Cardiology — MCQs

A 60-year-old woman with no past medical history has an elevated blood pressure of 165/80 mm Hg on routine evaluation. Repeated measurements over the next month confirm the elevated pressure. Physical examination, routine blood count, and biochemistry are all normal. For a patient with high blood pressure, select the most appropriate initial medication?

Q1148Easy

Which of the following is a BNP analogue?

Q1149Medium

A gradient between pulmonary artery wedge pressure and left ventricular end-diastolic pressure is seen in which of the following conditions?

Q1150Medium

Which of the following findings may be seen in a second-degree heart block?

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1141: The normal P wave is inverted in which lead?

A. Lead I
B. Lead II
C. Lead aVF
D. Lead aVR (Correct Answer)

Explanation: **Explanation:** The direction of the P wave on an ECG is determined by the vector of atrial depolarization. In a normal heart, the electrical impulse originates in the SA node (located in the high right atrium) and travels downwards and to the left toward the AV node [1]. **Why Lead aVR is correct:** Lead aVR is an augmented limb lead positioned on the right shoulder. Since the atrial depolarization vector moves **away** from the right shoulder (downward and leftward), the electrical activity is recorded as a negative deflection [1]. Therefore, a normal sinus P wave is **always inverted in lead aVR**. **Why the other options are incorrect:** * **Lead I:** This lead looks from the right arm to the left arm. Since the vector moves toward the left, the P wave is positive. * **Lead II:** This lead follows the primary axis of the heart (from right shoulder to left leg). Because the vector moves directly toward this lead, Lead II typically shows the **tallest and most upright** P wave [1]. * **Lead aVF:** This is an inferior lead looking upward from the feet. Since the vector moves downward toward the feet, the P wave is positive. **High-Yield Clinical Pearls for NEET-PG:** * **Sinus Rhythm Criteria:** A rhythm is defined as "sinus" only if the P wave is upright in leads I, II, and aVF, and inverted in aVR. * **Dextrocardia/Lead Reversal:** If you see an **upright P wave in aVR** and an inverted P wave in Lead I, suspect either limb lead reversal (most common) or Dextrocardia. * **Biphasic P waves:** The P wave may be biphasic in lead **V1**, where the initial positive deflection represents right atrial activity and the terminal negative deflection represents left atrial activity.

Question 1142: Severity of mitral stenosis is determined by:

A. Intensity of S1 heart sound
B. Diastolic murmur duration (Correct Answer)
C. Opening snap
D. Intensity of diastolic murmur

Explanation: ### Explanation The severity of Mitral Stenosis (MS) is primarily determined by the **duration of the diastolic murmur**, not its intensity. [2] **1. Why "Diastolic Murmur Duration" is correct:** In MS, the mid-diastolic murmur occurs due to a pressure gradient between the left atrium (LA) and left ventricle (LV). As the mitral valve orifice narrows (increased severity), it takes longer for the LA to empty into the LV. Consequently, the LA pressure remains higher than the LV pressure for a longer portion of diastole. Therefore, the **longer the duration** of the murmur (i.e., the closer it extends toward the S1), the more severe the stenosis. **2. Why other options are incorrect:** * **Intensity of S1:** While S1 is loud in mild-to-moderate MS due to mobile leaflets, it actually becomes **soft or muffled** in severe, calcified MS. Thus, intensity does not linearly correlate with severity. [2] * **Opening Snap (OS):** The presence of an OS indicates mobile leaflets. However, severity is determined by the **A2-OS interval**, not the OS itself. A shorter A2-OS interval indicates higher LA pressure and more severe MS. [1] * **Intensity of Diastolic Murmur:** Murmur intensity depends on the flow rate and pressure gradient. In very severe MS with low cardiac output, the murmur may actually become very soft (Silent MS). **Clinical Pearls for NEET-PG:** * **Signs of Severe MS:** Long diastolic murmur, short A2-OS interval (<0.07s), presence of pulmonary hypertension (loud P2), and a small pulse pressure. [1] * **The "Silent MS":** Occurs when the valve area is so small and cardiac output so low that the murmur is barely audible. * **Most common cause:** Rheumatic heart disease. * **Gold Standard for Diagnosis:** Echocardiography (Planimetry is the most accurate for valve area). [3]

Question 1143: What does the abbreviation AED stand for?

