Fetal bradycardia in early and late pregnancy

Bradycardia is a decrease in heart rate relative to the norm (60-90 beats per minute). A slight deviation does not affect a person's health, but is a signal of the development of pathology in the body. In the same way, the fetus's heartbeat in the womb should be within a certain range. A decrease to 110-120 beats indicates fetal bradycardia. Heart rate <100 beats per minute may be present in 5% of fetuses with arrhythmia. [ 1 ]

The standard obstetric definition of fetal bradycardia was a sustained FHR <110 bpm for at least a 10-minute period. FHRs vary with gestational age and decrease significantly as pregnancy progresses from a median of 141 bpm (interquartile range 135–147 bpm) <32 weeks' gestation to 137 bpm (interquartile range 130–144 bpm) >37 weeks' gestation.[ 2 ]

Causes fetal bradycardia

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

• low hemoglobin levels in the blood;
• infectious diseases;
• prolonged and severe toxicosis;
• umbilical cord entanglement;
• placental abruption;
• developmental defects of the embryonic organs;
• polyhydramnios or oligohydramnios;
• the effect of maternal antibodies on the conductivity of cardiac cells.
• consequence of combined spinal-epidural analgesia during induction of labor with oxytocin infusion. [ 3 ], [ 4 ]
• Premature amniotomy (40%) significantly correlates with fetal bradycardia. [ 5 ]

Brief episodes of transient fetal decelerations that resolve within minutes are common, especially in the second trimester, and are considered benign. Persistent fetal bradycardia during pregnancy may be due to sinus, low atrial or junctional bradycardia, blocked atrial bigeminy, or atrioventricular block and requires evaluation to differentiate them.

Risk factors

Factors that contribute to the development of fetal bradycardia include:

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

Pathogenesis

Irregular heart rhythm is associated with premature impulses reaching the myocardium. This is due to decreased automatism of the sinus node, located at the mouth of the vena cava, flowing into the right atrium. Such arrhythmia can be permanent or transient.

The latter is less dangerous, as it is caused by temporary disturbances in the functioning of the heart, for example, compression of blood vessels due to an awkward position of the fetus.

Persistent or pathological bradycardia threatens the fetus with prolonged hypoxia. Persistent 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 sustained bradycardia, which is usually attributed 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 obstetric emergency. Cardiac etiologies of sinus bradycardia are less common but include long QT syndrome due to extremely prolonged repolarization and congenital absence or dysfunction of the sinus node, such as in left atrial appendage isomerism (Ho et al., 1995). Cardiac causes are differentiated based on follow-up echocardiographic and postnatal electrocardiographic findings.

Multiple non-conducting PACs may result in an irregular, slow ventricular rate below 100 bpm. The heart rate becomes regular if every other beat is a blocked PAC, which defines non-conducting atrial bigeminy. On M-mode or Doppler tracing of atrial bigeminy, the atrial rate is irregular (alternating sinus and premature beats), while the ventricles beat regularly at a slow rate (60–80 bpm), which is half the atrial rate. Atrial bigeminy may persist for several hours but is clinically benign and will eventually resolve without treatment.

Irreversible complete heart block, the most common manifestation of conduction defect in the fetus, accounts for nearly half of all major fetal arrhythmias seen in fetal cardiology. On echocardiography, the atrial rate is normal and regular, but the ventricles beat independently at a much slower rate (40–80 bpm) due to a failure of AV conduction. Heart block is most often associated with either structural heart disease or maternal anti-Ro autoantibodies. This condition carries a significant mortality risk because the fetus must overcome a slow ventricular rate, loss of coordinated atrial contribution to ventricular filling, and possibly underlying cardiac disease or carditis. The presence of underlying structural heart disease, fetal edema, poor contractility, and a ventricular rate below 50 bpm are all associated with poor pregnancy outcome.

The most common association of fetal CHF with structural heart disease is unbalanced atrioventricular septal defect associated with left isomerism, which is almost universally fatal regardless of the choice of perinatal care. Fetal CHF without structural heart disease has a better prognosis and is mainly due to transplacental passage of maternal autoantibodies directed to the fetal ribonucleoproteins Ro/SSA. Anti-Ro antibodies are present in approximately 2% of pregnant women. In a similar percentage (1–2%) of fetuses, these antibodies will cause inflammation of the AV node and myocardium. The inflamed tissues may 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 fetal bradycardia is relatively rare. Underlying mechanisms include congenital biased atrial activation or acquired sinoatrial node injury. The sinus node rate may be suppressed, for example, by (1) left and right atrial isomerism, (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. Fetal therapy is not required for treatment of sinus or low atrial bradycardia, but observation is recommended.

