What is the management of fetal bradycardia?

Management of Fetal Bradycardia

The management of fetal bradycardia requires immediate identification of the underlying cause, with priority given to reversible causes, and prompt intervention to prevent adverse fetal outcomes.

Definition and Causes

Fetal bradycardia is defined as a sustained fetal heart rate below 110 beats per minute for more than 2-3 minutes (according to American College of Obstetricians and Gynecologists) or 5 minutes (according to International Federation of Gynecology and Obstetrics) 1.

Common causes include:

1. Reversible causes:

   • Maternal hypotension
   • Uterine hypertonus or hyperstimulation
   • Sustained umbilical cord compression
   • Supine hypotensive syndrome
   • Maternal hypothermia (often associated with urosepsis)
   • Blocked atrial extrasystoles

2. Irreversible causes:

   • Congenital complete heart block (most common cause of persistent fetal bradycardia)
   • Sinus node dysfunction
   • Structural cardiac abnormalities
   • Major placental abruption
   • Fetal hemorrhage (e.g., ruptured vasa previa)
   • Ruptured uterine scar with placental/fetal extrusion
   • Umbilical cord prolapse with sustained bradycardia

Management Algorithm

Step 1: Immediate Assessment and Reversible Causes

• Change maternal position to left lateral decubitus position to relieve potential aortocaval compression 2
• Assess for and correct maternal hypotension
• Stop any uterotonic agents if being administered
• Consider acute tocolysis if uterine hypertonus is present 1
• Evaluate for umbilical cord prolapse or compression
• Check maternal temperature and assess for signs of infection

Step 2: Determine Etiology

• Perform detailed ultrasound including fetal echocardiogram to evaluate for:

  • Structural cardiac abnormalities
  • Congenital heart block
  • Hydrops fetalis
  • Other anatomical abnormalities

• For persistent bradycardia, consider:

  • Maternal autoimmune disease screening (anti-Ro/SSA and anti-La/SSB antibodies) 2
  • Fetal karyotype and/or chromosomal microarray analysis, particularly if structural abnormalities are present
  • MCA Doppler to assess for fetal anemia 2

Step 3: Management Based on Etiology

For Acute, Reversible Causes:

• If bradycardia persists >10 minutes despite corrective measures: Consider emergency delivery (cesarean section) as this increases risk of hypoxic-ischemic injury 1

For Congenital Heart Block:

• If associated with structural heart disease or hydrops fetalis: Poor prognosis, consider delivery if near term 2
• If isolated congenital heart block with narrow QRS complex: Close monitoring, generally favorable outcome 2
• For immune-mediated heart block (anti-Ro/SSA antibodies):
  • Once third-degree AV block has developed, corticosteroid therapy has not shown benefit 2
  • In-utero therapy for bradyarrhythmia with hydrops is considered investigational 2

For Sinus Bradycardia:

• If normal intrauterine cord blood pH and oxygen tension can be demonstrated: Avoid emergency cesarean section 3
• Close monitoring with weekly heart rate assessment 4

For Blocked Atrial Extrasystoles:

• Monitor closely as this may evolve into supraventricular tachycardia and hydrops fetalis 4
• May resolve spontaneously without intervention

Step 4: Delivery Planning

• For persistent bradycardia with irreversible cause and near term: Consider delivery
• For isolated congenital complete heart block without structural abnormality: Close monitoring until term delivery is possible 5
• For bradycardia with hydrops fetalis: Consider earlier delivery if viable gestational age
• For women with complete heart block and symptoms: Consider temporary pacing during delivery 2

Special Considerations

• Fetal bradycardia due to maternal labetalol administration: Monitor fetal heart rate during uptitration, especially when doses exceed 800 mg/24h 6
• Neonates exposed to labetalol should be monitored for hypotension, hypoglycemia, and bradycardia 6
• Avoid atenolol in pregnancy due to risk of fetal growth restriction 6

Pitfalls and Caveats

1. Do not delay intervention for acute, profound bradycardia: Continuation of prolonged deceleration >10 minutes (terminal bradycardia) increases risk of hypoxic-ischemic injury 1

2. Differentiate between types of bradycardia: First trimester sinus bradycardia and those associated with major structural cardiac abnormalities have high fetal loss rates compared to bradycardia from atrial extrasystoles 4

3. Recognize that fetal bradycardia during urosepsis may be due to endotoxin release triggering cardiotoxic cytokines rather than maternal hypothermia alone 7

4. Avoid unnecessary emergency delivery: Not all persistent fetal bradycardias require urgent delivery, particularly isolated sinus bradycardia with normal pH and oxygen tension 3

5. Regular clinical audit of management of acute hypoxia, including "onset of bradycardia to delivery interval," may help identify system issues contributing to poor outcomes 1