Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Heart failure in infants and children
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Low-output or respiratory decompensation
Severe recession, hypoxaemia, gallop rhythm, hepatomegaly, weak pulses, altered consciousness, oliguria, hypotension or rising lactate indicates decompensated heart failure or cardiogenic shock and can deteriorate rapidly.
Action: Use ABCDE, call senior paediatric, cardiology and intensive-care teams, minimise distress, monitor continuously and obtain IV or IO access. Support ventilation, correct hypoglycaemia, obtain gas, lactate, ECG, chest radiograph and urgent echocardiography, and treat arrhythmia, sepsis or duct-dependent disease. Give fluid only in small reassessed aliquots when preload deficiency is plausible; use diuretic, vasoactive or mechanical support through specialist haemodynamic guidance.
Overview
Recognise age-specific heart failure, distinguish congestion from shock, identify congenital, myocardial and rhythm causes, and deliver stabilisation, nutritional support and specialist treatment with safe weight-based prescribing.
Cardiac output equals heart rate multiplied by stroke volume. Infants have limited ability to increase stroke volume, so severe bradycardia, sustained tachycardia and loss of feeding reserve can reduce output quickly.
Pressure overload occurs with aortic stenosis, coarctation or systemic hypertension; volume overload occurs with large shunts or regurgitant valves; intrinsic pump failure follows cardiomyopathy, myocarditis, ischaemia or metabolic disease.
Pulmonary overcirculation from a large VSD or PDA typically becomes symptomatic after pulmonary resistance falls. Duct-dependent left-sided obstruction instead presents during ductal closure with systemic shock and may have little pulmonary congestion initially.
Neurohormonal responses increase sympathetic tone, salt retention and vasoconstriction to preserve pressure. They temporarily support output but raise afterload and congestion, increasing respiratory and myocardial work.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
Infant heart-failure clue
A 2-month-old takes 45 minutes to finish each feed, pauses to breathe, sweats over the forehead and has dropped two weight centiles. Which additional finding most strongly supports heart failure?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Infants reveal exercise intolerance during feeding. Suck-swallow-breathe coordination fails, feeds lengthen, sweat appears and intake falls while metabolic demand rises. Serial growth is therefore a functional cardiac marker.
Hepatomegaly is a sensitive sign of systemic venous congestion in children. Peripheral oedema and raised jugular pressure are more common later or with chronic right-sided failure.
Tachypnoea has a broad differential including bronchiolitis, pneumonia, sepsis, anaemia and metabolic acidosis. Cardiac clues include feeding relation, gallop, murmur, hepatomegaly, abnormal pulses, cardiomegaly and poor growth.
An ECG may identify SVT, heart block, hypertrophy or myocardial injury but cannot assess output. Chest radiography shows heart size and pulmonary flow yet can be normal in early myocarditis or low-flow obstruction.
BNP or NT-proBNP can support congestion and trend response, but age, renal function, sepsis and congenital physiology affect concentration. A biomarker cannot replace echocardiography or bedside perfusion assessment.
Diuretics relieve fluid-related symptoms without correcting the cause. Excess diuresis can reduce preload, renal perfusion and growth, particularly in preload-dependent congenital circulation, so daily clinical and biochemical response matters.
Feeding plans balance respiratory safety and calories. Concentrating milk changes water and solute delivery and requires a dietitian; forcing oral feeds through tachypnoea risks aspiration and fatigue.
Advanced failure may need inotropes, vasopressors, non-invasive or invasive ventilation, extracorporeal support or ventricular assist devices. The correct agent depends on blood pressure, ventricular function and vascular resistance, so specialist haemodynamic decisions are essential.
Key points
Heart failure is inability of the cardiovascular system to meet metabolic needs without excessive filling pressures; children more often present with feeding, breathing, growth and perfusion problems than ankle oedema.
In early infancy, major causes include large left-to-right shunts, critical obstruction, cardiomyopathy, myocarditis and sustained SVT; in older children add repaired congenital disease, renal or systemic hypertension and acquired myocardial disease.
