Before Diagnosis: Initial Evaluation of the Pregnancy With Fetal Arrhythmia
Julia A. Drose
Bettina F. Cuneo
INTRODUCTION
The assessment of fetal arrhythmias begins not with the echocardiogram, but with a detailed history of the current pregnancy. Obstetrical, past medical, and family histories may give additional important clues to both the diagnosis and the severity of the arrhythmia. For example, a fetus with a normal rhythm a few days prior to presenting with a sustained tachycardia is less likely to be in heart failure than a fetus who was last evaluated weeks before and whose mother reports decreased fetal movement. A mother with a history of multiple fetal losses and a current pregnancy with a fetal heart rate (FHR) <3rd percentile for gestational age may be the proband of a family with undiagnosed mosaic or heterozygous long QT syndrome (LQTS) (FIG. 1.2.1).1,2,3 Alternatively, a mother with a history of Sjogren syndrome or a family history of autoimmune disease with FHR of 60 beats per minute may have anti-Ro/SSA antibodies and fetal atrioventricular (AV) block.4 The objective of this chapter is to review assessment of the pregnancy when a fetal arrhythmia is suspected.
 FIGURE 1.2.1 A fetus with sinus bradycardia. A: Graph depicting fetal heart rates (FHR, beats per minute [bpm]) versus gestational age (GA, weeks) from 3rd to 97th percentile. A fetus (red dots) with persistent FHR < 3rd percentile for GA but greater than standard definition of fetal bradycardia (FHR < 110 bpm) is shown. There was no family history of long QT syndrome; the mother and father’s QTc intervals were normal on 12-lead ECG. The mother had a history of two stillbirths at 21 and 23 weeks GA. B: The family pedigree following genetic testing. The fetal proband (green circle) had the longest QTc, but two of her siblings and her mother (black circles and squares) carried with KCNQ1 inherited variant. The two stillbirths are shown as triangles. The corrected QT intervals of each family member are shown in the circles and squares. |
HISTORY OF CURRENT PREGNANCY
The mother should be questioned for a detailed dietary history as well as prescribed and over-the-counter medications, including herbal remedies. Certain maternal medications can cause fetal arrhythmias. For example, beta-adrenergic blocking agents may cause fetal bradycardia, and excessive caffeine or other stimulants can cause tachyarrhythmia or ectopy.
It is helpful to know details about the FHR and rhythm that lead to a suspicion of fetal arrhythmia. If an irregular rhythm was heard prior to a sustained tachyarrhythmia, most likely a premature atrial contraction has initiated a run of supraventricular tachyarrhythmia (SVT). However, if the rhythm was irregular and the rate is now slow, the fetus could have progressed from 2° AV block to complete AV block, or from atrial ectopy to blocked atrial bigeminy.
Fetal arrhythmias can accompany any cardiac defect but can be anticipated with certain ones. AV block is associated with congenitally corrected transposition of the great vessels or left atrial isomerism (FIG. 1.2.2).5,6,7 The common association of accessory connections and Ebstein anomaly increases the likelihood of SVT or atrial flutter in a fetus with this defect (FIG. 1.2.3).8 Sinus bradycardia with normal FHR variability can occur in right and left atrial isomerism, due to abnormalities in the number and location of the sinoatrial node as well as with decreased FHR variability, frequently seen in the fetus with LQTS (FIG. 1.2.4).
 FIGURE 1.2.2 Intermittent and sustained atrioventricular (AV) block with structural cardiac defects. A: Congenitally corrected transposition of the great vessels. The right atrium (RA) gives rise to the left ventricle (LV), which is to the right and anterior of the right ventricle (RV). LA, left atrium. (Great vessels not shown.) B: Simultaneous atrial (a) and ventricular (V) M-mode of intermittent AV block in the fetus with congenitally corrected transposition of the great vessels. Arrows point to atrial contraction that is not conducted to the ventricle; the circle shows the absence of a ventricular contraction. Note the atrial rate is regular. a, atrium; V, ventricle. C: Fetal MCG rhythm tracing showing the intermittent AV block (arrows show p-waves not conducted to QRS). D: Left atrial isomerism with sustained AV block at 15 weeks of gestation. Note the thickened spongy-form myocardium especially the left ventricle (LV). RV, right ventricle. E: Simultaneous mitral inflow and aortic outflow spectral Doppler demonstrating the fetus in (D) has type 2, 2° AV block: the a-a′ intervals are regular, and every other atrial beat is conducted with an AV interval that is the same as the previous AV interval. |
 FIGURE 1.2.3 A fetus with Ebstein anomaly. A: The septal leaflet of the tricuspid valve is so inferiorly displaced the valve cannot be easily seen on the four-chamber view; instead the right atrium (RA), the atrioventricular groove (arrow) and the tricuspid valve orifice (***) are visualized. RA, right atrium. B: With slight anterior angulation, the tricuspid valve can be seen (red circle), displaced almost to the RV outflow tract. |
The fetal bradycardia associated with maternal anti-Ro/SSA autoantibodies is not always AV block. Rather, affected fetuses can present with sinus bradycardia or a junctional bradycardia, with atrial and ventricular rates being the same, or a junctional bradycardia with AV block (FIG. 1.2.5).9,10
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