Heart Failure in Children
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Direct answer
Heart failure in a child is a clinical syndrome read off the feeding mat rather than the treadmill: an infant who takes longer than 30 minutes per feed, sweats on the forehead while sucking, breathes at over 60 per minute and has an enlarging liver is in heart failure, whatever the cause. The cause is age-locked — duct-dependent congenital obstruction and hypoplastic left heart in the first week, coarctation as the duct closes, large left-to-right shunts (VSD, PDA, AVSD) at six to eight weeks as pulmonary resistance falls, then myocarditis and cardiomyopathy beyond a year. Treatment rests on diuretics, afterload reduction and inotropic support while the definitive fix — usually surgical — is arranged.
What you must remember
- Infant red flags: feeds longer than 30 minutes or sleep mid-feed, sweating on the brow during feeds, tachypnoea above 60, subcostal retractions, failure to thrive, and a gallop rhythm.
- The most reliable sign of worsening failure in an infant is an enlarging, tender liver — oedema and raised jugular venous pressure are late and hard to elicit in babies.
- Causes by age: first week — hypoplastic left heart syndrome, obstructed total anomalous pulmonary venous connection, duct-dependent lesions; one to six weeks — coarctation as the duct closes; six weeks to six months — large VSD, PDA, AVSD; beyond a year — myocarditis, dilated cardiomyopathy, rheumatic valve disease, anaemia.
- Physiology point worth a mark: left-to-right shunts produce heart failure only after pulmonary vascular resistance falls, which is why a large VSD is silent at birth and fails at two months.
- The Ross classification grades infant failure from feeding and respiratory indices — the infant NYHA equivalent.
- Investigations: chest radiograph (cardiothoracic ratio above 0.55 in infants, pulmonary venous congestion), ECG, echocardiography for anatomy and function, and BNP where available.
- Drug backbone: furosemide 1–2 mg/kg/dose, spironolactone, ACE inhibitors for afterload reduction, and digoxin — with paediatric dosing vigilance.
- Acute severe failure or cardiogenic shock: intravenous inotropes (milrinone, dopamine), oxygen and careful fluid management in intensive care; arrhythmia-driven failure needs rhythm control.
- Nutritional therapy is real therapy: high-calorie feeds up to 150 per cent of requirements, because these infants burn calories breathing.
- The cause decides the cure: prostaglandin E1 in duct-dependent obstruction, surgical repair of the defect, and disease-specific therapy for myocarditis, anaemia or arrhythmia.
- A forgotten Indian cause: severe chronic anaemia (high-output failure) and uncorrected shunts presenting late with advanced pulmonary vascular disease — echocardiography before it is too late.
A typical exam case
A ten-week-old ex-term infant has ten days of poor feeding and fast breathing: feeds take 40 minutes, she sweats over the forehead midway through, and she has crossed down two weight centiles. Respiratory rate is 68, liver span 7 cm, and a pansystolic murmur fills the lower left sternal edge — the textbook large VSD failing at the expected age. Recognise failure from the feeding history, confirm anatomy by echo, stabilise with furosemide and an ACE inhibitor while enriching calories, and refer for surgical closure rather than waiting for "growth".
The second scenario is the two-week-old who suddenly becomes grey and shocked with absent femoral pulses: coarctation with ductal closure — start prostaglandin E1 immediately, correct acidosis, and involve surgery. The third is the four-year-old with tachypnoea, a big heart on film and poor function on echo with normal anatomy after a viral prodrome: myocarditis — supportive intensive care, diuretics and inotropes with careful volume management. Each age carries its own answer sheet.
Where students slip
Importing adult symptomatology is the cardinal error: children rarely report orthopnoea, and waiting for oedema misses the diagnosis — feeding behaviour and liver size are the currency. The second error is ignoring the timeline: calling a duct-dependent lesion "failure to thrive" at two weeks, or expecting a large VSD to fail in the first week rather than at two months, loses the physiology mark. Third, fluid-restriction reflexes: infants with failure need more calories per kilogram, not dilute feeds — nutrition is therapy. And the dangerous slip is delaying prostaglandin in the shocked neonate while waiting for echocardiography.
Frequently asked questions
How does heart failure present in an infant?
As feeding difficulty — long feeds with sweating on the forehead, tachypnoea over 60 per minute, poor weight gain, hepatomegaly and a gallop — rather than exertional dyspnoea or oedema seen in adults.
Why do large left-to-right shunts cause heart failure at six to eight weeks and not at birth?
Because pulmonary vascular resistance is high at birth, limiting shunt flow; as it falls over the first weeks, the shunt enlarges and pulmonary overcirculation floods the heart into failure.
What is the Ross classification?
A paediatric heart failure severity score for infants built on feeding behaviour and respiratory rate — the infant equivalent of the NYHA functional class — used to grade and follow response to therapy.
Which drugs form the medical backbone of paediatric heart failure?
Loop diuretics (furosemide), aldosterone antagonists, ACE inhibitors, and digoxin, with intravenous inotropes such as milrinone for acute decompensation.