Infant features are tachypnoea, recession, prolonged or interrupted feeds, forehead sweating, poor weight gain and hepatomegaly. Older children report fatigue, reduced exercise, breathlessness, abdominal discomfort, oedema or palpitations.
Differentiate congestion from low output. Crackles, hepatomegaly and venous or pulmonary fluid indicate congestion; cool limbs, oliguria, altered mentation and lactate indicate inadequate perfusion, and both can coexist.
Initial assessment includes age-specific observations, four-limb pulses and pressure, saturation, weight trajectory, ECG, chest radiograph, blood count, electrolytes, renal, liver, glucose, gas, lactate and urgent echocardiography when unwell.
Echocardiography is the key structural and functional test, defining anatomy, ventricular function, valve disease, pressure estimates, shunts and pericardial fluid; a normal ejection fraction does not exclude abnormal filling or circulation-specific failure.
Aetiology
01
Congenital structural load
Large shunts, valve regurgitation, outflow obstruction and complex single-ventricle physiology create volume, pressure or mixing burdens that vary with age.
02
Myocardial disease
Dilated, hypertrophic or restrictive cardiomyopathy, myocarditis, neuromuscular and metabolic disorders directly impair contraction, relaxation or ventricular compliance.
03
Rhythm disturbance
Incessant SVT, atrial tachycardia, complete heart block or ventricular arrhythmia can reduce filling and output or cause reversible cardiomyopathy.
04
Acquired systemic stress
Sepsis, severe anaemia, renal failure, hypertension, endocrine disease and cardiotoxic treatment can precipitate failure in a normal or vulnerable heart.
Pathophysiology
1
Reduced forward output
Impaired contraction, filling, valve flow or rhythm lowers organ perfusion, producing fatigue, cool limbs, oliguria, acidosis and altered consciousness.
2
Elevated filling pressure
Back-pressure raises pulmonary or systemic venous hydrostatic pressure, leading to tachypnoea, oedema, hepatomegaly and feed intolerance.
3
Compensatory neurohormones
Sympathetic and renin-angiotensin activation preserves pressure and volume initially but increases afterload, sodium retention and myocardial oxygen demand.
4
Nutrition-work mismatch
Respiratory and cardiac work raises energy needs while tachypnoea and fatigue reduce safe intake, causing growth failure and weaker recovery reserve.
5
Age-limited cardiac reserve
Infants rely strongly on heart rate for output and tolerate extreme tachycardia, bradycardia or rapid loading changes poorly.
Clinical features and red flags
Infant feeding failure
Feeds become prolonged and interrupted by breathing, forehead sweat and exhaustion, with reduced volumes and poor centile gain.
Congestion
Tachypnoea, recession, crackles, hepatomegaly, gallop and oedema indicate raised pulmonary or systemic venous pressure.
Low output
Cool mottled limbs, weak pulses, prolonged refill, oliguria, lethargy and lactate elevation precede late hypotension.
Hypotension is a late sign in children; cool peripheries, weak pulses, prolonged refill, oliguria and rising lactate reveal low output earlier.
A newborn with shock or weak femoral pulses may have duct-dependent obstruction and needs prostaglandin-pathway assessment rather than routine heart-failure treatment alone.
Investigations
01Initial ABCDE, four-limb pulse and growth assessmentFirst step
Why
Separate congestion, low output, cyanosis and nutritional burden and detect duct-dependent obstruction.
Interpretation and limitations
Serial trends and age-specific values determine urgency; hypotension is not required for shock.
02Twelve-lead ECG and continuous rhythm monitoring
Why
Identify tachyarrhythmia, bradycardia, hypertrophy, conduction disease and injury patterns.
Interpretation and limitations
Document the rhythm before treatment when possible, but do not delay cardioversion in an unstable child.
03Blood gas, lactate and laboratory profile
Why
Assess perfusion and search for anaemia, infection, electrolyte, renal, hepatic, thyroid or metabolic drivers.
Interpretation and limitations
Rising lactate or organ injury marks severe delivery failure; results also determine medicine and fluid safety.
