Relation of Bradycardia and Blood Pressure of the Fetal Lamb in Utero to Mild and Severe Hypoxia

Abstract

Fetal lambs of mostly 130–145 days gestation age, were subjected to hypoxia by having the ewe breathe 13%, 10% and 6% oxygen. The umbilical artery and umbilical veins were catheterized with the fetus still in utero along with the maternal carotid artery. Blood pressures and heart rates were recorded, as well as maternal respiratory movement through an intrapleural trochar. Samples of ewe arterial and fetal venous bloods were taken for O₂ and CO₂ tension analysis by the Riley method. With mild or moderate hypoxia, umbilical artery mean and pulse pressures generally increase; fetal heart rate may increase, decrease, or fluctuate. With severe hypoxia, mean and pulse pressures in the umbilical artery decrease along with the fetal heart rate. When periodic breathing occurred in the ewe, reciprocal effects on the ewe and fetal circulations were observed; as the ewe heart rate and blood pressure went up during apnea, the fetal heart rate and blood pressure went down and vice versa when respiratory movements were resumed. Bradycardia in its initial stages may be momentarily stopped by injection of atropine into the fetus. The critical O₂ tension for depression of the fetal circulation is between 10–30 mm Hg. Bradycardia is not indicative of mild or moderate hypoxia; blood pressure improves with mild or moderate hypoxia; when blood pressure and heart rate both decline in severe hypoxia, it is indicative of fetal heart failure and imminent fetal death. The initial hypoxic bradycardia results from vagal activity since it can be blocked briefly by atropine and since the heart rate may fluctuate between beats from a slow to a fast rate. Fetal heart rate and blood pressure respond quickly to change of the gas content of the ewe's blood as demonstrated by changes occurring during periodic breathing in the ewe.