[Principles of cardiotocographic monitoring of the fetus in pregnancy].
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Biomedical subjects
Publications and source records attributed to M Hohmann.
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The effects of acute asphyxia on both the time course of blood flow changes in central and peripheral organs, including the skin, and the time course of changes in oxygen consumption were studied in 9 unanaesthetized fetal sheep in utero at 130 +/- 2 days of gestation during 4-min arrest of uterine blood flow. Blood flow distribution and total oxygen consumption were determined at 1-min intervals during asphyxia using isotope-labelled microspheres (15 micrograms diameter) and by calculating the decline of the arterial O2 content, respectively. During asphyxia peripheral blood flow including that to the skin, scalp, and choroid plexus decreased rapidly, whereas blood flow to the heart, brain stem and (in surviving fetuses only) adrenals increased slowly. Total oxygen consumption fell exponentially with time and was closely correlated with the fall in both arterial oxygen content and peripheral blood flow; the time courses of these changes were very similar to those of the decreasing blood flows to the skin and scalp. Blood flow within the brain was redistributed at the expense of the cerebrum and the choroid plexus; the total blood flow to the brain did not change. In the 5 fetuses that died during the recovery period adrenal blood flow failed to increase and, at the nadir of asphyxia, peripheral vessels dilated and central vessels constricted. We conclude that in fetal sheep near term during acute asphyxia the time course of changes in blood flow to central and peripheral organs is different; total oxygen consumption depends on arterial O2 content and peripheral blood flow; total blood flow to the brain does not change, but is redistributed towards the brain stem at the expense of the cerebrum and choroid plexus; fetal death is preceded by a failure of adrenal blood flow to increase, by peripheral vasodilatation, and by central vasoconstriction and skin blood flow validly indicates rapid changes in the distribution of blood flow and the changes in oxygen consumption that accompany it.
To improve the understanding of fetal responses to labour, we have ascertained whether reduced fetal skin blood flow after asphyxia reflects redistribution of the circulation, and if so, whether this can be detected by transcutaneous PO2 monitoring. We also studied the relation between plasma concentrations of catecholamines and organ blood flow. Eight experiments were conducted on 8 acutely-prepared fetal sheep in utero between 125 and 135 days of gestation. In each fetus 11 episodes of asphyxia were induced within 33 min by intermittent arrest of uterine blood flow for 90 s. The distribution of blood flow was measured before and after asphyxia (at 35.5 min) by the isotope-labelled microsphere method. Blood samples were drawn at 0, 33 (i.e. after 90 s recovery), and 40 min to determine blood gases, acid-base balance, and catecholamine concentrations. Fetal transcutaneous PO2, heart rate, arterial blood pressure, and arterial O2 saturation were recorded continuously. Repeated fetal asphyxia increased plasma catecholamine concentrations and caused a circulatory redistribution to the brain (181% change), adrenals (116% change), and lungs (105% change) at the expense of many peripheral organs, particularly of the skin (-61% change). The pattern of these changes was different from that observed by others in persistent hypoxia or asphyxia. The decrease in skin blood flow, which depressed transcutaneous PO2 and increased the arterial-transcutaneous PO2 difference, correlated with the decrease in blood flow to other peripheral organs and with an increase in blood flow to the brain stem. We conclude that reduced blood flow to the fetal skin after repeated episodes of asphyxia indicates circulatory redistribution, which can be detected by transcutaneous PO2 measurements. We suggest that monitoring of variables that depend on skin blood flow may improve fetal surveillance during complicated labour.
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UNLABELLED: Late cord clamping allows a redistribution of placental blood to the fetus within 3 minutes. A sufficient difference in hydrostatic pressure between placenta and fetus is the prerequisite for placental transfusion. Placental transfusion is reduced or diminished if the newborn baby is positioned above the placenta. Blood volume and blood pressure of the fetus are elevated after placental transfusion. The increased blood volume correlates with the effective renal blood flow. There is no difference between cardiovascular parameters 6 hours post partum in infants subjected to early or late clamping of the cord. Nevertheless, erythrocyte volume and oxygen capacity remain high during the first days of life in infants with late cord clamping. CONCLUSION: In normal deliveries the cord should be clamped after 1 to 2 minutes. In premature infants, however, placental transfusion is advantageous because the incidence of respiratory distress syndrome is lower with late clamping. If the fetus is hypoxic in utero, redistribution of the blood and placental transfusion takes place already before birth to improve the oxygen supply to the fetal tissue and resuscitatory measures can be undertaken immediately following birth.
