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“There’s a narrowing at the aortic outflow tract.” This describes aortic stenosis, not tricuspid atresia.

“The pulmonary veins don’t return to the left atrium.” This describes total anomalous pulmonary venous return (TAPVR), a separate congenital defect.

“There’s a narrowing at the entrance of the pulmonary artery.” This describes pulmonary stenosis, which can occur in some defects but is not the defining feature of tricuspid atresia.

A machinelike murmur is characteristic of patent ductus arteriosus (PDA), not tricuspid atresia. Murmurs in tricuspid atresia are usually related to VSD flow or pulmonary stenosis, not a machinelike PDA murmur.

Children with tricuspid atresia often increase their respiratory rate to compensate for hypoxia. Tachypnea, not bradypnea, is more likely.

Capillary refill is usually normal unless heart failure or shock develops. Delayed refill is not a defining characteristic of tricuspid atresia.

The red blood cell count is normal: This is incorrect because polycythemia is defined by an elevated red blood cell count.

There is little to no effect on the blood clotting system: Polycythemia can increase blood viscosity, which may predispose the child to thrombosis or stroke, so it does affect the blood clotting system indirectly.

The viscosity of the blood is unchanged: Increased RBCs thicken the blood, increasing viscosity, which can lead to complications like headaches, dizziness, stroke, and poor perfusion.

Arterial blood gas (ABG) analysis provides oxygen and CO₂ levels, but does not visualize cardiac anatomy or assess the presence of structural defects.

Pulmonary function tests assess lung function, not cardiac structure.

ECG detects electrical conduction abnormalities or chamber hypertrophy, but cannot define the precise anatomical defect like tricuspid atresia.

Blalock-Taussig operation is a palliative procedure, not definitive. It creates a shunt between the subclavian artery and pulmonary artery to increase pulmonary blood flow temporarily in congenital heart defects like TOF. It is often used in the neonatal period.

Jatene procedure is used to correct transposition of the great arteries (TGA), not tricuspid atresia.

Patch closure is typically used to repair septal defects (ASD, VSD), not to reroute circulation in single-ventricle defects like tricuspid atresia.

High-flow oxygen alone does not correct the structural defect or ensure adequate pulmonary blood flow. Excessive oxygen can even reduce pulmonary vascular resistance, decreasing blood flow to the lungs in ductal-dependent lesions.

Feeding is important for nutrition but cannot address immediate circulatory needs. Overfeeding may increase metabolic demand and worsen hypoxemia.

Administering furosemide for pulmonary edema is incorrect since pulmonary edema is not typically the primary issue in ductal-dependent tricuspid atresia. Furosemide would not improve systemic oxygenation in the immediate neonatal period.