Persistent fetal circulation

Persistent fetal circulation is a condition caused by a failure in the systemic circulation and pulmonary circulation to convert from the antenatal circulation pattern to the "normal" pattern.

Persistent fetal circulation
Other namesPersistent pulmonary hypertension of the newborn

In a fetus, there is high pulmonary vascular resistance and low pulmonary blood flow as the fetus does not use the lungs for oxygen transfer. When the baby is born, the lungs are needed for oxygen transfer and need high blood flow which is encouraged by low pulmonary vascular resistance.

It can be associated with pulmonary hypertension. Because of this, the condition is also widely known as persistent pulmonary hypertension of the newborn (PPHN).[1]


  • Normal vascular anatomy with functional vasoconstriction: This has a good prognosis, as it is reversible. Causes include hypoxia, meconium aspiration, and respiratory distress syndrome.
  • Decreased diameter of pulmonary vessels with hypertrophy of vessel walls: This has a poor prognosis, as it is a fixed abnormality. Causes include post-term pregnancy, placental insufficiency, and NSAID use by the mother.
  • Decreased size of pulmonary vascular bed: This has a poor prognosis, as it is a fixed abnormality. It is caused by space occupying lesions such as pleural effusions and diaphragmatic hernias.
  • Functional obstruction of pulmonary blood flow: This has a good prognosis if it is reversible. Causes include polycythemia and hyperfibrinogenemia.



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 persistent fetal circulation.


Treatment aims to increase the amount of oxygen in the blood and reverse any causes of hypoxia.

  • oxygen therapy
  • mechanical ventilation
  • Nitrous Oxide (NO·) Inhalation
  • Prostaglandins (intravenous)

The therapies available to manage PPHN include the high frequency ventilation, surfactant instillation, inhaled nitric oxide, and extracorporeal membrane oxygenation. These expensive and/or invasive modalities are unavailable in the developing countries where the frequency and mortality of PPHN is likely to be much higher. Therefore, oral sildenafil citrate, has been the alternative way of therapy. The cost comparison shows that sildenafil is lower in cost than iNO and more readily available. There is improvement in oxygenation when oral sildenifal is administered according to the studies found in the Official Journal of the American Academy of Pediatrics. The positive research results for varies studies indicates that oral sildenifal is a feasible source to improve oxygenation and survival in critical ill infants with PPHN secondary to parenchymal lung disease in centers without access to high-frequency ventilation, iNO, or ECMO.


It occurs in 1–2 infants per 1000 live births.[3]


  1. Mayock, Dennis E. (April 10, 2000). "Persistent Pulmonary Hypertension Of The Newborn". Archived from the original on October 12, 2010.
  2. Graves ED, Redmond CR, Arensman RM (March 1988). "Persistent pulmonary hypertension in the neonate". Chest. 93 (3): 638–41. doi:10.1378/chest.93.3.638. PMID 3277808.
  3. Chambers CD, Hernandez-Diaz S, Van Marter LJ, et al. (February 2006). "Selective serotonin-reuptake inhibitors and risk of persistent pulmonary hypertension of the newborn". The New England Journal of Medicine. 354 (6): 579–87. doi:10.1056/NEJMoa052744. PMID 16467545.

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