A. Automatic external defibrillator
B. Automated external defibrillator (Correct Answer)
C. Automatic electrical defibrillator
D. Automated electrical defibrillator

Explanation: **Explanation:** The correct term is **Automated External Defibrillator (AED)**. An AED is a portable, computerized medical device designed to be used by both medical professionals and laypeople during a cardiac arrest. It automatically analyzes the patient’s cardiac rhythm (specifically looking for shockable rhythms like Ventricular Fibrillation or Pulseless Ventricular Tachycardia) and delivers an electric shock to restore a functional heart rhythm [1]. **Analysis of Options:** * **Option B (Correct):** "Automated" is the precise term because the device uses internal algorithms to autonomously diagnose the rhythm and determine if a shock is indicated. "External" refers to the application of pads on the chest skin, as opposed to internal paddles used in surgery. * **Option A:** "Automatic" is a common misnomer. While the device performs tasks automatically, the official medical and manufacturing nomenclature is "Automated." * **Options C & D:** "Electrical" is redundant and incorrect in the title. While the device delivers an electrical current, the standard terminology focuses on its "External" application. **Clinical Pearls for NEET-PG:** 1. **Shockable Rhythms:** AEDs are programmed to recognize only two rhythms: **Ventricular Fibrillation (VF)** and **Pulseless Ventricular Tachycardia (pVT)** [1]. 2. **Non-shockable Rhythms:** Asystole and Pulseless Electrical Activity (PEA) [1]. In these cases, the AED will advise "No shock indicated," and CPR should be resumed immediately. 3. **Chain of Survival:** Early defibrillation is the most critical factor in improving survival rates for out-of-hospital cardiac arrest (OHCA) [1]. 4. **Safety:** Always ensure the patient is not in water and the chest is dry before applying AED pads to prevent electrical arcing.

Question 1144: Romana's sign is seen in which of the following?

A. Toxoplasma
B. Trypanosoma cruzi (Correct Answer)
C. Loaloa
D. Wuchereria

Explanation: **Explanation:** **Romaña’s sign** is a classic clinical hallmark of **Acute Chagas Disease**, caused by the protozoan parasite ***Trypanosoma cruzi***. It occurs when the parasite (transmitted via the feces of the Triatomine or "kissing" bug) enters through the conjunctiva or the skin near the eye. 1. **Why Trypanosoma cruzi is correct:** Romaña’s sign is characterized by **painless, unilateral periorbital edema**, conjunctivitis, and local lymphadenopathy (pre-auricular nodes). It represents the portal of entry for the parasite. If the parasite enters through a skin break elsewhere, the resulting inflammatory lesion is called a **Chagoma**. 2. **Why other options are incorrect:** * **Toxoplasma:** Typically presents with lymphadenopathy or chorioretinitis in immunocompromised hosts, but does not cause Romaña’s sign. * **Loa loa:** Known for **Calabar swellings** (transient, itchy dermal swellings) and the visible migration of the adult worm across the subconjunctiva [1]. * **Wuchereria bancrofti:** Causes lymphatic filariasis, leading to elephantiasis and hydrocele, but not acute periorbital edema. **High-Yield Clinical Pearls for NEET-PG:** * **Vector:** Triatomine bug (Reduviid bug). * **Chronic Chagas Disease:** Characterized by "Mega-syndromes"—**Dilated Cardiomyopathy** (most common cause in South America), **Megaesophagus**, and **Megacolon** [2]. * **ECG Finding:** Right Bundle Branch Block (RBBB) is a common conduction defect in Chagasic heart disease. * **Treatment:** Benznidazole or Nifurtimox [2].

Question 1145: Brugada syndrome is characterized by what ECG finding?

