Abstract
After a prolonged fetal heart rate deceleration induced by maternal aortic occlusion in acute sheep experiments the transcutaneous PO2 (tcPO2) showed a delayed recovery as compared with arterial oxygen saturation values (Künzel et al. 1979, 1980). An almost identical delayed recovery of the tcPO2 could be demonstrated by injecting norepinephrine into the sheep fetus, thus proving that the delayed response after asphyxia in combination with a fetal heart rate deceleration was probably due to increased sympathetic activity and release of catecholamines. This was the beginning of a series of clinical and experimental trials in which we tried to find out whether fetal heart rate monitoring, as to date the most accepted method of fetal surveillance, could be supplemented by the tcPO2 technique to obtain insights into
Transcutaneous PO2 (tcPO2) recordings from human fetuses 4h prior to birth. Two simplified Groups of measurements can be distinguished. In one group the tcPO2 remains more or less stable and decreases only in the last minutes before parturition to PO2 values between 6 and 18 mm Hg. In the second group of measurements, the tcPO2 decreases as early as 1–2 h antepartum. At the moment of delivery the tcPO2 was approximately zero. In 9 of 19 measurements, in which monitoring could be continued until delivery, the length of the tcPO2 “zero line” recorded antepartum was 2–90 min. (Jensen and Künzel 1980)
cardiovascular changes during asphyxiai impairment of the human fetus during parturition.
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References
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© 1985 Springer-Verlag Berlin Heidelberg
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Jensen, A., Künzel, W., Hohmann, M. (1985). Fetal Heart Rate and Fetal Deterioration: Clinical and Experimental Observations. In: Künzel, W. (eds) Fetal Heart Rate Monitoring. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70358-4_16
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DOI: https://doi.org/10.1007/978-3-642-70358-4_16
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