FIG 7.13 T2 maps in a fetus with transposition of the great arteries The brighter signal from the blood in the left ventricle and main pulmonary artery (MPA) than the blood in the right ventricle (RV) and aorta indicates a reduction in the oxygen saturation of blood supplied to the developing brain in the setting of ventriculoarterial discordance AAo, Ascending aorta; LV, left ventricle Congenital Heart Disease: Hemodynamic Consequences The effects of CHD on fetal oxygen delivery (DO2), oxygen consumption (VO2), fetal cerebral oxygen delivery (CDO2), and cerebral oxygen consumption are shown in Tables 7.5 and 7.6.23 Here, a range of different CHD types have been combined into a single group and compared with a large group of control fetuses To obtain blood oxygen content we estimated hemoglobin concentration based on gestational age appropriate reference data and converted T2 to oxygen saturation (SaO2) using prior experiments in which the relationship between the SaO2 of adult blood and T2 was determined.24,25 Using this approach, we found a reduction of 25% in fetal DO2 resulting from diminished umbilical vein flow and oxygen content.26 This reduction in fetal DO2 was associated with a corresponding drop in fetal VO2 As previously described, the reduction in fetal DO2 combined with interruption of the usual streaming of oxygenated blood from the placenta to fetal brain was associated with an average reduction in oxygen saturation of 10% in the ascending aorta In keeping with the concept of brain-sparing physiology described above, this reduction in ascending aortic saturation was associated with an increase in SVC flow, although this was only apparent when SVC flow was indexed to brain volume In our studies of lategestation CHD fetuses, their brains have been 10% to 15% smaller than those of normal controls, while fetal weight has not been significantly different When SVC flow and CDO2 are indexed to fetal weight, cerebral oxygen delivery and consumption are reduced in fetuses with CHD, while CDO2 and CVO2 indexed to fetal brain weight are not significantly different between fetuses with CHD and normal controls Table 7.5 Fetal Hemodynamics in Control and Congenital Heart Disease Fetuses by Magnetic Resonance Imaging Fetal gestational age (weeks) CHD (n = 40)a 36.5 ± 1.0 Normal (n = 46)a 36.5 ± 1.3 P Value Estimated fetal weight (kg) DO2 (indexed to fetal weight) (mL/min/kg) QUV (indexed to fetal weight) (mL/min/kg) UV SaO2 (%) AAo SaO2 (%) SVC flow (indexed to fetal weight) (mL/min/kg) SVC flow (indexed to fetal brain weight) (mL/min/g) a 3.0 ± 0.4 15.8 (13.9–20.9) 115.4 ± 32 73.5 (68.3–79.0) 48 (40–54) 128.5 (106.0–169.0) 1.41 ± 0.08 2.9 ± 0.4 21.0 (16.4–23.7) 130.2 ± 28 79.0 (73.8–83.0) 58 (52–64) 126.5 (103.0–151.3) 1.20 ± 0.06 003 03 01