young women?

A. AVN (Atrioventricular nodal reentrant tachycardia) (Correct Answer)
B. AV (Atrioventricular tachycardia)
C. Atrial fibrillation
D. Pre-excitation syndrome

Explanation: ### Explanation **Correct Option: A. AVNRT (Atrioventricular Nodal Reentrant Tachycardia)** AVNRT is the most common form of paroxysmal supraventricular tachycardia (PSVT) in the general population and is specifically the most common sustained tachycardia in **healthy young women** (typically occurring in the 2nd to 4th decades of life) [1]. * **Mechanism:** It involves a functional reentrant circuit within the AV node due to the presence of dual pathways: a **slow pathway** (short refractory period) and a **fast pathway** (long refractory period) [1], [2]. * **Clinical Presentation:** Patients typically present with sudden-onset palpitations, neck pulsations ("frog sign"), and a narrow-complex tachycardia on ECG with P-waves often buried within or immediately following the QRS complex [1]. **Incorrect Options:** * **B. AVRT (Atrioventricular Reentrant Tachycardia):** This involves an anatomical accessory pathway (e.g., Bundle of Kent) [3]. While common in younger patients, it is statistically less frequent than AVNRT. * **C. Atrial Fibrillation:** This is the most common *sustained* arrhythmia overall, but its incidence increases with age and underlying structural heart disease (e.g., hypertension, valvular issues). It is rare in "healthy young" individuals. * **D. Pre-excitation Syndrome (e.g., WPW):** This refers to the presence of an accessory pathway [3]. While it predisposes to AVRT, the syndrome itself is a substrate, not the tachycardia. **High-Yield Clinical Pearls for NEET-PG:** * **Acute Management:** Vagal maneuvers (first-line) followed by **IV Adenosine** (drug of choice). * **Definitive Treatment:** Radiofrequency ablation of the **slow pathway**. * **ECG Hallmark:** "Pseudo R' wave" in lead V1 or "Pseudo S wave" in inferior leads. * **Demographic Hint:** If the question mentions a young female with "pounding in the neck," think AVNRT.

Question 1002: Which of the following is NOT a management or diagnostic modality for Wolff-Parkinson-White syndrome?

A. Treadmill test (Correct Answer)
B. Electrophysiological studies
C. Oral beta blocker
D. Procainamide

Explanation: **Wolff-Parkinson-White (WPW) syndrome** is characterized by an accessory pathway (Bundle of Kent) that bypasses the AV node, leading to pre-excitation [1]. **Why Option A is the correct answer:** The **Treadmill Test (TMT)** is generally **not** a primary management or diagnostic modality for WPW. While exercise testing can sometimes be used to assess the refractory period of the accessory pathway (sudden disappearance of the delta wave at higher heart rates suggests a low-risk pathway), it is not used to diagnose the syndrome itself (which is done via ECG) or to manage it [4]. In fact, vigorous exercise can be dangerous in high-risk WPW patients as it may precipitate rapid conduction over the accessory pathway. **Analysis of Incorrect Options:** * **B. Electrophysiological Studies (EPS):** This is the gold standard for definitive diagnosis, risk stratification, and identifying the exact location of the accessory pathway prior to radiofrequency ablation [4]. * **C. Oral Beta Blockers:** These are used for long-term maintenance therapy in patients with orthodromic AVRT to slow conduction through the AV node [2]. (Note: They are contraindicated in WPW with Atrial Fibrillation). * **D. Procainamide:** This is the drug of choice for hemodynamically stable patients with **WPW and Atrial Fibrillation** because it increases the refractory period of the accessory pathway [2]. **High-Yield Clinical Pearls for NEET-PG:** 1. **ECG Triad:** Short PR interval (<0.12s), Delta wave (slurred upstroke of QRS), and Wide QRS complex [1]. 2. **Definitive Treatment:** Radiofrequency Ablation (RFA) of the accessory pathway. 3. **The "ABCD" Contraindication:** In WPW with AFib, avoid **A**denosine, **B**eta-blockers, **C**alcium channel blockers (Verapamil/Diltiazem), and **D**igoxin, as they block the AV node and paradoxically increase conduction through the accessory pathway, potentially leading to Ventricular Fibrillation [3].

