Extensive information about the circulatory physiology of the fetus and newborn has accumulated. The works of Barcroft (37), Dawes (38), Lind and associates (39), and Rudolph (40) should be consulted for details, but the central features are discussed here. The circulation before birth consists of parallel circuits (Fig. 33-1). Blood in the aorta may follow several routes to a capillary bed in the fetus or the placenta, back to the heart, passing through either ventricle, and out again to the aorta. The stream of newly oxygenated blood from the placenta passes through the umbilical vein, the ductus venosus, the inferior vena cava,
and the right atrium. Unlike the circulation after birth, the streams of oxygenated and unoxygenated blood are not completely separated, although the more oxygenated blood from the inferior vena cava is mostly diverted through the foramen ovale into the left atrium. Consequently, blood from the left ventricle entering the ascending aorta and coronary and carotid circulations is somewhat higher in oxygen than that entering the descending aorta from the right ventricle by way of the ductus arteriosus.

The volume pumped by the right ventricle is normally about 55% of the combined output of both ventricles. Because both ventricles pump against the systemic resistance, the level of pressure in the two ventricles is comparable. The resistance to blood flow through the lungs is relatively great; only minimal flow through the lungs occurs in utero, and almost all of the right ventricular output into the pulmonary artery passes through the ductus arteriosus to the descending aorta. The parallel arrangement of the ventricles allows fetal survival despite a wide variety of cardiac lesions. With total obstruction of either ventricle, the other ventricle assumes the entire cardiac output. Reversal of the pulmonary arterial and aortic streams of blood, as occurs in transposition of the great arteries, produces no deleterious effect on the fetus. Additionally, ductal or ascending aortic flow may reverse in the presence of severe semilunar valvar stenosis or atresia. Despite this remarkable ability to adapt, grow, and survive, the fetus is affected by limitations in myocardial contractility. Prolonged, severe pressure or volume loading of the heart or primary myocardial disease may result in congestive heart failure, manifested by hydrops fetalis. The interplay between the metabolic effects of congestion in the fetus and the possible compensatory role of the placenta is not understood. Because lesions that may be expected to cause gross intrauterine difficulty are tolerated surprisingly well, the postulate that the placenta helps compensate for the metabolic abnormalities resulting from congestive heart failure is tenable.