Effects of increased resistance to umbilical blood flow on fetal hemodynamic changes induced by maternal oxygen administration: A doppler velocimetric study on the sheep

Abstract

A fetal lamb model was used to investigate whether the effects of maternal O2administration on fetal blood gases and hemodynamics were modified when the fetoplacental circulation was compromised by stepwise compression of both umbilical veins. At basal state, O2 administration increased O2 saturation (SaO2) and the pul-satility index (PI) of the carotid artery Doppler wave form (p < 0.01). The first compression decreased left ventricular output (-21 ± 16%, mean ± 1 SD, p < 0.01) and umbilical mean velocity (-22 ± 28%, p < 0.01) but did not modify carotid pH, SaO2, or the PI in any of the arteries studied. At this level of compression, O2 administration increased carotid SaO2 (p < 0.01) but did not affect carotid PI. After a second compression, left ventricular output and umbilical mean velocity were even more reduced [-39 ± 21% (p < 0.01) and -53 ± 23% (p < 0.01), respectively]. With this compression, carotid pH, Sao2, and PI decreased, whereas umbilical and descending aorta PI increased. O2 administration at this level of compression increased carotid SaO2 (p < 0.01) but did not modify carotid PI. Throughout the three stages of the experiment, O2 administration did not affect umbilical PI, descending aorta PI, or umbilical mean velocity. A good linear relationship (r = 0.77, p < 0.001) was demonstrated between left ventricular O2 delivery and carotid PI. Thus, at basal state, O2 administration induced velocity changes compatible with an increase in cerebral vascular resistance. With an increase in umbilical vein resistance, this response was no longer demonstrated, even at a level of vein compression not significantly affecting carotid, umbilical, or descending aorta PI. These results support future use of fetal Doppler velocimetry during maternal hyperoxygenation as a method to evaluate fetal O2 reserve and fetoplacental hemodynamic function. © 1993 International Pediatric Research Foundation, Inc.