Pulmonary hypertension (PH) is a serious and potentially life-threatening condition in neonates, often resulting from impaired transition from fetal to postnatal circulation. Although traditionally associated with elevated pulmonary vascular resistance and hypoxemic respiratory failure, PH in infants who are preterm encompasses a spectrum of pathophysiologic mechanisms and can be broadly categorized into 3 phenotypes: precapillary, postcapillary, and flow driven. Each phenotype presents with distinct hemodynamic features and clinical implications. Although pulmonary vasodilators such as inhaled nitric oxide remain a cornerstone of therapy for PH, their efficacy and safety vary significantly depending on the underlying phenotype and etiology. In this narrative review, we examine the evolving understanding of PH in infants who are premature and propose a physiologically grounded framework for diagnosis, phenotyping, and individualized management.
Gilbert et al. (Sun,) studied this question.