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side of the heart, estimated at half of the returning flow The degree of shunting in the human fetus is less, being estimated at between one-quarter and twofifths.49 The determinants of shunting include the differing resistances of the portal vasculature and venous duct, along with other influences such as blood viscosity, umbilical venous pressure, and mechanisms of neural and endocrine control The waveforms measured within the venous duct have been found to remain normal for long periods during placental compromise, reflecting its essential role in the fetal circulation.65 Patterns in the umbilical vein also act as a barometer of fetal well-being These are caused by the dilation of the venous duct in response to fetal hypoxemia that reduces impedance and allows pressure waves to travel in a retrograde fashion from the right atrium to the umbilical vein resulting in venous pulsations Absent or reversal of flow in the venous duct is usually an ominous sign (Fig 6.10) It reflects fetal hypoxemia and has been shown to predict fetal death or adverse perinatal outcome.61–63 and usually prompts emergency delivery by cesarean section An alternative etiology for absent or reversed end-diastolic flow in the venous duct is increased central venous pressure, seen particularly where there is obstruction within the right heart, such as pulmonary atresia with severe tricuspid regurgitation (Video 6.9) This may also result in fetal hydrops and intrauterine death.66–68 FIG 6.10 Series of Doppler recordings in the venous duct illustrating worsening cardiac function (A) The normal pattern shows forward flow toward the right atrium throughout the cardiac cycle (B) Impaired ventricular filling is associated with absent end-diastolic flow in the waveform (C) Worsening function is characterized by a reversal of flow coincident with the “a” wave of atrial contraction Flow to the Brain Doppler waveforms signifying normal brain flow in the middle cerebral artery are characterized by an expected peak systolic velocity (in centimeters per second) of approximately twice the fetal gestational age and a positive diastolic tail (see Fig 6.8A) Abnormality of the Doppler waveforms signified fetal hypoxemia,69 but initial reports that flow waveforms in the anterior cerebral artery were better able to predict adverse neurodevelopmental outcome have not been substantiated.70,71 In sheep studies the pulsatility in the middle cerebral artery was found to correlate poorly with peripheral vascular resistance,72 but the clinical application of the cerebral to placental resistances in the human fetus remains a subject of debate.64,73 One of the most practical applications of the middle cerebral artery measurement is in the noninvasive detection of fetuses with anemia, where an increase in the peak systolic velocity with normal diastolic velocity has been described.74 The velocity is proportional to the reduction in hematocrit and directs management decisions to provide life-saving fetal therapy intrauterine transfusion.75 In fetuses with intrauterine growth restriction, a “brain-sparing” phenomenon comprising increased diastolic velocities in the middle cerebral artery, producing a low pulsatility index, has been described (see Fig 6.8B) At delivery, brain sparing was associated with hypoxemia and abnormal systemic venous flows with acidemia and adverse perinatal outcome.61–63 Growth-restricted fetuses with abnormal venous flow have worse perinatal outcome compared with those where the abnormality in flow is confined to the umbilical or middle cerebral arteries In fetuses with low middle cerebral arterial pulsatility, an abnormal systemic venous Doppler signal indicates further deterioration.76 A combination of Doppler indexes, shown to be predictive of the optimal time for delivery of the sick fetus, has been studied to identify whether they are predictive of early cerebral injury, when combined with imaging techniques.77 Evidence of cerebral redistribution, as measured by the ratio of the pulsatility indexes of the umbilical artery to the middle cerebral artery, was associated with reduced total volume of the brain Autoregulatory arterioles are sensitive to the local concentration of metabolic products but will not function if the surrounding tissue is metabolically inactive This may misleadingly manifest as a “normalization” of cerebral Doppler flow waveforms in terminally sick fetuses just prior to their intrauterine death.78 However, newer techniques using MRI may be able to provide noninvasive in vivo assessment of fetal cerebral metabolism and its response to adverse intrauterine conditions and congenital malformations Blood oxygen–dependent MRI measures the relative state of oxygenation in the fetus by comparing the differencing magnetic properties of the oxygenated and deoxygenated hemoglobin This can be detected using T2-weighted imaging and has been evaluated in both sheep and human studies.79–83