Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 131: In a preterm baby with patent ductus arteriosus, which of the following statements is true, EXCEPT?

A. Narrow pulse pressure (Correct Answer)
B. Necrotizing enterocolitis
C. Continuous murmur
D. Congestive heart failure

Explanation: In a Patent Ductus Arteriosus (PDA), blood shunts from the high-pressure aorta to the low-pressure pulmonary artery during both systole and diastole. **Explanation of the Correct Answer:** * **Option A (Narrow pulse pressure):** This is the **incorrect** statement (and thus the correct answer). In PDA, the runoff of blood from the aorta into the pulmonary artery during diastole causes a significant drop in diastolic blood pressure. Conversely, the stroke volume increases to compensate for the left-to-right shunt, maintaining or slightly increasing systolic pressure. This results in a **Wide Pulse Pressure**, not a narrow one. Clinically, this manifests as "bounding pulses" (Water-hammer pulse). **Explanation of Incorrect Options:** * **Option B (Necrotizing enterocolitis):** Large PDAs cause a "ductal steal" phenomenon, diverting blood away from the systemic circulation. Reduced mesenteric perfusion increases the risk of **NEC** in preterm infants. * **Option C (Continuous murmur):** The classic physical finding is a **Gibson’s murmur** (continuous machinery murmur), heard best at the left infraclavicular area. Note: In very small preterms, it may only be systolic initially. * **Option D (Congestive heart failure):** The increased pulmonary venous return leads to volume overload of the left atrium and left ventricle, potentially resulting in **CHF**. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Intravenous **Indomethacin** or **Ibuprofen** (NSAIDs) are used to close a PDA by inhibiting prostaglandins. Paracetamol is an emerging alternative. * **Maintenance:** If a duct-dependent lesion is present (e.g., Transposition of Great Arteries), **Alprostadil (PGE1)** is given to keep the ductus open. * **Chest X-ray:** Shows cardiomegaly and increased pulmonary vascular markings.

Question 132: What is the average blood pressure of a 1-year-old child?

A. 120/80 mmHg
B. 75/50 mmHg
C. 95/50 mmHg (Correct Answer)
D. 60/30 mmHg

Explanation: **Explanation:** The blood pressure (BP) in children is significantly lower than in adults and increases progressively with age, height, and weight. For a **1-year-old child**, the average (50th percentile) blood pressure is approximately **95/50 mmHg**. **Why Option C is correct:** Blood pressure is determined by cardiac output and systemic vascular resistance. In infants and toddlers, the arterial walls are more compliant and the stroke volume is smaller compared to adults. According to standard pediatric reference charts (like the Nelson Textbook of Pediatrics), the systolic BP at birth is ~60–70 mmHg, rising to ~95 mmHg by age 1, and reaching adult levels by late adolescence. **Analysis of Incorrect Options:** * **Option A (120/80 mmHg):** This is the standard normal BP for a healthy **adult**. In a 1-year-old, this would represent severe Stage 2 hypertension. * **Option B (75/50 mmHg):** This range is more characteristic of a **neonate** (newborn) or an infant under 3 months of age. * **Option D (60/30 mmHg):** This is typical for a **preterm neonate**. In a 1-year-old, this value would indicate profound hypotension or shock. **High-Yield Clinical Pearls for NEET-PG:** * **Formula for Systolic BP (1–10 years):** A quick bedside rule for the 50th percentile systolic BP is **90 + (2 × age in years)**. For a 1-year-old: 90 + 2 = 92 mmHg (closest to 95). * **Hypotension Definition:** In a child aged 1–10 years, systolic BP **< 70 + (2 × age in years)** is considered hypotension. * **Cuff Size:** The most common cause of an erroneous BP reading is incorrect cuff size. The bladder should cover **80–100%** of the arm circumference and **40%** of the arm width. * **Right Arm Preference:** BP should ideally be measured in the right arm to avoid false readings in cases of Coarctation of the Aorta.

Question 133: All of the following may occur in Noonan's syndrome except?

