Ensuring the safety of mothers and infants in the twenty-first century, early detection of fetal abnormalities and giving timely and correct treatment are issues of importance to all countries in the world. China’s national policy of eugenics, the direction of improving the quality of the birth population and reducing low age mortality have placed higher demands on obstetricians, gynecologists and pediatricians. Fetal echocardiography is a non-invasive fetal monitoring technique that has been developed in the last 20 years to provide more in-depth and detailed fetal cardiovascular information. Fetal cardiac ultrasound began in the developed world in the 1970s with M-mode ultrasound, but our King’s New Room Professor observed the fetal heartbeat with A-mode ultrasound in the 1960s. The application of 2D ultrasound and Doppler technology has brought the fetal diagnosis of congenital cardiovascular disease to a new and more perfect level, further promoting the development of neonatal precardiology and the therapeutics of fetal precardiac disease, including fetal precardiac surgery and catheter intervention of fetal precardiac. Fetal cardiac ultrasound involves the monitoring of fetal hemodynamic function and cardiac anatomy and morphology, therefore, fetal cardiac ultrasound plays a key role not only in the diagnosis and interventional treatment of precocious heart, but also in the diagnosis of fetal arrhythmia and cardiac insufficiency and monitoring of therapeutic effects. The development of perinatal cardiology is a joint effort of fetal ultrasound, fetal cardiac sonographers, pediatric cardiologists, perinatal medicine and obstetricians, and genetic pathologists, and requires multidisciplinary collaboration. I. Fetal congenital heart disease Congenital heart disease children account for 8 to 12 per 1000 births, which means that there are 120,000 to 200,000 children born with congenital heart disease in China every year, of which about 20% or more are born with complex congenital heart disease that cannot be treated well with current treatments or are prone to die early after birth, which does not yet include congenital heart disease that can have a better recent surgical outcome, but has a high rate of long-term re congenital heart disease with a high rate of surgery (Table 1). The problem reflected in the birth of these babies in China is that precocious heart disease was the number one cause of infant death in 2002 (birth asphyxia was second and preterm low birth weight was third), and Beijing has been number one for 6 years. In areas with less developed medical systems, it is possible that other causes of death after birth dominate, but congenital cardiovascular disease is at least in the top four. Beijing monitors common and key genetic diseases, congenital diseases and infectious diseases, venereal diseases, and mental illnesses annually, monitoring nearly 160,000 people each year and detecting 35 diseases, with a congenital and genetic disease detection rate of about 1 percent. The top three in order are: high myopia in both eyes, congenital heart disease, and congenital red-green blindness in both eyes. Among them, congenital heart disease has the highest rate of disability and death. In recent years, with the continuous improvement of congenital surgical techniques, surgical methods, surgical materials, and the development of extracorporeal circulation and myocardial protection techniques more suitable for infants, the number of complex congenital heart disease species that can be surgically corrected has been increasing, the age limit has been gradually reduced, and the number of neonatal surgeries has been rising. In addition, due to a better understanding of the physiological changes caused by cardiac surgery and more reasonable postoperative management, the survival rate after surgery is increasing and the complications and mortality rate are gradually decreasing. At the same time, the development of pediatric cardiology, close collaboration with cardiac surgery, and the development of mosaic therapy have brought the treatment of congenital heart disease to a new stage. Many children with serious and complicated congenital heart disease are already in a critical state when they are admitted to the hospital due to the lack of awareness or delay in diagnosis of the congenital heart disease, and most of them lose the precious time for surgery and die. Some data show that about 70% of neonatal deaths due to precocious heart disease occur within one week after birth, which means that a clear prenatal diagnosis of cardiac anomalies is necessary to save these lives by getting the correct treatment in time after delivery. For example, hypoplastic left heart syndrome, complete transposition of the great arteries with intact ventricular septum, and pulmonary atresia are all arterial duct-dependent complex congenital heart diseases. Without a clear prenatal diagnosis, they often die early in the postnatal period due to late postnatal diagnosis and untimely application of prostaglandin E, which causes the ducts to tend to be atretic or atretic. Severe aortic stenosis, pulmonary stenosis, and aortic constriction, if diagnosed prenatally and treated postnatally with timely catheter intervention balloon angioplasty, can receive very satisfactory near and long-term results. If treatment is delayed or due to serious complications such as heart failure and arrhythmias can lead to death or leave behind secondary malformations that are difficult to recover, such as ventricular hypertrophy and myocardial fibrosis, resulting in lifelong disability. Some scholars believe that certain cardiac malformations are secondary, such as right ventricular dysplasia may be secondary to pulmonary atresia or very severe pulmonary stenosis with continuous fetal ventricular septum (1-3.5% of precardiac disease), and left heart dysplasia syndrome (7.9% of