[Fetal monitoring in pregnancy and labor. Conclusions concerning causality of early childhood brain damage].
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Biomedical subjects
Publications and source records attributed to H P Diemer.
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This pilot study involved 20 cycles contributed by six apparently healthy women. They were all experienced users of the symptothermal method of NFP and trained as NFP-teachers. In a double-blind study NFP-parameters like S-19 = F1, appearance of any mucus = F2 and appearance of fertil mucus = F3 also peak mucus symptom +4 = L1 and 3. day of high basal body temperature = L2 are related to ovulation detected by ultrasonic measurement of follicular growth and hormonal values (LH, total Oestrogen in urine). We have focused on the calculation of the first day and the end of the fertile phase. In relation to the maximal follicular diameter (mfd = day 0) the LH-peak was located at day -0,7. The peak mucus symptom was observed at day -0,58. F1 was seen 10,4 +/- 2,6 days, F2 6,2 +/- 2,6 days, F3 2,8 +/- 1,4 days before day 0. L1 was located at 3,37 +/- 1,74 days, L2 4,1 +/- 1,95 days after day 0. Using at least 2 indicators as recommended with the symptothermal method none of 19 cycles failed to detect the beginning of the fertile phase, but 3 out of 20 failed to detect the end. In 19 out of 20 cycles natural signals observed by the participants indicated ovulation. It must be mentioned that all our women were highly motivated persons.
None of the betamimetics have a exclusively tocolytic effect. By stimulating the cardiovascular beta-receptor, they also cause a substantial increase in the heart rate and a decrease in blood pressure. We administered 4--5 micrograms/min of Fenoterol to 13 patients during the first stage of labour. This led to complete inhibition of labour. To reduce cardiac side effects, a primarily cardiac beta-blocker (5 mg Atenolol or 20 mg Metoprolol) was also given. The maternal and fetal heart rates were measured by ECG and by fetal scalp-electrode, respectively. The fetal heart rate remained largely unchanged, both during the Fenoterol infusion as well as during the additional administration of the beta-blocker. The maternal heart rate, which increased under the influence of the Fenoterol, fell (p less than or equal to 0.01) but did not return to normal. In all cases the beta-blockade led to a brief increase in uterine activity.
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Measurements of resistances were performed on different parts of coronary vessels, including spontaneous collaterals in anesthetized dogs, following ligation and embolization of the descending branch of the left coronary artery. The normal situation was compared with the state of maximal pharmacological dilatation. The pharmacological dilatation decreased the collateral resistance by 24% in spite of the fact that the collaterals supplied an infarcted area in this case; the precollateral resistance, which chiefly consists of large vessels was also diminished. The collateral perfusion pressure is not only dependent on the aortic pressure, but also on the flow rate in the corresponding large coronary vessel and thereby on the ratio of precollateral to postcollateal resistance. A decrease of the collateral perfusion pressure causes an insufficient perfusion of the area supplied by the collaterals only when the pressure fall is not compensated for by an adequate decrease in the collateral resistance and when the ratio of the collateral to the nutritive resistance increases. Thus, both, the extent of the pressure fall across the precollateral resistance and the dilating capacity of the collaterals determine whether is not a pharmacological dilatation of the coronary vascular bed results in an insufficient supply of an infarcted area, i.e. in a so called "Steal-phenomenon". The results show further, that the given physical model of the microcirculation satisfactorily approximates the observed behaviour of the vascular system.
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