Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Ventricular and atrial septal defects
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Septal defect with decompensated heart failure
A large defect can present in infancy with severe tachypnoea, feeding exhaustion, diaphoresis, hepatomegaly, poor perfusion or failure to gain weight as pulmonary vascular resistance falls.
Action: Assess and support airway, breathing and circulation, give oxygen only for documented hypoxaemia, obtain ECG, chest radiograph, blood tests and urgent echocardiography, and involve paediatrics and paediatric cardiology. Correct hypoglycaemia and dehydration carefully, treat infection or arrhythmia, and begin specialist-directed diuretic and nutritional support while definitive closure is planned.
Overview
Differentiate ventricular from atrial septal defects, connect murmur and symptom timing to shunt physiology, and identify which children need observation, heart-failure support or catheter or surgical closure.
Ventricular defects are classified by location, including perimembranous, muscular, inlet and outlet types. Location matters because of proximity to the conduction system, atrioventricular valves or aortic cusps and because spontaneous closure rates differ.
A small restrictive VSD maintains a large pressure difference and a fast, loud jet while limiting shunt volume. A large nonrestrictive defect equalises ventricular pressures, allows substantial pulmonary flow and increases pulmonary arterial pressure.
Symptoms rarely begin at birth in an isolated large VSD because neonatal pulmonary vascular resistance initially restricts flow. As resistance falls, pulmonary overcirculation increases and feeding-related heart failure becomes evident.
Atrial defects include secundum defects at the fossa ovalis, primum defects near atrioventricular valves and sinus venosus defects near caval entry. A patent foramen ovale is a flap-like fetal remnant, not missing septal tissue, and usually has no significant childhood shunt.
Practice
Two practice questions
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Paediatrics and child healthOriginal SBA
Large VSD in infancy
A 7-week-old has tachypnoea, sweating during feeds, hepatomegaly and poor weight gain. A lower-left systolic murmur is present but not especially loud. Which explanation best fits?
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. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Because atrial pressures are low, an ASD does not usually create a loud murmur through the hole. Extra flow across the pulmonary valve creates the systolic sound, and prolonged right-ventricular ejection delays pulmonary valve closure to produce fixed splitting.
Clinical assessment records feed duration, growth centiles, respiratory infections, exercise tolerance and palpitations. Look for a hyperdynamic precordium, hepatomegaly and signs of pulmonary congestion in a symptomatic infant.
Echocardiography must identify more than diameter. It defines rims, relation to valves and veins, ventricular pressure, right- or left-heart loading, pulmonary flow and additional lesions such as aortic arch obstruction or atrioventricular septal defect.
Diuretics reduce congestion and nutritional strategies replace calories lost to increased work of breathing. ACE inhibition is selected by paediatric cardiology for particular physiology; it is not automatic treatment for every left-to-right shunt.
Spontaneous closure is common for small muscular VSDs and possible for perimembranous defects, whereas a true ASD generally persists. Observation is safe only when growth, pressure, chamber size and valve function remain acceptable.
Catheter device closure avoids sternotomy in anatomically suitable secundum ASDs and selected muscular VSDs. Device position, residual shunt, arrhythmia, erosion risk and antiplatelet plan require specialist follow-up.
Surgical repair is preferred for large or poorly positioned VSDs, primum or sinus venosus ASDs and lesions needing associated valve or venous repair. Timing balances operative risk against irreversible pulmonary vascular injury and growth burden.
After successful uncomplicated closure, follow-up intensity varies. Residual shunt, pulmonary hypertension, valve regurgitation, conduction disease or prosthetic material requires continuing congenital cardiac surveillance.
Key points
A VSD connects the ventricles; a pressure gradient produces a left-to-right systolic jet after birth, usually heard as a harsh pansystolic murmur at the lower left sternal edge.
An ASD connects the atria; the shunt is driven mainly by ventricular compliance and causes right-sided volume loading, often with an upper-left systolic flow murmur and fixed wide S2 splitting rather than a loud defect jet.
Small muscular VSDs frequently close spontaneously. A large nonrestrictive VSD may cause heart failure at 4–8 weeks as pulmonary resistance falls and may be surprisingly quiet.
Most children with secundum ASD are asymptomatic. Examination, ECG and echocardiographic right-heart volume loading reveal haemodynamic importance.
Initial tests are saturation, growth and feeding assessment, full cardiovascular examination and paediatric echocardiography; ECG and chest radiography help describe chamber and pulmonary-flow consequences.
Echocardiography confirms location, size, shunt direction, pressure effects, chamber dimensions and associated lesions and guides whether observation or closure is appropriate.
Treat infant heart failure with specialist-directed diuresis and high-energy feeding while monitoring renal function, electrolytes and growth; medicine does not close the anatomical defect.
Close a VSD when heart failure or growth failure persists despite treatment, pulmonary pressure or volume burden is important, or aortic regurgitation or another complication develops.
