Cardiology Practice Questions

Q: All of the following are true about Right Ventricular Infarcts, except?

Normal JVP. In Right Ventricular Infarction (RVI), the hallmark pathophysiology is **acute right-sided heart failure**. This leads to a sudden backup of pressure into the systemic venous circulation [3]. **1. Why "Normal JVP" is the correct (false) statement:** The most sensitive and characteristic clinical sign of RVI is an **elevated Jugular Venous Pressure (JVP)** [2]. Because the right ventricle fails to pump blood effectively into the pulmonary circulation, blood backs up into the superior vena cava. A normal JVP in a patient with suspected RVI is highly unlikely and should prompt a search for an alternative diagnosis. **2. Explanation of other options:** * **Nocturia:** In right-sided failure, dependent edema accumulates in the lower limbs during the day. At night, when the patient lies supine, this fluid is redistributed, increasing renal perfusion and venous return, leading to increased urine production (nocturia). * **Ascites:** Chronic or severe acute right heart failure leads to systemic venous congestion, causing hepatic congestion and fluid leakage into the peritoneal cavity (ascites) [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Triad of RVI:** Hypotension, Clear Lungs (absence of pulmonary edema), and Elevated JVP. * **Kussmaul’s Sign:** A paradoxical rise in JVP during inspiration is frequently seen in RVI. * **Diagnosis:** The most specific finding is **ST-elevation in lead V4R** (Right-sided ECG). * **Management Contraindication:** Avoid **Nitrates, Diuretics, and Morphine**, as they decrease preload. RVI is "preload dependent." * **Treatment of choice:** Aggressive **IV fluid resuscitation** (Normal Saline) to maintain right ventricular filling pressure [1].

Q: Besides ECG, what other studies are required to diagnose Brugada syndrome?

Echocardiography. Brugada syndrome is a genetic channelopathy (primarily involving the $SCN5A$ sodium channel gene) that predisposes patients to ventricular arrhythmias and sudden cardiac death. The diagnosis is fundamentally based on a characteristic ECG pattern (Type 1: coved ST-segment elevation $\geq$ 2mm in V1-V2) in the **absence of structural heart disease.** **Why Echocardiography is the correct answer:** The definition of Brugada syndrome requires the exclusion of underlying structural abnormalities that could mimic the ECG pattern or independently cause arrhythmias (e.g., Arrhythmogenic Right Ventricular Cardiomyopathy - ARVC). **Echocardiography** is the mandatory first-line imaging study used to confirm that the heart is structurally normal, thereby fulfilling the diagnostic criteria. **Analysis of Incorrect Options:** * **A. Stress test:** Exercise typically decreases the ST elevation in Brugada patients (as heart rate increases, the ST elevation often diminishes). It is not a diagnostic requirement. * **B. Holter monitor:** While useful for detecting paroxysmal arrhythmias or nocturnal agonal respiration, it cannot confirm the "structurally normal heart" requirement for diagnosis. * **C. Angiogram:** Invasive coronary angiography is generally not required unless there is a high suspicion of coronary artery disease mimicking the ECG changes (Pseudo-Brugada). **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Demographics:** Most common in young males of Southeast Asian descent. * **Triggers:** Fever, sodium channel blockers (e.g., Ajmaline, Flecainide), and alcohol. Fever-induced ECG changes are a classic board presentation. * **Management:** The only proven effective treatment for symptomatic patients or survivors of cardiac arrest is an **Implantable Cardioverter Defibrillator (ICD).** Quinidine can be used as an adjunct for electrical storms.

Q: Which of the following is an electrocardiographic feature of pulmonary hypertension?

