Fetal bradycardia in early and late pregnancy

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Last reviewed: 16.04.2020

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Bradycardia is called a decrease in heart rate relative to normal (60-90 beats per minute). A slight deviation does not affect the state of human health, but is a signal of the development of pathology in the body. Similarly, the fetal heart rate in the womb should be in a certain range. Lowering it to 110-120 beats indicates a fetal bradycardia. A heart rate of <100 beats per minute may be present in 5% of fetuses with arrhythmia. [1]

The standard obstetric determination of the fetus of bradycardia was sustained FHR <110 beats per minute for at least a 10-minute period. FHRs depend on gestational age and decrease significantly as pregnancy progresses from a median of 141 beats per minute (interquartile range 135–147 beats per minute) <32 weeks of gestation to 137 beats per minute (interquartile range 130–144 beats per minute)> 37 weeks pregnancy. [2]

Causes of the bradycardia in the fetus

There are quite a few reasons why such a diagnosis may develop. Among them:

  • low hemoglobin in the blood;
  • infectious diseases;
  • prolonged and severe toxicosis;
  • cord entwining;
  • detachment of the placenta;
  • malformations in the development of the organs of the embryo;
  • many or low water;
  • the effect of maternal antibodies on the conductivity of the cells of the cardiac system.
  • consequence of combined spinal-epidural analgesia during labor induction with oxytocin infusion. [3], [4]
  • premature amniotomy (40%) significantly correlates with bradycardia in the fetus. [5]

Brief episodes of transient fetal slowdowns that occur within a few minutes are often noted, especially in the second trimester, and are considered benign. Permanent fetal bradycardia during pregnancy may be due to sinus, low atrial or connective bradycardia blocked by atrial bigeminia or atrioventricular block and needs to be evaluated to distinguish between them.

Risk factors

Factors contributing to the occurrence of fetal bradycardia include:

  • unhealthy lifestyle of a woman: smoking, alcohol, poor nutrition, lack of fresh air;
  • taking medications that adversely affect the fetus;
  • chronic pathologies of the expectant mother, especially the heart and lungs;
  • living in ecologically disadvantaged areas;
  • severe stressful situations.


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. [6]

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.

Symptoms of the bradycardia in the fetus

It is very difficult to suspect fetal bradycardia in the womb. In a born child, the first signs are expressed by the following symptoms: the newborn freezes, the skin turns pale, acquires a bluish tint, sometimes there are convulsions, apnea - respiratory arrest.

  • Early and late bradycardia

Fetal bradycardia in early pregnancy (up to 8 weeks) is highly likely to indicate a chromosomal abnormality. This may be a harbinger of Patau syndrome (the presence of the pathological 13th chromosome), Down (trisomy on the 21st chromosome), Edwards (tripling of 18 pairs of chromosomes).

Heart rhythm disturbances in the first trimester of pregnancy indicate diseases of the cardiovascular system. This is how congenital heart defects manifest themselves.

In the second and third semester of pregnancy, bradycardia most often indicates placental insufficiency when the blood flow in it is disturbed. The fetus does not sufficiently receive the nutrients necessary for its development, oxygen, hypoxia sets in. All organs, including the heart, suffer from this.

  • Bradycardia during childbirth

The normal course of childbirth and the same condition of the fetus does not cause significant deviations in the heart rhythm, regardless of its presentation. A decrease in the basal rhythm to 100 beats per second and lower for 5-6 minutes indicates fetal hypoxia. In this case, doctors have to make a decision about emergency delivery.

Complications and consequences

Sinus bradycardia is almost always associated with serious impaired development of the child in the womb. This is fraught with the threat of premature birth, possible bleeding in the 3rd trimester of pregnancy. A child can be born with a congenital heart disease, have deformities.

Progressive bradycardia before recording 68-56 beats per minute can cause fetal death. The overall mortality rate will be 20% (37% if termination of pregnancy is taken into account). Risk factors for mortality were congenital heart defects, hydrops, and / or ventricular dysfunction. [7]

Diagnostics of the bradycardia in the fetus

Chromosomal abnormality is determined using a blood test for hCG and PAPP-A (double test). The diagnosis is clarified by a chorionic biopsy, amniocentesis and cordocentesis.

Starting from 18 weeks of pregnancy, the doctor with a stethoscope listens to the heartbeat of the fetus. For a more accurate diagnosis, instrumental methods are used: magnetocardiography of the fetus,  [8] ultrasound, CTG (cardiotocography). [9]

The leading, and sometimes the main method for determining heart rhythm disturbances is ultrasound scanning. For differentiation with other pathologies, its various modes are used:

  • in the M-mode, the ventricle and atrium are examined, their rhythms of contractions are determined;
  • Pulse-wave doppleography captures the artery and vein and can record the flow of blood to the mitral valve and its outflow into the aorta, observe the renal, pulmonary, umbilical cord vessels.

Large heart abnormalities, including bradycardia, are detected at 18-22 weeks of gestation.

Cardiotocography is performed after 32 weeks. Using special sensors applied to the pregnant woman’s stomach, the fetal cardiac activity is recorded for 15-45 minutes and scored up to 10. An indicator of 6-7 points indicates fetal hypoxia, below 6 - its critical condition.

Fetal electrocardiogram (fECG) can detect QRS signals in the fetus from the 17th week of pregnancy; however, the technique is limited by the minimum size of the fetal signal relative to the noise ratio. This is affected by early pregnancy, maternal noise such as uterine contractions, the degree of electrical insulation caused by surrounding tissues (vernix caseosa), and skin resistance. [10]

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Treatment of the bradycardia in the fetus

Short episodes of bradycardia, which last no more than 2 minutes, are considered benign, transient, do not require constant monitoring, treatment and, as a rule, do not lead to complication of pregnancy.

A more severe form of pathology sometimes requires intrauterine surgery, sometimes correction is carried out after the birth of the child.

With placental insufficiency, the expectant mother is treated in a hospital, prescribing drugs that improve the utero-placental blood flow, as well as aimed at treating the underlying disease that led to this condition.

The rationale for the treatment of isolated intrauterine development of chronic hepatitis B fetus is primarily aimed at containing antibody-mediated myocardial inflammation, increasing fetal cardiac output and improving survival. Maternal administration of dexamethasone has been shown to improve incomplete fetal AV block, myocardial dysfunction, and cavity effusion. Beta sympathomimetics, such as salbutamol and terbutaline, can be used to increase fetal heart rate and myocardial contractility. Published data from a hospital for sick children in Toronto (Jaeggi et al., 2004) suggest an increase in survival of over 90% for HBV antibody-related if a maternal high dose of dexamethasone was started during diagnosis of the anomaly and maintained during pregnancy, and if β- an adrenergic drug was added at a fetal heart rate below 50–55 beats per minute. [11]


A mild form of bradycardia can be prevented by such preventive measures as avoiding stress, walking in the fresh air, observing sleep patterns, eating healthy foods that include foods rich in vitamins and minerals, and quitting smoking and alcohol.


Favorable postnatal outcomes have children with transient bradycardia. With the sinus part of the newborn, a therapeutic or cardiac surgical correction is required. For those for whom the cause of the pathology lies in neurological, respiratory, hemodynamic disorders, metabolic acidosis, an unfavorable outcome is possible - serious health problems and even death. In the case of prolonged intrauterine bradycardia of the fetus, delivery by emergency cesarean section within 25 minutes improved the long-term neurological outcome in the newborn. [12] Childbirth in a special perinatal center improves prognosis.

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