Cardiology — MCQs
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An 11-day-old neonate presented with difficulty in breathing, poor feeding, and sweating during feeding. On examination, weak femoral pulses, bounding radial pulses, radio-femoral delay, a loud S2, systolic ejection clicks or thrills in the suprasternal notch were noted. A systolic murmur was heard along the left sternal border at the 3rd and 4th intercostal spaces, transmitting to the left infrascapular area and to the neck. Arterial blood gas of the lower limbs revealed severe acidosis compared to the upper limbs, and SpO2 (upper limb) > SpO2 (lower limb). Chest X-ray findings are not specified. Which of the following needs to be given urgently to the neonate to save their life?
A child presents with a history of mental retardation. On examination, findings include dolichocephaly, low-set ears, micrognathia, clenched hands with overlapping fingers, simian crease, and rocker-bottom feet. What is the most common cardiac lesion expected in this patient?
What is the most important determinant in Tetralogy of Fallot?
Ductus arteriosus dependent blood flow is mandatory in all of the following congenital heart diseases EXCEPT:
What is the relationship between the S1 ejection click and severe pulmonary stenosis?
Which of the following cyanotic heart diseases is associated with left axis deviation and left ventricular hypertrophy?
Which type of Atrial Septal Defect (ASD) is associated with a murmur similar to Mitral Regurgitation (MR) and left axis deviation?
Which condition presents with a single second heart sound?
What is the commonest type of cyanotic heart disease?
A physician monitoring a newborn infant's heart sounds using a stethoscope hears the characteristic murmur of a patent ductus arteriosus. How soon after birth should this murmur normally disappear?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 51: An 11-day-old neonate presented with difficulty in breathing, poor feeding, and sweating during feeding. On examination, weak femoral pulses, bounding radial pulses, radio-femoral delay, a loud S2, systolic ejection clicks or thrills in the suprasternal notch were noted. A systolic murmur was heard along the left sternal border at the 3rd and 4th intercostal spaces, transmitting to the left infrascapular area and to the neck. Arterial blood gas of the lower limbs revealed severe acidosis compared to the upper limbs, and SpO2 (upper limb) > SpO2 (lower limb). Chest X-ray findings are not specified. Which of the following needs to be given urgently to the neonate to save their life?
- A. Prostaglandin E1 (PGE1) (Correct Answer)
- B. Prostaglandin E2 (PGE2)
- C. Prostaglandin F2-alpha (PGF2-alpha)
- D. Prostaglandin D2 (PGD2)
Explanation: ### Explanation **Diagnosis: Preductal Coarctation of the Aorta (Critical Coarctation)** The clinical presentation of an 11-day-old neonate with heart failure (poor feeding, sweating), **radio-femoral delay**, and differential cyanosis/acidosis (upper limb SpO2 > lower limb SpO2) is pathognomonic for **Critical Coarctation of the Aorta**. In this condition, the systemic circulation to the lower body depends entirely on the patency of the **Ductus Arteriosus**. As the ductus begins to close physiologically around the first or second week of life, the neonate develops sudden-onset shock and severe metabolic acidosis. **1. Why Prostaglandin E1 (PGE1) is Correct:** PGE1 (Alprostadil) is a potent vasodilator that prevents the closure of or reopens the ductus arteriosus (**Ductal-dependent systemic circulation**). By maintaining a "Patent Ductus Arteriosus" (PDA), blood can bypass the aortic obstruction to perfuse the lower body, stabilizing the neonate until surgical correction can be performed. **2. Why Incorrect Options are Wrong:** * **PGE2:** While it has some vasodilatory properties, it is primarily used in obstetrics for cervical ripening and is not the standard of care for maintaining ductal patency. * **PGF2-alpha:** This is a potent vasoconstrictor used to control postpartum hemorrhage; it would be contraindicated here as it could worsen pulmonary hypertension. * **PGD2:** This prostaglandin is involved in sleep regulation and allergic inflammation; it has no role in neonatal cardiac emergencies. **3. Clinical Pearls for NEET-PG:** * **Differential Cyanosis:** Seen in PDA with Reversal of Shunt or Preductal Coarctation (Pink upper body, blue lower body). * **Reverse Differential Cyanosis:** Seen in Transposition of the Great Arteries (TGA) with PDA (Blue upper body, pink lower body). * **Chest X-ray:** Look for the **"3" sign** (indentation of the aorta) or **Rib Notching** (usually seen in older children, not neonates). * **Drug of Choice:** PGE1 is the life-saving initial management for all ductal-dependent lesions (e.g., Hypoplastic Left Heart, Transposition, Critical PS/AS).