T wave inversion. Explanation: Pulmonary hypertension (PH) leads to chronic pressure overload of the right ventricle (RV), resulting in **Right Ventricular Hypertrophy (RVH)** and right atrial enlargement. **Why T wave inversion is correct:** In pulmonary hypertension, the hypertrophied and strained right ventricle undergoes repolarization abnormalities [1]. This manifests as **T wave inversions in the right precordial leads (V1–V3)** and sometimes the inferior leads (II, III, aVF) [1]. This is known as the "Right Ventricular Strain Pattern" and is a hallmark ECG finding of chronic RV pressure overload [1]. **Analysis of Incorrect Options:** * **B. Presence of U wave:** Typically associated with **hypokalemia**, bradycardia, or certain medications (e.g., Digoxin, Class IA antiarrhythmics). It is not a feature of PH. * **C. SI, Q3, T3 pattern:** While this is a classic board-exam finding for right heart strain, it is specifically associated with **Acute Pulmonary Embolism** (acute cor pulmonale) rather than the chronic changes of pulmonary hypertension [1]. It is also relatively insensitive. * **D. PR prolongation:** This represents a first-degree AV block, usually seen in conditions affecting the conduction system (e.g., hyperkalemia, beta-blocker use, or rheumatic fever), not typically PH. **High-Yield NEET-PG Pearls for Pulmonary Hypertension ECG:** 1. **Right Axis Deviation (RAD):** Often > +110°. 2. **P-pulmonale:** Tall, peaked P waves (>2.5 mm) in lead II (Right Atrial Enlargement). 3. **R/S ratio in V1:** > 1 (Dominant R wave in V1 is a classic sign of RVH) [1]. 4. **Right Bundle Branch Block (RBBB):** Often seen due to RV stretching [1].

Q: Which drug should be avoided in hypertrophic obstructive cardiomyopathy?

Digoxin. Explanation: In Hypertrophic Obstructive Cardiomyopathy (HOCM), the primary pathophysiology involves a dynamic left ventricular outflow tract (LVOT) obstruction. This obstruction is worsened by factors that increase myocardial contractility or decrease ventricular volume [1]. Why Digoxin is avoided: Digoxin is a positive inotrope. By increasing the force of myocardial contraction [2], it narrows the outflow tract during systole and exacerbates the Systolic Anterior Motion (SAM) of the mitral valve. This leads to an increase in the pressure gradient across the LVOT, worsening the obstruction and clinical symptoms. Therefore, Digoxin (and other inotropes like Dobutamine) is strictly contraindicated. Analysis of other options: * Beta-blockers (Option C): These are the first-line treatment for HOCM [3]. They are negative inotropes and negative chronotropes; they reduce the heart rate (increasing diastolic filling time) and decrease contractility, thereby reducing the LVOT gradient. * Verapamil (Option B): A non-dihydropyridine calcium channel blocker used as a second-line agent. It improves diastolic filling and reduces the pressure gradient. * Amiodarone (Option A): Often used in HOCM patients to manage or prevent atrial fibrillation and ventricular arrhythmias, which are common complications [1]. NEET-PG High-Yield Pearls: 1. Avoid "Triple D": Digoxin, Diuretics (in high doses), and Dilators (Nitrates/ACE inhibitors) should be avoided as they worsen the obstruction. 2. Squatting/Handgrip: These maneuvers increase afterload/preload, which decreases the HOCM murmur intensity. 3. Valsalva/Standing: These maneuvers decrease venous return (preload), which increases the HOCM murmur intensity. 4. Drug of Choice: Propranolol (Beta-blocker) [3].

Q: The systolic ejection murmur in hypertrophic obstructive cardiomyopathy is diminished when a patient:

Lies down. **Explanation:** The murmur in **Hypertrophic Obstructive Cardiomyopathy (HOCM)** is a systolic ejection murmur caused by dynamic left ventricular outflow tract (LVOT) obstruction. The intensity of this murmur depends on the **Left Ventricular (LV) volume**: * **Decreased LV volume** (less preload/afterload) → Increases obstruction → **Louder murmur.** * **Increased LV volume** (more preload/afterload) → Decreases obstruction → **Softer murmur.** **Why "Lies down" is correct:** When a patient lies down (supine position) or performs passive leg raising, there is an **increase in venous return (preload)** to the heart. This increased volume fills the LV, pushing the hypertrophied septum away from the mitral valve, thereby widening the LVOT and **diminishing** the murmur. **Analysis of Incorrect Options:** * **Valsalva Maneuver (Option A):** During the strain phase, venous return decreases. This reduces LV volume, worsening the obstruction and **increasing** the murmur intensity. * **Amyl Nitrite (Option C):** This is a potent vasodilator that decreases afterload and venous return. The resulting smaller LV cavity **increases** the murmur. * **Standing up (Option D):** Sudden standing causes venous pooling in the lower limbs, decreasing preload. This reduces LV volume and **increases** the murmur. **High-Yield Clinical Pearls for NEET-PG:** 1. **The "Rule of Two":** HOCM and Mitral Valve Prolapse (MVP) are the only two murmurs that get **louder** with Valsalva and Standing (maneuvers that decrease preload) [1]. 2. **Handgrip Exercise:** Increases afterload, which pushes the septum away from the LVOT, **decreasing** the HOCM murmur (unlike Aortic Stenosis, where it stays the same or decreases). 3. **Squatting:** Increases both preload and afterload, **decreasing** the HOCM murmur.

