Cardiac arrhythmias and conduction disorders occur in the antenatal period in 1–5% of pregnancies. 10–20% of fetal arrhythmias are life-threatening to the fetus. The causes of the development of cardiac arrhythmia in the fetus may be associated with structural defects of the heart, with congenital pathology of the cardiac conduction system, with abnormalities of depolarization and repolarization of cardiomyocytes, may be determined by genetic ion channelopathy. There are quite a few regions of the heart that can generate ectopic impulses. The origin of these areas can often be explained by the stages of embryological development of the heart. All cardiomyocytes of the developing heart initially have the properties of a pacemaker cell, but most of them differentiate into a cardiac muscle cell. Only small populations of myocytes that form the sinus node, atrioventricular node, and bundle of Hiss are blocked from differentiation and remain at the embryologic level of development. The persistence of nodal tissue in the working myocardium is thought to contribute to the development of arrhythmias. Because of their embryologic origin, these areas may exhibit automaticity, have increased susceptibility to ectopic impulses, and slow conduction, creating the conditions for arrhythmias. The mechanisms of differentiation of cardiomyocytes into either a working cell or cardiac conduction cell phenotype have not yet been fully defined. Transcription factors that regulate the development of the cardiac conducting system have now been identified and mutations in some of them cause conduction defects. Genetic defects and pre- and postnatal diseases can cause dysfunction of pacemakers and conduction pathways, which emphasizes the clinical need to understand the molecular and cellular mechanisms of their development. Knowledge of the pathways and mechanisms of fetal arrhythmias largely determines the possibility of their medical treatment and assists in genetic counseling.