Question 52: A child presents with a history of mental retardation. On examination, findings include dolichocephaly, low-set ears, micrognathia, clenched hands with overlapping fingers, simian crease, and rocker-bottom feet. What is the most common cardiac lesion expected in this patient?
- A. Atrial Septal Defect (ASD)
- B. Ventricular Septal Defect (VSD) (Correct Answer)
- C. Patent Ductus Arteriosus (PDA)
- D. Pulmonary stenosis
Explanation: ### Explanation **Diagnosis: Edwards Syndrome (Trisomy 18)** The clinical presentation described—**dolichocephaly** (prominent occiput), **low-set ears**, **micrognathia**, **clenched hands with overlapping fingers** (2nd and 5th fingers over 3rd and 4th), and **rocker-bottom feet**—is classic for **Edwards Syndrome (Trisomy 18)**. **1. Why VSD is the Correct Answer:** Congenital heart disease (CHD) occurs in over 90% of infants with Edwards Syndrome. Among these, **Ventricular Septal Defect (VSD)** is the most common cardiac lesion. It is frequently associated with polyvalvular disease (involving the mitral or aortic valves). **2. Analysis of Incorrect Options:** * **Atrial Septal Defect (ASD):** While ASDs occur in Edwards Syndrome, they are less frequent than VSDs. ASD (specifically Ostium Primum type) is more characteristically associated with **Down Syndrome (Trisomy 21)**. * **Patent Ductus Arteriosus (PDA):** PDA is common in Edwards Syndrome and is a hallmark of **Congenital Rubella Syndrome**, but it ranks second to VSD in Trisomy 18. * **Pulmonary Stenosis:** This is a component of Tetralogy of Fallot (TOF) or seen in **Noonan Syndrome**, but it is not the primary lesion in Edwards Syndrome. **3. High-Yield Clinical Pearls for NEET-PG:** * **Trisomy 21 (Down):** Most common CHD is **Endocardial Cushion Defect** (AVSD), followed by VSD. * **Trisomy 13 (Patau):** Presents with midline defects (holoprosencephaly, cleft lip/palate, polydactyly). Most common CHD is **VSD**. * **Turner Syndrome (45,XO):** Most common CHD is **Bicuspid Aortic Valve** (most common overall) and **Coarctation of the Aorta** (classic exam answer). * **Williams Syndrome:** Associated with **Supravalvular Aortic Stenosis**. * **DiGeorge Syndrome:** Associated with **Truncus Arteriosus** and interrupted aortic arch.
Question 53: What is the most important determinant in Tetralogy of Fallot?