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The cardiovascular and metabolic responses during acute fetal hypoxia were studied in 7 pregnant sheep near term. Complete reduction of uterine flow (UBF) for 180 s was performed in 13 experiments by inflating a balloon positioned in the maternal aorta. Fetal heart rate (FHR), systolic and diastolic blood pressure (BP) and fetal arterial oxygen saturation (SO2) were measured continuously. Blood samples were taken at short intervals and analyzed for pH, PCO2, PO2, SO2, base excess and lactate. Following the reduction of UBF, FHR began to rise after 4.7 +/- 14.4 (SD)s and fell after 31.3 s paralleled by the rise of the BP after 23.2 +/- 8.2 (SD)s. The fall of FHR was not related to the SO2 at control, but to the decline of the SO2 by 10-15%. There was no critical limit of SO2 at which the FHR started to fall and the BP began to rise. The rise of the FHR after UBF had been released was significantly correlated to the rise of SO2. Lactate production during hypoxia was related to the slope of the SO2 decline, i.e., to the fetal O2 consumption. The total metabolic response during hypoxia and recovery given by the pH area was correlated to the SO2 at control. No correlation between dip area of FHR and PH area could be established.
To our knowledge there is no study that answers the question, whether low blood pressure itself or the fall of blood pressure during standing have a negative effect on pregnant women. These patients suffer from signs of reduced central and/or peripheral blood flow like fatigue, headache, cold extremities, paresthesia, flickering, black outs and dizziness. In addition, it is of interest whether frequency, occurrence and intensity of these hypotensive symptoms alter during pregnancy. In a longitudinal study 12 hypotensive pregnant women were compared with 13 normotensive and later on in a randomized study 102 clinical healthy pregnant women were tested with a modified orthostatic test over defined time periods during pregnancy. Blood pressure and heart rate were registered in one minute intervals over 30 minute period with an automatic Dinamap measuring device. This period was subdivided in a 10 minutes lying period, 10 minutes standing period followed by a 10 minutes lying period. In addition, the pregnant women were asked about frequency, occurrence and intensity of typical hypotensive symptoms. The frequency of subjective symptoms were related to low blood pressure (p less than 0.001) but not to the fall in blood pressure during standing. The occurrence of different hypotensive symptoms (p less than 0.05) and their intensity (p less than 0.01) were most often in early pregnancy and decreased until term. We conclude that the subjective symptoms were twice as much during early pregnancy than during late pregnancy and were more often in patients with low blood pressure. Furthermore, fatigue, headache and cold extremities occur frequently during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
This study was designed for two purposes. The first was to establish an in-vitro technique for the comparative study of isolated capacitance veins during pregnancy. Secondly, to test the hypothesis that pregnancy is associated with an increase in venous compliance and the unstressed volume of the veins. Capacitance-size mesenteric veins were mounted in a pressurized myograph system equipped with a video dimension analyzing system and a servo pressure control unit, which was modified for venous studies. After equilibration, the transmural pressure was changed from 2 to 10 mmHg in 2 mmHg increments every 15 minutes. The calculated change in volume over this pressure range consisted of both a change in vessel diameter and in axial length. The veins from the nonpregnant rats exhibited a greater change in axial length than those from the pregnant rats (21% vs. 14%). Unexpectedly, the compliance (change in volume/change in pressure) of the veins from the pregnant rats was significantly less (42%) than those from the nonpregnant rats. However, the basic component of the change in vascular capacitance, the unstressed volume, was significantly greater in the veins from the pregnant rats (100%). We conclude that pregnancy causes alterations in the wall of the capacitance veins, which results in an apparent increase in volume at the expense of wall compliance. Secondly, the pressurized myograph system is a valuable tool for studying the physiology of the capacitance veins during pregnancy under rigorously controlled conditions.
