Neonatal Pulmonary Hypertension: Integrating Developmental, Inflammatory, Gut, Fetomaternal, and Cardio‐Pulmonary Biology Into Bedside Care

ABSTRACT Neonatal pulmonary hypertension (NPH) is best understood as a dynamic multisystem syndrome rather than an isolated pulmonary vascular disorder. Disruption of postnatal pulmonary vascular transition occurs within a broader biological network that includes developmental lung‐vascular biology, placental and fetomaternal influences, infection and inflammation, myocardial adaptation, and emerging gut‐lung‐vascular signaling pathways. This narrative review summarizes current evidence and expert consensus to reframe NPH across the spectrum of acute maladaptation, developmental lung disease and underdevelopment phenotypes, and prematurity‐associated mixed physiology encountered in the neonatal intensive care unit, including infants who remain hospitalized beyond 28 days of life. Pulmonary arterial pressure in the newborn reflects the interaction of pulmonary vascular resistance, pulmonary blood flow, and left atrial pressure. Targeted neonatal echocardiography is essential for phenotype recognition, real‐time hemodynamic assessment, and treatment selection. Developmental lung biology, genetic susceptibility, prenatal programming, inflammatory injury, and emerging gut‐lung interactions converge to produce pulmonary vascular dysfunction, abnormal pulmonary vascular adaptation, and right ventricular pressure overload. Understanding these interacting systems supports physiology‐guided bedside care that integrates respiratory, cardiovascular, and systemic management strategies. Management should therefore move beyond reflex vasodilation toward individualized respiratory support, physiology‐guided hemodynamic optimization, selective use of pulmonary vasodilators, and longitudinal surveillance of the developing heart‐lung unit.