Abstract
Despite scientific advancement, hypoxemic respiratory failure remains a major challenge in contemporary neonatal intensive care. Dysregulation of the pulmonary vascular bed and failure of the normal postnatal decline in pulmonary vascular resistance (PVR) lead to acute pulmonary hypertension (aPH), traditionally referred to as persistent pulmonary hypertension (PH) of the newborn. The hemodynamic consequences of excessive right ventricular (RV) afterload due to elevated PVR include RV dysfunction, reduced left ventricular (LV) preload, low cardiac output, and systemic hypoperfusion with associated low systemic arterial pressure (SAP).
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