1.Fetal circulating oxygen: The partial pressure of umbilical vein oxygen in the fetal circulation is about 32 mmHg and the partial pressure of umbilical artery oxygen is about 15 mmHg, which is much lower than the postnatal level, but the fetal oxygen saturation can be maintained at a high level because of the leftward shift of oxygen dissociation curve during fetal period (Figure 5-2). Umbilical vein oxygen saturation is about 80% and drops to about 70% after mixing with the blood flow from the inferior vena cava and hepatic veins. The Euclidean valve at the anterior edge of the inferior vena cava opening produces a laminar flow in the middle of the right atrium, so that most of the more oxygenated inferior vena cava blood is introduced into the left atrium through the foramen ovale fissure, and the oxygen saturation drops to about 65% in the left atrium after mixing with a small portion of the blood returning from the pulmonary veins, which do not yet have a gas exchange function. The oxygen saturation of the superior vena cava is only 40%, and after entering the right atrium and mixing with the blood returning from the inferior vena cava, the oxygen saturation rises to about 55% at the level of the right ventricle, and after entering the main pulmonary artery, most of the blood enters the descending aorta through the arterial catheter, and after mixing again with the more oxygenated blood from the ascending aorta, the oxygen saturation increases to 60%, supplying the lower part of the fetal body and the placenta [1,2,5]. This shows that the arteriovenous blood flow in the fetal circulation is not clear-cut, and the efficiency of the circulation is naturally not as high as that in adults, but during intrauterine development it is necessary to take care of the characteristics of placental oxygen uptake and to switch to a circulatory reroute with pulmonary oxygen uptake immediately after birth, so the fetal circulation is both effective and flexible in opening and closing. 2, fetal circulation pressure and blood flow rate: fetal sheep research data show [6,7] that during pregnancy the umbilical vein pressure is about 8-10 mmHg, portal vein pressure is about 5-6 mmHg, superior vena cava, inferior vena cava and right atrial pressure is about 2-3 mmHg, left atrial pressure is about 1-2 mmHg, the average ventricular pressure increases gradually with the progress of pregnancy, 25-30 mmHg at 60 days of gestation, and 60-70 mmHg at term. The human fetal ventricular pressure is slightly higher than the fetal sheep ventricular pressure. The velocity of inferior vena cava blood flow in the fetal circulation is approximately 15 cm/s, and the velocity of venous catheter blood flow is approximately 55-60 cm/s. This characteristic allows relatively high velocity blood flow in the venous catheter to pass through the foramen ovale directly into the left atrium. The velocity of the pulmonary artery trunk is higher than that of the ascending aorta in the human fetus, and the variation in velocity and waveform between the two is similar to that of the fetal sheep data, but the difference in velocity between the pulmonary artery trunk and the ascending aorta is slightly lower in the human fetus. Because the pulmonary circulation is not open during the fetal period, most of the blood flow from the pulmonary artery trunk enters the descending aorta through the arterial duct, and thus the arterial duct blood flow velocity is significantly higher than that of the branch pulmonary arteries. 3. Fetal cardiac output and its distribution in the fetal circulation: Unlike the equal left and right cardiac output after birth, the fetal cardiac output is defined as the total amount of blood excreted by both ventricles, i.e., the joint cardiac output. The ratio of left and right ventricular cardiac output in human fetuses in late gestation is about 1:1.2-1.3, i.e., the left cardiac output is 200 ml/(kg.min), the right cardiac output is 250 ml/(kg.min), and the joint cardiac output is 450 ml/(kg.min). The placental vascular resistance is the lowest in the fetal circulation and receives the largest part of the fetal cardiac output (about 55% in early and middle pregnancy and decreases to about 40% in late pregnancy, i.e. 250-180 ml/(kg.min), which facilitates the exchange of substances between the fetus and the mother. In the early and middle stages of pregnancy, the pulmonary artery receives only 10-15% of the right heart output, i.e., 35 ml/(kg.min), and thus the pulmonary artery branches are thinly developed. At the time of delivery, pulmonary artery blood