A. Hypertrophic cardiomyopathy
B. Cryptorchidism
C. Infertility in females (Correct Answer)
D. Autosomal dominant transmission

Explanation: **Explanation:** Noonan’s syndrome is an **autosomal dominant** multisystem disorder often referred to as the "Male Turner Syndrome" due to phenotypic similarities. It is primarily caused by mutations in the **RAS-MAPK signaling pathway** (most commonly the **PTPN11 gene**). **Why "Infertility in females" is the correct answer:** Unlike Turner Syndrome (45,XO), where streak ovaries lead to primary infertility, females with Noonan’s syndrome (usually 46,XX) typically have **normal ovarian function and are fertile**. In contrast, **males** with Noonan’s syndrome often suffer from infertility due to gonadal dysfunction associated with bilateral cryptorchidism. **Analysis of incorrect options:** * **Hypertrophic Cardiomyopathy (HCM):** This is a classic association. While Pulmonary Stenosis (dysplastic valve) is the most common cardiac lesion, HCM occurs in approximately 20-30% of cases. * **Cryptorchidism:** Undescended testes are seen in up to 80% of affected males, frequently leading to impaired spermatogenesis. * **Autosomal dominant transmission:** Noonan’s syndrome follows an AD pattern, though many cases arise from *de novo* mutations. **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** Usually normal (46,XY or 46,XX). * **Cardiac Profile:** Pulmonary Valve Stenosis (most common) > HCM > ASD. * **Facial Features:** Low-set ears, hypertelorism, downward-slanting palpebral fissures, and webbed neck. * **Hematology:** Increased risk of bleeding diathesis (Factor XI deficiency) and Juvenile Myelomonocytic Leukemia (JMML). * **Triad for Diagnosis:** Short stature, characteristic facies, and congenital heart disease.

Question 134: What is the most common cause of heart block in infants?

A. Systemic lupus erythematosus (SLE)
B. Surgery for congenital heart disease (Correct Answer)
C. Viral myocarditis
D. Rheumatic fever

Explanation: **Explanation:** The most common cause of heart block in infants and children is **iatrogenic injury during surgery for congenital heart disease (CHD)**. During corrective procedures for defects like Ventricular Septal Defects (VSD), Atrioventricular Canal Defects, or Tetralogy of Fallot, the conduction system (specifically the Bundle of His) is anatomically close to the surgical site. Sutures or mechanical trauma during the repair can lead to transient or permanent complete heart block. **Analysis of Options:** * **A. Systemic Lupus Erythematosus (SLE):** This is the most common cause of **congenital** (in-utero) complete heart block due to the transplacental passage of maternal anti-Ro (SSA) and anti-La (SSB) antibodies. However, in the overall pediatric population, post-surgical causes are statistically more frequent. * **C. Viral Myocarditis:** While myocarditis can cause arrhythmias and conduction delays due to myocardial inflammation, it is a less common cause of permanent heart block compared to surgical trauma. * **D. Rheumatic Fever:** This typically presents in older children (school-age) rather than infants. While it characteristically causes a **first-degree heart block** (prolonged PR interval), it rarely progresses to complete heart block in the acute phase. **High-Yield Clinical Pearls for NEET-PG:** * **Congenital Heart Block:** Strongly associated with maternal **SLE**; 100% of these infants have mothers with anti-Ro/SSA antibodies. * **Post-Surgical Block:** If a heart block persists for more than **7–10 days** after cardiac surgery, a permanent pacemaker is usually indicated. * **Most common site of injury:** The Bundle of His, especially during VSD closure.

Question 135: Pulmonary blood flow is decreased in which of the following conditions?

A. Tetralogy of Fallot (Correct Answer)
B. Ebstein's anomaly
C. Common atrium
D. Transposition of the great arteries with intact ventricular septum

