Congenital heart disease with increased blood flow commonly leads to the development of increased reactivity and pulmonary arterial hypertension by mechanisms that remain unclear. We hypothesized a shear stress paradigm of hemodynamic reactivity and network remodeling via the persistence and/or exacerbation of a fetal diameter bifurcation phenotype (parent diameter d₀ and daughters d₁d₂ with <2 in ( d₁/ d₀) +( d₂/ d₀) =1 and area ratio <1 in =(d₁²+d₂²)/d₀²) that mechanically acts as a high-resistance-magnifier/shear stress-amplifier to blood flow. Evidence of a hemodynamic influence on network remodeling was assessed using a lamb model of high-flow induced secondary pulmonary hypertension where an aortopulmonary graft is surgically placed in one of twins in utero (Shunt-twin) but not in the other twin (Control-twin). Eight weeks after birth arterial casts were made of the left pulmonary arterial circulation. Bifurcation diameter measurements down to 0.010 mm in the Shunt-twin and Control-twin were then compared to those of an un-operated fetal cast. Network organization, cumulative resistance and pressure/shear stress distributions were evaluated via a fractal model whose dimension D₀ delineates hemodynamic reactivity. The Fetus and Control-twin fractal dimensions differed: Fetus D₀=1.72, a high-resistance/shear stress amplifying condition; Control-twin (D₀=2.02), an area-preserving transport configuration. The Shunt-twin (D₀=1.72) maintained a fetal design, but paradoxically remodeled diameter geometry to decrease cumulative resistance relative to the Control-twin. Our results indicate that fetal/neonatal pulmonary hemodynamic reactivity remodels in response to shear stress, but the response to elevated blood flow and pulmonary hypertension involves the persistence and exacerbation of a fetal diameter bifurcation phenotype that facilitates endothelial dysfunction/injury.