Congenital heart disease presenting in the newborn — branching viva

Station opening

Examiner: "Tell me the single bedside decision that frames every newborn with suspected congenital heart disease, and why it matters." [6]

Strong candidate (must-hit)

• The decision is whether the lesion is duct-dependent: whether systemic or pulmonary blood flow can only occur through an open ductus arteriosus. It matters because the ductus closes functionally over 24 to 48 hours, so a duct-dependent baby who looks well initially will collapse — with shock (left obstruction) or cyanosis (right obstruction) — as the duct closes. Making that call early and starting prostaglandin before the echo is the difference between a planned transfer and an arrest. [6]

Weak candidate

• "We look for a murmur and do an echocardiogram." [6]

Branch A — The day-three collapsed neonate

Examiner: "A term infant who passed the screen and was well at discharge returns on day 3 with poor feeding, weak femoral pulses and a metabolic acidosis. What is your diagnosis, your immediate drug, and the principle that governs its timing?" [9]

Strong

• Diagnoses a duct-dependent obstructive lesion — coarctation or interrupted aortic arch until proven otherwise — because the baby was well while the duct supplied the lower body and has collapsed as the duct closed, with weak femoral pulses and acidosis. The immediate drug is prostaglandin E1 (alprostadil) 0.01 to 0.05 mcg/kg/min intravenously. The governing principle is to start it before the echocardiogram: the echo confirms but does not treat, and waiting risks irreversible collapse. Anticipates prostaglandin-induced apnoea and readies intubation. [9]

Weak

• "It is probably sepsis — I would give fluids and antibiotics and wait for the blood cultures." [6]

Branch B — The positive pulse-oximetry screen

Examiner: "A routine screen at 24 hours reads 88 percent in the right hand and 87 percent in the foot in an asymptomatic baby. What are the thresholds, what do you do, and what is the common trap?" [4]

Strong

• A saturation below 90 percent in any limb is a positive screen mandating urgent cardiology assessment regardless of how well the baby looks. Acts now: assess the baby, give oxygen, start prostaglandin if a duct-dependent lesion is suspected, and arrange urgent echo and cardiology referral — not a repeat or discharge. The common trap is being falsely reassured by the well appearance, which is exactly why screening exists. States that a passed screen does not exclude CHD (sensitivity about 76 percent), and that the deceptively well baby is the one who collapses later. [4] [7]

Weak

• "The baby looks well, so I would repeat the screen tomorrow." [4]

Branch C — The cyanotic newborn and the hyperoxia test

Examiner: "A cyanotic newborn with minimal distress fails to improve in 100 percent oxygen. The radiograph shows an egg on a string. What is the diagnosis, the mechanism, and the limitation of the hyperoxia test?" [10]

Strong

• Diagnoses d-transposition of the great arteries — the commonest cause of neonatal cyanosis — with parallel circulations requiring mixing at the atrial or ductal level; the egg on a string is the radiograph sign. Explains that the hyperoxia test supports a right-to-left shunt when the PaO2 fails to rise, but is not specific because persistent pulmonary hypertension of the newborn behaves similarly, so it is interpreted with the work of breathing, the radiograph, the pre/post-ductal difference and the echo. Anticipates that antenatal detection of d-TGA, though improved, is imperfect. [2] [10]

Weak

• "The cyanosis is from lung disease — start antibiotics and CPAP." [2]

Branch D — The retrieval and the prostaglandin trap

Examiner: "You have started prostaglandin and are arranging retrieval. What side-effects do you warn the team about, and how do you decide on intubation?" [9]

Strong

• Warns that prostaglandin predictably causes apnoea, pyrexia, hypotension and, with longer use, gastric-outlet effects; because apnoea can be abrupt, intubation equipment is ready and many teams electively intubate before a long retrieval. Cites the Browning Carmo experience that low-dose prostaglandin can maintain the duct safely for transport, often without routine ventilation when the dose is low and the baby is stable — the threshold for intubation is individualised to dose, transfer distance and airway stability. [9]

Weak

• "Prostaglandin is safe — I would transfer the baby extubated without monitoring for apnoea." [9]

Close

Examiner: "Summarise your approach to the newborn with suspected congenital heart disease in one sentence." [6]

Strong

• "I split the presentation at the bedside into cyanotic versus duct-dependent, start prostaglandin E1 the moment a duct-dependent lesion is suspected — before the echo — feel the femoral pulses in every baby, and organise echocardiography and retrieval to a cardiac centre in parallel, while covering sepsis and anticipating prostaglandin-induced apnoea." [1] [6] [9]