UNLABELLED: To analyze the variability of fetal heart rate (FHR) after a temporary definite hypoxia, uterine blood flow (QUT) was totally reduced in 8 pregnant sheep. In 13 experiments the reduction lasted 60 sec and in 13 further experiments 180 sec. The normalization of FHR after reduction of QUT was compared with the change of fetal blood pressure (BP) and fetal oxygen saturation (SO2). RESULTS: During reduction of QUT the fall of FHR and the decrease of SO2 was significant (r = -0,43, 2 alpha less than 0,05). With the start of normalization there was a temporary correlation between the increase of FHR and the restauration of SO2 after 12-18 sec (r = 0,79, 2 alpha less than 0,001). Thus the initial rise of FHR might be caused by the chemoreceptors. Above all after longer reduction of QUT there were three typical reactions during the recovery period: increase of FHR and BP, short fall of FHR and BP and increase of FHR and continous fall of BP. The start of normalization of FHR after reduction of QUT depends on the restauration of SO2. Because of the variable FHR response it is not possible to describe the duration of the preceding hypoxia.
Deceleration of the fetal heart rate are indications of fetal distress, which are commonly seen in connection with uterine contractions. The aim of the investigation was, whether nasal application of oxytocin (Syntocinon, Sandoz AG) is sufficient for the induction of contractions for an oxytocin-challenge-test. 232 oxytocin-challenge-tests in 85 risk patients between 29th-42nd week of gestation were analyzed in a retrospective and prospective way. The amounts of oxytocin nasal spray necessary for stimulating contractions were compared to the gestational age and maternal body weight (1 spray snuff = 4 IU Oxytocin). 20 pregnant women were given 8 IU oxytocin nasal spray after 10 minutes CTG-registration without any contractions. The incidence of induced contractions per ten minutes period were calculated. The amount of oxytocin nasal spray necessary for the stimulation of contractions decreased in relation to the increased gestational age and maternal body weight (oxytocin spray = 2.751-0.051 X (gestational age)-0.014 X (body weight), p less than 0.01). After a single application of 8 IU oxytocin nasal spray at least one contraction occurred in 13 out of 20 cases within the first 10 minutes. Between the 20th-30th minute the induced uterine contractions reached a maximum of 3 contractions per 10 minutes. No persisting contractions were observed. The application of 8 IU of oxytocin nasal spray is sufficient to induce in about 95% of the cases an oxytocin-challenge-test which gives information concerning the actual state of the fetus at risk.
Uterine blood flow decreases during uterine contractions. Under physiological conditions there is however an uterine hemodynamic buffer mechanism to guarantee a sufficient oxygen supply to the fetus even during uterine contractions. Heart rate decelerations occur therefore not during the period of cervical dilation but in the second stage of labor. In disorders of pregnancy uterine blood flow is primarily reduced and the slightest uterine contraction exhibits signs of fetal hypoxia, i.e. deceleration of fetal heart rate. Heart rate decelerations signify the possibility of the deterioration of the fetal acid base status. But the degree of fetal acidosis can be estimated only by fetal scalp blood sampling. A valuable tool to predict fetal hazard is to measure the transcutaneous PO2. Numerous hypoxic episodes decrease not only the arterial PO2 but also the skin blood flow which demonstrates a reduced peripheral circulation. This, however, is an indication of severe fetal stress in utero.
This study was designed to answer three questions: 1. Is there a change in systolic blood pressure, diastolic blood pressure and heart rate during pregnancy? 2. Are there alterations of these parameters during standing? 3. Is there a relationship between mean arterial blood pressure and heart rate at rest and during standing? In a randomized study 161 clinically healthy pregnant women between 8th and 41st week of pregnancy were tested with a modified orthostatic test over defined time periods during pregnancy. Systolic and diastolic blood pressure and heart rate were registered in one minute intervals over a 30 minute period with an automatic Dinamap measuring device. This period was subdivided in a 10 minutes lying period, 10 minutes standing period followed by a 10 minutes lying period. There was a marked increase in systolic and diastolic blood pressure at rest with the beginning of the 34th week of gestation (p < 0.05 and p < 0.01). Despite this, maternal heart rate continued to rise over the whole course of pregnancy (p < 0.01). Furthermore, women with a fall in heart rate on standing were only seen in late pregnancy. Finally, pregnant women with a low mean arterial blood pressure (< or = 85 mmHg) did not experience a fall in blood pressure on standing more frequently than normal controls (> 85 mmHg). We conclude that a fall in blood pressure on standing is not dependent on blood pressure at rest during pregnancy.