A. ST elevation (Correct Answer)
B. Prolonged PR interval
C. Prolonged QT interval
D. Tall T waves

Explanation: Explanation: Brugada Syndrome is an autosomal dominant genetic disorder caused by a mutation in the SCN5A gene, which encodes the cardiac sodium channel. This leads to a defect in the inward sodium current, primarily affecting the right ventricular outflow tract (RVOT). Why ST elevation is correct: The hallmark ECG finding in Brugada Syndrome is coved-type ST-segment elevation (≥2 mm) followed by a negative T-wave in the right precordial leads (V1–V3). This is known as the Type 1 Brugada pattern. It is often described as having a "shark fin" or "saddle-back" appearance. These changes occur due to an imbalance between inward and outward currents during the early repolarization phase of the action potential. Why other options are incorrect: * Prolonged PR interval: Associated with first-degree AV block or conditions like hyperkalemia and Lyme disease [3], but not the diagnostic hallmark of Brugada. * Prolonged QT interval: Characteristic of Long QT Syndrome (LQTS), which predisposes to Torsades de Pointes [2]. Brugada typically has a normal QT interval. * Tall T waves: Usually seen in hyperkalemia (peaked T waves) [3] or the hyperacute phase of myocardial infarction [1]. High-Yield Clinical Pearls for NEET-PG: * Demographics: Most common in young males of Southeast Asian descent. * Clinical Presentation: Sudden cardiac death (SCD) due to polymorphic ventricular tachycardia or ventricular fibrillation, often occurring during sleep or while at rest. * Triggers: Fever, alcohol, and certain drugs (e.g., sodium channel blockers) can unmask the ECG pattern. * Management: The only proven effective treatment for symptomatic patients or those at high risk is an Implantable Cardioverter Defibrillator (ICD).

Question 1146: A 70-year-old man with hypertension presents with severe chest pain and diaphoresis. On examination, he has bounding pulses with wide pulse pressure. A diastolic murmur is heard along the right sternal border. Which of the following is the possible etiology?

A. Aortic dissection (Correct Answer)
B. STEMI with papillary muscle dysfunction
C. Myocarditis with functional regurgitation
D. Flash pulmonary edema

Explanation: ### Explanation The clinical presentation of severe chest pain, diaphoresis, and **wide pulse pressure** in an elderly hypertensive patient is highly suggestive of **Acute Aortic Regurgitation (AR)** secondary to **Aortic Dissection (Type A)** [2]. **1. Why Aortic Dissection is Correct:** In a patient with aortic dissection, the intimal tear can extend retrograde into the aortic root, causing disruption of the aortic valve apparatus [4]. This leads to acute AR, characterized by a **diastolic murmur** and **bounding pulses** (due to a large stroke volume being ejected into the aorta and then rapidly leaking back into the left ventricle) [1]. Notably, a diastolic murmur heard specifically at the **right sternal border** (rather than the left) strongly suggests aortic root pathology, such as dissection or aneurysm, rather than primary valvular disease. **2. Why Other Options are Incorrect:** * **B. STEMI with papillary muscle dysfunction:** This typically results in acute **Mitral Regurgitation (MR)**, which presents with a *systolic* murmur at the apex, not a diastolic murmur at the right sternal border [3]. * **C. Myocarditis:** While it can cause heart failure and functional MR/TR due to chamber dilation, it does not typically present with sudden-onset wide pulse pressure or a right-sided diastolic murmur. * **D. Flash pulmonary edema:** This is a clinical manifestation (often due to bilateral renal artery stenosis or acute LV failure) rather than a primary etiology for the physical findings described. **3. High-Yield Clinical Pearls for NEET-PG:** * **Right Sternal Border Murmur:** Always think of Aortic Root Dilatation or Dissection. * **Stanford Classification:** Type A involves the ascending aorta (requires surgery); Type B involves only the descending aorta (managed medically) [2]. * **Gold Standard Investigation:** CT Angiography (stable patients) or Transesophageal Echocardiogram (unstable patients) [4]. * **Classic Triad:** Sudden "tearing" chest pain, pulse/BP asymmetry between arms, and a new murmur of AR.

Question 1147: A 60-year-old woman with no past medical history has an elevated blood pressure of 165/80 mm Hg on routine evaluation. Repeated measurements over the next month confirm the elevated pressure. Physical examination, routine blood count, and biochemistry are all normal. For a patient with high blood pressure, select the most appropriate initial medication?

