Fetal Arrhythmia Diagnosis and Pharmacologic Management

Abstract

One of the most successful achievements of fetal intervention is the pharmacologic management of fetal arrhythmias. This management usually takes place during the second or third trimester. While most arrhythmias in the fetus are benign, both tachy- and bradyarrhythmias can lead to fetal hydrops or cardiac dysfunction and require treatment under certain conditions. This review will highlight precise diagnosis by fetal echocardiography and magnetocardiography, the 2 primary means of diagnosing fetuses with arrhythmia. Additionally, transient or hidden arrhythmias such as bundle branch block, QT prolongation, and torsades de pointes, which can lead to cardiomyopathy and sudden unexplained death in the fetus, may also need pharmacologic treatment. The review will address the types of drug therapies; current knowledge of drug usage, efficacy, and precautions; and the transition to neonatal treatments when indicated. Finally, we will highlight new assessments, including the role of the nurse in the care of fetal arrhythmias. The prognosis for the human fetus with arrhythmias continues to improve as we expand our ability to provide intensive care unit-like monitoring, to better understand drug treatments, to optimize subsequent pregnancy monitoring, to effectively predict timing for delivery, and to follow up these conditions into the neonatal period and into childhood. Coordinated initiatives that facilitate clinical fetal research are needed to address gaps in knowledge and to facilitate fetal drug and device development.

Keywords: antiarrhythmic drugs; arrhythmia; congenital heart block; fetal arrhythmia; fetal echocardiography; fetal magnetocardiography; fetal pharmacology; fetal tachycardia; long QT syndrome; torsades de pointes.

Figure 1

Fetal SVT. (a) Heart rate trend over 5 minutes. In this case, the fetus is in SVT at about 194/min for nearly the entire tracing. Sinus bradycardia at 110/min is likely due to the transplacental effects of digoxin and flecainide. (b) cardiac time intervals in both sinus rhythm and SVT with 1:1 VA conduction. Note that the QRS is wider during SVT, likely related to flecainide effect. (c) Aberrantly conducted PAC that initiates SVT. Note that T‐wave inversion is present. This could be due to digoxin. Dig, digoxin; fMCG, fetal magnetocardiogram; GA, gestational age; PAC, premature atrial contraction; SVT, supraventricular tachycardia.

Figure 2

24‐week GA fetus with complex 2:1 isoimmune AV block, HR 75/min. (a) The signal averaged wave form, which documents 2 P waves for each QRS and a stable but prolonged PR interval. (b) Slow ventricular tachycardia is shown, which is common during the first several weeks of AV block. (c) Image shows that this fetus also had periods of rapid ventricular tachycardia and complete AV block with wide QRS escape rhythm (complete bundle branch block). These unstable findings are most common during the early adaptive phase, when the fetus is adjusting to the sudden drop in heart rate associated with AV block. AV, atrioventricular; CBBB, complete bundle branch block; GA, gestational age; VT, ventricular tachycardia.

Figure 3

29‐week GA fetus with familial LQTS type 2. The top tracing shows low fetal heart rates of 52/min due to functional 2:1 AV block. Irregular tachycardia is seen (left half) with rates of 100‐200/min. The bottom panel shows the rhythm associated with the higher rates, which is torsades de pointes and not sinus rhythm with ectopy as suspected by referral echocardiogram. AV, atrioventricular; FHR, fetal heart rate; fMCG, fetal magnetocardiogram; GA, gestational age; LQTS, long QT syndrome; TdP, torsades de pointes; VT, ventricular tachycardia.