Fetal Supraventricular Tachycardia

Fetal supraventricular tachycardia is a regular fetal heart rate of 220 to 300 beats per minute with 1 to 1 atrioventricular conduction, most often caused by a reentry circuit through an accessory pathway. It is the commonest fetal tachyarrhythmia. Sustained disease for more than 50 percent of the time leads to heart failure and hydrops, and untreated hydrops carries high mortality.

• Risk factors: structural heart disease, Wolff-Parkinson-White syndrome, maternal thyroid disease, maternal stimulant use.
• Usually discovered at 24 to 32 weeks.
• Outcome with treatment is usually good.

Women are usually asymptomatic, and the fetal rate is found to be fast on auscultation. Hydrops may produce a large uterus for dates, reduced fetal movements and polyhydramnios.

• Persistent fetal rate above 200 beats per minute without variation.
• Fundal height large from ascites or polyhydramnios in hydrops.
• Differential diagnosis: sinus tachycardia (rate 160 to 200 beats per minute with variability), atrial flutter, ventricular tachycardia, fetal hypoxia, chorioamnionitis, maternal drug effect.
• Complications: heart failure, hydrops fetalis, polyhydramnios, preterm birth, stillbirth, neonatal cardiomyopathy, neonatal death.

The approach is M mode or Doppler timing of atrial and ventricular contractions with a search for hydrops.

• Ventricular rate 220 to 300 beats per minute with 1 to 1 conduction; short ventriculoatrial interval (shorter than the atrioventricular interval) suggests reentry; long ventriculoatrial interval suggests slower mechanisms.
• Fetal echocardiography for structure, ventricular function, atrioventricular valve regurgitation and effusions; scan for ascites, pleural and pericardial effusion, skin oedema.
• Maternal ECG, TSH, free T4, electrolytes, creatinine, liver enzymes and magnesium before drugs.
• Cardiotocography shows no variability and a flat fast baseline.

The principle is maternal drug therapy to convert or slow the rate, started early when hydrops is present or tachycardia is sustained.

• Supportive: admit for drug loading with continuous maternal ECG and pulse monitoring; maternal potassium above 4.0 mmol/L and magnesium above 0.8 mmol/L before drugs; fetal rhythm and hydrops scan every 1 to 3 days until controlled.
• Pharmacological: without hydrops: digoxin 0.5 mg oral 8-hourly for 3 doses then 0.25 mg oral 12-hourly, aiming for a maternal serum level of 1.0 to 2.0 nanograms/mL, with conversion expected in 3 to 7 days; flecainide 100 mg oral 8-hourly (maximum 300 mg daily, stopped if maternal QRS widens by 25 percent or more) or sotalol 80 mg oral 12-hourly increased to 160 mg 12-hourly for failure of digoxin; with hydrops: start flecainide 100 mg oral 8-hourly (maximum 300 mg daily), or digoxin with flecainide together; betamethasone 12 mg IM twice, 24 hours apart, between 24 and 34 weeks and 6 days if delivery is likely; neonatal treatment of persistent tachycardia: adenosine 150 micrograms/kg rapid IV bolus, increased by 50 micrograms/kg every 2 minutes to a maximum of 300 micrograms/kg.
• Procedures: ice to the face (vagal manoeuvre) for neonatal tachycardia; synchronised cardioversion 0.5 to 1 J/kg for unstable newborn; delivery by induction or caesarean section at term or at once after 34 weeks if therapy fails and hydrops worsens, in a unit with neonatal cardiology.
• Special groups: maternal long QT, structural heart disease or conduction disease contraindicates flecainide and sotalol and needs digoxin alone or specialist drug choice; women with hyperthyroidism need antithyroid drugs.
• Red flags: hydrops, rate above 250 beats per minute, reduced fetal movements, maternal palpitations or syncope on drugs, QRS widening, bradycardia.
• Follow-up: fetal rhythm and hydrops scan every 1 to 2 weeks after conversion; maternal drug levels and ECG weekly; newborn ECG at birth, and again at 1 week.