Explanation: ### Explanation The fundamental concept in pediatric cardiology for NEET-PG is distinguishing between **Cyanotic Congenital Heart Diseases (CCHD)** with increased vs. decreased pulmonary blood flow (PBF). **Why Tetralogy of Fallot (TOF) is Correct:** TOF is the classic example of a CCHD with **decreased pulmonary blood flow**. The pathophysiology is governed by **Right Ventricular Outflow Tract (RVOT) obstruction** (infundibular stenosis). This obstruction creates high resistance to blood entering the pulmonary arteries. Consequently, deoxygenated blood is shunted from right to left across the large Ventricular Septal Defect (VSD), leading to oligaemic lung fields on X-ray. **Analysis of Incorrect Options:** * **Ebstein’s Anomaly:** While it can cause cyanosis due to a right-to-left shunt at the atrial level, the pulmonary blood flow is typically variable but not primarily "decreased" in the same obstructive sense as TOF. However, in severe cases, it can mimic decreased flow, but TOF remains the definitive textbook answer for this category. * **Common Atrium:** This is a form of ASD where there is a large left-to-right shunt, leading to **increased pulmonary blood flow** and eventual pulmonary hypertension. * **Transposition of the Great Arteries (TGA):** In TGA, the pulmonary artery arises from the left ventricle. Unless there is associated pulmonary stenosis, TGA (especially with an intact septum) typically presents with **increased pulmonary blood flow** because the low-resistance pulmonary circuit receives blood directly from the systemic-fed left ventricle. **High-Yield Clinical Pearls for NEET-PG:** * **Decreased PBF (Oligaemic lungs):** TOF, Tricuspid Atresia, Pulmonary Atresia. * **Increased PBF (Plethoric lungs):** TGA, TAPVC, Truncus Arteriosus, Single Ventricle. * **TOF X-ray:** "Boot-shaped heart" (Coeur en sabot) due to an upturned apex (RVH) and a concave pulmonary bay. * **Management:** Squatting position in "Tet spells" increases systemic vascular resistance (SVR), forcing more blood through the RVOT into the lungs.

Question 136: Which of the following conditions is worsened by prostaglandin E infusion?

A. Pulmonary atresia without VSD
B. Hypoplastic left heart syndrome
C. Obstructive TAPVC (Correct Answer)
D. Aortic arch interruption

Explanation: **Explanation:** The primary goal of **Prostaglandin E1 (PGE1)** infusion is to maintain the patency of the **Ductus Arteriosus (DA)**. This is life-saving in ductal-dependent congenital heart diseases but contraindicated in specific conditions. **Why Obstructive TAPVC is the correct answer:** In Total Anomalous Pulmonary Venous Connection (TAPVC), all pulmonary veins drain into the systemic venous circulation (right atrium) instead of the left atrium. In the **obstructive** form (commonly infradiaphragmatic), there is severe resistance to pulmonary venous return. This leads to massive pulmonary congestion and edema. Administering PGE1 opens the ductus arteriosus, which increases pulmonary blood flow. In the presence of an obstruction to venous outflow, this extra blood "backs up" into the lungs, **worsening pulmonary edema** and clinical hypoxia. **Analysis of Incorrect Options:** * **A. Pulmonary Atresia without VSD:** This is a **ductal-dependent pulmonary circulation** lesion. PGE1 is mandatory to allow blood to flow from the aorta through the ductus to the lungs for oxygenation. * **B. Hypoplastic Left Heart Syndrome (HLHS):** This is a **ductal-dependent systemic circulation** lesion. PGE1 is essential to allow the right ventricle to pump blood to the systemic circulation via the ductus. * **D. Aortic Arch Interruption:** Similar to HLHS, the lower body depends on the ductus for perfusion. PGE1 is life-saving to prevent cardiogenic shock and renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **PGE1 Indications:** Cyanotic lesions with decreased pulmonary flow (e.g., TOF, Tricuspid Atresia) and Acyanotic lesions with decreased systemic flow (e.g., Coarctation of Aorta, HLHS). * **PGE1 Side Effects:** The most common side effect is **Apnea** (requires readiness for intubation), followed by fever and flushing. * **TAPVC X-ray Sign:** "Snowman" or "Figure of 8" appearance (seen in Supracardiac TAPVC).

Question 137: All of the following are cyanotic heart diseases, EXCEPT?

