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a Chapter 22 Doppler Velocimetry in Maternal Alloimmunization 341<br />

cause of fetal anemia. Intermittent, low-frequency 3-<br />

to 5-Hz sinusoidal variations of the fetal heart rate<br />

are more likely a result of stressed cardiac neuroregulation<br />

than actual changes in fetal blood flow [21,<br />

22].<br />

The inability of the medullary centers to control<br />

the fetal heart rate results in a sinusoidal heart rate<br />

pattern. Observations of fetal heart rate in severe anemia,<br />

fetal brain maldevelopment, cytomegalovirus infection<br />

and during alfaprodine or pancuronium bromide<br />

administration as reported by various authors<br />

appear to confirm this mechanism [23, 24].<br />

In the absence of significant hypoxia a mechanism<br />

of sinusoidal heart rate pattern is not well understood.<br />

It is likely that more than one compensatory<br />

mechanism is involved in such a severely affected fetus.<br />

Decreased fetal blood viscosity, increased blood<br />

volume, increased preload, baroreceptor, and volume<br />

receptor stimulation all affect fetal heart rate. Hecher<br />

et al. [15] reported increased fetal blood viscosity<br />

after fetal intravascular transfusion that occurred only<br />

in whole blood but not in serum, suggesting that it is<br />

increased erythrocyte mass that leads to increased<br />

blood viscosity. In anemic fetuses the cumulative effects<br />

of increased blood volume and decreased blood<br />

viscosity may lead to increased venous blood return<br />

and increased preload as reflected by the preload index<br />

in inferior vena cava velocimetry.<br />

No systematic studies of Doppler velocimetry during<br />

sinusoidal rhythm have been reported. In our one<br />

case fetal Doppler velocimetry in umbilical artery,<br />

descending aorta, MCA, and inferior vena cava were<br />

recorded. The elevation of ªaº wave in the inferior<br />

vena cava was noted, and fetal anemia was confirmed<br />

by cordocentesis. Subsequently, sinusoidal rhythm<br />

was relieved by fetal intravascular transfusion with<br />

the return of the inferior vena cava Doppler waveform<br />

to normal values shortly after transfusion. Association<br />

of abnormal Doppler velocimetry with a sinusoidal<br />

heart rate pattern has not been definite and<br />

needs more observations; however, the presence of<br />

fetal sinusoidal rhythm has been reported consistently<br />

as an ominous sign and an emergency requiring<br />

prompt diagnosis and treatment [21].<br />

Changes in Fetal Systemic Arterial<br />

Blood Flow<br />

Fig. 22.1. Sinusoidal fetal heart rate pattern<br />

Doppler Flow Velocity Measurements<br />

Fetal blood flow velocity is the parameter that can be<br />

adequately measured, provided that the angle of insonation<br />

is known and laminar blood flow is taken into<br />

consideration [25]. Accuracy of these measurements<br />

depends on the angle of insonation, < 608 being acceptable<br />

[26]. Volumetric flow measurements are also<br />

possible but require accurate data on the size of the<br />

vessel that are not easy to obtain. With current technology,<br />

they are not of practical use in fetal Rh disease.<br />

According to the law of physics, low viscosity<br />

ªthinnedº fetal blood in anemia flows faster in fetal<br />

blood vessels [16]. With unchanged peripheral resistance<br />

that translates into increased systolic and diastolic<br />

velocities. A similar increase in both systolic<br />

and diastolic blood flow velocities may be an explanation<br />

for generally unchanged S/D ratios and other<br />

indices in fetal arterial circulation. An increase in<br />

blood flow velocity does occur and to measure this<br />

change in flow the maximum velocity (or ªpeak<br />

velocityº) may be a more appropriate measurement<br />

[17]. This single measurement of absolute velocity at<br />

its maximum peak is angle dependent and as such requires<br />

consistency in the technique of measurements.<br />

In extreme conditions, in a terminally ill fetus, additional<br />

factors (hypoxia, neural regulation) may be<br />

affecting blood flow distribution and blood flow<br />

velocity in specific vessels, but it is not observed in<br />

mild to moderate anemia.<br />

Fetal Aortic Arch<br />

Increased fetal blood flow velocity in the aortic arch<br />

can be expected in anemic fetuses consistent with increased<br />

blood flow velocity in the fetal descending<br />

aorta but specific studies are lacking. The standard<br />

measurements have not been established for this<br />

complex blood flow velocity pattern that varies according<br />

to changing physiologic conditions [26].<br />

Fetal Descending Aorta<br />

An example of blood flow velocity measured in the<br />

fetal aorta in an anemic fetus is presented in Fig.<br />

22.2.

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