precardiac disease) may be associated with severe fetal aortic stenosis or restrictive foramen ovale. Due to the lack of a ventricle, any postnatal treatment can only maintain a lifelong single ventricle circulation. Therefore, research on fetal catheter intervention and fetal cardiac surgery to avoid or mitigate secondary cardiac malformations, and fetal cardiac insufficiency has become a clinical research hotspot in the last decade or so. Fetal arrhythmias are often first detected by auscultation, but fetal echocardiography is currently the only means to determine their nature and impact on the fetus. Because of the limited duration of ultrasound monitoring, the duration of fetal arrhythmias cannot be determined. Electronic monitoring of fetal heart rate can provide a long time course of instantaneous fetal heart rate and average heart rate, which can assist in determining the duration of tachycardia or bradycardia, but cannot determine the nature of the arrhythmia, and requires a larger gestational age. Therefore, the combination of both can better evaluate the clinical significance of fetal arrhythmias and guide the choice of treatment plan, and is also the easiest and most reliable way to follow up the outcome. Fetal arrhythmias are tachyarrhythmic, slow and irregular. Fetal tachycardia: the fetal heart rate exceeds 160 bpm. mild tachycardia 160-180 bpm, severe tachycardia >180 bpm. the forms are supraventricular fetal tachycardia, atrial tachycardia, atrial fibrillation, ventricular tachycardia, etc. In addition to arrhythmic factors, such as fetal hypoxia, fetal maternal transfusion syndrome, twin fetal transfusion syndrome, and maternal hyperthyroidism are also causes of fetal tachycardia. Fetal tachycardia includes sinus tachycardia, supraventricular tachycardia, atrial fibrillation or atrial flutter, and ventricular tachycardia. The diagnosis is made by ultrasound based on the fetal heart rate, rhythm, and whether the atria and ventricles are in agreement with each other. Fetal tachycardia can be intermittent and recurrent, or it can be continuous. Supraventricular tachycardia is common in fetuses, with more than 90% being atrioventricular and less than 10% being intraventricular. The prognosis is good in cases without fetal edema. In a group of 30 cases of fetal supraventricular tachycardia, 27 cases were followed up for 1-7.25 years after birth, except for 2 cases that died of preterm birth and 1 case that died of irregular digoxin use, 23 cases recovered sinus rhythm within 1 year after birth without recurrence, and only 1 case had recurrent tachycardia after 6 years, suggesting that fetal supraventricular tachycardia has a good prognosis and should be treated actively and not given up easily. Atrial fibrillation or atrial flutter shows extremely fast atrial beats up to 400 bpm, but slow ventricular rate, mostly around 200 bpm, which is rare clinically, and atrial flutter has a good prognosis. Persistent fetal tachycardia can lead to fetal edema, fetal heart failure, and pericardial, thoracic, or abdominal effusion. Fetal supraventricular tachycardia should be clearly diagnosed by aggressive fetal and fetal cardiac ultrasound, except for possible causes of structural cardiac abnormalities, and should be treated aggressively if it is clear that persistent supraventricular tachycardia alone is present. Depending on whether there is fetal edema, the mother is given oral or intravenous digoxin (1st line) for 48-72 hours saturation (0.25-0.5mg , q8h ) or 6-7 days saturation method, and later maintenance amount 0.25-0.2mg g8h, the mother’s blood concentration requires higher 2.0-2.5ng/ml. if there is no fetal edema, the fetal blood digoxin concentration is 80-100&# of the mother’s blood concentration. xFF05;. In the absence of fetal edema, the mother can be followed up on an outpatient basis with only the oral slow saturation digoxin method. With fetal edema, inpatient treatment is required plus 2nd or 3rd line antiarrhythmic drugs, with the first choice of flecainide 100mg po q(6)-8h, maternal blood concentration 0.4-1.0& micro; g/ml, fetal blood concentration is 70-80&# xFF05; of the mother. Fetal and fetal heart ultrasound twice a week is required to determine fetal status and to enhance monitoring of the mother, requiring the involvement of a cardiologist in the treatment. Other antiarrhythmic agents such as amiodarone, cardioplegia, escitalopram, etc. have been reported. The preferred route of administration is via mother-placenta-fetus. If treatment is ineffective or if the fetus has severe heart failure or is too young to survive early delivery, the amniotic cavity, umbilical vein, or fetal abdominal wall injection routes may be used. Other tachyarrhythmias are not described in this article, but caution is needed in giving drug therapy. Fetal bradycardia, with fetal heart rate below 120 bpm, is seen in paroxysmal sinus bradycardia (increased vagal tone), persistent sinus bradycardia (abnormal sinus node function, maternal hypothermia, long QT syndrome), 2nd or 3rd degree AV block, and additionally commonly in premature atrial beats that are not transmitted inferiorly. A limit of 120-110 bpm is usually without adverse consequences. Below 100 bpm, the possibility of congenital heart disease such as atrial defect, ventricular defect, and left atrial heterogeneity should be considered. Complete fetal AVB with a ventricular rate of 40-80 bpm and a normal atrial rate with a slowed ventricular rate on M ultrasound is most often associated with fetal heart failure and may be associated with congenital heart disease. The prognosis for a fetus with congenital 3rd degree AVB is poor. Simple 3rd degree AVB is common in mothers with immune disorders or just positive immune antibodies. The chance of having a child with 3rd degree AVB in the first trimester is 5-8 in mothers with positive anti-SSA and SSB antibodies, but up to 15 in the second trimester. Sinus bradycardia can be caused by extra-fetal cardiac factors, such as fetal hypoxia, fetal head pressure, high intrauterine pressure, and also by fetal sympathetic-parasympathetic imbalance and vagal hyperactivity, especially around 20 weeks of gestation. Fetal irregular heartbeat: This includes atrial premature arrhythmias, ventricular premature arrhythmias or tachyarrhythmias with atrioventricular block. Occasional preterm contractions are not clinically significant. In a group at Yale University with 984 fetal arrhythmias, 878 (89%) had preterm contractions. Fetal cardiac anatomical abnormalities should be noted in fetuses with arrhythmias. 