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

Abstract

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.

Successful prenatal treatment with continuous chronic maternal hyperoxygenation therapy in hypoplastic left heart in two pregnancies: Case report

“…The possibility of adverse impulse on brain development in CMH was also discussed by Rudolph 22 in a fetal lamb study. With a reduction in cerebral blood flow, even though the cerebral oxygen supply was maintained, cerebral glucose delivery and consumption was significantly reduced.…”

Non‐invasive in‐utero quantification of vascular reactivity in human placenta

“…Many studies aimed at measuring placental vascular properties non-invasively use maternal hyperoxygenation stimuli. These studies have been inconclusive, in part owing to large variations in the fetal response to maternal hyperoxia [39][40][41][42][43][44][45][46][47][48] . Hyperoxygenation is a complex stimulus, decreasing maternal cardiac output and triggering hyperventilation, potentially impacting both maternal and fetoplacental perfusion 49 .…”

Hypoplastic Left Heart Syndrome: Is There a Role for Fetal Therapy?

“…Other fetal complications like constriction of the arterial duct or retinopathy may also be considered but were not reported in human studies on chronic MH. Due to the lack of data in the field of chronic MH and possibly associated fetal complications, the recommendation of a recent review was that studies on MH should be curtailed (69).…”