ASSESSMENT OF THE FETAL POT CHANGES BY CEREBRAL AND UMBILICAL DOPPLERON LAMB FETUSES DURING ACUTE-HYPOXIA

The objective of the present study was to validate one or a combinatio n of fetal Doppler parameters in order to assess acute fetal hypoxia i n an ovine model. Acute hypoxia was induced by reducing umbilical, or maternal aortic flow (approx. 70%). A CW Doppler probe was fixed on th e fetal cervical skin, facing the internal carotid artery and the feta l abdominal skin adjacent to the umbilical arteries. (The angle betwee n Doppler beam and flow vector remained constant,) A ''Doptek 3000'' s pectrum analyser was used to measure the maximal and mean Doppler freq uencies. Heart rate (HR), umbilical blood flow (UBF), carotid blood fl ow (CBF), umbilical RI(URI), cerebral RI(CRI)and cerebroplacental rati o (CPR = CRI/URI) were calculated in real time. A catheter was inserte d into the fetal femoral artery, for blood gas (Po-2, Pco(2) pH) and b lood pressure (BP) measurements. After 1 min of aorta compression (70% aortic flow reduction), the URI increased by 10% (P < 0.05), and the UBF decreased by 10% (P < 0.05), but the CRI decreased by 20% (P < 0.0 2), and the CBF did not change significantly. Fetal Po-2 and CPR fell down after 1 min (59% and 38%, respectively; P < 0.001), although stro ng fetal heart rate decelerations were observed. The blood pressure, P co(2) and pH did not change significantly during this test. Throughout the 12 min of cord compression (70% umbilical flow reduction) the URI increased (70% to 80% P < 0.001), and the UBF decreased (approx. 60%; P < 0.001), but the CRI decreased (approx. 25%; P < 0.01), and the CB F remained constant(+/-5%; ns). Fetal Po-2 and CPR all decreased durin g the compression (30% to 44% and 40% to 60%, respectively; P < 0.001) . HR, pH and Pco(2) did not change significantly. During cord compress ion the blood pressure did not change significantly. In both cases, th e CPR decreased significantly (P < 0.001) with the Pot in the same dir ection and with a comparable amplitude (-30% to -50%). Nevertheless, t he drop in CPR was greater during cord compression than during aorta c ompression, probably because the compression of the cord induced a cen tral hypovolemia in addition to the hypoxia. The CPR was found to be t he hemodynamic parameter that followed most closely the Pot acute chan ges. The amplitude of the variations of this parameter (-30% to -50%) were quite similar to those of the Pot during the period of acute hypo xia. A good correlation was found between the absolute values of CPR a nd Pot (aorta compression: r = 0.65; cord compression: r = 0.70).