To help with diagnosis, the clinician can watch out for predisposing factors, such as: birth asphyxia, meconium aspiration, use of NSAIDs (non steroidal anti-inflammatory drugs) and SSRIs (selective serotonin reuptake inhibitors) by the mother, and early onset sepsis or pneumonia. To diagnose a fetus with pulmonary hypertension, PVR must be higher than systemic vascular resistance, resulting in high afterload and decreased systemic blood flow. This causes a significant decrease in oxygen concentration, which clinically manifests as insufficient blood flow to the lower body, while there is adequate<unk>  to the head and right side of the body. Other echocardiographic findings in PPHN include right ventricular hypertrophy, deviation of the ventricular septum, tricuspid regurgitation, and shunting at the patent foramen ovale. Other clinical signs that may signify PPHN are respiratory distress, partial pressure of oxygen greater than 100 mg and elevated partial pressure of carbon dioxide. A gradient of 10% or more in oxygenation saturation between simultaneous preductal and postductal arterial blood gas values in absence of structural heart disease documents<unk> . Since this may be a sign of other conditions,<unk>  must also be characterized by enlargement of right and left ventricles often confirmed through a definitive ECG.<unk>  in neonates can be reversible or irreversible depending on the classified etiology listed above. If related to pulmonary disorders, the amount of lung damage dictates whether or not treatment is efficacious in reversing newborn lung insufficiency. Other causes for acute pulmonary hypertension include: infection, endocrine disorders, and drug injury. Examples of cases with newborns who with sustained fetal<unk>  are pulmonary hypoplasia and genetic abnormalities.
Persistent fetal circulation
Alveolar capillary dysplasia
Neonatal sepsis
Foetal cerebral redistribution
Umbilical cord compression
Shaken baby syndrome
Fetal distress
Placental insufficiency