ABSTRACT
Normally, within minutes after birth, pulmonary vascular resistance (PVR) rapidly falls from high fetal levels. This allows pulmonary blood flow to increase nearly tenfold and enables the lung to assume its postnatal role in gas exchange. Severe hypoxaemia characterises the course of severe neonatal respiratory failure. Hypoxaemia may result from intrapulmonary or extrapulmonary shunting. Intrapulmonary shunting is associated with severe parenchymal lung disease (e.g., surfactant deficiency), bacterial pneumonia, and meconium aspiration pneumonitis; generally amenable to exogenous surfactant, and/or ventilator strategies aimed at adequate lung volume recruitment. Severe hypoxaemia commonly relates to persistent pulmonary hypertension of the neonate (PPHN) [1]. Persistently raised PVR results in extrapulmonary shunting of desaturated blood across the patent ductus arteriosus, foramen ovale, or both, and sustained pulmonary hypertension in right ventricular dysfunction and critical hypoxia. To cut the vicious cycle of hypoxia and increased barotraumatism due to hyperventilation commonly used in this setting, there was no other alternative than to put the lung “at rest” using extracorporeal membrane oxygenation and waiting for the PVR to spontaneously decrease. Therefore, interventions aimed at selective pulmonary vasodilation could be beneficial.
