Maternal hyperoxygenation for the human fetus: should studies be curtailed?

Pediatr Res. 2020 Mar;87(4):630-633. doi: 10.1038/s41390-019-0604-4. Epub 2019 Oct 10.


Congenital hypoplasia of left heart structures in fetuses frequently progresses with gestational development. Interference with cerebral development is common in these fetuses. Chronic maternal hyperoxygenation (MHO) has been recommended to increase left ventricular size and to limit cerebral damage. The effects of MHO on cerebral blood flow and metabolism have been studied in normal fetuses and fetuses with left heart hypoplasia. Maternal hyperoxygenation increases fetal pulmonary blood flow. This is associated with reduction of foramen ovale flow, thus limiting the increase in left ventricular output. Modest increase in the size of left heart structures has been reported, but in another study, no significant improvement occurred. In sheep fetuses increased oxygenation results in marked reduction of cerebral blood flow, with no change in oxygen delivery or consumption by the brain, but significant reduction in cerebral glucose delivery and consumption. In one study of fetuses with left heart hypoplasia, chronic MHO was associated with decrease in head size. The effectiveness of MHO in improving left ventricular development is controversial. MHO is, however, associated with reduction of cerebral blood flow and possible interference with cerebral development. In view of this it is recommended that all studies of chronic maternal hyperoxygenation be curtailed.

Publication types

  • Review

MeSH terms

  • Animals
  • Aorta, Thoracic / embryology
  • Brain / blood supply*
  • Brain / embryology
  • Cerebrovascular Circulation*
  • Disease Models, Animal
  • Female
  • Humans
  • Hypoplastic Left Heart Syndrome / embryology
  • Hypoplastic Left Heart Syndrome / physiopathology
  • Hypoplastic Left Heart Syndrome / therapy*
  • Morphogenesis
  • Oxygen Inhalation Therapy* / adverse effects
  • Pregnancy
  • Risk Assessment
  • Treatment Outcome
  • Ventricular Function, Left*
  • Ventricular Remodeling*