Question 1003: Which of the following conditions causes heart failure with reduced ejection fraction?

A. Restrictive cardiomyopathy
B. Hemochromatosis
C. Amyloidosis
D. Dilated Cardiomyopathy (Correct Answer)

Explanation: Heart failure is clinically categorized based on the Left Ventricular Ejection Fraction (LVEF). **Heart Failure with Reduced Ejection Fraction (HFrEF)**, also known as systolic heart failure, is defined by an LVEF ≤40% [3]. **1. Why Dilated Cardiomyopathy (DCM) is correct:** DCM is the prototypical cause of HFrEF. It is characterized by ventricular chamber enlargement and impaired contractility (systolic dysfunction) [1]. The weakened myocardium cannot pump blood effectively, leading to a reduced stroke volume and a low ejection fraction. Common etiologies include genetics, viral myocarditis, alcohol, and peripartum states [1]. **2. Why the other options are incorrect:** * **Restrictive Cardiomyopathy (RCM):** This condition is characterized by rigid ventricular walls that resist filling [2]. While the stroke volume may be low, the contractility is usually preserved in early stages, leading to **Heart Failure with Preserved Ejection Fraction (HFpEF)** [2]. * **Amyloidosis:** This is the most common cause of restrictive cardiomyopathy. Deposition of amyloid fibrils in the interstitium leads to stiff ventricles and diastolic dysfunction (HFpEF). * **Hemochromatosis:** Iron deposition typically causes a restrictive pattern (HFpEF) initially. While it can progress to a dilated pattern in advanced stages, it is classically associated with restrictive physiology in the context of board exams. **High-Yield Clinical Pearls for NEET-PG:** * **HFpEF (Diastolic HF):** LVEF ≥50%. Common causes include Hypertension (most common), Aging, and Restrictive Cardiomyopathy. * **HFrEF (Systolic HF):** LVEF ≤40%. Common causes include Ischemic Heart Disease (most common) [2] and Dilated Cardiomyopathy [1]. * **Echo Finding in DCM:** "Eccentric hypertrophy" (sarcomeres added in series) [1]. * **Echo Finding in Pressure Overload (HTN/AS):** "Concentric hypertrophy" (sarcomeres added in parallel).

Question 1004: Which of the following ECG findings in an asymptomatic athlete's heart should be considered pathological?

A. Increased amplitude of QRS
B. Second-degree (Mobitz 2) heart block (Correct Answer)
C. Prominent U wave
D. Sinus bradycardia

Explanation: ### Explanation In highly trained athletes, chronic intense physical activity leads to physiological remodeling of the heart, known as **Athlete’s Heart**. This involves increased vagal tone and chamber enlargement, which manifest as specific ECG changes. **Why Mobitz Type 2 is the Correct Answer:** ECG findings in athletes are categorized into **Normal (Training-related)** and **Abnormal (Pathological)**. * **Mobitz Type 2 Second-degree AV Block** is always considered **pathological** [1]. It indicates a conduction system disease (usually infra-nodal) and carries a high risk of progression to complete heart block [1]. It is not a result of high vagal tone and requires further investigation (e.g., echocardiography, cardiac MRI, or electrophysiology studies). **Analysis of Incorrect Options:** * **A. Increased QRS Amplitude:** This is a common, benign finding in athletes reflecting physiological left ventricular hypertrophy (LVH) due to volume or pressure loads during exercise. * **C. Prominent U Wave:** Often seen in athletes due to bradycardia or physiological repolarization changes; it is considered a normal variant in this population. * **D. Sinus Bradycardia:** This is the most common ECG finding in athletes (often <40 bpm). It results from increased resting parasympathetic (vagal) tone and is considered physiological. **High-Yield Clinical Pearls for NEET-PG:** * **Normal/Benign findings in athletes:** Sinus bradycardia, Sinus arrhythmia, First-degree AV block, and **Mobitz Type 1 (Wenckebach)** [1]. These typically disappear with exercise or sympathetic stimulation. * **Abnormal/Pathological findings:** T-wave inversion (V2-V6), ST-segment depression, Pathological Q waves, and **Mobitz Type 2** [1]. * **Key Distinction:** If an athlete has Mobitz Type 1, it is usually benign; if they have Mobitz Type 2, it is always a "red flag."

