Supraventricular Tachyarrhythmias
Stacy Ann Stratemann Killen
Frank A. Fish
INTRODUCTION
The supraventricular tachyarrhythmias (SVT) include incessant and/or paroxysmal episodes of increased fetal heart rates ≥180 beats per minute (bpm). SVT may be confined to the atria as seen in atrial ectopic tachycardia (AET) or atrial flutter (AF). Alternatively, SVT may be due to a reciprocating rhythm involving both the atria and ventricles utilizing the atrioventricular (AV) node and an accessory connection, as exemplified by atrioventricular reentrant tachycardia (AVRT) and permanent junctional reciprocating tachycardia (PJRT). In this chapter, the abbreviation “SVT” refers to all the supraventricular tachyarrhythmias. This chapter will describe the mechanism, presentation, and assessment of fetal SVT, which complicate 0.5% of pregnancies and is associated with morbidity and mortality.1,2,3
TACHYCARDIA EVALUATION
Echocardiographic evaluation of fetal tachycardias, using M-mode (through atria and ventricles) and spectral Doppler (left ventricular inflow and outflow, superior vena cava and ascending aorta/innominate vein and transverse aorta, pulmonary artery and pulmonary vein), should seek to determine the atrial and ventricular rates, the relationship of atrial and ventricular contractions, and the onset and termination of tachycardia.4,5,6,7,8,9 Atrial and ventricular M-mode or spectral Doppler venous and atrial flow signals infer atrial (A) and ventricular (V) contractions5 and are analogous to P-wave and R-wave seen on an electrocardiogram (ECG).
Fetal position, activity, and image resolution can limit echocardiographic assessment of fetal rhythm. When simultaneous assessment of atrial and ventricular motion cannot be made by traditional M-mode, color M-mode allows the aortic outflow Doppler signal to overlie the M-mode atrial signal; mechanical and flow events are displayed simultaneously9 (FIG. 3.2.1). This technique can be especially helpful in understanding atrial and ventricular relationships during tachycardia.
 FIGURE 3.2.1 Color M-mode during atrial flutter. The atrial contractions (bottom line, green arrows) occur at twice the rate of the ventricular contractions (top line, yellow arrows). (Reprinted from Detterich JA, Pruetz J, Sklansky MS. Color M-mode sonography for evaluation of fetal arrhythmias. J Ultrasound Med. 2012;31(10):1681-1688.) |
Echocardiography can also assess the effects of tachycardia on hemodynamics. Notching in the umbilical vein, hydrops, and atrioventricular valve insufficiency are all signs of a compromised fetus. Even after sinus rhythm has been restored, Doppler waveforms may take several days to normalize (FIG. 3.2.2).
Other techniques to assess fetal tachycardia include fetal magnetocardiography and fetal electrocardiography, which are described in Part 2, Chapter 3 and Part 6, Chapter 1, respectively.
 FIGURE 3.2.2 Spectral Doppler findings during and immediately after supraventricular tachyarrhythmia (SVT). A: Umbilical artery (UA) (top) and umbilical vein (UV) in a severely hydropic fetus during SVT. Note the notching in the vein and the reduced end-diastolic flow in the artery. B: Mitral inflow (above baseline)/aortic outflow (below baseline) in a fetus with recently converted atrial flutter. The velocity of the mitral A-wave, which normally should be higher than the velocity of the E-wave, is diminished, probably due to atrial fatigue after prolonged atrial flutter. A-wave velocity increased after several weeks in sinus rhythm. The AV interval in this fetus is prolonged (˜180 ms) secondary to antiarrhythmic treatment. C: Ductus venosus in the same fetus. The A-wave is very close to baseline. This finding improved in several days after tachycardia conversion. |
TACHYCARDIA MECHANISMS
Fetal SVT represents about 10% of fetal arrhythmias.1,10 Associated congenital heart disease occurs in ˜5% to 10% of fetuses with SVT.1,10 Morbidity is a function of fetal gestational age and the proportion of time in tachycardia. Interestingly, AVRT has a longer cycle length (slower heart rate) in the fetus than in the neonate.11 AVRT (60%-70%) and AF (30%) are the most commonly observed SVT types.12,13
This chapter will focus on four primary mechanisms that produce SVT (TABLE 3.2.1):
Atrioventricular reentrant tachycardia (AVRT) is a short ventriculoatrial (VA) tachycardia that involves the AV node for antegrade conduction and a retrograde-conducting accessory AV connection.
Permanent junctional reciprocating tachycardia (PJRT), a long VA tachycardia, is a variant of AVRT with reentry across a concealed slow retrograde-conducting accessory connection.
Atrial ectopic tachycardia (AET), another long VA tachycardia, is due to enhanced automaticity of atrial tissue rather than reentry.
Atrial flutter (AF), which is due to macro-reentry within the atrial myocardium and is characteristically associated with AV block of varying degree.
These mechanisms are identified in the fetus by the respective heart rates and timing relationships of the atria and ventricles (TABLE 3.2.2).
Atrioventricular Reentrant Tachycardia (Figs. 3.2.3 and 3.2.4)
AVRT, the most common type of fetal SVT, may demonstrate sudden onset (paroxysmal) and termination of tachycardia. AVRT is a reentrant or reciprocating (the terms can be used interchangeably) tachycardia involving the atria, ventricles, AV node, and an accessory connection.14 AVRT has a fixed 1:1 relationship between atrial and ventricular contraction with rates of 210 to 320 bpm. Typically, there is little heart rate variability. Onset is most commonly between 18- and 32-weeks gestation. The typical form of AVRT involves ventricular activation occurring through the normal conduction system and atrial re-activation initiated via an accessory AV connection. The accessory connection completes a reentrant circuit, and reciprocating antegrade-retrograde conduction perpetuates the circuit.13 Characteristically, the VA interval is shorter than the AV interval (“short VA” tachycardia). Thus, the VA interval is less than half of the cardiac cycle length and the VA/AV ratio is <1. The tachycardia rate is related to the relative
conduction properties of the accessory connection and the AV node. Tachycardia onset is triggered by an initiating event, usually a PAC,15,16 and begins abruptly. There may be repeated self-limited episodes or tachycardia may remain incessant. If either the AV node or the accessory connection fails to transmit a single impulse, reentry terminates, which is the reason that antiarrhythmic agents that slow conduction across the AV node often successfully terminate reentrant SVT.
conduction properties of the accessory connection and the AV node. Tachycardia onset is triggered by an initiating event, usually a PAC,15,16 and begins abruptly. There may be repeated self-limited episodes or tachycardia may remain incessant. If either the AV node or the accessory connection fails to transmit a single impulse, reentry terminates, which is the reason that antiarrhythmic agents that slow conduction across the AV node often successfully terminate reentrant SVT.
TABLE 3.2.1 ETIOLOGIES OF FETAL SUPRAVENTRICULAR TACHYARRHYTHMIA | ||
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TABLE 3.2.2 CHARACTERISTICS OF FETAL SUPRAVENTRICULAR TACHYCARDIAS | |||||||||||||||||||||||||
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