Aetiology
01
Septation during development
Incomplete formation or fusion of atrial or ventricular septal components leaves a communication whose position reflects the disrupted embryological structure.
02
Genetic associations
Trisomy 21, 22q11 deletion and other chromosomal or single-gene conditions increase septal defects, often with additional cardiac anatomy.
03
Maternal risk context
Pre-existing diabetes and selected fetal exposures are associated with congenital cardiac malformation, although most isolated defects have no single identified cause.
Pathophysiology
1
Ventricular pressure shunt
After pulmonary resistance falls, left-ventricular pressure drives blood through a VSD, increasing pulmonary flow and left-heart volume return.
2
Atrial compliance shunt
Greater right-ventricular compliance draws blood across an ASD during the cardiac cycle, enlarging right atrium, right ventricle and pulmonary flow.
3
Pulmonary vascular exposure
A large VSD exposes pulmonary vessels to high flow and pressure much earlier than a low-pressure ASD, accelerating vascular remodelling.
4
Growth-energy imbalance
Tachypnoea and feeding effort increase caloric expenditure while limiting intake, creating faltering growth despite an anatomically normal gastrointestinal tract.
Clinical features and red flags
Small restrictive VSD
A thriving infant or child has a loud harsh pansystolic lower-left sternal murmur without heart-failure signs.
Large VSD
Tachypnoea, feeding sweat, prolonged feeds, poor growth, hyperdynamic precordium and hepatomegaly appear as pulmonary resistance falls.
Secundum ASD
An asymptomatic child may have an upper-left ejection systolic murmur, fixed wide S2 splitting and right-ventricular impulse.
Primum ASD
Lower septal anatomy, atrioventricular valve regurgitation and possible conduction-axis abnormality suggest a partial atrioventricular septal defect.
A new early diastolic murmur or increasing aortic regurgitation on imaging changes closure urgency in VSD.
Red flags requiring action
Tachypnoea at rest, recession, sweating or tiring during feeds, hepatomegaly, poor weight gain or recurrent respiratory admissions indicates important pulmonary overcirculation.
Shock, cyanosis or marked desaturation is not explained by an uncomplicated isolated ASD or VSD and requires urgent search for additional anatomy, pulmonary hypertension, infection or respiratory disease.
Investigations
01Initial growth and physiological assessmentFirst step
Why
Identify heart failure, desaturation and cumulative nutritional burden.
Interpretation and limitations
Crossing down weight centiles, tachypnoea and hepatomegaly indicate clinically important flow even if murmur intensity seems modest.
02Twelve-lead ECG
Why
Assess chamber loading, axis, rhythm and conduction.
Interpretation and limitations
Left or biventricular hypertrophy can accompany large VSD; incomplete right-bundle pattern and right-axis findings may accompany secundum ASD.
03Chest radiograph
Why
Assess heart size and pulmonary vascularity in a symptomatic child.
Interpretation and limitations
Cardiomegaly with plethoric lung fields supports significant shunting but a normal film does not exclude a smaller lesion.
Restrictiveness, right-ventricular pressure, pulmonary pressure estimates and volume loading guide observation and closure planning.
05Cardiac MRI or catheter haemodynamics
Why
Differential diagnosis
01
Innocent flow murmur
A soft posture-sensitive sound with normal S2, ECG, growth and cardiac dimensions lacks the fixed splitting or harsh defect features.
02
Atrioventricular septal defect
Common atrioventricular junction, valve regurgitation and inlet septal components distinguish this lesion, especially in a child with trisomy 21.
03
Pulmonary valve stenosis
An ejection click, outflow gradient and no right-sided volume shunt differentiate pulmonary stenosis from the flow murmur of ASD.
04
Patent arterial duct
A continuous infraclavicular murmur with bounding pulses and descending-aortic runoff points away from an isolated intracardiac defect.
05
Primary lung or feeding disease
Wheeze, aspiration, infection or swallowing dysfunction can cause tachypnoea and poor growth but does not explain septal flow on echocardiography.
Management
01Symptomatic infantRelieve congestion and restore growthFirst stepA large VSD causes tachypnoea, hepatomegaly, poor feeding or faltering growth.+
1Obtain urgent paediatric cardiology assessment and echocardiographic definition of shunt and pressure.
2Use specialist-prescribed diuretic therapy, high-energy feeds and feeding support with renal, electrolyte and growth monitoring.
3Plan closure when symptoms or growth remain unacceptable, pressure burden is important or medicine cannot be safely reduced.
02VSD surveillanceObserve only low-burden defectsA restrictive VSD has no chamber loading, pulmonary hypertension, aortic regurgitation or growth effect.+
1Record site and relation to aortic and atrioventricular valves and review for spontaneous closure.
2Reassess murmur, growth and echocardiographic valve or chamber effects at the specialist interval.
Complications
01
Congestive heart failure
A large VSD produces pulmonary oedema, feeding intolerance, hepatomegaly and growth failure during vulnerable early infancy.