Question 1005: A 45-year-old tall, thin male presents with acute onset of chest pain radiating into the back. In the emergency room, his right radial pulse is bounding, but his femoral pulses are absent. What is the most likely diagnosis?

A. Aortic insufficiency
B. Aortic dissection (Correct Answer)
C. Ventricular fibrillation
D. Mitral insufficiency

Explanation: The clinical presentation is classic for an **Aortic Dissection (Stanford Type B or DeBakey Type III)** [1]. The patient’s habitus (tall and thin) suggests an underlying connective tissue disorder like **Marfan Syndrome** [2], a major risk factor for aortic pathology [1]. **Why Aortic Dissection is correct:** The hallmark of aortic dissection is sudden, "tearing" or "ripping" chest pain radiating to the back [1]. The pathognomonic sign in this case is the **pulse deficit** (asymmetric pulses). A dissection flap can propagate down the aorta, physically obstructing the orifice of major arterial branches [3]. Here, the flap has likely spared the right subclavian artery (bounding radial pulse) but has occluded the distal aorta or iliac arteries, leading to absent femoral pulses [2]. **Why the other options are incorrect:** * **Aortic Insufficiency:** While a dissection involving the aortic root (Type A) can cause acute AI, it would not explain the absence of femoral pulses [4]. * **Ventricular Fibrillation:** This is a cardiac arrest rhythm leading to sudden collapse and absence of *all* pulses, not a localized pulse deficit. * **Mitral Insufficiency:** Acute MI presents with pulmonary edema and a holosystolic murmur, not back pain or asymmetric pulses. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Digital Subtraction Angiography (DSA), but **CT Angiography** is the investigation of choice in emergency settings [3]. * **Transesophageal Echocardiogram (TEE):** Best for hemodynamically unstable patients [3]. * **Management:** Immediate BP control using **IV Labetalol** (target systolic BP 100–120 mmHg) to reduce shear stress (dP/dt). * **Classification:** Type A (involves ascending aorta) requires surgery; Type B (descending only) is usually managed medically [1].

Question 1006: A 30-year-old male presents with severe chest pain, breathlessness, and hypotension. ECG shows ST elevation in V3, V4, V5, and V6 leads. What is the best treatment for this patient?

A. Streptokinase
B. t-PA
C. Heparin
D. Percutaneous Transluminal Coronary Angioplasty (PTCA) (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Percutaneous Transluminal Coronary Angioplasty (PTCA)** **Why it is correct:** The patient presents with classic signs of an **Antero-lateral ST-Elevation Myocardial Infarction (STEMI)** (ST elevation in V3-V6) complicated by **cardiogenic shock** (hypotension and breathlessness). According to the current ACC/AHA and ESC guidelines, **Primary Percutaneous Coronary Intervention (PCI/PTCA)** is the gold standard treatment for STEMI [1]. It is superior to fibrinolysis in terms of achieving higher patency rates of the infarct-related artery, lower rates of re-infarction, and reduced intracranial hemorrhage. In patients with hemodynamic instability or cardiogenic shock, PTCA is mandatory regardless of the time delay, as it significantly improves survival [1]. **Why the other options are incorrect:** * **A & B (Streptokinase and t-PA):** These are fibrinolytic agents. While they are used in STEMI if PCI cannot be performed within 120 minutes of medical contact, they are less effective than PTCA. Furthermore, in cardiogenic shock, fibrinolysis is less effective due to poor systemic perfusion [1]. * **C (Heparin):** Heparin is an anticoagulant used as an adjunct therapy in STEMI to prevent further thrombus formation, but it cannot achieve the rapid mechanical reperfusion required to save the myocardium and stabilize the patient. **High-Yield Clinical Pearls for NEET-PG:** * **Door-to-Balloon Time:** Should be **<90 minutes** (at a PCI-capable center) or **<120 minutes** (if transfer is required). * **Door-to-Needle Time (Fibrinolysis):** Should be **<30 minutes**. * **Indications for PTCA over Fibrinolysis:** Cardiogenic shock, contraindications to bleeding, or late presentation (12–24 hours with ongoing ischemia). * **ECG Localization:** V3–V4 (Anterior wall/LAD), V5–V6 (Apex/Lateral/LAD or LCx).

