Paediatrics chapters
Congestive cardiac failure in children
How heart failure shows itself in infants and older children, the causes at each age, the tests that confirm it, and the step-by-step treatment with diuretics, digoxin, inotropes and supportive care, including digoxin toxicity.
- Heart failure is a heart that cannot pump enough blood for the body's needs; in infants it shows as fast breathing, sweating and tiring on feeds, poor weight gain and an enlarged liver.
- The three cardinal signs are cardiomegaly, tachypnoea and hepatomegaly; causes depend on age: left-to-right shunts and duct-dependent lesions in infancy, rheumatic heart disease, myocarditis and acute nephritis in older children.
- Treat the cause, give oxygen, propped-up position, calorie-dense feeds, furosemide (plus spironolactone), digoxin, and dopamine or dobutamine if perfusion is poor.
On this page
Overview
Congestive cardiac failure (CCF) is a state in which the heart cannot deliver enough cardiac output to meet the body's metabolic needs. In children it is most often caused by congenital heart disease in infancy and by acquired disease (rheumatic carditis, myocarditis, acute nephritis, severe anaemia) in older children.
Infants do not complain of breathlessness; they show it as difficulty feeding, sweating, fast breathing and failure to gain weight. Spotting this early and finding the cause is the key skill.
Pathophysiology in brief
- Cardiac output = stroke volume x heart rate.
- When output falls, the body compensates: sympathetic activity (faster, stronger beats, vasoconstriction), and reduced kidney blood flow switches on renin, aldosterone and ADH, retaining salt and water.
- These help at first but later add preload and afterload, so the heart dilates and hypertrophies.
- Past a point, further stretching weakens contraction: decompensated failure.
- Left-sided failure congests the lungs (fast breathing, crackles); the right side then fails, causing liver enlargement and, later, oedema.
Sweating in infants comes from sympathetic overactivity.
Common paediatric causes
| Age | Causes |
|---|---|
| Fetus | Severe anaemia (haemolysis, fetomaternal bleed), SVT, complete heart block |
| Newborn and infant | Large left-to-right shunts (VSD, PDA, AV canal), left-sided obstruction (coarctation, hypoplastic left heart), mixing lesions (truncus arteriosus, single ventricle), SVT, viral myocarditis, asphyxial cardiomyopathy, metabolic causes (hypoxia, hypoglycaemia, acidosis, anaemia, sepsis), fluid overload |
| Older children | Rheumatic fever and rheumatic heart disease, acute hypertension (acute glomerulonephritis), viral myocarditis, cardiomyopathy, cor pulmonale, severe anaemia |
Timing gives the clue. Failure in the first days suggests a duct-dependent left-sided obstruction (hypoplastic left heart, critical coarctation) or an arrhythmia. Failure after a few weeks suggests a large left-to-right shunt (VSD, PDA), because the shunt grows as pulmonary resistance falls.
In an older Pakistani child with fever, joint pains and a new murmur, think rheumatic carditis. In a child with haematuria, oedema and high blood pressure, think acute nephritis.
Clinical diagnosis
Cardinal signs
- Cardiomegaly (displaced apex, enlarged heart on X-ray).
- Tachypnoea (left-sided congestion).
- Hepatomegaly (right-sided congestion).
Other symptoms and signs
| Infants | Older children |
|---|---|
| Feeding difficulty | Easy fatigue, effort intolerance |
| Sweating on feeds | Breathlessness, orthopnoea |
| Poor weight gain, failure to thrive | Peripheral oedema, raised JVP |
| Irritability, restlessness | Crackles at the lung bases |
| Tachycardia, gallop rhythm | Tachycardia, gallop rhythm |
| Recurrent chest infections | Weight gain from fluid |
| Weak pulses, pallor | Weak pulses, pallor |
Nelson notes that a chest X-ray without cardiomegaly usually rules out heart failure. A fast-breathing infant with a normal-sized heart more likely has lung disease or sepsis.