A. Thiazide diuretics (Correct Answer)
B. Spironolactone
C. Clonidine
D. Prazosin

Explanation: **Explanation:** The patient presents with **Isolated Systolic Hypertension (ISH)**, defined as a systolic blood pressure (SBP) ≥140 mmHg with a diastolic blood pressure (DBP) <90 mmHg. This condition is common in elderly patients due to age-related arterial stiffness and decreased compliance of the aorta [1]. **Why Thiazide Diuretics are Correct:** According to standard guidelines (JNC 8 and AHA/ACC), **Thiazide-type diuretics** (e.g., Chlorthalidone, Hydrochlorothiazide) are considered first-line agents for the management of uncomplicated hypertension. In the elderly and those with ISH [1], Thiazides have been proven in landmark trials (like the SHEP study) to significantly reduce the risk of stroke, heart failure, and cardiovascular mortality [2]. They are preferred due to their efficacy, low cost, and favorable safety profile as initial monotherapy [1]. **Why Other Options are Incorrect:** * **B. Spironolactone:** This is a potassium-sparing diuretic (aldosterone antagonist). It is generally reserved as a fourth-line agent for **resistant hypertension** or specifically indicated for patients with heart failure with reduced ejection fraction (HFrEF). * **C. Clonidine:** A centrally acting alpha-2 agonist. It is not a first-line drug due to its side effect profile (sedation, dry mouth) and the risk of **rebound hypertension** if doses are missed. * **D. Prazosin:** An alpha-1 blocker. It is not used as first-line monotherapy for hypertension because it does not provide the same degree of cardiovascular protection as Thiazides or ACE inhibitors. It is primarily used in patients with concomitant Benign Prostatic Hyperplasia (BPH). **NEET-PG High-Yield Pearls:** * **First-line classes for HTN:** Thiazides, ACE inhibitors, ARBs, or Calcium Channel Blockers (CCBs) [1]. * **Best Thiazide:** Chlorthalidone is often preferred over Hydrochlorothiazide due to its longer half-life and more potent BP-lowering effect. * **Side Effects of Thiazides:** Hyper**G**lycemia, Hyper**L**ipidemia, Hyper**U**ricemia, and Hyper**C**alcemia (Mnemonic: **GLUC**), along with Hypokalemia and Hyponatremia.

Question 1148: Which of the following is a BNP analogue?

A. Eplerenone
B. Nesiritide (Correct Answer)
C. Levosimendan
D. Coenzyme Q

Explanation: **Explanation:** **Correct Answer: B. Nesiritide** Nesiritide is a **recombinant human B-type Natriuretic Peptide (BNP)**. It works by binding to the particulate guanylate cyclase receptor in vascular smooth muscle and endothelial cells, leading to increased intracellular cyclic GMP (cGMP) [1]. This results in potent **vasodilation** (reducing both preload and afterload) and **natriuresis** (excretion of sodium by the kidneys) [1], [2]. It is primarily used in the management of acutely decompensated heart failure (ADHF) with dyspnea at rest. **Analysis of Incorrect Options:** * **A. Eplerenone:** This is a selective **mineralocorticoid receptor antagonist (MRA)**. It is a potassium-sparing diuretic used to reduce mortality in chronic heart failure (HFrEF), but it is not a BNP analogue. * **C. Levosimendan:** This is a **calcium sensitizer** and an inodilator. It increases cardiac contractility by sensitizing troponin C to calcium and causes vasodilation by opening ATP-sensitive potassium channels. * **D. Coenzyme Q:** This is an antioxidant and a component of the mitochondrial electron transport chain. While sometimes used as a supplement in heart failure, it has no structural or functional relation to BNP. **High-Yield Clinical Pearls for NEET-PG:** * **BNP vs. NT-proBNP:** BNP is the active hormone (shorter half-life), while NT-proBNP is the inactive N-terminal fragment (longer half-life, more stable for diagnostic testing). * **Sacubitril/Valsartan (ARNI):** Sacubitril is a **neprilysin inhibitor** that prevents the breakdown of endogenous BNP. Note that BNP levels will rise during ARNI therapy, so NT-proBNP should be used for monitoring instead. * **Nesiritide Side Effects:** The most common side effect is dose-related **hypotension**. It may also be associated with a transient increase in serum creatinine.

Question 1149: A gradient between pulmonary artery wedge pressure and left ventricular end-diastolic pressure is seen in which of the following conditions?

