Abstract
BackgroundHypoxia delays brain maturation and contributes to neurodevelopmental morbidity in fetuses with congenital heart defects (CHDs). Maternal hyperoxygenation (MH) can, in theory, promote oxygen/nutrient delivery to the fetal brain, owing to an improved heart structure/function and increased fetal oxygen content. We aimed to determine whether MH alters fetal cerebral hemodynamics in fetuses with CHD.MethodsTwenty-eight fetuses with borderline small left hearts and 28 age-matched normal fetuses were enrolled and subdivided by gestational age (GA): 23+ 0 ~ 27+ 6 weeks and 28+ 0 ~ 36+ 6 weeks. The middle cerebral artery pulsatility index (MCA-PI), vascular index (VI), flow index (FI) and vascular/flow index (VFI) were measured with baseline room air, after 10 min of MH and after 10 min of recovery for all subjects.ResultsMCA-PI, VI, FI and VFI did not differ with MH in the normal fetuses. In fetuses with borderline small left hearts, MCA-PI increased and VI, FI and VFI significantly decreased during the 3rd trimester (from 1.44 ± 0.27, 3.19 ± 0.87, 56.91 ± 9.19, and 1.30 ± 0.33 at baseline to 1.62 ± 0.15, 2.37 ± 0.37, 45.73 ± 4.59, and 0.94 ± 0.15 during MH, respectively, P < 0.05), but this response was not apparent during mid-gestation (p > 0.05). These parameters returned to the baseline levels during the recovery phase. The change in cerebral perfusion depended on the baseline MCA-PI and increased the combined cardiac index (CCOi).ConclusionsMH alters the cerebral hemodynamics of fetuses with borderline small left hearts during the third trimester. Further investigation is needed to determine whether MH may benefit brain growth and neurodevelopment in this high-risk population.
Highlights
Hypoxia delays brain maturation and contributes to neurodevelopmental morbidity in fetuses with congenital heart defects (CHDs)
We aimed to determine 1) whether a short period of Maternal hyperoxygenation (MH) could transiently alter fetal cerebral hemodynamics in fetuses with borderline small left hearts and 2) the potential factors that might affect the response to MH
Population characteristics In total, 28 borderline small left heart fetuses and 28 age-matched normal control fetuses were enrolled in the study
Summary
Hypoxia delays brain maturation and contributes to neurodevelopmental morbidity in fetuses with congenital heart defects (CHDs). Maternal hyperoxygenation (MH) can, in theory, promote oxygen/nutrient delivery to the fetal brain, owing to an improved heart structure/function and increased fetal oxygen content. Recent studies have demonstrated neurodevelopmental morbidity in fetuses with congenital heart defects (CHDs). Our previous study [10] showed an elevated combined cardiac index (CCOi) and myocardial deformation during MH in fetuses with a small aortic isthmus. These data suggested that MH can, in theory, promote oxygen/nutrient delivery to the fetal brain, owing to improved heat structure/function and increased umbilical PO2 [11]. We hypothesized that fetal cerebral hemodynamics would be altered during MH therapy in cases of CHD
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