439: the Effect of Maternal Hyperoxygenation on Fetal Myocardial Mechanics and Hemodynamics in Control Fetuses and Those with Left-Heart Hypoplasia

Primary: Characterize the effect of acute maternal hyperoxygenation (MHO) on LV and RV myocardial mechanics (strain and strain rate). Secondary: 1) Characterize the effect of MHO on loading conditions as reflected by: middle cerebral artery (MCA) pulsatility index (PI), umbilical artery (UA) PI, pulmonary artery (PA) PI, aortic and pulmonary cardiac output, and pulmonary vein VTI over 1 second. 2) Characterize the differential impact of MHO on control fetuses and on those with left heart hypoplasia (LHH) We performed a post-hoc analysis of 31 fetal echocardiograms performed in 15 subjects (9 control and 6 with LHH) between 26 and 36 weeks gestation as part of a previous, pilot study which tested the effect of MHO on fetal growth of left-sided structures. Control fetuses were assessed 1-4 times throughout gestation. Fetuses with LHH were assessed once. Oxygen was administered via 8L non-rebreather face mask for minimum of 10 minutes. A blinded observer traced the LV and RV long axis for analysis of myocardial deformation (Fig 1A) at 3 time points: baseline, during MHO, and recovery (10 minutes after oxygen discontinuation). M-mode of the AV valves was used to mark onset of systole, and aortic valve spectral Doppler was used to mark ejection time (Fig 1B). Offline measurements were made using Syngo Velocity Vector Imaging. To assess changes in the echocardiographic parameters between conditions, a mixed linear regression model to account for repeated measures was used in the control group. The Wilcoxon sign-rank test was used for the LHH group. P-values of <0.05 were deemed significant. MHO resulted in lower LV strain and strain rate were and higher RV strain and strain rate in both control and LHH groups. With removal of MHO, opposite effects were observed, although LV values did not return all the way to baseline. PA PI decreased and pulmonary vein VTI increased in response to MHO, suggesting decreased pulmonary vascular resistance and increased pulmonary venous return. There was no significant effect of MHO on MCA or UA PI. The differential effect of MHO on LV and RV mechanics suggest that changes in deformation indices may be explained by increases in LV preload and decreases in RV afterload. The time period for recovery of fetal hemodynamics from MHO is not well defined, and may be longer than 10 minutes.