Impact of Maternal Hyperoxygenation on Myocardial Deformation and Loading Conditions in Fetuses with and without Left Heart Hypoplasia

Background: Maternal hyperoxygenation (MHO) is used in a variety of clinical applications, but its impact on fetal cardiovascular physiology is poorly understood. Our aims were to describe the effects of MHO on myocardial deformation parameters and on ultrasound-based metrics of preload and afterload and to assess the differential effect of MHO on fetuses with left heart hypoplasia (LHH). We hypothesized that the effects of MHO would be modulated by loading conditions and that fetuses with LHH would be more sensitive to changes in preload and afterload induced by MHO.

Methods: We performed a post hoc analysis of 36 fetal echocardiograms performed as part of a pilot study of MHO in LHH (n = 9) and control (n = 9) fetuses. Oxygen was administered via 8 L face mask for 10 minutes. Right ventricular (RV) and left ventricular (LV) longitudinal strain and strain rate, estimated aortic and pulmonary cardiac output, pulmonary vein velocity-time integral (VTI) and pulsatility indices (PI) of the middle cerebral artery (MCA), pulmonary arteries (PA), and umbilical artery (UA) were measured at three time points: baseline, during MHO, and 10 minutes after removal of MHO.

Results: Maternal hyperoxygenation induced decreases in LV strain and strain rate and increases in RV strain and strain rate. Pulmonary artery PI decreased and pulmonary vein VTI increased, suggesting decreased pulmonary vascular resistance and increased pulmonary venous return. Most findings did not return to baseline after removal of MHO. We found no significant effect of MHO on MCA or UA PI. Left heart hypoplasia cases demonstrated similar effects of MHO in control cases, with larger changes in pulmonary vein VTI and LV strain rate.

Conclusion: The effects 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 ill-defined.