A. Tetralogy of Fallot (TOF)
B. Patent Ductus Arteriosus (PDA) (Correct Answer)
C. Tricuspid Atresia
D. Eisenmenger's complex

Explanation: **Explanation:** Congenital Heart Diseases (CHD) are broadly classified into **Acyanotic** (Left-to-Right shunt) and **Cyanotic** (Right-to-Left shunt) based on whether deoxygenated blood enters the systemic circulation. **Why PDA is the correct answer:** **Patent Ductus Arteriosus (PDA)** is a classic **Acyanotic CHD**. In a PDA, the high-pressure aorta shunts oxygenated blood back into the lower-pressure pulmonary artery (Left-to-Right shunt). Since oxygenated blood is recirculated to the lungs rather than deoxygenated blood entering the systemic flow, the patient remains "pink" (non-cyanotic) unless complications like Eisenmenger syndrome develop later. **Analysis of Incorrect Options:** * **Tetralogy of Fallot (TOF):** The most common cyanotic CHD after infancy. It involves pulmonary stenosis and a VSD, leading to a Right-to-Left shunt and systemic cyanosis. * **Tricuspid Atresia:** A cyanotic CHD where the absence of the tricuspid valve necessitates an ASD and VSD/PDA for survival. Deoxygenated systemic blood must mix with pulmonary venous blood to reach the left side, causing cyanosis. * **Eisenmenger’s Complex:** This occurs when a long-standing acyanotic shunt (like VSD) causes pulmonary hypertension, leading to a **reversal of shunt** (Right-to-Left). Once the shunt reverses, the patient becomes clinically cyanotic. **High-Yield Clinical Pearls for NEET-PG:** * **The 5 T’s of Cyanotic CHD:** **T**OF, **T**ransposition of Great Arteries (TGA), **T**ricuspid Atresia, **T**runcus Arteriosus, and **T**otal Anomalous Pulmonary Venous Connection (TAPVC). * **PDA Murmur:** Characteristically described as a **"Machinery murmur"** (continuous) heard best at the left infraclavicular area. * **Drug of Choice:** **Indomethacin** or **Ibuprofen** (NSAIDs) are used to close a PDA in prematures; **Alprostadil (PGE1)** is used to keep it open in ductal-dependent cyanotic lesions.

Question 138: Which of the following conditions is typically not seen in adults?

A. Kawasaki disease (Correct Answer)
B. Henoch-Schönlein purpura
C. Susac syndrome
D. Takayasu arteritis

Explanation: **Explanation:** The correct answer is **Kawasaki Disease (KD)**. **Why Kawasaki Disease is the correct answer:** Kawasaki Disease is an acute, febrile, medium-vessel vasculitis that is almost exclusively a disease of **young children**. Approximately 85% to 90% of cases occur in children under the age of 5, with a peak incidence between 6 months and 2 years. While rare "adult-onset Kawasaki disease" cases are documented in literature, it is classically defined in pediatric medicine as a childhood condition. In the context of competitive exams like NEET-PG, it is the hallmark "pediatric" vasculitis. **Analysis of Incorrect Options:** * **Henoch-Schönlein Purpura (HSP):** Although it is the most common vasculitis in children, it frequently occurs in adults (often presenting with a more severe clinical course and higher risk of renal complications). * **Susac Syndrome:** This is a rare endotheliopathy characterized by the triad of encephalopathy, branch retinal artery occlusions, and sensorineural hearing loss. It typically affects young adults (ages 20–40), predominantly females. * **Takayasu Arteritis:** Known as "pulseless disease," this large-vessel vasculitis primarily affects the aorta and its branches. It is most commonly seen in young women under the age of 40. **NEET-PG High-Yield Pearls:** * **KD Diagnosis:** Requires Fever for ≥5 days + 4 out of 5 criteria (Conjunctivitis, Rash, Edema/Erythema of hands/feet, Adenopathy, Mucositis/Strawberry tongue). * **Complication:** Coronary artery aneurysms are the most dreaded complication; 2D-Echo is the investigation of choice. * **Treatment:** IVIG (2g/kg) + High-dose Aspirin. Note: This is one of the few instances where Aspirin is used in children despite the risk of Reye’s syndrome.

Question 139: What are the potential complications of a large patent ductus arteriosus (PDA)?

