Hemodynamic factors affecting uterine artery Doppler waveform pulsatility in sheep

Quantitative analysis of vascular resistance from the Doppler time-velocity waveform relies on measuring arterial pulsatility. However, input pressure waveform pulsatility, impedance, and resistance have all been found to effect artery flow waveform pulsatility in circulatory mathematic models and in umbilical sheep preparations in vivo. The present study used an in vivo sheep preparation to determine that embolization of the uteroplacental circulation and maternal angiotensin II administration caused changes in the uterine Doppler time-velocity waveform pulsatility that were dependent on input pressure waveform pulsatility, fundamental impedance, and resistance changes. Uteroplacental vascular embolization increased vascular resistance and the uterine artery Doppler waveform resistive index; the mean component of flow (mean pressure/resistance) decreased. Decreased uterine artery Doppler resistive index occurred despite angiotensin II-induced vasoconstriction and increased vascular resistance because the pulse component of flow (pulse pressure/impedance) decreased.     

Fetal endocrine responses to chronic placental embolization in the late-gestation ovine fetus

OBJECTIVE: The purpose of this study was to examine the effect of chronic fetal placental embolization on the fetal corticotropin, cortisol, and catecholamines concentrations and on myometrial contractility pattern. STUDY DESIGN: Fourteen fetal sheep were studied (seven embolized, seven controls) for 10 days between 0.84 and 0.91 of gestation. Daily injections of nonradioactive microspheres were performed to decrease fetal arterial oxygen content by 30% to 35% of the preembolization value. Umbilical artery Doppler flow velocity waveforms were measured daily. RESULTS: Chronic fetal placental embolization produced progressive fetal hypoxemia (p < 0.001) with changes in umbilical artery Doppler flow velocity waveforms indicative of a 25% increase in placental vascular resistance (p < 0.01). In response to chronic fetal hypoxemia there was a progressive increase in baseline fetal plasma norepinephrine concentration (p < 0.001). There was a transient fourfold to fivefold increase in baseline fetal plasma cortisol levels concomitant with a significant decrease in baseline immunoreactive corticotropin between days 7 and 9 of embolization (both p < 0.05), with a return to control values by day 10. There was a 57% increase in myometrial contracture frequency in the embolized group when compared with controls (p = 0.001). CONCLUSIONS: During repetitive chronic placental damage that led to fetal hypoxemia, the fetal endocrine environment changed with time in a direction that would prevent the onset of premature activation of the hypothalamic-pituitary-adrenal axis and premature delivery.     

DNA synthesis is dissociated from the immediate-early gene response in the post-ischemic kidney

OBJECTIVE: Fetal growth and development are closely related to normal placental growth and function. We performed a study to determine the effect of a 10-day period of fetal hypoxemia induced by umbilical-placental hypoperfusion on tissue deoxyribonucleic acid synthesis rates in the 0.84 to 0.91 of gestation ovine fetus and placenta. STUDY DESIGN: Daily fetal placental embolization was performed in four chronically catheterized sheep fetuses until fetal arterial oxygen content decreased by approximately 30% compared with preembolization values. Five control fetuses received vehicle only. On experimental day 10, the deoxyribonucleic acid synthesis rate was determined by injecting tritiated thymidine (1 mCi/kg) intravenously approximately 8 hours before the end of the study. RESULTS: Fetal arterial oxygen decreased from 3.2 +/- 0.1 (SEM) mmol/L preembolization to 2.2 +/- 0.2 mmol/L on day 10 (p < 0.001) and remained unchanged in controls. On day 10 deoxyribonucleic acid synthesis rates were significantly reduced in embolized fetuses compared with controls, by 38% in cotyledons (83.0 +/- 15.1 vs 133.7 +/- 9.9 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), 28% in the left ventricular wall (36.8 +/- 3.7 vs 51.0 +/- 4.7 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), and 45% in the quadriceps muscle (15.4 +/- 4.0 vs 28.1 +/- 3.0 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05). Tritiated thymidine autoradiography demonstrated that cotyledonary deoxyribonucleic acid synthesis occurred exclusively in the fetal trophoblasts cells. CONCLUSION: We concluded that a reduction in cotyledonary, quadriceps muscle, and left ventricular myocardium deoxyribonucleic acid synthesis rates are the earliest adaptive mechanisms of fetal growth associated with development of umbilical-placental insufficiency. We speculate that alteration in the myocardial deoxyribonucleic acid synthesis rate could be a major contributing factor in the deterioration of fetal myocardial function associated with increased placental vascular resistance.     

