Heart Failure Treatment In the fetal circulation, the two ventricles and their respective arterial outlets are functionally disposed in parallel with the aorta and pulmonary artery being connected via a widely patent arterial duct The stroke volume each ventricle generates is determined mainly by myocardial properties (compliance and contractility) and loading conditions (preload and afterload) In the prenatal circulation, a normal or near normal cardiac output can be maintained even with only one functional ventricle Fetal CHF results from the inability of both ventricles to fill and eject enough blood to meet the needs of the developing fetus.113 The fetal echocardiographic findings depend on the severity of the cardiac dysfunction and include cardiomegaly, valvar regurgitation, systemic venous congestion, effusions, and preferential shunting of blood flow to the brain, heart, and adrenals in those cases with advanced CHF Disorders other than tachyarrhythmias and bradyarrhythmias that may present in fetal heart failure include myocardial diseases, structural cardiac abnormalities, abnormal cardiac loading conditions, and ischemia For many of these conditions, potentially life-saving prenatal treatment will not be available This is usually the situation for those fetuses with low-output failure secondary to a poorly tolerated primary cardiomyopathy114 or structural heart disease,115–119 although treatment with transplacental digoxin to improve cardiac systolic function has occasionally been attempted.120,121 Moreover, high-dose indomethacin has been used in a handful of fetuses with the Ebstein anomaly, right heart failure, severe tricuspid and pulmonary regurgitation; this succeeded in improving the fetal systemic perfusion and allowing in utero survival by restricting the arterial ductal flow reversal (unpublished authors’ data) If CHF is secondary, treatment of the primary cause, if possible, is the best strategy.113 This includes CHF secondary to anemia, twin-twin transfusion syndrome, or a fetal arrhythmia (see earlier) Supplementary Oxygenation Acute and Chronic Cardiovascular Effects It has been known since the 1930s that the administration of supplemental inhaled oxygen to the mother during labor increases the oxygen content of blood in the umbilical cord.122–124 However, oxygen is not routinely given during suspected intrapartum fetal distress due to the lower umbilical cord pH values (