Clinical evaluation of fetal cardiac ultrasound in fetal arrhythmias Fetal arrhythmias are often first detected by auscultation, but to determine their nature and impact on the fetus, fetal echocardiography is currently the only means of examination. 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. Therefore, the combination of the two can better evaluate the clinical significance of fetal arrhythmias and guide the choice of treatment plan, which is also the easiest and most reliable way to follow up the outcome. Fetal arrhythmias are fast, slow and irregular. (1) Fetal tachycardia: the fetal heart rate exceeds 160 bpm, mild tachycardia 160-180 bpm, and severe tachycardia >180 bpm, in the form of 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. This suggests that the prognosis for fetal supraventricular tachycardia is good and should be treated aggressively and not easily abandoned. Atrial fibrillation or atrial tachycardia shows extremely fast atrial beats, up to 400 bpm, but a slow ventricular rate, mostly around 200 bpm. 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 heart ultrasound, except for possible etiologies, and should be aggressively treated if it is clear that it is purely persistent. Depending on whether there is fetal edema, the mother should be given oral or intravenous digoxin (1st line) for 48-72 hours saturation (0.25-0.5mg, q8h) or 6-7 days saturation, and later maintenance doses of 0.25-0.2mgg8h, with a higher maternal blood concentration requirement of 2.0-2.5ng/ml. If there is no fetal edema, the fetal blood digoxin concentration is 80-100% of the maternal blood concentration. In the absence of fetal edema, the mother can be followed up on an outpatient basis with the oral slow saturation digoxin method only. In the presence of fetal edema, hospitalization is required for the addition of 2nd or 3rd line antiarrhythmic drugs, preferably Flecainide 100mg po q(6)-8h, maternal blood concentration 0.4-1.0µg/ml, fetal blood concentration is 70-80% of maternal blood concentration. Fetal and fetal heart ultrasound twice a week is required to determine fetal status and to enhance monitoring of the mother, with the involvement of a cardiologist. Other antiarrhythmic agents such as amiodarone, cardioplegia, and fibrate 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. Fetal bradycardia 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 also in premature atrial beats that are not transmitted inferiorly. Fetal heart rate below 120 bpm. mild 120-100 bpm, severe <100 bpm. complete AV block with ventricular rate of 40-80 bpm, M ultrasound showing normal atrial rate and slowed ventricular rate, most often with fetal heart failure, may be associated with precordial disease, poor prognosis in fetuses with precordial 3rd degree AV block. Sinus bradycardia can be caused by extra-fetal cardiac factors, such as fetal hypoxia, fetal head pressure, and high intrauterine pressure. Fetal cardiac irregularities include atrial bradycardia, ventricular bradycardia, or tachyarrhythmias with AV 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 examined in fetuses with arrhythmias, and 10% of fetal tachycardias are associated with cardiac anatomical abnormalities. Fetal arrhythmias need to be diagnosed and treated in a multidisciplinary manner, taking into account clinical and fetal heart rate monitoring and combined anomalies, and pregnancy should not be easily terminated.