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502 D. Maulik<br />

Fig. 33.23. Pulmonary arterial Doppler<br />

waveforms show a premature cardiac<br />

contraction followed by a compensatory<br />

pause (arrows). Note the relative<br />

increase in the peak velocity of the<br />

post-compensatory wave, confirming<br />

the existence of the Frank-Starling<br />

mechanism in the fetal heart<br />

sion. The mechanism of reentrant tachyarrhythmia<br />

consists of circus electric activity encompassing atrial<br />

and ventricular conduction systems, most frequently<br />

involving an accessory bypass tract. The atrial impulse<br />

first is conducted to the A-V node and then<br />

into the His-Purkinje system accessory pathway and<br />

ventricles. The accessory pathway transmits the impulse<br />

from the ventricle to the atrium, thereby completing<br />

the reentry circuit (Fig. 33.24). This pattern<br />

comprises the most common type of reentrant SVT<br />

encountered in the fetus and neonate. When the accessory<br />

pathway transmits the impulse in a downward<br />

direction (antegrade), Wolff-Parkinson-White<br />

syndrome results. For the A-V nodal reentry, the slow<br />

tract within the node (a pathway) conducts the impulse<br />

antegradely and the fast track (b pathway) conducts<br />

the impulse retrogradely, which then completes<br />

the ring-like conduction pathway of the circus movement.<br />

Although there are other reentry mechanisms,<br />

they are infrequently seen in the fetus. Reentrant SVT<br />

is more amenable to therapeutic intervention.<br />

The automatic SVT is caused by the presence of<br />

ectopic atrial foci that stimulate the tachyarrhythmic<br />

activity of the ventricles. Atrial fibrillation and flutter<br />

are related to the atrial circus movement, which produces<br />

atrial tachyarrhythmia, a variable transmission<br />

of which results in ventricular tachyarrhythmia.<br />

These classes of SVT are rare in the fetus and are associated<br />

with a worse prognosis than the reentrant<br />

variety.<br />

It is noteworthy from the perinatal perspective that<br />

fetal SVT is often associated with cardiac malformations,<br />

including Ebstein's anomaly, tricuspid atresia,<br />

corrected transposition, and cardiomyopathy,<br />

although most infants are without any such complications.<br />

In addition, viral infections, specifically cytomegalovirus<br />

and coxsackie B, have been implicated.<br />

Fig. 33.24. Electrophysiology of the reentrant supraventricular<br />

tachyarrhythmia involving the accessory bypass tract.<br />

SA sinoatrial, AV atrioventricular<br />

The condition is usually recognized during fetal<br />

heart rate auscultation or electronic monitoring. The<br />

definitive diagnosis is achieved during fetal echocardiographic<br />

examination. Duplex imaging-guided M-<br />

mode sonography remains the most important modality<br />

permitting determination of the atrial and ventricular<br />

rates. Figure 33.25 presents a color M-mode<br />

demonstration of the atrial contribution to the tachyarrhythmic<br />

process. M-mode echocardiography<br />

may also be useful for assessing ventricular hypertrophy<br />

or dilation and spectral Doppler interrogation for<br />

establishing atrial and ventricular rates by the simultaneous<br />

interrogation of either the A-V flow and ventricular<br />

outflow of the aorta and inferior vena cava<br />

(see above). Finally, the importance of a detailed 2D<br />

echocardiographic examination cannot be overemphasized,<br />

as it allows targeted evaluation of the struc-

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