Persistence of the fetal circulation (PFC) was initially described as a syndrome of central cyanosis in term newborn infants resulting from right-to-left shunting of blood via persisting fetal channels which mimicked structural heart disease. Subsequently, this abnormal hemodynamic pattern has been recognized as a complication of a spectrum of neonatal disease. The designation PFC has achieved wide acceptance; however, other terminology may be encountered, including persistence of the transitional circulation and persistent pulmonary hypertension of the newborn.


Muscular pulmonary arterioles are constricted in the term fetus. If these vessels fail to dilate at birth, or if constriction recurs, pulmonary hypertension (PHN) ensues, with consequent elevation of right ventricular and right atrial pressures. Right-to-left (R→L) shunting of blood across the foramen ovale occurs when right atrial pressure exceeds left atrial pressure. R→L shunting through the ductus arteriosus requires pulmonary arterial pressure to exceed systemic pressure, as well as patency of the ductus (see Fig 1).

PHN may independently be responsible for myocardial dysfunction by imposing an abnormal workload on the right ventricle or by adversely affecting right coronary artery blood flow with consequent subendocardial ischemia. The physiology of PFC is presented schematically in Fig 2.

There are two potential pathways to PFC (see Fig 3).

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