Symptoms fetal bradycardia

It is very difficult to suspect fetal bradycardia in the womb. In a newborn, 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 - cessation of respiratory movements.

• Bradycardia in early and late pregnancy

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

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

In the second and third trimesters of pregnancy, bradycardia most often indicates placental insufficiency, when blood flow in it is disrupted. The fetus does not receive the nutrients and oxygen necessary for its development to a sufficient degree, and hypoxia occurs. All organs, including the heart, suffer from this.

• Bradycardia during labor in the fetus

Normal labor and the same condition of the fetus do not cause significant deviations in the heart rate, regardless of its presentation. A decrease in the basal rhythm to 100 beats per second or less for 5-6 minutes indicates fetal hypoxia. In this case, doctors have to decide on emergency delivery.

Complications and consequences

Sinus bradycardia is almost always associated with serious developmental disorders of the child in the womb. This is fraught with the threat of premature birth, possible bleeding in the 3rd trimester of pregnancy. The child may be born with a congenital heart defect, have deformities.

Progressive bradycardia to 68-56 bpm can cause fetal death. Overall mortality can 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 fetal bradycardia

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

Starting from the 18th week of pregnancy, the doctor listens to the fetal heartbeat with a stethoscope. For more accurate diagnostics, instrumental methods are used: fetal magnetocardiography, [ 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 M-mode the ventricle and atrium are examined and their contraction rhythms are determined;
• Pulse-wave Doppler ultrasound captures the artery and vein and can record the blood flow to the mitral valve and its outflow into the aorta, and observe the renal, pulmonary, and umbilical vessels.

Major cardiac abnormalities, including bradycardia, are detected at 18-22 weeks of pregnancy.

Cardiotocography is performed after 32 weeks. Using special sensors placed on the pregnant woman's abdomen, the fetus's cardiac activity is recorded for 15-45 minutes and assessed in points up to 10. An indicator of 6-7 points indicates fetal hypoxia, below 6 - its critical condition.

Fetal electrocardiogram (fECG) can detect fetal QRS signals as early as 17 weeks of gestation; however, the technique is limited by the minimum fetal signal to noise ratio. This is influenced by early pregnancy, maternal noise such as uterine contractions, the degree of electrical insulation caused by surrounding tissue (vernix caseosa), and skin resistance.[ 10 ]

Treatment fetal bradycardia

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

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

In case of placental insufficiency, the expectant mother is treated in a hospital, prescribing drugs that improve uteroplacental blood flow, as well as those aimed at treating the underlying disease that led to this condition.

The rationale for treatment of isolated intrauterine fetal CHB is primarily aimed at inhibiting antibody-mediated myocardial inflammation, increasing fetal cardiac output, and improving survival. Maternal dexamethasone has been shown to improve fetal incomplete atrioventricular block, myocardial dysfunction, and pleural effusion. Beta-sympathomimetics such as salbutamol and terbutaline can be used to increase fetal heart rate and myocardial contractility. Published data from the Hospital for Sick Children in Toronto (Jaeggi et al., 2004) suggest improved survival above 90% for antibody-associated CHB if high-dose maternal dexamethasone was initiated at the time of diagnosis of the anomaly and maintained throughout pregnancy and if a β-adrenergic agent was added when the fetal heart rate was below 50–55 bpm. [ 11 ]

Prevention

Mild bradycardia can be prevented by such preventive measures as avoiding stress, walking in the fresh air, maintaining a sleep schedule, eating a healthy diet with foods rich in vitamins and minerals, and quitting smoking and drinking alcohol.

Forecast

Children with transient bradycardia have a favorable postnatal outcome. In the case of sinus bradycardia, some newborns require therapeutic or cardiac surgery correction. For those whose pathology is caused by neurological, respiratory, hemodynamic disorders, metabolic acidosis, an unfavorable outcome is possible - severe 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 of the newborn. [ 12 ] Delivery in a special perinatal center improves the prognosis.