Q: An arteriovenous fistula can lead to which of the following complications, except?

Cardiac arrhythmias. An arteriovenous (AV) fistula is an abnormal communication between an artery and a vein, bypassing the high-resistance capillary bed. This leads to significant hemodynamic changes characterized by **high-output heart failure**. **Why "Cardiac Arrhythmias" is the correct answer:** While chronic volume overload from an AV fistula can eventually lead to chamber enlargement (atrial or ventricular dilation), which *may* predispose a patient to arrhythmias, **cardiac arrhythmias are not a direct or characteristic hemodynamic complication** of an AV fistula itself. The primary pathology is mechanical and volume-related rather than electrical. **Analysis of incorrect options:** * **Increased Preload:** The shunting of blood from the high-pressure arterial system directly into the low-pressure venous system increases venous return to the right heart, directly increasing preload. * **Increased Cardiac Output:** To compensate for the decreased systemic vascular resistance (SVR) caused by the shunt, the stroke volume and heart rate increase, leading to a high-output state [1]. * **Sinus Tachycardia:** This occurs as a compensatory mechanism to maintain blood pressure in the face of reduced SVR and is a hallmark of the hyperdynamic circulation associated with AV fistulas. **Clinical Pearls for NEET-PG:** 1. **Nicoladoni-Branham Sign:** Compression of the AV fistula leads to a sudden decrease in heart rate (bradycardia) and an increase in blood pressure; this is a diagnostic clinical sign. 2. **Wide Pulse Pressure:** Due to decreased diastolic pressure (shunting) and increased systolic pressure (increased stroke volume). 3. **Heart Failure:** AV fistulas are a classic cause of **High-Output Heart Failure** (others include Beriberi, Hyperthyroidism, and Paget’s disease).

Q: Dilated cardiomyopathy does not develop in which of the following conditions?

Alkaptonuria. ### Explanation **Correct Answer: B. Alkaptonuria** **Why Alkaptonuria is the correct answer:** Alkaptonuria is an autosomal recessive metabolic disorder caused by a deficiency of the enzyme **homogentisate 1,2-dioxygenase**. This leads to the accumulation of homogentisic acid, which deposits in connective tissues (ochronosis). In the heart, this deposition typically causes **valvular heart disease**—most commonly **Aortic Stenosis** due to calcification of the valve leaflets—and coronary artery disease. It does **not** typically cause Dilated Cardiomyopathy (DCM). **Analysis of Incorrect Options:** * **A. Duchenne Muscular Dystrophy (DMD):** Absence of dystrophin in cardiac myocytes leads to progressive fibrosis. DCM is a hallmark feature of DMD, often appearing in the second decade of life [2]. * **C. Sarcoidosis:** This is an infiltrative/granulomatous disease. While it often presents as restrictive cardiomyopathy or conduction blocks, it frequently progresses to **DCM** due to extensive myocardial scarring and remodeling. * **D. Keshan Syndrome:** This is a specific form of **DCM** caused by **Selenium deficiency**. It was traditionally endemic in areas of China with selenium-poor soil. **High-Yield Clinical Pearls for NEET-PG:** * **Alkaptonuria Triad:** Black urine (on standing), Ochronosis (bluish-black pigmentation of sclera/ear cartilage), and large joint arthritis. * **Most common cause of DCM:** Idiopathic (Genetic/Familial in ~30% of cases) [1]. * **Reversible causes of DCM:** Alcohol, Tachycardia-induced, Peripartum cardiomyopathy, and Selenium/Thiamine deficiency [1]. * **DMD vs. BMD:** Cardiac involvement is more common and occurs earlier in Duchenne than in Becker muscular dystrophy [3].

Q: A 26-year-old man presents with a chronic cough, headaches, and leg aches upon exertion. He is a smoker. A chest X-ray reveals notching of his ribs. Which of the following undiagnosed congenital defects may be responsible for these findings?