A. Aortic regurgitation
B. Constrictive pericarditis
C. Left atrial myxoma (Correct Answer)
D. Pulmonary thromboembolism

Explanation: ### Explanation **Underlying Concept:** Normally, the **Pulmonary Artery Wedge Pressure (PAWP)** is a surrogate for **Left Atrial Pressure (LAP)** [2]. In the absence of mitral valve disease, LAP is equal to **Left Ventricular End-Diastolic Pressure (LVEDP)** because the mitral valve is open during diastole, creating a continuous column of blood. A gradient between PAWP and LVEDP indicates an **obstruction at the level of the mitral valve** or within the left atrium [1]. **Why Left Atrial Myxoma is Correct:** A **Left Atrial Myxoma** acts as a physical "ball-valve" obstruction. During diastole, the tumor prolapses into or obstructs the mitral orifice, preventing blood from flowing freely into the left ventricle. This causes a rise in LAP (and thus PAWP) while the LVEDP remains normal or low, creating a significant pressure gradient. This mimics the hemodynamics of **Mitral Stenosis** [1]. **Analysis of Incorrect Options:** * **Aortic Regurgitation:** Here, blood flows back from the aorta into the LV during diastole. This increases LV volume and pressure, often causing LVEDP to be *higher* than LAP (due to premature mitral valve closure). * **Constrictive Pericarditis:** This is characterized by **diastolic equalization of pressures**. The PAWP, LVEDP, and Right Ventricular End-Diastolic Pressure (RVEDP) all become elevated and equal (within 5 mmHg). * **Pulmonary Thromboembolism:** This causes a "pre-capillary" pathology. While Pulmonary Artery Pressure increases, the PAWP and LVEDP typically remain normal and equal, as the pathology is proximal to the pulmonary capillaries. **High-Yield Clinical Pearls for NEET-PG:** * **PAWP > LVEDP Gradient:** Seen in Mitral Stenosis, Left Atrial Myxoma, and Cor Triatriatum [1]. * **LVEDP > PAWP Gradient:** Seen in Aortic Regurgitation and decreased LV compliance (e.g., restrictive cardiomyopathy). * **Myxoma Triad:** Constitutional symptoms (fever/weight loss), Embolic phenomena, and Obstructive symptoms (mimicking MS; "Tumor Plop" sound on auscultation).

Question 1150: Which of the following findings may be seen in a second-degree heart block?

A. Change in QRS complex morphology
B. Atrial rate more than ventricular rate
C. Prolonged conduction time
D. All of the above (Correct Answer)

Explanation: **Explanation:** Second-degree heart block is characterized by intermittent failure of the AV node or His-Purkinje system to conduct atrial impulses to the ventricles. This leads to specific ECG changes that validate all the given options. 1. **Atrial rate more than ventricular rate (Option B):** This is the hallmark of second-degree block. Because some P waves are "dropped" (not followed by a QRS complex), there are more P waves than QRS complexes, making the atrial rate higher than the ventricular rate. 2. **Prolonged conduction time (Option C):** In **Mobitz Type I (Wenckebach)**, there is progressive prolongation of the PR interval until a beat is dropped. Even in **Mobitz Type II**, the underlying conduction system disease often results in a baseline prolonged PR interval or delayed conduction through the bundle branches. 3. **Change in QRS complex morphology (Option A):** This is particularly relevant in **Mobitz Type II** block. This type usually occurs infra-nodally (at the Bundle of His or Purkinje fibers). It is frequently associated with a **wide QRS complex** (Bundle Branch Block), whereas Mobitz Type I usually presents with a narrow QRS. **High-Yield Clinical Pearls for NEET-PG:** * **Mobitz Type I (Wenckebach):** Site of block is usually the **AV Node**. It is often reversible, associated with increased vagal tone or inferior wall MI, and usually has a benign prognosis. * **Mobitz Type II:** Site of block is **infra-nodal**. It is more dangerous as it can suddenly progress to Complete Heart Block (3rd degree). It often requires a permanent pacemaker. * **Vagal Maneuvers:** Carotid sinus massage worsens Mobitz Type II but may improve Mobitz Type I.

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Cardiology — MCQs

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