- A. Right Ventricular Hypertrophy (RVH)
- B. Sub-pulmonic stenosis (Correct Answer)
- C. Pansystolic murmur
- D. Enlargement of the heart
Explanation: **Explanation:** Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease. It consists of four classic components: Ventricular Septal Defect (VSD), Overriding of the Aorta, Right Ventricular Outflow Tract Obstruction (RVOTO), and Right Ventricular Hypertrophy (RVH). **Why Sub-pulmonic Stenosis is the Correct Answer:** The severity of the clinical presentation and the degree of cyanosis in TOF are primarily determined by the **severity of the RVOTO (Sub-pulmonic stenosis)**. This obstruction dictates the amount of blood flow to the lungs and the degree of right-to-left shunting across the VSD. If the stenosis is mild, the shunt may be left-to-right ("Pink Fallot"); if severe, it causes significant cyanosis and "Tet spells." **Analysis of Incorrect Options:** * **Right Ventricular Hypertrophy (RVH):** This is a secondary adaptation due to the high-pressure workload caused by the RVOTO and the large VSD. It is a result, not the primary determinant of the disease's severity. * **Pansystolic Murmur:** In TOF, the VSD is typically large and non-restrictive, meaning it does not produce a loud murmur. The characteristic murmur in TOF is actually a **crescendo-decrescendo ejection systolic murmur** caused by the pulmonic stenosis. * **Enlargement of the Heart:** TOF typically presents with a **normal-sized heart** on X-ray. The classic "Coeur-en-sabot" (boot-shaped heart) appearance is due to an upturned apex (from RVH) and a concave pulmonary segment, not global cardiomegaly. **High-Yield Clinical Pearls for NEET-PG:** * **Tet Spells:** Caused by an acute increase in RVOTO. Management includes the **Knee-chest position** (increases systemic vascular resistance) and Oxygen. * **X-ray finding:** Boot-shaped heart with **oligemic lung fields**. * **ECG finding:** Right axis deviation and RVH. * **Squatting:** Children squat to increase peripheral resistance, which decreases the right-to-left shunt and improves oxygenation.
Question 54: Ductus arteriosus dependent blood flow is mandatory in all of the following congenital heart diseases EXCEPT:
- A. Truncus arteriosus (Correct Answer)
- B. Hypoplastic left heart syndrome
- C. Transposition of the great arteries with intact ventricular septum
- D. Obliterated aortic arch
Explanation: **Explanation:** In pediatric cardiology, **ductal-dependent lesions** are congenital heart defects where the patency of the Ductus Arteriosus (DA) is essential for either systemic or pulmonary circulation. **1. Why Truncus Arteriosus is the Correct Answer:** In **Truncus Arteriosus**, a single large vessel arises from both ventricles, supplying the systemic, pulmonary, and coronary circulations. Because there is a common outflow tract, blood can reach the lungs and the body regardless of whether the ductus arteriosus is open or closed. While it is a cyanotic heart disease, it is **not** ductal-dependent for survival. **2. Analysis of Incorrect Options (Ductal-Dependent Lesions):** * **Hypoplastic Left Heart Syndrome (HLHS):** This is a ductal-dependent **systemic** circulation lesion. The left side of the heart cannot support systemic flow; thus, blood must flow from the pulmonary artery through the ductus to the aorta to perfuse the body. * **TGA with Intact Ventricular Septum:** This is a ductal-dependent **mixing** lesion. Since the systemic and pulmonary circulations are in parallel (rather than series), the ductus (or an ASD) is mandatory to allow oxygenated blood to reach the systemic circulation. * **Obliterated (Interrupted) Aortic Arch:** This is a ductal-dependent **systemic** circulation lesion. There is no luminal continuity between the ascending and descending aorta; the lower body is entirely dependent on right-to-left flow through the ductus. **Clinical Pearls for NEET-PG:** * **Management:** Prostaglandin E1 (Alprostadil) infusion is the immediate life-saving treatment to keep the ductus open in these conditions. * **Ductal-dependent Pulmonary flow:** Includes Pulmonary Atresia and Critical Pulmonary Stenosis. * **Ductal-dependent Systemic flow:** Includes HLHS, Critical Coarctation of the Aorta, and Interrupted Aortic Arch.
Question 55: What is the relationship between the S1 ejection click and severe pulmonary stenosis?
- A. In severe pulmonary stenosis, the gap increases.
- B. In severe pulmonary stenosis, the gap reduces. (Correct Answer)
- C. In severe pulmonary stenosis, there is no change.
- D. In severe pulmonary stenosis, the ejection click comes before.
