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a Chapter 37 Evaluation of Pulmonary and Ductal Vasculature 551
as described above. Therefore a decrease in the PI of
the ductus arteriosus (below the normal values of
1.9±3.0) is suggestive of ductal constriction.
Normal Doppler Waveforms
The normal Doppler waveform in the fetal ductus arteriosus
is characterized by high systolic velocity and
low diastolic velocity from the main pulmonary artery
to the descending aorta (Fig. 37.1). This velocity
is the highest systolic one in the normal fetus that
can be obtained by Doppler interogation of the fetal
circulation and has a distinctive waveform. Color
Doppler sonography is useful for obtaining continuous-wave
Doppler images of the ductus in the ductal
arch region where the velocity is highest. Aliasing in
the ductal arch marks the site of peak velocity in a
fetal sagittal imaging plane. It has been shown that
maximal ductal blood velocity increases from 25 to
32 weeks' gestation [1], and data from our center
based on a prospective longitudinal study from 121
examinations on 41 normal pregnant women showed
a linear increase in systolic velocity from 14 to 40
weeks' gestation (Fig. 37.2). The ductal velocity was
toward the descending aorta during systole (65±
140 cm/s) and diastole (15±35 cm/s). The PI of the
ductal velocity did not change with gestation
(mean Ô2 standard deviations: 2.46 Ô 0.52).
Ductal Constriction After Therapy
for Preterm Labor
Second and third trimester fetuses have an increase
in ductal blood velocities with increasing gestational
age. The reasons for the increasing ductal blood
velocity are complex: The ductal velocities are a function
of multiple variables, including ductal wall caliber
and compliance, systolic and diastolic ductal flow,
and right ventricular function. Blood velocities of the
fetal ductus arteriosus must be considered in relation
to gestational age for correct interpretation.
Exposure to nonsteroidal antiinflammatory agents,
with the prototype being indomethacin, can lead to
constriction of the ductus and alterations in human
cardiovascular physiology. This change is presumed
due to inhibition of fetal prostaglandins. However, as-
Fig. 37.2. Ductus ateriosus flow and pulsatility index in fetuses
exposed to terbutaline (n=10), fetuses with ductal
constriction (n=22), and fetuses with hypoplastic left heart
syndrome (n =14) compared with normal range (mean Ô 2
SD) versus gestational age. (Reprinted from [13] with permission)