Case Report
A 3 month old, 5.5 kg, male infant with incessant SVT since fetal life
presented to the Emergency Room (ER) with grunting, respiratory distress
and decreased feeding for two days. He had a low grade fever, runny nose
and a cough two weeks prior to presentation. There were other ill
contacts in the household. On examination he had signs and symptoms of
heart failure with a heart rate (HR) of 150 beats per minute(bpm),
respiratory rate 50 per minute and liver 3 cm below the costal margin.
An electrocardiogram showed a long RP tachycardia and Echocardiogram
revealed an ejection fraction of 22%. Laboratory work was significant
for a Brain Natriuretic Peptide (BNP) of 10,000 and a viral respiratory
panel positive for Parainfluenza and Coronavirus NL63 but negative for
all the other Coronavirus including COVID-19.
The infant was well known to the electrophysiology service for incessant
SVT since fetal life. SVT was first diagnosed at 32 weeks of gestation
on a fetal ultrasound with heart rates in the 180s-200s. Treatment
during fetal life had been attempted with flecainide and digoxin and the
baby was delivered early at 35 weeks for mild fetal hydrops. In the
postnatal period SVT rates were in the 200s and rate but not rhythm
control (HR:140s-150s/bpm) was achieved with high doses of amiodarone
(20 mg/kg/day) and procainamide (60 mic/kg/min) infusions and oral
sotalol. The infant was transitioned to oral flecainide, amiodarone and
sotalol was switched to a beta blockers in view of concerns with
combining QTc prolonging drugs. The SVT continued to be incessant but at
lower rates of 120-130 bpm as an outpatient and the patient was
monitored closely for the first 2 months with a 30 day remote telemetry
monitor(Biotel™, Malvern PA) and an owlet sock (OwletTM, Lehi, UT). Serial outpatient echocardiograms
showed that at the two month checkup the infant’s ejection fraction had
dropped from 60% at discharge at three weeks of age to 50%. The infant
did not return for follow up for the 2.5 month check due to inter
current viral respiratory illnesses in the family and the home monitors
showed that the average heart rates were increasing from the 120s to the
140s. At three months he presented to the ER with the above picture. He
was started on milrinone and furosemide and from an antiarrhythmic
standpoint, was loaded with digoxin, another short load of amiodarone PO
followed by maintenance amiodarone and his beta blockers
increased. Flecainide was discontinued in view of the deterioration in
cardiac function. On this regimen he had an unresponsive staring episode
that lasted a few seconds. His heart rates were low in the 70s and his
digoxin level was elevated at 4.1. A decision was made to take him to
the Electrophysiology laboratory for a catheter ablation. 72 hrs prior
to the planned ablation the oral amiodarone, digoxin and beta blockers
were stopped and he was placed an on esmalol infusion to keep his heart
rates under 130 bpm. The esmalol was titrated upto 150
microgram/kg/minute and was stopped 30 mins prior to the ablation.