Question 1007: A 65-year-old man is about to undergo an elective hip replacement. A pre-operative ECG is taken. Based upon the ECG, which of the following jugular venous pressure (JVP) abnormalities is most likely to be present?

A. Absent A waves (Correct Answer)
B. Cannon A waves
C. Giant V waves
D. Rise in JVP during inspiration

Explanation: ***Absent A waves*** - In **atrial fibrillation**, there is no coordinated **atrial contraction**, resulting in the absence of A waves in the JVP tracing. - The **chaotic atrial activity** prevents the normal atrial systolic contribution to venous return, eliminating the A wave component. *Cannon A waves* - These occur in **complete heart block** or **AV dissociation** when the atria contract against closed tricuspid valves. - They represent **intermittent large A waves** when atrial and ventricular contractions are not synchronized, not seen in atrial fibrillation. *Giant V waves* - These are characteristic of severe **tricuspid regurgitation**, where blood regurgitates back into the right atrium during ventricular systole. - The **enlarged V waves** reflect increased right atrial pressure during systole, unrelated to atrial fibrillation rhythm abnormalities. *Rise in JVP during inspiration* - This describes **Kussmaul's sign**, typically seen in **constrictive pericarditis** or **cardiac tamponade**. - It represents impaired venous return due to **rigid pericardial constraint**, not related to the rhythm disturbance of atrial fibrillation.

Question 1008: Electrical alternans in ECG is characteristic of which condition?

A. Severe bronchial asthma
B. Pericardial effusion (Correct Answer)
C. Severe left ventricular failure
D. Aortic regurgitation

Explanation: Explanation: **Electrical Alternans** is a pathognomonic ECG finding characterized by beat-to-beat variations in the amplitude or axis of the QRS complexes (and sometimes P or T waves). [1] **Why Pericardial Effusion is correct:** In large pericardial effusions (especially **Cardiac Tamponade**), the heart is suspended in a fluid-filled sac. This allows the heart to physically "swing" back and forth within the pericardium with each contraction. As the heart moves closer to and further away from the chest wall electrodes, the electrical voltage recorded on the ECG fluctuates, creating the characteristic alternating heights of the QRS complexes. [1] **Why the other options are incorrect:** * **Severe Bronchial Asthma:** May show "P-pulmonale" (tall P waves) or right axis deviation due to lung hyperinflation, but not electrical alternans. * **Severe Left Ventricular Failure:** Often presents with low voltage QRS or signs of left ventricular hypertrophy (LVH), but the heart does not swing to cause alternans. * **Aortic Regurgitation:** Typically shows signs of LVH with volume overload (deep Q waves in lateral leads) and a widened pulse pressure, but no electrical alternans. **NEET-PG High-Yield Pearls:** * **Beck’s Triad (Cardiac Tamponade):** Hypotension, Jugular Venous Distension (JVD), and Muffled heart sounds. * **Pulsus Paradoxus:** A classic clinical sign of tamponade (drop in systolic BP >10 mmHg during inspiration). * **Total Electrical Alternans:** When P, QRS, and T waves all show alternans, it is highly specific for cardiac tamponade. [1] * **Low Voltage QRS:** Also commonly seen in pericardial effusion due to the insulating effect of the fluid. [1]

Question 1009: Malignant hypertension can lead to all of the following except?