Differential diagnosis
Conditions that also cause fast breathing, crackles and a palpable liver in an infant:
| Condition | How to tell it apart |
|---|---|
| Severe lung disease (bronchiolitis, pneumonia) | Fever, cough, wheeze; normal heart size on X-ray |
| Sepsis with multi-organ failure | Unwell, poorly perfused baby; heart size normal |
| Severe anaemia | Marked pallor, low haemoglobin; failure eases with slow packed cell transfusion |
| Renal failure / nephritis with fluid overload | Oedema, hypertension, abnormal urine and creatinine |
| Metabolic causes in the newborn | Hypoxia, hypoglycaemia, acidosis on blood gas and glucose |
Many of these coexist with heart failure (for example, pneumonia in a child with a large VSD).
Investigations
| Test | What it shows |
|---|---|
| Chest X-ray | Cardiomegaly; lung vessels vary with the cause; perihilar haziness or pulmonary oedema in severe failure |
| ECG | Ventricular hypertrophy; ischaemic changes in cardiomyopathy; low-voltage QRS with ST-T changes in myocarditis or pericarditis; the best test for a rhythm cause (SVT, heart block) |
| Echocardiography | Ventricular function, structural lesions, effusion; Doppler estimates output |
| Blood gas | Low oxygen with pulmonary oedema; respiratory and/or metabolic acidosis in severe failure |
| Bloods | Haemoglobin, electrolytes (potassium, calcium), glucose, renal function, cultures if infection suspected |
Management
Remove or treat the cause wherever possible (close the shunt, control the arrhythmia, treat anaemia or hypertension, treat rheumatic carditis).
General and supportive measures
- Rest; strict bed rest is rarely needed, but frequent rest and good sleep are.
- Position: older children sit or lie propped up at about 20-30 degrees.
- Oxygen when hypoxic or distressed.
- Feeding: extra calories are vital, as metabolic needs are high and intake is poor. Use nasogastric feeds if the infant is too tired to suck.
- Salt: no salt-restricted formula for infants; in older children limit salt to about 0.5 g a day.
- Fluids: restrict to about two thirds of normal maintenance (around 75 mL/kg/day) in admitted patients.
- Monitor vital signs (hourly in the first 24 hours), input-output chart and weight; keep haemoglobin, potassium, calcium and pH normal.
- Treat infections promptly.
- Anaemia: slow packed cell transfusion, 10 mL/kg.
Drugs
| Drug | Dose (Akbar) | Points |
|---|---|---|
| Furosemide | 1-2 mg/kg/dose IV, then 2 mg/kg/day in two doses | Relieves pulmonary congestion and oedema; watch potassium |
| Spironolactone | 1-3 mg/kg/day in two doses | Potassium-sparing; combined with furosemide |
| Digoxin | See below | Positive inotrope; slows heart rate |
| Dopamine / dobutamine | Infusion, started low and titrated | When BP or urine output stays low or response is poor; switch to dobutamine if dopamine fails |
| Vasodilators (captopril; nitroprusside IV) | Captopril: start low after a small test dose; Akbar gives up to 6 mg/kg/day in 4 divided doses. Nitroprusside IV 0.5-8 µg/kg/min | Reduce afterload; useful in left ventricular disease |
Digoxin
Digitalisation (total digitalising dose, TDD, oral):
| Age | TDD |
|---|---|
| Preterm | 20 micrograms/kg |
| Term neonate (to 1 month) | 20-30 micrograms/kg |
| Infant or child | 25-40 micrograms/kg |
| Adolescent or adult | 0.5-1 mg in divided doses |
Give half the TDD first, then a quarter every 12 hours twice.
Maintenance: 5-10 micrograms/kg/day, split into two doses. The IV dose is 75% of the oral dose.
TDD at 30 micrograms/kg = 30 x 10 = 300 micrograms (oral)
First dose = 1/2 x 300 = 150 micrograms; then 75 micrograms at 12 h and 75 micrograms at 24 h
IV TDD would be 75% x 300 = 225 micrograms
Maintenance 5-10 micrograms/kg/day = 50-100 micrograms/day, given in two doses
Digoxin toxicity
- Symptoms: loss of appetite, nausea and vomiting, colour vision changes.
