Maternal hyperoxygenation in congenital heart disease

Abstract

The importance of prenatal diagnosis and fetal intervention has been increasing as a preventative strategy for improving the morbidity and mortality in congenital heart disease (CHD). The advancements in medical imaging technology have greatly enhanced our understanding of disease progression, assessment, and impact in those with CHD. In particular, there has been a growing focus on improving the morbidity and mortality of fetuses diagnosed with left-sided lesions. The disruption of fetal hemodynamics resulting from poor structural developmental of the left outflow tract during cardiogenesis is considered a major factor in the progressive lethal underdevelopment of the left ventricle (LV). This positive feedback cycle of inadequate flow and underdevelopment of the LV leads to a disrupted fetal circulation, which has been described to impact fetal brain growth where systemic outflow is poor and, in some cases, the fetal lungs in the setting of a restrictive interatrial communication. For the past decade, maternal hyperoxygenation (MH) has been investigated as a diagnostic tool to assess the pulmonary vasculature and a therapeutic agent to improve the development of the heart and brain in fetuses with CHD with a focus on left-sided cardiac defects. This review discusses the findings of these studies as well as the utility of acute and chronic administration of MH in CHD.

Keywords: Fetal; congenital heart disease (CHD); diagnosis; maternal hyperoxygenation (MH); therapy.

Figure 1

Spectrum of left ventricular (LV) hypoplasia as a result of abnormal blood flow-directed remodelling secondary to primary LV outflow obstructive lesions occurring during cardiogenesis. Mild forms of LV hypoplasia are supportive for biventricular repair whereas severe forms of LV hypoplasia require single ventricle palliation repair [image adapted with permission from (19)].