Synopsis
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.
- 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.
- 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.
Key red flags
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.
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.
Investigation priorities
Identify heart failure, desaturation and cumulative nutritional burden.
Management branches
A large VSD causes tachypnoea, hepatomegaly, poor feeding or faltering growth.
- Obtain urgent paediatric cardiology assessment and echocardiographic definition of shunt and pressure.
- Use specialist-prescribed diuretic therapy, high-energy feeds and feeding support with renal, electrolyte and growth monitoring.
- Plan closure when symptoms or growth remain unacceptable, pressure burden is important or medicine cannot be safely reduced.