Systemic pressure rises from: Removal of placenta from circulation and rise in left
ventricular output, aided by increased preload on LV from higher pulmonary blood flow
returning to LA and LV.
Closure of fetal shunts: Increase in left atrial pressure from higher pulmonary venous
return leads to functional closure of PFO and cessation of right to left atrial shunt.
Drop in PA pressure and constriction of PDA from higher oxygen tension lead to
cessation of right to left PDA shunt and eventual anatomical closure of PDA.
PATHOPHYSIOLOGY OF PPHN:
Abnormally constricted lung vasculature: The failure of normal adaptation Some cases
of idiopathic PPHN may be related to maternal intake of medications that cause fetal
ductal constriction (NSAID) or pulmonary vasoconstriction (NSAID and/or SSRI intake).
The pathophysiology specific to common parenchymal lung diseases associated with
PPHN are described below.
Meconium aspiration syndrome:
Meconium causes mechanical obstruction to the airways →resulting in air trapping,
hyperinflation, ↑ risk for pneumothorax, inactivation of surfactant, release of
vasoconstrictors. Chemical pneumonitis leads to release of cytokines and leukotrienes
that can increase pulmonary vasoconstriction. Recognition of the role of surfactant
inactivation in MAS lead to clinical trials of surfactant replacement therapy for neonates