04Chest radiograph
Why
Assess cardiac silhouette, pulmonary vascularity, oedema, effusion and respiratory alternatives.
Interpretation and limitations
Cardiomegaly supports chronic volume or pump failure, but a normal silhouette does not exclude acute myocarditis or obstruction.
Differential diagnosis
01
Respiratory infection
Coryza, wheeze, crackles and fever suggest infection, but hepatomegaly, cardiomegaly or a gallop warrants parallel cardiac evaluation.
02
Sepsis
Shock, tachycardia and organ dysfunction overlap; cultures, inflammatory assessment and early antibiotics are required when infection remains possible.
03
Anaemia
Low oxygen-carrying capacity produces tachycardia and high-output failure; a full blood count identifies this treatable driver.
04
Renal or hepatic disease
Fluid retention and oedema can arise outside the heart, distinguished by urine, protein, albumin, renal and liver evaluation plus echocardiography.
05
Feeding or metabolic disorder
Aspiration, reflux and inborn errors cause poor growth or tachypnoea but may also trigger decompensation in occult cardiac disease.
Management
01DecompensatedSupport output and breathingFirst stepThe child has respiratory failure, poor perfusion, acidosis, altered consciousness or hypotension.+
1Call intensive-care and cardiology support, monitor continuously and provide airway and ventilation assistance.
2Obtain ECG, gas, lactate and urgent echocardiography while treating hypoglycaemia, sepsis, arrhythmia or duct-dependent disease.
3Use small reassessed fluid, diuretic or vasoactive treatment according to congestion, preload and ventricular physiology rather than a generic shock bolus sequence.
02CongestedRelieve fluid safelyPulmonary or systemic congestion is present with sufficient perfusion.+
1Confirm weight, renal function, sodium and potassium and identify the structural or myocardial cause.
2Use specialist-prescribed furosemide and monitor urine, weight, breathing and biochemical response.
Complications
01
Cardiogenic shock
Progressive output failure causes acidosis, renal and hepatic injury, cerebral hypoperfusion and cardiac arrest if support is delayed.
02
Respiratory failure
Pulmonary oedema, effusions and fatigue can require non-invasive or invasive ventilation while underlying haemodynamics are corrected.
03
Faltering growth and development
Chronic calorie deficit, hypoxaemia and repeated hospital admission impair somatic growth, feeding skills and longer-term neurodevelopment.
04
Arrhythmia and thrombosis
Dilated chambers, low flow and central venous lines increase tachyarrhythmia and intracardiac or venous thrombus risk.
05
Medicine toxicity
Diuretics and vasoactive drugs can cause electrolyte loss, renal injury, hypotension or rhythm disturbance without close weight-based monitoring.
Monitoring and follow-up
In acute care, trend work of breathing, saturation, pulse quality, blood pressure, urine output, mental state, gas and lactate at a frequency matched to instability.
Measure daily weight and strict fluid balance during decongestion, interpreting weight loss alongside perfusion and renal function.
Check urea, creatinine, sodium and potassium after furosemide initiation or dose change and during vomiting, diarrhoea or reduced intake.
Plot growth and review actual calories, feed time and route at every chronic visit; record developmental and oral-motor progress.
Use serial echocardiography, ECG and rhythm monitoring according to cause, and reassess sooner with new symptoms or medicine intolerance.
Ensure a written emergency, medicine and follow-up plan and coordinate primary care, cardiac nursing, dietetics, pharmacy and congenital transition.
Special situations
Feeding is infant exercise
Sweating, tachypnoea and exhaustion during milk intake are the infant equivalent of exertional limitation and should be observed directly.
Hepatomegaly beats ankle oedema
The liver enlarges early with systemic venous pressure, while peripheral oedema may be absent in significant childhood heart failure.
Shock precedes hypotension
Children maintain pressure through vasoconstriction, so cool limbs, oliguria and lactate reveal inadequate output before a cuff reading falls.
Tachycardia may be the cause
Incessant SVT can create ventricular dysfunction that improves after durable rhythm control, making an ECG essential.
