[The correlation of glucose-concentration and acid-base-balance of the maternal and fetal blood during labor (author's transl)].

The aim of the present paper was to investigate if the glucose concentration of the fetal blood is reduced already during parturition. It was further of interest if there is a relationship between the glucose concentration in the maternal blood and the acid-base-balance of the maternal and the fetal blood, respectively. The observations comprised 40 patients during labor. Blood was sampled from the hyperemized fetal scalp and the umbilical artery. The maternal blood was collected from the hyperemized earlobe and fingertip, respectively. The blood was analyzed for pH, PCO2, base excess and blood glucose. The dip area (DA) was taken from the cardiogram and measured by planimetry. During labor the blood glucose increased in the fetal blood from 67 mg% (SD 12) to 87 mg% (SD 23) (2 alpha less than 0,001) and in the maternal blood from 88 mg% (SD 14) to 113 mg% (SD 29) (2 alpha less than 0,02). There was a significant correlation between the fetal and maternal blood glucose concentrations. The increase of the fetal glucose concentration is, however, less with increasing maternal blood glucose. (b = 0,66). The base excess in the maternal and fetal blood fell significantly. The rise of the maternal and fetal base excess (= base deficit) was related to the increase of the glucose concentration (2 alpha less than 0,001). If the base excess was zero, the fetal and the maternal blood glucose was 46 mg% and 78 mg%, respectively. The difference between the maternal and fetal blood glucose was 28 mg%. With increasing DA the fetal blood glucose increased (2 alpha less than 0,001.). From the observations it is concluded that there developes no hypoglycemia during parturition. This is due to the correlation found between fetal and maternal blood glucose and due to the rise in fetal blood glucose during hypoxia. Obviously, the decrease in fetal glucose following delivery is caused by a lack of glycogen which is enduced during labor and strengthened by a deficit of enteral glucose supply.