10% of fetal tachycardias are associated with cardiac anatomical abnormalities. The fetal arrhythmia should be analyzed together with clinical and fetal heart rate monitoring and combined anomalies. Fetal cardiac insufficiency is commonly associated with abnormal heart development, hemolysis, intrauterine growth retardation (IUGR), fetal arrhythmia, maternal disease (diabetes), and overdue pregnancy. Fetal ultrasound has been much studied for fetal heart function and is the best tool to evaluate fetal heart function and to detect fetal cardiac insufficiency earlier than fetal heart rate changes and treat it early. Ultrasound manifestations of fetal heart failure: (1) fetal heart enlargement; (2) fetal heart area/thorax area ? 0.4 (normal 0.25-0.33); (3) one atrium/ventricle is larger than the other; (4) ventricular wall thickness is greater than in fetuses of the same age; (5) regurgitation of fetal heart valves; (6) decreased cardiac ejection fraction (left ventricular EF? 50％ (normal 50％-80％); (7) fetal edema; (8) persistent bradycardia ( 70bpm) or tachycardia (?200bpm); (9) increased velocity of the inferior vena cava a-peak reversal; (10) redistribution of blood flow (loss of diastolic blood flow in the umbilical artery, renal artery, etc.). The mother is taking digoxin or treating the cause, and fetal cardiac ultrasound is also available to follow the effects of treatment. Fetal edema and plasma cavity effusion have clear ultrasound manifestations and more etiologies, but cardiovascular malformations and cardiac rhythm should be carefully examined to exclude their abnormalities IV. Fetal cardiac tumors and cardiomyopathies Fetal cardiac tumors account for 0.14％ of fetal cardiac ultrasound, the most common myocardial rhabdomyosarcoma accounts for 89％ and the incidence is followed by teratoma, fibroma, and hemangioma. Cardiomyopathies such as dilated cardiomyopathy, hypertrophic cardiomyopathy, and endocardial elastosis can also be demonstrated. Since these heart diseases can cause heart failure and arrhythmias during the fetal period and have a poor prognosis after birth, termination of pregnancy can be considered if the fetal heart is clearly diagnosed by ultrasound. In one case, the fetal diagnosis of myocardial densification insufficiency was cautious, we had a case of fetal right heart densification insufficiency with massive tricuspid regurgitation, treated with postnatal cardiac dilatation, 2 years later, the tricuspid regurgitation was small, the right ventricle was nearly normal, and the comb-like myocardium was significantly shortened. Heart failure was controlled, and after treatment of chronic cardiac insufficiency, the left ventricular comb myocardium was significantly shortened. Because of the development of the world science and the leap forward in medical electronics, the electronic monitoring of the fetus was advanced and fetal diseases including fetal heart disease could be carried out. It is because of the growing awareness of diseases in the fetal period that both functional and structural diseases are associated with the treatment and regression of diseases after birth, which inevitably affects the diagnosis, treatment and regression of neonatal diseases. As the diagnosis of diseases in the fetal period continues to develop, and different countries and nationalities have different concepts of fetal life, they will naturally adopt different treatment methods, which will inevitably affect the spectrum of human diseases in the future, some of which will be significantly reduced or disappear, such as chromosomal diseases, gene-related diseases, cardiac tumors, cardiomyopathies, complex precordial heart, complex malformations of the nervous system such as anencephaly, limb malformations, and many others. For human eugenics is undoubtedly a good thing, saving a lot of social resources and family burdens, but to eliminate congenital complex malformations and diseases that can have obvious abnormalities in the fetal period, and to eliminate life after birth with severe disabilities in the fetal period is the direction of our medical development or our human tragedy. When does life begin? Does life begin when the sperm and egg are united or does it begin when the fetus leaves the mother to survive on its own? Different people will have different opinions. What will our world be like if in the future, thanks to the development of medicine, all the people who come into the world are elites? After all, the existence of the underprivileged is the soil and cradle of human love. Although I was one of the first to advocate the development and strengthening of fetal heart disease diagnosis and treatment, and the development of this profession under the national policy of eugenics in China, I have not yet reached a conclusion on what is right from an ethical point of view. At least today, with the current upsurge in the development of fetal malformation diagnosis, consultation and treatment in China, I do not want it to become a great leap forward. It is necessary to collapse our hearts, to consider the problem more, to reduce the impetuous and fashionable ills, to be scientific, to be responsible for our human beings, to be responsible for every life.