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a Chapter 35 Doppler Echocardiographic Assessment of Fetal Cardiac Failure 531
galy and venous distention. It also showed a significant
increase in cardiac output and evidence of mitral
and tricuspid regurgitation. Velocity flow studies
remained stable throughout the pregnancy and a
gradual improvement in the hydrops in the recipient
twin was seen. After birth, a neonatal echocardiogram
showed cardiomegaly, poor contractility, and mitral
and tricuspid regurgitation in the recipient twin. The
donor twin had normal cardiac output and velocity
measurements. These authors recommended serial
cardiac velocity flow studies in all cases of suspected
twin±twin transfusions [104]. Cardiomegaly and tricuspid
valve regurgitation are consistent findings
seen in the recipient twin as it deteriorates [108].
Some investigators have attempted to identify
pregnancies at risk for twin±twin transfusion by evaluating
blood flow in the first trimester. Matias et al.
evaluated 20 monochorionic twin pairs in the first
trimester and felt that the presence of an increased
nuchal fold and abnormal ductus venosus blood flow
(reversed A wave) was highly predictive of the development
of twin±twin transfusion syndrome later in
pregnancy [109].
Intrauterine Growth Restriction
True IUGR is a pathological process that affects normal
fetal growth and results in an infant whose growth is
less than its inherent potential [109±114]. A number
of chronic maternal medical conditions, such as the hemoglobinopathies
or significant heart disease, result in
decreased oxygen delivery to the fetus and lead to
IUGR. Other maternal diseases, especially those in
which hypertension is a component, or abnormalities
of the placenta can also cause IUGR. Problems such
as congenital anomalies or intrauterine infection damage
the developing fetus and decrease its growth. These
pathological processes can diminish the normal inherent
growth potential of the fetus. This, in turn, can result
in chronic fetal hypoxia and eventual fetal heart
failure and death. The combined use of ultrasonic fetal
weight estimation, fetal anthropometric ratios, and
Doppler ultrasound has been shown to be a reasonably
accurate method of diagnosing and following fetuses
with IUGR. This topic is discussed more fully in the
chapter on IUGR and Doppler.
True IUGR caused by abnormalities in uteroplacental
perfusion is characterized by selective changes
in peripheral vascular resistance that can be evaluated
using any of the angle-independent indices of Doppler
velocity flow studies in the fetal peripheral vessels
[112]. The author's experience has shown that
umbilical artery Doppler velocity studies have been a
significant help in the diagnosis and management of
IUGR [13, 111].
The role of Doppler velocity flow studies in the
heart and great vessels is not fully known. Increased
placental resistance and increased systemic resistance
due to hypoxia that may be seen in IUGR may lead
to increased right heart work and decreased right
ventricular flow. A redistribution of cardiac output in
IUGR results in a decreased left ventricle afterload
due to the cerebral vasodilatation, and an increased
right ventricle afterload due to the systemic vasoconstriction
[114±116]. Furthermore, hypoxemia may impair
myocardial contractility, while the polycythemia
that is usually present might alter blood viscosity and
therefore preload. A number of investigators have
shown alterations in velocity flow in the heart with
impaired ventricular filling causing an increased A/E
ratio at the level of the atrioventricular valves, lower
peak velocity in the aorta and pulmonary arteries, increased
aortic and decreased pulmonary time-to-peak
velocities, and a relative increase of left cardiac output
associated with decreased right cardiac output
[110±114]. These changes are compatible with a preferential
shift of cardiac output in favor of the left
ventricle, leading to improved perfusion to the brain,
the ªbrain-sparingº effect.
As the fetus deteriorates, peak velocity and cardiac
output gradually decline and cardiac filling is impaired.
An increase in reverse flow in the inferior
vena cava during atrial contraction may occur and
the fetus continues to deteriorate which, in turn, will
lead to pulsations in the umbilical vein. Rizzo et al.
have speculated that the fetal heart adapts to placental
insufficiency in order to maximize brain substrates
and oxygen supply [14]. With progressive deterioration
of the fetal condition, this protective
mechanism is overwhelmed by the fall in cardiac output
and fetal distress occurs. These findings suggest
that the study of cardiac and great vessel blood flow
patterns will be a useful tool for longitudinal monitoring
of the fetal condition in pregnancies complicated
by uteroplacental insufficiency. Makikallio et al.
have shown that the development of retrograde flow
in the aortic isthmus of IUGR fetuses indicated high
right ventricular afterload [116].
Diabetes Mellitus
Infants of diabetic mothers have long been recognized
as being at risk for cardiac enlargement, heart failure,
and stillbirth. Cardiac hypertrophy and a transient
type of hypertrophic subaortic stenosis have been described
in these infants. Although many investigators
feel that fetal cardiac hypertrophy in infants of diabetic
mothers is due to poor maternal glucose control
with resultant fetal hyperinsulinemia, Rizzo et al.
have described a progressive thickening of the interventricular
septum and right and left ventricular