Coarctation of the aorta. **Explanation** The clinical presentation of rib notching, headaches, and claudication (leg aches upon exertion) in a young adult is a classic triad for **Coarctation of the Aorta (Post-ductal type).** **Why Coarctation of the Aorta is correct:** In coarctation, there is a narrowing of the aortic arch, typically distal to the origin of the left subclavian artery [1]. To bypass this obstruction, the body develops extensive **collateral circulation**. Blood flows from the subclavian arteries into the internal thoracic arteries, then into the **posterior intercostal arteries** to reach the descending aorta. The increased pressure and volume cause these intercostal arteries to become dilated and tortuous. As they pulsate against the lower borders of the ribs, they cause pressure atrophy of the bone, visible on a chest X-ray as **"rib notching"** (usually affecting the 3rd to 8th ribs). Headaches occur due to upper limb hypertension, while leg aches result from decreased perfusion to the lower extremities. **Why the other options are incorrect:** * **Eisenmenger’s Syndrome:** This is the reversal of a left-to-right shunt due to pulmonary hypertension. It presents with cyanosis and clubbing, not rib notching. * **Tetralogy of Fallot (TOF):** A cyanotic heart disease characterized by a "boot-shaped heart" (coeur en sabot) on X-ray, not rib notching. * **Transposition of Great Vessels (TGA):** Presents in neonates with severe cyanosis and an "egg-on-a-string" appearance on X-ray. **High-Yield NEET-PG Pearls:** * **Rib Notching:** Not seen in the 1st and 2nd ribs because their intercostal arteries arise from the costocervical trunk (proximal to the coarctation). * **X-ray Sign:** Look for the **"3" sign** on the chest X-ray (formed by the pre-stenotic dilation, the coarctation, and the post-stenotic dilation). * **Clinical Sign:** **Radio-femoral delay** and a significant BP systolic difference between upper and lower limbs.

Question 1

All of the following are true about Right Ventricular Infarcts, except?

Accepted Answer

Normal JVP

Answer

Nocturia

Answer

Nocturia

Answer

Ascites

Question 2

Which of the following results in broad complex tachycardia?

Accepted Answer

Antidromic conduction in Accessory pathway mediated tachycardia

Answer

Orthodromic conduction in accessory pathway mediated tachycardia

Answer

AV nodal re-entrant tachycardia

Answer

Atrial fibrillation

Question 3

Besides ECG, what other studies are required to diagnose Brugada syndrome?

Accepted Answer

Echocardiography

Answer

Stress test

Answer

Holter monitor

Answer

Angiogram

Question 4

Which of the following is an electrocardiographic feature of pulmonary hypertension?

Accepted Answer

T wave inversion

Answer

Presence of U wave

Answer

SI, Q3, T3 pattern

Answer

PR prolongation

Question 5

Which drug should be avoided in hypertrophic obstructive cardiomyopathy?

Accepted Answer

Digoxin

Answer

Amiodarone

Answer

Verapamil

Answer

Beta blockers

Question 6

The systolic ejection murmur in hypertrophic obstructive cardiomyopathy is diminished when a patient:

Accepted Answer

Lies down

Answer

Performs the Valsalva maneuver

Answer

Inhales amyl nitrite

Answer

Stands up

Question 7

The severity of Mitral stenosis is clinically best decided by?

Accepted Answer

Length of the diastolic murmur

Answer

Intensity of the diastolic murmur

Answer

Loudness of the first heart sound

Answer

Split of the second heart sound

Question 8

An arteriovenous fistula can lead to which of the following complications, except?

Accepted Answer

Cardiac arrhythmias

Answer

Sinus tachycardia

Answer

Increased preload

Answer

Increased cardiac output

Question 9

Dilated cardiomyopathy does not develop in which of the following conditions?

Accepted Answer

Alkaptonuria

Answer

Duchenne muscular dystrophy

Answer

Sarcoidosis

Answer

Keshan Syndrome

Question 10

A 26-year-old man presents with a chronic cough, headaches, and leg aches upon exertion. He is a smoker. A chest X-ray reveals notching of his ribs. Which of the following undiagnosed congenital defects may be responsible for these findings?

Accepted Answer

Coarctation of the aorta

Answer

Eisenmenger's syndrome

Answer

Tetralogy of Fallot

Answer

Transposition of great vessels

Cardiology — MCQs

Cardiology — MCQs

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