Do not wait for hypotension before diagnosing cardiogenic shock.
02
Do not label tachypnoea bronchiolitis without examining pulses, liver, growth and heart rhythm.
03
Do not give repeated large fluid boluses to a congested child without haemodynamic reassessment.
04
Do not diurese a duct-dependent or preload-dependent circulation blindly.
05
Do not use adult tablet doses or interchange oral-liquid concentrations by volume.
06
Do not force oral feeds through severe tachypnoea or fatigue.
07
Do not judge response by breathing alone while weight, urine, electrolytes or perfusion worsens.
08
Do not delay advanced-centre referral until multiorgan failure is established.
Acute management is cause and physiology directed: ventilation support, careful preload, diuresis for congestion, rhythm conversion, treatment of infection or myocarditis and urgent repair of critical structural disease.
Licensed oral Frusol paediatric dosing is 1–3 mg/kg once daily, maximum 40 mg/day, titrated to response by the specialist; formulation strength, renal function, sodium and potassium require checking.
Nutrition is treatment: use energy-dense feeds, small frequent volumes, nasogastric support and dietetic input when safe oral intake cannot meet growth requirements.
Chronic disease-modifying medicines in children depend on diagnosis, ventricular physiology, age and evidence and should be initiated and titrated by paediatric heart-failure specialists rather than copied from an adult pathway.
Escalate refractory failure to a specialist centre for advanced imaging, catheter haemodynamics, genetic or metabolic evaluation, mechanical circulatory support and transplant assessment.
A sustained tachyarrhythmia can both imitate and cause heart failure; obtain a rhythm strip before assuming all tachycardia is compensatory.
Chest pain, troponin elevation, ventricular arrhythmia or sudden deterioration after viral illness raises myocarditis and requires intensive cardiac monitoring.
Faltering growth, feed duration over roughly 30 minutes, diaphoresis or recurrent admissions represents clinically important chronic burden even when resting saturation is normal.
05
Urgent paediatric echocardiography
Why
Define anatomy, systolic and diastolic function, valves, shunts, pressures and pericardial fluid.
Interpretation and limitations
This directs cause-specific therapy; circulation-specific failure can be important despite a conventionally preserved ejection fraction.
06Advanced aetiology testing
Why
Investigate cardiomyopathy, myocarditis, metabolic or genetic disease when initial anatomy does not explain failure.
Interpretation and limitations
Cardiac MRI, genetics, metabolic assays, catheterisation or biopsy are specialist-selected because timing and yield depend on phenotype.
3
Reduce or pause treatment and reassess when hypotension, oliguria, electrolyte disturbance or excessive weight loss suggests over-diuresis.
03NutritionMake growth a treatment targetFeeding work or fluid limits prevent adequate weight gain.+
1Observe a feed and assess swallow-breathe coordination, duration, volume and aspiration risk.
2Use small frequent energy-dense feeds with paediatric dietetic input and nasogastric support when oral intake is unsafe or inadequate.
3Track weight, length, head growth, electrolytes and fluid balance and adjust around surgery or decompensation.
1Transfer early to a paediatric heart-failure and congenital centre for haemodynamic and aetiological definition.
2Consider inotrope, ventilation, extracorporeal or ventricular-assist support according to physiology and reversibility.
3Initiate transplant assessment alongside genetic, metabolic, rehabilitation and family support when recovery or repair is unlikely.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Relieves pulmonary or systemic congestion by promoting sodium and water excretion while the underlying structural, rhythm or myocardial cause is treated.
Furosemide oral solution (Frusol 20 mg/5 mL)
Licensed paediatric oral dose is 1–3 mg/kg once daily, titrated to the required response, with a maximum total dose of 40 mg/day; administer in the morning where possible and measure the correct product concentration precisely.
Check weight, hydration, blood pressure, urine output, urea, creatinine, sodium and potassium. Over-diuresis can reduce preload and growth; review nephrotoxic drugs, ototoxicity risk, sulfonamide hypersensitivity and formulation excipients, and never interchange liquid strengths volume-for-volume.