The pulmonary vascular resistance is elevated during intrauterine life but decreases rapidly following uncomplicated birth, to facilitate the transition of oxygenation from the placenta to the newborn lungs. Failure of the pulmonary vascular resistance to decrease after birth can result in significant complications and severe hypoxaemia and cyanosis, a condition described as persistent pulmonary hypertension of the newborn. Similarly, an elevated pressure of the pulmonary artery can result from chronic intrauterine lung hypoplasia such as in congenital diaphragmatic hernia, or following a prolonged postnatal developmental arrest of the pulmonary vascular network in infants who were born prematurely and suffered significant and prolonged respiratory disease. Hypoxaemia can also occur as the result of intrapulmonary shunting, which happens in non-ventilated but perfused lung segments, and is the result of recirculation of deoxygenated blood from the pulmonary into the systemic circulation.