02
Pulmonary vascular disease
Uncorrected major shunting can fix pulmonary resistance and eventually reverse flow, making closure dangerous and causing cyanosis.
03
Aortic valve regurgitation
An outlet or perimembranous VSD can draw an aortic cusp into the defect, progressively impairing valve closure.
04
Arrhythmia and conduction disease
Atrial dilatation, surgery or device placement can lead to atrial arrhythmia or heart block requiring long-term review.
05
Infective endocarditis
High-velocity jets, residual defects and prosthetic material can support endocardial infection despite the absence of routine dental prophylaxis for most patients.
Monitoring and follow-up
Record weight gain, feed duration, respiratory rate and liver size frequently in a symptomatic infant; treatment success must include growth, not just quieter breathing.
Check urea, creatinine, sodium and potassium after starting or changing diuretics and whenever intake, vomiting or intercurrent illness changes.
Use serial echocardiography to follow defect size, chamber loading, pulmonary pressure, aortic or atrioventricular valve function and residual shunt.
After device closure, follow the centre's plan for antiplatelet duration, endocarditis advice, activity and imaging for device position or residual leak.
Ask older children about exercise capacity and palpitations and obtain rhythm monitoring when symptoms or atrial enlargement raises concern.
Ensure a named congenital follow-up and transition plan when residual anatomy, pulmonary hypertension, valve disease or arrhythmia risk persists.
Special situations
Murmur intensity can invert severity
A tiny VSD produces a fast loud jet, whereas a large pressure-equalising VSD can be softer but cause severe pulmonary overcirculation.
ASD sound comes from flow
The characteristic systolic murmur reflects increased pulmonary-valve flow, while fixed S2 splitting reflects prolonged right-ventricular ejection.
PFO is not ASD
A patent foramen ovale is a potentially open flap without missing septal tissue and usually does not volume-load a child's right heart.
Anatomy chooses closure route
Adequate rims permit many secundum ASDs to accept a device; primum and sinus venosus defects need surgical repair of associated anatomy.
Pressure can end operability
Once pulmonary vascular resistance becomes irreversibly high, closing the communication may worsen right-heart failure rather than cure disease.
Common pitfalls
01
Do not equate the loudest VSD murmur with the largest shunt.
02
Do not wait for cyanosis before recognising heart failure from a left-to-right defect.
03
Do not call fixed S2 splitting an innocent pulmonary flow murmur.
04
Do not treat a PFO and a true ASD as interchangeable anatomy.
05
Do not continue diuretics without monitoring renal function, electrolytes, intake and growth.
06
Do not close a shunt with suspected fixed pulmonary vascular disease before specialist haemodynamic assessment.
07
Do not overlook aortic regurgitation developing beside a perimembranous or outlet VSD.
08
Do not give routine dental antibiotic prophylaxis solely for an uncomplicated septal defect.
Close a significant secundum ASD with right-heart volume loading, usually electively; a suitable rimmed secundum defect may use a transcatheter device, whereas primum and sinus venosus defects require surgery.
Routine antibiotic prophylaxis for dental procedures is not recommended simply because an ASD or VSD exists; follow the current NICE and specialist plan, particularly around prosthetic material.
A large VSD may have a softer murmur than a small restrictive defect; severe symptoms must outweigh apparent murmur loudness.
A new diastolic sound at the left sternal edge in a child with VSD can indicate aortic cusp prolapse and aortic regurgitation requiring expedited review.
Exertional syncope, sustained palpitations, oedema or declining exercise capacity in an older child with an unrepaired ASD suggests haemodynamic or rhythm complications.
Trisomy 21 with an apparent septal lesion warrants careful definition of atrioventricular septal anatomy and earlier pulmonary vascular risk.
Resolve shunt size, pulmonary resistance or anatomy when echocardiography is incomplete or intervention is planned.
Interpretation and limitations
These are specialist tests; invasive resistance measurement is crucial when pulmonary vascular disease could make closure unsafe.
3
EscalationEscalate new aortic regurgitation, endocarditis, pressure elevation or functional limitation for closure discussion.
03ASD closureTreat right-heart volume loadingA persistent ASD creates significant right atrial and ventricular enlargement.+
1Confirm subtype, pulmonary venous anatomy, rims and pulmonary pressure before intervention.
2Use transcatheter device closure for a suitable secundum defect; use surgery for primum, sinus venosus or unsuitable anatomy.
3Follow the device or surgical plan for imaging, rhythm surveillance, antiplatelet treatment and activity after the procedure.
04Advanced pressureMeasure before closingPulmonary vascular disease or bidirectional or right-to-left shunting is suspected.+
1Refer to a specialist congenital and pulmonary-hypertension centre for full haemodynamic assessment.
2Do not assume closure is beneficial when pulmonary resistance is fixed because removing the pressure-relief shunt may be dangerous.
3Create an individual long-term plan covering oxygenation, exercise, pregnancy counselling and complication monitoring.