- Heart: bradycardia (below 100/min in infants, below 80/min in young children, below 60/min in older children), ventricular ectopics, any degree of heart block; ECG shows a long PR interval and ST changes.
- Precipitants: hypokalaemia (Nelson); renal impairment (Akbar: digoxin is contraindicated in renal failure).
- Treatment: stop digoxin, continuous ECG monitoring, potassium replacement unless there is heart block, atropine for sinus bradycardia, phenytoin or lidocaine for ventricular arrhythmias, and digoxin-specific Fab fragments as the treatment of choice in serious toxicity.
Low potassium makes digoxin toxicity more likely, so a child on furosemide plus digoxin needs potassium checked; spironolactone helps hold it up.
Complications and poor prognostic indicators
Complications:
- Growth failure.
- Recurrent chest infections (pneumonia).
- Circulatory collapse and shock, for example when an infection strikes a child with dilated cardiomyopathy (Nelson).
- Pulmonary hypertension and Eisenmenger syndrome in long-standing shunts.
- Drug problems: digoxin toxicity, low potassium from loop diuretics.
Signs of a poor outlook: neither textbook gives a scoring list. In words, the outlook is worse when:
- Failure does not respond to full medical treatment, and low BP or low urine output needs inotropes.
- Pulmonary pressure keeps rising in a shunt lesion (heading towards irreversible pulmonary vascular disease).
- The cause cannot be corrected, such as cardiomyopathy, which carries a high mortality, so cardiac transplantation is considered (Nelson).
Prevention and long-term follow-up
- Early diagnosis and timely repair of congenital lesions before failure and pulmonary vascular disease set in.
- Prevent rheumatic fever: treat streptococcal sore throat, and give secondary penicillin prophylaxis to those who have had it.
- Treat anaemia, hypertension and infections early.
- Follow-up: weight and growth charts, heart rate, liver size, electrolytes on diuretics, signs of digoxin toxicity, and serial echocardiography; endocarditis prevention and dental care where indicated.
Expect: the three cardinal signs (cardiomegaly, tachypnoea, hepatomegaly); feeding difficulty and sweating as early infant signs; causes by age, especially large VSD or PDA in infancy and rheumatic carditis or acute nephritis in older children; the fetal causes (anaemia, SVT, heart block); the timing clue (first days = left obstruction, weeks = shunt); X-ray cardiomegaly and echo for function; furosemide and spironolactone doses; digoxin loading and maintenance with the IV dose at 75% of oral; digoxin toxicity features, precipitation by low potassium, and Fab fragments; when to add dopamine or dobutamine; slow packed cell transfusion for anaemic failure.
Quick revision
- CCF = output below metabolic need; infants show feeding difficulty, sweating, tachypnoea, poor weight gain.
- Cardinal signs: cardiomegaly, tachypnoea, hepatomegaly.
- Infancy: shunts (VSD, PDA), duct-dependent lesions, SVT, myocarditis. Older: rheumatic carditis, nephritis, myocarditis, anaemia.
- Supportive: oxygen, propped up, calorie-dense or NG feeds, fluid to two thirds maintenance.
- Furosemide 1-2 mg/kg/dose; spironolactone 1-3 mg/kg/day.
- Digoxin: half TDD, then quarter twice 12-hourly; maintenance 5-10 micrograms/kg/day; IV = 75% of oral.
- Toxicity: vomiting, bradycardia, block; low K precipitates; Fab fragments.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why do infants with heart failure sweat during feeds?
Feeding is hard work for them, and the high sympathetic drive of heart failure causes sweating along with fast breathing and tiredness.
Why does a large VSD cause heart failure at a few weeks rather than at birth?
Pulmonary resistance is high at birth and falls over the first weeks, so the left-to-right shunt and lung blood flow increase gradually.
Why is potassium checked in a child on digoxin and furosemide?
Furosemide lowers potassium, and low potassium makes digoxin toxicity and arrhythmias much more likely.
When are dopamine or dobutamine used?
When blood pressure or urine output stays low, or the child does not respond to diuretics, digoxin and supportive care.