22 Supraventricular Tachycardia
A 30-year-old African American woman, gravida 1, was referred at 25 weeks by the high-risk obstetrician for rapid fetal heart rate during a routine obstetrics appointment. The mother had Wolff–Parkinson–White (WPW) syndrome and had had successful catheter ablation. She is currently not on any antiarrhythmic medication.
2. Heart rate is 228 bpm, with equal atrial and ventricular rates (Fig. 22-1), suggesting 1:1 ventriculoatrial (VA) or atrioventricular (AV) conduction with a short VA interval (86 ms).
9. Tricuspid and mitral valve holosystolic regurgitation is present (Fig. 22-2), with the additional finding of ascites fluid.
b. The mother was fully evaluated by adult cardiology with a baseline electrocardiogram (ECG) and echocardiogram to exclude obvious cardiac pathology that would place her at risk in administering antiarrhythmic medications. Thyroid function testing was normal.
c. Management of the fetal SVT was discussed with the mother and her partner. It was explained that in more than 80% of patients, control of the dysrhythmia is possible, but occasionally this requires more than one medication and monitoring until the mother is on a sufficient dose of the medication that controls the fetal dysrhythmia.
d. With or without rhythm control, there is a small risk of a sudden fetal event or the development of fetal hydrops (particularly without control) as well as risks of other morbidities (e.g., stroke).
c. Valve function for increasing degrees of tricuspid and mitral regurgitation. The dP/dt (change in pressure per change in time) can be assessed on AV valve regurgitation jets. Normal is greater than 1000 mm Hg per second, and a poor prognosis is associated with values less than 400 mm Hg per second.
c. Ventricular tachycardia in the fetus is relatively rare and accounts for less than 5% of fetal tachycardia. One clue to this diagnosis is a tachycardia rate of less than 225 bpm with signs of congestive heart failure (CHF).
2. Fetal arrhythmia can occur at any gestational age, but it is most commonly seen after 24 weeks of pregnancy. Tachycardia before 20 weeks of gestation raises the likelihood of infection or maternal drug ingestion or hyperthyroidism.
3. The risk of tachycardia is highest in fetuses with multiple blocked atrial premature beats leading to a low ventricular rate (atrial bigeminy). The vast majority of fetuses with atrial and ventricular premature beats without tachycardia have uneventful prenatal and postnatal outcome. Intermittent SVT should be monitored to assess what portion of the whole day the fetus is in SVT (Fig. 22-3).
3. Fetal atrial ectopic (AET) and permanent (paroxysmal) junctional reciprocal tachycardia (PJRT) often persist after birth, and long-term antiarrhythmic therapy or electrophysiologic intervention may be necessary.
4. At 1 year of age, roughly one third of fetal SVT patients remain clinically symptomatic. One third do not have clinical tachycardia, but tachycardia can be induced using esophageal stimulation. In one third, tachycardia can no longer be induced, and presumably the bypass tract no longer conducts.
2. If monitoring of the fetal heart rate by ultrasound, continuous wave Doppler, or cardiotocography reveals, at any point, fetal arrhythmia (an irregular, rapid, or slow fetal heart rate), one should consider referring the mother for further evaluation by fetal ultrasound and fetal echocardiography. For persistently high or low rates at assessment, the referral should be immediate, given the potential risk of compromise and need for accurate diagnosis to plan management and intervention where possible.
3. Polyhydramnios and fetal hydrops can lead to detection of an underlying fetal tachyarrhythmia and should be considered in the setting where there is unexplained fetal hydrops. One might even consider continuous fetal heart rate monitoring or frequent Doppler assessment every day to exclude or confirm fetal tachyarrhythmia as a primary cause.
2. The high incidence of atrioventricular reentry tachycardia (AVRT) or, similarly, unidirectional reciprocating accessory pathway tachycardia (URAP) during fetal and neonatal life and its decrease due to the spontaneous disappearance of SVT can suggest immaturity of the myocardium. In particular, these tachycardias suggest a delayed development of the annulus fibrosus and/or prolonged persistence of accessory AV pathways.
a. Atrial flutter is generated within the atria by an atrial reentrant circuit and is observed mainly during the third trimester. This supports the hypotheses of an atrial macroreentry as an underlying mechanism of fetal atrial flutter.
c. Incessant heart rates as high as 300 bpm can lead to hydrops in 2 to 3 days (Fig. 22-4) and manifest umbilical venous pulsations.
4. The pathophysiology in SVT of the human fetus includes an impeded ventricular filling due to a short, inadequate diastolic period. This can alter the ventricular filling either directly or by changes in diastolic ventricular function due to inadequate oxygen supply by the reduced myocardial flow. Both mechanisms can elevate the venous pressure, resulting in increased rates of transcapillary fluid filtration into the interstitial space and significant reduction of lymphatic flow. This inadequate reduction in lymphatic drainage results in interstitial edema and finally hydrops (Box 22-1).