PE22.1-11 | Cardiovascular System — Graded Quiz

In PDA, blood runs from the aorta to pulmonary artery throughout diastole (continuous murmur). Diastolic run-off causes a low diastolic BP, widening the pulse pressure and producing bounding pulses.

PDA hallmarks: continuous machinery murmur (left infraclavicular), wide pulse pressure, bounding pulses — all due to aortic run-off in diastole; indomethacin closes PDA in preterm neonates; surgical/catheter ligation in older children.

Increased SVR raises diastolic BP (narrow pulse pressure). Mitral regurgitation and RV failure are not the mechanism of wide pulse pressure in PDA.

In ASD, the inter-atrial communication equalises right and left atrial pressures; RV filling does not vary with respiration (normally RV fills more on inspiration, advancing P2 towards A2). The fixed equalization means P2 stays delayed equally throughout the respiratory cycle: fixed split S2.

Fixed split of S2 = pathognomonic of ASD; due to equalization of LA/RA pressures preventing respiratory variation in RV filling → constant delay of P2 relative to A2.

Fixed split is not due to increased PVR (that eventually causes P2 to equal or precede A2 in Eisenmenger). LBBB causes paradoxical splitting. RV dysfunction causes delayed P2 that varies with respiration.

Propranolol IV 0.1 mg/kg (over 10 minutes) relieves infundibular spasm in TOF by reducing catecholamine-mediated dynamic RVOTO and slowing heart rate, both of which reduce the R-to-L shunt and improve oxygenation. Sodium bicarbonate and phenylephrine (increasing SVR) are adjuncts.

Tet-spell stepwise management: knee-chest position → oxygen → morphine 0.1–0.2 mg/kg IV → propranolol 0.1 mg/kg IV → IV fluids → NaHCO₃ for acidosis → phenylephrine if refractory. Oral propranolol 1–4 mg/kg/day prevents recurrence until corrective surgery.

Furosemide worsens pre-load depletion (hypovolaemia) making tet-spells worse. Digoxin increases contractility and worsens dynamic obstruction. Calcium gluconate has no role in tet-spells.

In d-TGA, the aorta arises from the RV (carries deoxygenated blood) and the PA from the LV (carries oxygenated blood) — the circulations run in parallel, not in series. Without a point of mixing (PFO, PDA, or VSD), oxygenated and deoxygenated blood never intermix and the neonate cannot survive.

d-TGA: aorta from RV, PA from LV → parallel circulations → life-incompatible without mixing. Management: PGE1 to maintain ductus, balloon atrial septostomy (Rashkind) for immediate stabilization, arterial switch operation (Jatene) within first 2 weeks.

The aorta does carry deoxygenated blood, but it is mixing (not quantity) that determines viability. LV function is normal at birth. Ductus size is not the core issue — even a small mixing lesion provides some oxygenation.

Captopril (ACE inhibitor) reduces afterload and neurohormonal activation in paediatric cardiac failure; starting dose 0.1–0.5 mg/kg/dose 2–3 times daily titrated up. ACE inhibitors improve cardiac remodelling and are the standard third agent after digoxin and diuretic.

Paediatric cardiac failure: digoxin (inotrope) + furosemide (preload) + captopril (afterload); spironolactone for hypokalaemia. Dose all agents by weight. Monitor renal function and electrolytes with ACE inhibitors and diuretics.

Spironolactone is an aldosterone antagonist/diuretic useful for hypokalaemia or as adjunct diuresis but is not the primary afterload-reducing agent. Beta-blockers (atenolol) and calcium channel blockers (nifedipine) are not first-line for cardiac failure in infants.

Aspirin 50–100 mg/kg/day (max 4–6 g/day) in 4 divided doses is used for arthritis and mild-moderate carditis; corticosteroids (prednisolone 2 mg/kg/day) are used for severe carditis with cardiac failure. For Sydenham chorea: haloperidol or sodium valproate are drugs of choice; aspirin is NOT effective and should not be used for chorea.

ARF anti-inflammatory: aspirin 50–100 mg/kg/day (arthritis, mild carditis); prednisolone 2 mg/kg/day (severe carditis/cardiac failure). Sydenham chorea = haloperidol or sodium valproate; aspirin is NOT used for chorea.

Aspirin is effective for arthritis/carditis; ibuprofen has not been studied as well. Aspirin is INEFFECTIVE for Sydenham chorea (and contraindicated in children due to Reye's syndrome risk for viral co-infections); chorea usually self-resolves but may be treated with haloperidol or valproate.

HACEK organisms are fastidious, slow-growing gram-negative rods that are the classic cause of culture-negative endocarditis, requiring prolonged incubation (2–3 weeks) and special media. They account for a significant proportion of culture-negative IE in children.

Modified Duke Criteria: culture-negative IE triggers workup for HACEK organisms, Coxiella, Bartonella, and Candida. Minimum 3 blood cultures from different sites before antibiotics; if negative after 5 days, request prolonged incubation and serological testing.

Streptococcus viridans is the most common cause of IE overall and grows readily in standard blood cultures. S. aureus is rapidly growing. Enterococcus grows in standard cultures.

Stage 1 HTN in an obese adolescent without target-organ damage or secondary cause identified should initially be managed with lifestyle modification (weight reduction, DASH diet with sodium restriction, aerobic exercise ≥30–60 min/day) for 4–6 weeks before pharmacotherapy is considered.

Paediatric Stage 1 HTN: lifestyle modification first (weight, salt, exercise); pharmacotherapy if lifestyle fails, Stage 2 HTN, symptomatic, or target-organ damage. ACE inhibitors/ARBs (especially with CKD/diabetes), calcium-channel blockers, or thiazides are first-choice agents.

Immediate pharmacotherapy without a lifestyle trial is not indicated for Stage 1 HTN without symptoms. IV labetalol is for hypertensive emergencies with end-organ damage. Renal biopsy is not the next step — non-invasive renal artery Doppler/MRA precedes biopsy.

Cardiothoracic ratio (CTR) = maximum transverse cardiac diameter divided by maximum transverse thoracic diameter on a PA CXR. A CTR >0.5 in children >2 years suggests cardiomegaly. In infants <2 years, the normal CTR can be up to 0.55 due to the relative thymic size and thoracic shape.

CTR >0.5 on PA CXR = cardiomegaly in children >2 years; normal CTR in infants can be up to 0.55. Always obtain PA (not AP) films for accuracy; supine/AP positioning artificially magnifies the cardiac shadow.

The cardiac silhouette and sternal-edge rules are imprecise. The standard is the CTR. In infants the normal CTR upper limit is 0.55, not 0.5.

Right ventricular dominance is NORMAL in the paediatric ECG: at birth, the RV is dominant (due to equal pulmonary and systemic resistance in fetal life); right-axis deviation and a dominant (tall) R wave in V1 are normal up to ~3–6 months, gradually transitioning to left-axis dominance by school age. This is the classic paediatric-vs-adult ECG difference.

Key paediatric ECG differences from adult: RV dominance (tall R in V1, right-axis deviation) normal in infants; shorter intervals (HR faster → shorter PR, QRS, QT); right-axis shifts to left-axis by ~3–6 years. RVH in an older child with CHD is a red flag.

QTc 0.44 s is the upper limit of normal in children (same as adults). P-wave duration >0.12 s and PR >0.20 s are abnormal at any paediatric age (these suggest LAE and 1st-degree AVB respectively).