flow increases significantly, reaching one-third of the right ventricular expulsion, i.e., 80-90 ml/(kg.min), and the pulmonary artery then develops rapidly, accompanied by an increase in cerebral blood flow and a decrease in placental blood flow. The coronary circulation accounts for about 3% of the joint cardiac output, i.e. 13-15 ml/(kg.min), and the blood supply to the head and upper part of the torso accounts for about 20% of the joint cardiac output, i.e. 90 ml/(kg.min). In the middle and late stages of pregnancy, blood flow to all organs of the fetal sheep gradually increases with the progress of pregnancy, and the human fetus changes in a similar way. In addition, the size of the fetal heart chambers and the internal diameter of the great vessels can be used to reflect the blood flow through this area and its development. During fetal heart development, if there is a congenital structural heart malformation that would result in abnormal blood flow, the chambers and vessels of the heart with insufficient blood flow will likely undergo dysplasia or even stagnation and cause the malformation to continue to worsen in utero, which is the rationale for prenatal intervention for some severe congenital heart diseases, such as hypoplastic left heart syndrome and severe pulmonary stenosis. Through appropriate intrauterine treatment to change the abnormal blood flow caused by cardiovascular anomalies and establish a normal fetal hemodynamic state, it can delay, prevent or reverse the occurrence of fetal ventricular dysplasia and delayed development of the body/pulmonary vascular bed, meet the requirements of the body and pulmonary circulation after birth, and improve the prognosis of fetuses with severe cardiovascular anomalies. 4. Factors affecting fetal cardiac output: Influencing factors include heart rate, ventricular pre/post load and myocardial functional status. The data of fetal sheep study shows that if the heart rate of fetal sheep increases from 140 beats/min to 160 beats/min, the fetal ventricular expulsion increases by 15-20%. When the fetal heart rate exceeds 300-320 beats/min, the fetal ventricular filling time and ejection time are both insufficient, thus decreasing the cardiac output. Stimulation of the fetal vagus nerve slows the fetal heart rate by 15%, with a corresponding decrease in fetal ventricular blood output, and a significant decrease in fetal cardiac output when the heart rate is too low. The effect of human fetal heart rate variability on cardiac output is the same as in fetal lambs. An increase in fetal afterload will result in a decrease in fetal cardiac output, and a low preload such as right atrial pressure and right ventricular end-diastolic pressure will result in a significant decrease in cardiac output. An appropriate increase in preload, such as a 2-3 mmHg increase in atrial pressure, will result in a significant increase in cardiac output, but a continued increase in right atrial pressure will not result in a continued increase in cardiac output. In contrast, a sustained increase in afterload will result in a gradual decrease in cardiac output with subsequent increases in load, regardless of the level of atrial pressure. Myocardial contractility factors affecting fetal cardiac output include: low myocardial tone, low myocardial T-tubule system, poorly organized myocardial fibers, low sarcoplasmic reticulum calcium uptake, low myocardial sympathetic nerve distribution, small myocardial cell size, and low mitochondria, sarcoplasmic reticulum, myofilaments, and α and β-adrenergic receptors at the same initial length. The main source of energy for cardiomyocytes is glucose, not fatty acids. In increased myocardial workload cardiac hypertrophy, fetuses may have cardiomyocyte replication, i.e., an increase in cardiomyocyte number, whereas in adults there is only an increase in cardiomyocyte volume. Fetal myocardium has a low contractile component, myocardial systolic and diastolic function is much lower than in mature myocardium, and fetal cardiomyocytes are in an optimal length myocyte state. According to Frank-Starling’s law, increasing cardiac output by increasing cardiac volume per beat is very limited, and a high circulatory dynamics can only be maintained by increasing heart rate and biventricular work. A significant increase (e.g., fetal tachyarrhythmia) or significant decrease (e.g., intrauterine distress) in fetal heart rate can lead to a dramatic decrease in cardiac output, and under the combined effect of single or multiple factors, the fetal heart are more susceptible to heart failure.