CARDIOVASCULAR CONDITIONS · NEONATAL
The newborn heart
Many heart defects look well at birth and only declare themselves as the duct closes - then as cyanosis, collapse or heart failure. The skill is spotting duct-dependent disease early and separating cardiac from respiratory cyanosis.
START HERE
The first few minutes
Recognise
Cyanosis not relieved by oxygen, shock or poor perfusion, a murmur, or absent femoral pulses.
Pre/post-ductal sats
Low or differential saturations; the hyperoxia test helps separate cardiac from respiratory cyanosis.
Assess
Femoral pulses, perfusion, liver, four-limb BP; ECG, CXR and a blood gas (acidosis suggests shock).
Stabilise
If a duct-dependent lesion is possible, start prostaglandin (PGE1); support ABC, avoid hyperoxia in single-ventricle lesions.
Escalate
Arrange urgent echocardiography and cardiology, and call NETS for retrieval to a cardiac centre.
BROWSE THE CONDITIONS
Conditions in this section
Duct-dependent cyanotic lesions
The blue baby - TGA, pulmonary atresia, severe Fallot, tricuspid atresia.
Duct-dependent systemic lesions
Collapse as the duct closes - HLHS, critical coarctation, critical AS, interrupted arch.
Transposition of the Great Arteries
Parallel circulations; profound cyanosis needing prostaglandin ± balloon septostomy.
Patent Ductus Arteriosus
Left-to-right shunt, common in preterm infants; bounding pulses, active precordium.
Heart Failure & Large Shunts
VSD / AVSD - heart failure at 4-6 weeks as pulmonary resistance falls.
Supraventricular Tachycardia
Narrow-complex tachycardia >220/min; vagal manoeuvres, then adenosine.
Total Anomalous Pulmonary Venous Drainage
Cyanosis with respiratory distress; obstructed TAPVD is a surgical emergency.
The Neonatal Murmur
Innocent vs pathological; check pulses, saturations and feeding before reassuring.
CLINICAL REASONING
Telling them apart at a glance
| Presentation | Typical timing | Key signs | Discriminating clue | First step |
|---|---|---|---|---|
| Duct-dependent cyanotic (TGA) | Birth-hours | Profound cyanosis, soft/no murmur | Fails the hyperoxia test | Prostaglandin |
| Duct-dependent systemic (HLHS, CoA) | Collapse days 1-14 | Shock, weak/absent femorals, acidosis | Lower post-ductal sats; absent femorals | Prostaglandin |
| Obstructed TAPVD | Birth-hours | Cyanosis + respiratory distress, pulmonary oedema | Does not improve (may worsen) with PGE1 | Urgent surgery |
| PDA (preterm) | Days | Bounding pulses, active precordium, murmur | Preterm + wide pulse pressure | Fluids/treatment per unit |
| Large L-to-R shunt (VSD) | 4-6 weeks | Tachypnoea, sweating, poor feeding, hepatomegaly | Presents later, acyanotic | Diuretics, refer |
| SVT | Any | HR >220, narrow complex, little variability | Fixed, very fast rate | Vagal → adenosine |
| Innocent murmur | Any | Soft systolic murmur, well baby | Normal pulses, sats and feeding | Reassure / review |
When to call NETS
If a duct-dependent lesion is on the table, call early - and start prostaglandin while you wait.
- Suspected duct-dependent lesion, or cyanosis not responding to oxygen
- Shock or collapse with metabolic acidosis
- Any baby started on, or needing, prostaglandin
- SVT not responding, or any need for a cardiac opinion
Take-home message: Neonatal heart disease shows up as cyanosis, collapse or heart failure - and the lesions that kill early are duct-dependent. Use pre- and post-ductal saturations and the hyperoxia test to separate cardiac from respiratory cyanosis, always check femoral pulses, and if a duct-dependent lesion is possible, start prostaglandin and call NETS while arranging an urgent echo.
For educational purposes only. Always align management to current ANZCOR/NRP guidelines and your local SCN/NICU or NETS protocols.