Explanation: **Explanation:** The **pulmonary ejection click** occurs due to the sudden tensing of the stenotic pulmonary valve leaflets as they reach their maximum excursion during ventricular systole. The timing of this click is determined by the pressure in the right ventricle (RV) relative to the pulmonary artery (PA). **1. Why the gap reduces (Correct Answer):** In **severe pulmonary stenosis**, the RV pressure rises much more rapidly during early systole to overcome the high resistance of the valve. Because the RV pressure reaches the opening threshold (PA diastolic pressure) much earlier, the valve opens sooner after the first heart sound (S1). Consequently, the interval between S1 and the ejection click shortens. In extremely severe cases, the click may even merge with S1 or disappear. **2. Analysis of Incorrect Options:** * **Option A:** An increased gap is seen in **mild pulmonary stenosis**, where RV pressure rises more slowly, delaying the opening of the valve. * **Option C:** The timing of the click is dynamic and directly correlates with the severity of the pressure gradient. * **Option D:** The ejection click is a systolic event; it cannot occur before S1 (which marks the beginning of systole). **High-Yield Clinical Pearls for NEET-PG:** * **The Respiratory Paradox:** The pulmonary ejection click is the **only** right-sided sound that **decreases in intensity during inspiration**. This happens because increased venous return during inspiration raises RV end-diastolic pressure, causing the valve to "float" upward prematurely, reducing its excursion during systole. * **Severity Markers:** As PS severity increases: 1. The S1-Click interval **decreases**. 2. The systolic murmur becomes **longer** and peaks **later** in systole. 3. The S2 split becomes **wider** (delayed P2) and the P2 component becomes **softer**.
Question 56: Which of the following cyanotic heart diseases is associated with left axis deviation and left ventricular hypertrophy?
- A. Transposition of great vessels
- B. Truncus arteriosus
- C. Tricuspid atresia (Correct Answer)
- D. Total anomalous pulmonary venous drainage
Explanation: **Explanation:** In the context of cyanotic congenital heart disease (CCHD), the presence of **Left Axis Deviation (LAD)** and **Left Ventricular Hypertrophy (LVH)** on an ECG is a classic "high-yield" finding diagnostic of **Tricuspid Atresia**. 1. **Why Tricuspid Atresia is correct:** In Tricuspid Atresia, there is no communication between the right atrium and right ventricle. Blood must flow through an ASD to the left atrium and then into the **Left Ventricle (LV)**. The LV becomes the main pumping chamber for both systemic and pulmonary circulations (via a VSD or PDA), leading to LV volume overload and hypertrophy. The right ventricle is typically hypoplastic, causing the electrical axis to shift leftward. 2. **Why other options are incorrect:** * **Transposition of Great Vessels (TGA):** Typically presents with Right Axis Deviation (RAD) and Right Ventricular Hypertrophy (RVH) because the RV remains the systemic ventricle. * **Truncus Arteriosus:** Usually presents with biventricular hypertrophy or normal axis; it does not characteristically show isolated LAD. * **TAPVC:** Characterized by severe right-sided pressure and volume overload, leading to marked RAD and RVH. **High-Yield Clinical Pearls for NEET-PG:** * **The "LAD + Cyanosis" Duo:** If a neonate is cyanotic and the ECG shows LAD, think **Tricuspid Atresia** or **Tricuspid Stenosis**. * **X-ray finding:** Tricuspid atresia often shows a "Wall-to-Wall" heart or a "sitting duck" appearance (though less specific than the ECG). * **Management:** Requires a staged surgical approach: Blalock-Taussig shunt → Glenn procedure → Fontan procedure.
Question 57: Which type of Atrial Septal Defect (ASD) is associated with a murmur similar to Mitral Regurgitation (MR) and left axis deviation?
