Congenital Heart Disease (CHD): Hemodynamic Effects of Acute Maternal Hyperoxygenation in the Fetus
Congenital heart disease (CHD) is predominantly detected before birth. Using echocardiography and MRI, this study will determine whether acute exposure to maternal hyperoxygenation (MH) leads to measurable increases in fetal cerebral oxygenation from baseline in fetuses with CHD. The study aims to determine whether MH could be used as a chronic in-utero treatment strategy to promote brain growth/maturation to birth and to improve postnatal neurodevelopmental outcomes, and identify the types of CHD most likely to benefit from chronic MH.
• Pregnant mothers ≥18 years of age
• Written maternal informed consent
• Fetal diagnosis of one of the CHDs (1-3) as listed below and intention of active treatment after birth:
‣ Single ventricular (SV) lesions: hypoplastic left heart syndrome (HLHS); pulmonary atresia with intact ventricular septum (PA/IVS); tricuspid atresia (TA); unbalanced AV septal defect (AVSD); double inlet ventricle (DILV); and severe form of Ebstein's anomaly (EA) of the tricuspid valve associated with functional or anatomical right outflow obstruction. HLHS will include aortic stenosis with mitral stenosis, aortic atresia with mitral stenosis or mitral atresia. Pulmonary or aortic obstruction is defined as a condition with minimal or absent antegrade flow across the respective valve. Severe forms of EA is defined as lesion without anterograde pulmonary flow in the setting of severe tricuspid regurgitation.
⁃ Bi-ventricular lesions with right ventricular outflow tract obstruction (BV/RVOTO); tetralogy of Fallot (TOF), TOF-like double outlet right ventricle (DORV), and pulmonary atresia with ventricular septal defect (PA/VSD).
⁃ Bi-ventricular lesions with transposed great arteries (TGA w/ VSD; TGA w/o VSD; DORV with TGA)