A. Endocardial valvulitis
B. Eisenmenger syndrome
C. Congestive heart failure (CHF)
D. All of the above (Correct Answer)

Explanation: **Explanation:** A Patent Ductus Arteriosus (PDA) is a persistent communication between the descending thoracic aorta and the pulmonary artery. In a large PDA, the high-pressure gradient causes a massive **left-to-right shunt**, leading to specific hemodynamic complications. **1. Why "All of the Above" is correct:** * **Congestive Heart Failure (CHF):** Large shunts cause volume overload of the left atrium and left ventricle (LV). This leads to LV dilatation and eventual failure, typically presenting in infancy with tachypnea, poor feeding, and failure to thrive. * **Eisenmenger Syndrome:** Chronic exposure of the pulmonary vasculature to high pressure and high flow leads to pulmonary hypertension and irreversible obstructive pulmonary vascular disease. Eventually, pulmonary pressure exceeds systemic pressure, causing the shunt to reverse (**right-to-left**), leading to differential cyanosis. * **Endocardial Valvulitis (Infective Endocarditis):** The high-velocity jet through the ductus causes turbulence that damages the endothelial lining of the pulmonary artery. This creates a nidus for bacterial vegetation, making PDA a significant risk factor for endarteritis/endocarditis. **Clinical Pearls for NEET-PG:** * **Murmur:** Classically a **continuous "machinery" murmur**, loudest at the left infraclavicular area (Gibson’s murmur). * **Pulse:** "Water-hammer" or bounding pulses due to a wide pulse pressure (diastolic runoff into the pulmonary artery). * **Drug of Choice:** **Indomethacin or Ibuprofen** (NSAIDs) are used to close a PDA in preterms by inhibiting prostaglandins. * **Differential Cyanosis:** In Eisenmengerized PDA, cyanosis is seen in the lower limbs but not the upper limbs (specifically the right arm), as the ductus joins the aorta distal to the left subclavian artery.

Question 140: A patient with a moderate ventricular septal defect (VSD) in chronic congestive cardiac failure (CCF) develops clubbing without cyanosis. What is the most likely diagnosis?

A. Shunt reversal
B. Long standing pulmonary edema
C. Subacute bacterial endocarditis (SABE) (Correct Answer)
D. Pulmonary arterial hypertension

Explanation: ### Explanation The correct diagnosis is **Subacute Bacterial Endocarditis (SABE)**. **1. Why SABE is the Correct Answer:** In a patient with a moderate VSD, the presence of **clubbing without cyanosis** is a classic clinical pointer toward SABE. While clubbing is frequently associated with cyanotic congenital heart diseases (e.g., Tetralogy of Fallot), in acyanotic conditions like VSD, it typically signifies a complication. SABE causes chronic inflammation and the release of growth factors (like PDGF) from platelet-fibrin vegetations, leading to digital clubbing. Since the shunt remains left-to-right, the patient remains acyanotic. **2. Why Other Options are Incorrect:** * **Shunt Reversal (Eisenmenger Syndrome):** This occurs when pulmonary hypertension becomes severe enough to reverse the shunt (right-to-left). While this causes clubbing, it **must** be accompanied by central cyanosis. * **Long-standing Pulmonary Edema:** Chronic congestion leads to dyspnea and rales but does not cause digital clubbing. * **Pulmonary Arterial Hypertension (PAH):** PAH itself does not cause clubbing unless it progresses to shunt reversal (Eisenmenger syndrome), at which point cyanosis would be mandatory. **3. High-Yield Clinical Pearls for NEET-PG:** * **VSD & SABE:** Small to moderate VSDs have a higher risk of SABE than large VSDs because the high-velocity jet creates more turbulence and endocardial damage. * **Clubbing in Cardiology:** Always differentiate between **Cyanotic Clubbing** (TOF, Eisenmenger) and **Acyanotic Clubbing** (SABE, Atrial Myxoma). * **Most Common Site for SABE in VSD:** Vegetations usually form on the **tricuspid valve** or the margins of the defect on the right ventricular side due to the "jet effect." * **Prophylaxis:** Current guidelines do not recommend routine antibiotic prophylaxis for uncomplicated VSDs unless there is a prior history of endocarditis or prosthetic material used in repair.

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Congenital Heart Diseases: Cyanotic

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Congenital Heart Diseases: Acyanotic

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Rheumatic Heart Disease

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Kawasaki Disease

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Infective Endocarditis

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Myocarditis and Cardiomyopathies

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Arrhythmias in Children

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Heart Failure in Children

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Pulmonary Hypertension

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Systemic Hypertension

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Dyslipidemia in Children

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Cardiac Evaluation and Diagnostics

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Cardiology — MCQs

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