o_1977r8vv9vk1ts2ms0kd8pksa.pdf

a Chapter 29 Doppler Ultrasound Examination of the Fetal Coronary Circulation 437
Fig. 29.12. Systolic and diastolic peak blood flow measurements
in three cases of severe fetal anemia. In cases 1 and
3 velocities were obtained in hydropic fetuses prior to
transfusion. In case 1 a hematocrit of 9% was corrected to
39.8% and in case 3 from 14% to 42.8%. In the second
case of maternal trauma, repeated transfusions were necessary
on days 1 and 5 for hematocrit levels of 21% and
24%, respectively. (From [43])
drops, and hemolytic disease [43, 64]. Peak diastolic
velocities as high as 1 m/s and peak systolic velocities
of 0.5 m/s may be observed, significantly exceeding
those observed in any other fetal condition. Blood
flow velocities are responsive to maternal oxygen
therapy and fetal blood transfusion and fall below the
visualization threshold after normalization of the fetal
hematocrit (Fig. 29.12). With the development of fetal
hydrops, a decrease in coronary sinus dynamics is
observed. This finding is analogous to observations
in adults with heart failure where coronary sinus caliber
changes are attenuated presumably due to elevations
in coronary venous pressures [45].
Ductus Arteriosus Constriction
Constriction of the ductus arteriosus is one of the reported
fetal complications of maternal indomethacin
therapy for preterm labor. As a conduit for the right
ventricle to the systemic circulation, constriction of
this vessel raises afterload and therefore cardiac work
and oxygen requirement. In severe constriction tricuspid
insufficiency and abnormal venous indices
may develop. In such severe cases color- and pulsedwave
Doppler of coronary artery blood flow is possible.
While the peak velocities are not significantly
elevated, the gestational age at visualization is determined
by the onset of the clinical condition. With
resolution of ductus arteriosus constriction following
discontinuation of indomethacin, coronary blood flow
could no longer be visualized.
Other Fetal Conditions
Acute changes in fetal oxygenation and cardiac preand
afterload also cause arterial and venous redistribution
in favor of the organs essential for fetal life.
These ªheart-, brain-, and adrenal gland-sparingº
phenomena have been described in different animal
models. The few observations made by Doppler ultrasound
in the human fetus support the presence of the
same protective mechanisms. Transient ªbrain- and
heart-sparingº phenomena were observed in a 30-
week fetus following acute bradycardia after umbilical
fetal blood sampling. Sudden visualization of coronary
blood flow, ªbrain-sparing,º and highly pulsatile
precordial venous flow persisted for a long period
after the 12-min bradycardia [65]. Changes in coronary
sinus dynamics have been documented in a fetus
with supraventricular tachycardia [45]. It is likely
that more observations of alterations in coronary arterial
and venous dynamics will be reported as familiarity
with the examination technique and advances
in ultrasound technology facilitate examination.
Clinical Applications
in Fetal Cardiac Abnormalities
Due to the vascular properties of the coronary arterial
circulation abnormalities frequently develop in cardiac
lesions that are associated with disturbed intracardiac
pressure/volume relationships during organogenesis.
Owing to the embryologic development of
coronary sinus abnormalities involving this vessel,
anomalous central venous drainage (both systemic
and/or pulmonary) is frequently present. Ultrasound
biometry and assessment of coronary sinus dynamics
has clinical relevance and may be the only apparent
clue pointing in the direction of such anomalies.
Ventriculocoronary Connections
in the Human Fetus
Ventriculocoronary connections are frequently noted
in fetuses and newborns with pulmonary atresia, hypoplastic
right ventricle, intact ventricular septum, or
restrictive ventricular septal defect [66]. In cases of
hypoplastic left heart with aortic atresia, intact ventricular
septum and patent mitral valve ventriculocoronary
connections may also be present but are less
common. The genesis of these vascular abnormalities
is discussed above. The abnormal coronary channels
may provide a conduit to release intraventricular
pressures and may partially avert hypoplasia and fibroelastosis;
however, coronary blood flow dynamics
may be significantly compromised, impacting on
prognosis and approach to postpartum surgical man-