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Introduction

Persistent pulmonary hypertension of the newborn (PPHN) is characterized by persistently elevated pulmonary vascular resistance (PVR) that leads to right-to-left shunting of deoxygenated blood through fetal circulatory pathways (eg, ductus arteriosus, foramen ovale), resulting in a gradient between preductal and postductal oxygen saturations.

Pathogenesis

Fetal circulation is characterized by high PVR (due to hypoxic vasoconstriction) and low systemic vascular resistance (SVR) (due to in-parallel connection to low-resistance placental circulation via the umbilical arteries and vein) ( Figure 1).  Therefore, in utero, PVR is greater than SVR, and the majority of blood is shunted from the high-resistance pulmonary circulation into the low-resistance systemic circulation (ie, right-to-left shunting), through the ductus arteriosus and foramen ovale.  After birth, pulmonary expansion and aeration normally leads to diffuse pulmonary vasodilation and decreased PVR.

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