A. Hypertensive retinopathy
B. Respiratory failure (Correct Answer)
C. Renal failure
D. Hemolytic blood picture

Explanation: **Explanation:** Malignant hypertension (now often categorized under **Hypertensive Emergency**) is defined by severely elevated blood pressure (typically >180/120 mmHg) associated with acute, life-threatening end-organ damage. **Why Respiratory Failure is the correct answer:** While malignant hypertension can cause **Acute Pulmonary Edema** (due to left ventricular failure), it does not typically present as primary respiratory failure. Respiratory failure is a dysfunction of gas exchange (Type I or II), whereas the pulmonary involvement in hypertension is a hemodynamic/mechanical issue. Therefore, it is not considered a classic diagnostic hallmark of malignant hypertension compared to the other options. **Analysis of other options:** * **Hypertensive Retinopathy:** This is a defining feature. [1] Malignant hypertension is classically characterized by Grade III (flame-shaped hemorrhages, cotton wool spots) or **Grade IV (papilledema)** retinopathy. * **Renal Failure:** The kidneys are primary targets. [1] The pathological process of **fibrinoid necrosis** in the afferent arterioles leads to acute kidney injury (AKI), proteinuria, and hematuria. * **Hemolytic Blood Picture:** Severe hypertension causes mechanical damage to red blood cells as they pass through fibrin-deposited small vessels. This results in **Microangiopathic Hemolytic Anemia (MAHA)**, characterized by schistocytes on a peripheral smear. **High-Yield Clinical Pearls for NEET-PG:** * **Pathological Hallmark:** Fibrinoid necrosis of arterioles. [1] * **Drug of Choice:** IV Labetalol or Nicardipine. (Note: Use Sodium Nitroprusside with caution due to cyanide toxicity). * **BP Reduction Goal:** Reduce Mean Arterial Pressure (MAP) by no more than 25% within the first hour to prevent cerebral ischemia. * **Key Triad:** Severe hypertension + Papilledema + Encephalopathy/Renal failure. [1]

Question 1010: A 48-year-old male patient with an anterior myocardial infarction underwent primary angioplasty with a bare metal stent. What duration of antiplatelet therapy will you advise for discharge?

A. Dual antiplatelets for 12 months, then aspirin long-term (Correct Answer)
B. Ticagrelor for 1 month, then aspirin long-term
C. Aspirin for 1 month, then ticagrelor long-term
D. Ticagrelor alone is adequate long-term

Explanation: The management of Acute Coronary Syndrome (ACS), such as an ST-Elevation Myocardial Infarction (STEMI), requires **Dual Antiplatelet Therapy (DAPT)** to prevent stent thrombosis and recurrent ischemic events. **1. Why Option A is Correct:** According to current ACC/AHA and ESC guidelines, all patients undergoing Percutaneous Coronary Intervention (PCI) for **ACS** should receive DAPT (Aspirin + a P2Y12 inhibitor like Ticagrelor, Prasugrel, or Clopidogrel) for at least **12 months**, regardless of the stent type (Bare Metal Stent or Drug-Eluting Stent). After 12 months, the P2Y12 inhibitor is typically discontinued, and Aspirin is continued indefinitely for secondary prevention. **2. Why Other Options are Incorrect:** * **Option B & C:** One month of DAPT is insufficient for ACS patients. While 1 month was historically considered for Bare Metal Stents (BMS) in stable ischemic heart disease, the high-risk nature of an **Infarction (ACS)** mandates a full year of therapy to allow for vascular healing and stabilization of other non-culprit plaques. * **Option D:** Monotherapy with Ticagrelor is not the standard of care post-PCI for the first 12 months; Aspirin remains the cornerstone of long-term secondary prevention. **Clinical Pearls for NEET-PG:** * **Stent Type vs. Indication:** In *Stable Ischemic Heart Disease*, DAPT duration depends on stent type (1 month for BMS, 6 months for DES). However, in **ACS**, the duration is always **12 months** regardless of stent type. * **P2Y12 Choice:** In ACS, Ticagrelor or Prasugrel are preferred over Clopidogrel due to superior efficacy, unless there is a high bleeding risk. * **Triple Therapy:** If the patient also has Atrial Fibrillation, they require "Triple Therapy" (DAPT + Oral Anticoagulant), usually for a shortened period (1 week to 1 month) followed by "Double Therapy" [1] to minimize bleeding risk.

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Cardiology — MCQs

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