Abstract：
A disruption in the well-orchestrated fetal-to-neonatal cardiopulmonary transition at birth results in the clinical conundrum of severe hypoxemic respiratory failure associated with elevated pulmonary vascular resistance (PVR), referred to as persistent pulmonary hypertension of the newborn (PPHN). In the past three decades, the advent of surfactant, newer modalities of ventilation, inhaled nitric oxide, other pulmonary vasodilators, and finally extracorporeal membrane oxygenation (ECMO) have made giant strides in improving the outcomes of infants with PPHN. However, death or the need for ECMO occurs in 10-20% of term infants with PPHN. Better understanding of the etiopathogenesis of PPHN can lead to physiology-driven management strategies. This manuscript reviews the fetal circulation, cardiopulmonary transition at birth, etiology, and pathophysiology of PPHN.
摘要：
出生时精心安排的胎儿到新生儿心肺转换的中断导致与肺血管阻力（PVR）升高相关的严重低氧性呼吸衰竭的临床难题。称为新生儿持续性肺动脉高压（PPHN）。在过去的三十年里，表面活性剂的出现，较新的通风方式，吸入一氧化氮，其他肺血管扩张剂，最后,体外膜氧合(ECMO)在改善PPHN患儿的预后方面取得了巨大进展.然而,死亡或需要ECMO发生在10-20%的PPHN足月婴儿中。更好地了解PPHN的病因可以导致生理学驱动的管理策略。这篇手稿回顾了胎儿循环，出生时的心肺过渡，病因学,和PPHN的病理生理学。
