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PE22.1-11 | Cardiovascular System — Practice Quiz
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A 6-month-old infant is brought with breathlessness during feeds and recurrent chest infections. Examination shows a harsh pansystolic murmur at the left lower sternal border. Chest X-ray reveals cardiomegaly with increased pulmonary vascular markings. Which haemodynamic change best explains the pulmonary plethora in this infant?
VSD causes a left-to-right shunt; oxygen-rich blood recirculates through the pulmonary circuit, increasing pulmonary blood flow and producing vascular plethora on CXR.
Acyanotic CHD with L-to-R shunt (VSD, ASD, PDA) increases pulmonary blood flow producing plethora on CXR; the larger the shunt the greater the cardiomegaly.
R-to-L shunts cause cyanosis, not pulmonary plethora. LVOTO and mitral stenosis are not the primary mechanisms here.
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A 2-year-old with a large VSD is noted to have progressive cyanosis over the past 3 months. Echocardiography now shows right ventricular hypertrophy and reversal of the shunt direction. Which complication has occurred?
Eisenmenger syndrome is the irreversible pulmonary vascular obstructive disease arising from a long-standing L-to-R shunt; pulmonary pressure equalises or exceeds systemic pressure causing shunt reversal and cyanosis.
Any large L-to-R shunt (VSD, ASD, PDA) can cause Eisenmenger syndrome if uncorrected; early repair prevents this irreversible complication.
TOF is a congenital defect with specific anatomy not arising from a VSD. IE causes fever/emboli. Pulmonary atresia is a structural abnormality, not a complication of isolated VSD.
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A 3-year-old boy is brought to casualty having a severe hypercyanotic episode: he is squatting on his own, deeply cyanosed, and screaming. His diagnosis is Tetralogy of Fallot. Which is the MOST appropriate immediate management?
Tet-spell management: knee-chest position increases SVR and reduces R-to-L shunt; morphine blunts sympathetic drive; propranolol IV relieves infundibular spasm and slows HR, all reducing the dynamic obstruction.
Four components of TOF: VSD, overriding aorta, RVOTO (infundibular PS), RVH. Tet-spell management focuses on increasing SVR, reducing infundibular spasm (knee-chest, morphine, propranolol, oxygen, bicarbonate if acidotic).
Digoxin and frusemide are used in cardiac failure, not tet-spells. Atropine increases HR making the dynamic infundibular obstruction worse.
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A 5-day-old neonate with suspected transposition of great arteries has SpO₂ of 55% despite 100% oxygen. While awaiting balloon atrial septostomy, which pharmacological agent maintains ductal patency?
PGE1 (alprostadil) 0.05–0.1 mcg/kg/min IV infusion maintains or reopens the ductus arteriosus in duct-dependent congenital heart disease (TGA, PA, critical PS, HLHS), allowing mixing and maintaining systemic oxygenation until definitive intervention.
In duct-dependent cyanotic CHD (TGA, pulmonary atresia, critical PS), PGE1 infusion at 0.05–0.1 mcg/kg/min is life-saving while awaiting interventional or surgical repair; monitor for apnoea.
Indomethacin is a prostaglandin inhibitor used to CLOSE a PDA — the opposite of what is needed here. Digoxin and furosemide have no role in acute ductal management.
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A 4-month-old infant with large VSD presents with tachypnoea, hepatomegaly, gallop rhythm, and poor weight gain. Which weight-based drug regimen is MOST appropriate for initial medical management of cardiac failure?
Paediatric cardiac failure is managed with digoxin (positive inotropy) 5–10 mcg/kg/day + furosemide (diuretic) 1–2 mg/kg/day, both weight-based. ACE inhibitors (captopril) may be added as afterload reduction.
Paediatric cardiac failure treatment is weight-based: digoxin 5–10 mcg/kg/day + furosemide 1–2 mg/kg/day ± captopril; never prescribe adult fixed doses to infants or children.
Propranolol alone is not first-line for cardiac failure (it is used for tet-spells, SVT, thyrotoxicosis). High-dose IV furosemide monotherapy is not standard; adult-dose tablets are never used in infants.
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A 7-year-old boy from a low-income family presents with migratory arthritis, carditis, Sydenham chorea, and subcutaneous nodules 3 weeks after a sore throat. ASO titre is elevated. Which set of diagnostic criteria applies?
The 2015 Revised Jones Criteria (AHA) have two tiers — high-risk (developing nations with high ARF prevalence, like India) and low-risk populations — with lower echocardiographic thresholds in high-risk settings. The Modified Duke Criteria are for infective endocarditis.
