The irregular rhythm of the contractions of the heart is associated with premature pulses entering the myocardium. This is due to a decrease in the automatism of the sinus node, located at the mouth of the vena cava, flowing into the right atrium. Such arrhythmia is constant or transient.
The latter is less dangerous, because It is caused by temporary disturbances in the functioning of the heart, such as constricting blood vessels due to the uncomfortable position of the fetus.
Persistent or pathological bradycardia threatens the fetus with prolonged hypoxia. Permanent intrauterine bradycardia is rare in the prenatal period. It is usually associated with sinus bradycardia due to fetal distress, atrial extrasystoles, and congenital complete heart block. 
Most important is the observation of persistent bradycardia, which usually refers to one of the following mechanisms: (1) sinus bradycardia; (2) atrial bigemia; and (3) complete heart block (CHB).
Sinus bradycardia, secondary to progressive fetal hypoxia, is an emergency obstetric situation. The cardiac etiology of sinus bradycardia is less common, but includes prolonged QT syndrome due to extremely prolonged repolarization and congenital absence or dysfunction of the sinus node, for example, in the left atrial appendage isomerism (Ho et al., 1995). The causes of cardiac activity differ on the basis of control echocardiographic and postnatal electrocardiographic data.
Numerous non-performed PACs can result in an irregular, slow ventricular rate below 100 beats per minute. A heart rate becomes regular if every second beat is a blocked PAC, which determines not conducted atrial bigeminia. In M-mode or Doppler recording of atrial bigemia, the atrial frequency is irregular (alternating sinus and premature strokes), while the ventricles beat regularly at a slow pace (60–80 beats per minute), which is half the atrial frequency. Atrial beheminia may persist for several hours, but is clinically benign and will eventually disappear without treatment.
Irreversible complete heart block, the most common manifestation of conduction disturbances in the fetus, accounts for almost half of all major fetal arrhythmias observed by fetal cardiology. On echocardiography, the atrial frequency is normal and regular, but the ventricles beat independently much more slowly (40–80 beats per minute) due to a failure in the electrical conductivity of the AV. Heart block is most often associated with either structural heart disease or maternal anti-Ro autoantibodies. This condition is associated with a significant risk of mortality, because the fetus needs to overcome a slow ventricular rhythm, loss of a coordinated atrial contribution to ventricular filling and, possibly, concomitant heart disease or carditis. Identification of the main structural heart disease, fetal edema, poor contractility and ventricular frequency below 50 beats per minute - all this is associated with a poor pregnancy outcome.
The most common association of fetal chronic heart failure of the fetus with structural heart disease is an unbalanced defect in the atrioventricular septum associated with left isomerism, which is almost universally lethal, regardless of the choice of perinatal care. Fetal hCG without structural heart disease has a better prognosis and is mainly associated with the transplacental passage of maternal autoantibodies directed to fetal ribonucleoproteins Ro / SSA. Antibodies against Ro are present in approximately 2% of pregnant women. In a similar percentage (1-2%) of the fetuses, these antibodies will cause inflammation of the AV node and myocardium. Inflamed tissues can then heal with fibrosis, which can cause heart block, endocardial fibroelastosis, and dilated cardiomyopathy. Heart block, the most common cardiovascular complication associated with antibodies (Jaeggi et al., 2010).
Persistent bradycardia of the fetus is relatively rare. Key mechanisms include congenital displaced atrial activation or acquired damage to the sinoatrial node. The frequency of the sinus node can be suppressed, for example, due to (1) isomerism of the left and right atria, (2) inflammation and fibrosis in the normal sinus node in patients with viral myocarditis or collagen vascular disorders (SSA / Ro [+] or SSA / Ro and SSB / La [+] antibodies) or (3) maternal treatment with β-blockers, sedatives, or other drugs. For treatment of sinus or low atrial bradycardia, fetal therapy is not required, but observation is recommended.