- A. ASD secundum
- B. ASD primum (Correct Answer)
- C. Floppy mitral valve
- D. ASD secundum with rheumatic MR
Explanation: **Explanation:** **ASD primum** (a type of partial Atrioventricular Septal Defect) is the correct answer due to its unique anatomical and electrophysiological characteristics: 1. **Mitral Regurgitation (MR) Murmur:** ASD primum is almost universally associated with a **cleft in the anterior mitral leaflet**. This cleft results in mitral regurgitation, which produces a holosystolic murmur at the apex radiating to the axilla, mimicking isolated MR. 2. **Left Axis Deviation (LAD):** In most ASDs (like secundum), the axis is shifted to the right. However, in ASD primum, there is a congenital displacement of the AV node and the bundle of His. This leads to early activation of the left ventricle, resulting in a characteristic **Left Axis Deviation** on ECG (often -30° to -90°). **Analysis of Incorrect Options:** * **ASD secundum (A):** The most common type of ASD. It typically presents with **Right Axis Deviation (RAD)** and a Right Bundle Branch Block (RBBB) pattern. It does not involve the mitral valve. * **Floppy mitral valve (C):** While this causes MR, it is not an atrial septal defect and does not typically present with the specific ECG findings or shunting associated with ASDs. * **ASD secundum with rheumatic MR (D):** Known as **Lutembacher Syndrome** (classically MS, but can include MR). While it features both an ASD and a murmur, it does not explain the congenital LAD seen in primum defects. **High-Yield Clinical Pearls for NEET-PG:** * **ASD primum** is strongly associated with **Down Syndrome** (Trisomy 21). * **ECG Triad for ASD Primum:** Prolonged PR interval (1st-degree heart block), Left Axis Deviation, and RBBB. * **Physical Exam:** Look for a "fixed wide split S2" (common to all ASDs) PLUS an apical holosystolic murmur (unique to primum).
Question 58: Which condition presents with a single second heart sound?
- A. Tetralogy of Fallot (TOF) (Correct Answer)
- B. Hypertension
- C. Pulmonary edema
- D. Myocardial infarction (MI)
Explanation: **Explanation:** The second heart sound (S2) is produced by the closure of the aortic (A2) and pulmonary (P2) valves. A **single S2** occurs when one component is either absent, significantly delayed, or obscured. **Why TOF is the correct answer:** In Tetralogy of Fallot, there are two primary reasons for a single S2: 1. **Pulmonary Stenosis:** The severe narrowing of the right ventricular outflow tract results in a very soft, delayed, or completely inaudible P2. 2. **Aortic Overriding:** The aorta is positioned more anteriorly and is dilated, which often masks the faint pulmonary component. Consequently, only the loud A2 is heard, resulting in a single S2. **Analysis of Incorrect Options:** * **Hypertension:** Systemic hypertension typically causes a **loud A2** (accentuated S2) due to the high pressure closing the aortic valve forcefully, but both components are usually present. * **Pulmonary Edema:** This is a clinical state of fluid alveolar congestion. While it may be associated with an S3 gallop, it does not inherently cause a single S2. * **Myocardial Infarction (MI):** MI may lead to a soft S1 or a paradoxical splitting of S2 (if it causes a Left Bundle Branch Block), but it is not a classic cause of a single S2. **NEET-PG High-Yield Pearls:** * **Single S2 Mnemonic (P-A-T):** **P**ulmonary atresia, **A**ortic stenosis (severe), **T**runcus arteriosus, and **T**etralogy of Fallot. * **Loud S2:** Seen in Pulmonary Hypertension (loud P2) and Systemic Hypertension (loud A2). * **Fixed Wide Splitting:** Pathognomonic for Atrial Septal Defect (ASD). * **Paradoxical Splitting:** Seen in LBBB and severe Aortic Stenosis (P2 occurs before A2).
Question 59: What is the commonest type of cyanotic heart disease?