ARF diagnosis uses 2015 Revised Jones Criteria; India is a high-risk country, allowing lower thresholds (polyarthralgia as major). Evidence of preceding GAS infection (elevated ASO, throat culture) is essential alongside ≥2 major or 1 major + 2 minor criteria.
The original 1944 Jones criteria are outdated. WHO 2004 criteria apply to recurrent ARF (not first diagnosis). The Modified Duke Criteria are used for infective endocarditis.
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A child diagnosed with Acute Rheumatic Fever has been prescribed secondary prophylaxis. Which is the recommended regimen for a child at HIGH RISK of recurrence (e.g., established rheumatic heart disease)?
Benzathine penicillin G 1.2 MU IM (600,000 U if <27 kg) every 3–4 weeks is the gold-standard secondary prophylaxis; duration is at least 10 years or until age 25 (whichever is longer) for those with carditis/established RHD. Aspirin treats arthritis/fever, not prophylaxis.
Secondary prophylaxis of ARF: benzathine penicillin G IM every 3–4 weeks; minimum 10 years or to age 25 for carditis; no aspirin for chorea (use haloperidol/sodium valproate); primary streptococcal pharyngitis treatment = penicillin V for 10 days.
Amoxicillin is used for primary treatment of streptococcal pharyngitis. Aspirin is used for anti-inflammatory relief (arthritis), NOT prophylaxis; notably aspirin is NOT used for chorea. No prophylaxis is incorrect — recurrences cause progressive valve damage.
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A 9-year-old with congenital heart disease develops persistent fever for 3 weeks, new-onset regurgitant murmur, and splinter haemorrhages. Blood cultures yield viridans streptococci on 3 of 3 sets. By the Modified Duke Criteria, what is the classification?
The Modified Duke Criteria: DEFINITE IE = 2 major, or 1 major + 3 minor, or 5 minor. Major criteria: ≥2 positive blood cultures with typical organism (viridans streptococci = typical); new valve regurgitation on echo. Minor: fever ≥38°C, predisposing condition (CHD), vascular phenomena (splinter haemorrhages). Here: 2 major criteria (bacteraemia + new murmur implies echo-positivity) = Definite IE.
Modified Duke Criteria: Major = typical organism in 2+ cultures OR echocardiographic evidence (vegetation/abscess/new dehiscence/new valvular regurgitation); Minor = fever, predisposing condition, vascular phenomena, immunological phenomena, blood culture not meeting major. DEFINITE = 2 major, or 1 major + 3 minor, or 5 minor.
The criteria are designed to classify even when echo is not yet done; 3/3 positive blood cultures with typical organisms alone is a major criterion.
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During a school health screening, a 12-year-old boy's blood pressure is found to be 136/86 mmHg on repeated measurements. His BMI is at the 85th percentile. According to paediatric hypertension guidelines, which statement is CORRECT?
Paediatric hypertension is defined as BP ≥95th percentile for age, sex, and height on at least 3 separate occasions (using age-sex-height normative tables, e.g., NHBPEP/AAP 2017 tables). The adult 140/90 threshold does not apply to children.
Paediatric hypertension: BP ≥95th percentile for age/sex/height on ≥3 occasions (AAP 2017 normative tables). First-line management is lifestyle modification; antihypertensives for Stage 2 or target-organ damage. Renal causes (renovascular, CKD) must be excluded in children.
Adult BP thresholds (140/90 or 160/100) do NOT apply to children; paediatric norms are age-, sex-, and height-specific. A single reading never warrants pharmacotherapy.
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While performing cardiovascular examination in a 3-year-old, the examiner finds a pansystolic murmur at the left lower sternal border (grade 3/6), with a thrill. The child is acyanotic. Chest X-ray shows cardiomegaly and pulmonary plethora. The ECG shows left ventricular hypertrophy. Which single investigation will BEST confirm the diagnosis and guide surgical planning?
2D echocardiography with colour Doppler is the investigation of choice for CHD: it confirms defect anatomy, quantifies shunt direction and size, assesses ventricular function, and measures PA pressures — all necessary for surgical planning.
2D echocardiography with colour Doppler is the cornerstone investigation for CHD in children; it defines anatomy, quantifies shunts, measures PA pressures, and guides timing of surgery or catheter intervention.
Cardiac catheterisation was the gold standard historically but is now reserved for haemodynamic measurement when echo is inconclusive. CTPA is for pulmonary embolism. Radionuclide scans are not first-line for structural CHD.
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