OBJECTIVE: To compare fetal ductus venosus blood flow velocities in anemic fetuses and normal controls and to study the effect of intravascular transfusion on ductus venosus flow velocities. METHODS: Fetal ductus venosus flow velocities were measured using pulsed Doppler ultrasound in 21 anemic fetuses immediately before and after intravascular transfusion and again the day after transfusion. The control group consisted of 21 normal fetuses matched for gestational age. RESULTS: In the anemic fetuses, ductus venosus flow velocities were significantly higher than in controls. Transfusion initially resulted in even higher flow velocities. The following day, ductus venosus flow velocities decreased to values comparable to those in the control group. The ratio of peak to minimum velocity was higher in the anemic fetuses. CONCLUSION: Our finding of increased ductus venosus blood flow in anemic fetuses supports the theory that in fetal anemia, venous return and therefore cardiac preload is increased. High peak to minimum velocity ratio may reflect increased atrial pressure as a sign of imminent congestive heart failure. Because blood passing through the ductus venosus is directed into the left atrium, increased ductus venosus blood flow in the anemic fetus may be an essential compensatory mechanism to maintain oxygen supply to vital organs such as the heart and brain.
OBJECTIVE: To compare fetal ductus venosus blood flow velocities in anemic fetuses and normal controls and to study the effect of intravascular transfusion on ductus venosus flow velocities. METHODS: Fetal ductus venosus flow velocities were measured using pulsed Doppler ultrasound in 21 anemic fetuses immediately before and after intravascular transfusion and again the day after transfusion. The control group consisted of 21 normal fetuses matched for gestational age. RESULTS: In the anemic fetuses, ductus venosus flow velocities were significantly higher than in controls. Transfusion initially resulted in even higher flow velocities. The following day, ductus venosus flow velocities decreased to values comparable to those in the control group. The ratio of peak to minimum velocity was higher in the anemic fetuses. CONCLUSION: Our finding of increased ductus venosus blood flow in anemic fetuses supports the theory that in fetal anemia, venous return and therefore cardiac preload is increased. High peak to minimum velocity ratio may reflect increased atrial pressure as a sign of imminent congestive heart failure. Because blood passing through the ductus venosus is directed into the left atrium, increased ductus venosus blood flow in the anemic fetus may be an essential compensatory mechanism to maintain oxygen supply to vital organs such as the heart and brain.