- A. Atrial Septal Defect (ASD)
- B. Ventricular Septal Defect (VSD)
- C. Tetralogy of Fallot (TOF) (Correct Answer)
- D. Patent Ductus Arteriosus (PDA)
Explanation: ### Explanation **Correct Answer: C. Tetralogy of Fallot (TOF)** **Why it is correct:** Congenital heart diseases (CHD) are broadly classified into **Acyanotic** (left-to-right shunt) and **Cyanotic** (right-to-left shunt). **Tetralogy of Fallot (TOF)** is the most common cyanotic heart disease beyond the neonatal period. It consists of four classic features: Ventricular Septal Defect (VSD), Overriding of the aorta, Right Ventricular Outflow Tract Obstruction (RVOTO/Pulmonary stenosis), and Right Ventricular Hypertrophy (RVH). The degree of cyanosis in TOF is primarily determined by the severity of the pulmonary stenosis. **Why the other options are incorrect:** * **A, B, and D (ASD, VSD, and PDA):** These are all **Acyanotic** heart diseases characterized by left-to-right shunting. While they are more common overall than cyanotic defects, they do not cause cyanosis unless Eisenmenger syndrome (reversal of shunt) develops later in life. * **VSD** is the overall most common congenital heart disease. * **ASD** is the most common CHD to present in adulthood. **NEET-PG High-Yield Pearls:** * **Most common cyanotic CHD at birth (Neonatal period):** Transposition of the Great Arteries (TGA). * **Most common cyanotic CHD overall (Infancy/Childhood):** Tetralogy of Fallot (TOF). * **X-ray finding in TOF:** "Boot-shaped heart" (Coeur en sabot) due to an upturned apex from RVH and a concave pulmonary segment. * **Management of "Tet Spells":** Knee-chest position (increases systemic vascular resistance), Oxygen, Morphine, and Beta-blockers. * **Most common overall CHD:** Ventricular Septal Defect (VSD).
Question 60: A physician monitoring a newborn infant's heart sounds using a stethoscope hears the characteristic murmur of a patent ductus arteriosus. How soon after birth should this murmur normally disappear?
- A. 1-2 months
- B. 1-2 weeks
- C. 1-2 days
- D. Immediate closure (Correct Answer)
Explanation: **Explanation:** The **Ductus Arteriosus (DA)** is a vital fetal structure connecting the pulmonary artery to the descending aorta, bypassing the non-functional fetal lungs. The transition from fetal to neonatal circulation involves two distinct stages of closure: 1. **Functional Closure:** This occurs **immediately after birth** (usually within 10–15 hours in term infants). Upon the first breath, pulmonary vascular resistance drops and systemic resistance increases, reversing the shunt. Simultaneously, increased arterial oxygen tension ($PaO_2$) and a decrease in circulating Prostaglandin $E_2$ (due to placental removal and lung metabolism) trigger the smooth muscle of the DA to constrict. Therefore, any murmur associated with a physiological PDA should disappear within the first day of life. 2. **Anatomical Closure:** This involves fibrosis and the formation of the **Ligamentum Arteriosum**, which typically takes **2–3 weeks**. **Analysis of Options:** * **Option A & B (1-2 months/weeks):** These timeframes represent pathological persistence. If the ductus remains patent beyond the first week, it is considered a Patent Ductus Arteriosus (PDA), often requiring medical (Indomethacin/Ibuprofen) or surgical intervention. * **Option C (1-2 days):** While functional closure can take up to 24–48 hours in some healthy infants, the physiological process is initiated immediately. In the context of "normal" disappearance for exam purposes, "Immediate" is the preferred descriptor for the cessation of the shunt. **Clinical Pearls for NEET-PG:** * **Murmur:** PDA presents as a **"Machinery-type" continuous murmur**, loudest at the left infraclavicular area. * **Drug of Choice:** **IV Indomethacin or Ibuprofen** (NSAIDs) are used to close a PDA by inhibiting prostaglandin synthesis. * **Maintenance:** **Alprostadil (PGE1)** is used to keep the ductus open in cyanotic heart diseases (e.g., Transposition of Great Arteries). * **Association:** PDA is highly associated with **Congenital Rubella Syndrome** and **Prematurity**.
Practice by Chapter
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