Gait patterns in children with hemiplegic spastic cerebral palsy

Our objective was to study uterine and umbilical artery flow resistance during the oxytocin challenge test (OCT). The study population was 21 women with suspected placental insufficiency; one woman was excluded because of a positive OCT with reactive fetal heart rate pattern. We carried out simultaneous electronic fetal heart rate monitoring and Doppler velocimetry of uterine and umbilical artery flow during the OCT. The uterine artery flow resistance increased significantly during contractions in both OCT-positive (n = 5) and OCT-negative (n = 15) cases compared with basal values, but the increase was significantly higher in positive cases. The umbilical artery flow resistance increased significantly during contractions in OCT-positive cases, but was almost unchanged in negative cases. During uterine inactivity, there were no differences between the groups for any vessel. This study showed that fetal heart rate decelerations during the OCT are associated with rapid and exaggerated increases of vascular resistance in both uterine and umbilical arteries. The causal relationship is unknown, but the findings indicate pathophysiological mechanisms revealed only during uterine contractions.     

Causality and control: key to the experiment

Maternal betamethasone administration causes a transient but considerable reduction in fetal body and breathing movements and in fetal heart rate variation. The aim of the present prospective study was to investigate whether there is evidence of circulatory changes in fetal, placental or uterine arteries, consistent with hypoxemia. Eighteen women at risk for preterm delivery received betamethasone to enhance fetal lung maturation. Doppler studies were performed before treatment, and 24 and 72 h after the second dose of betamethasone. Blood flow velocity waveforms were obtained from both uterine arteries, umbilical arteries, fetal descending aorta, fetal renal artery, and fetal cerebral arteries. No significant changes occurred in the pulsatility index of any of these blood vessels, suggesting that the transient reduction in fetal heart rate variation and fetal body and breathing movements following maternal betamethasone administration is not mediated through fetal hypoxemia.     

Effect of dehydroepiandrosterone sulfate on fetal middle cerebral artery flow velocity waveforms in term pregnancy

OBJECTIVE: To investigate whether bolus injection of dehydroepiandrosterone sulfate (DHAS) is associated with changes in fetal middle cerebral artery flow velocity waveforms in term pregnancy. METHODS: Ten normal full-term pregnant women received the administration of a 200-mg intravenous dose of DHAS in 20 ml of 5% dextrose. Ten normal full term pregnant women received 20 ml 5% dextrose as controls. Color Doppler flow imaging and pulsed Doppler ultrasonographic assessments were made on fetuses in each group before and 10 min, 30 min, 60 min, 90 min. and 120 min after DHAS or dextrose administration. The pulsatility index (PI) values for the middle cerebral artery, and umbilical artery, and fetal heart rate were recorded. RESULTS: In the DHAS group, middle cerebral artery PI decreased from baseline by 24% (p<.05) after 10 min, and the mean reduction was 22% (p<.05) after 30 min. The PI returned to the baseline value 60 min later. In the control group, there was no change in middle cerebral artery PI. No change was found in umbilical artery PI or fetal heart rate in the control or DHAS group. CONCLUSION: DHAS induces a significant decrease in the fetal middle cerebral artery PI, which suggests a possible decrease in fetal cerebral vascular impedance in term pregnancy.     

Newborn acid-base status and umbilical cord morphology

OBJECTIVE: To assess the relation between umbilical cord morphology and intrapartum fetal status and umbilical cord blood gases at birth. METHODS: In a prospective study of 134 consecutive newborns and their umbilical cords, relations were investigated between umbilical cord morphologic characteristics (umbilical cord length, number of vascular coils, coiling index, and vessel length index) and intrapartum fetal heart rate (FHR) decelerations, color of amniotic fluid, operative delivery for suspected fetal acidosis, umbilical vessel blood gases, and acid-base status. RESULTS: Statistically significant linear correlations were found between umbilical venous pH and the umbilical cord length (r = 0.30; 95% confidence interval [CI] 0.13, 0.46; P < .001), number of vascular coils (r = 0.27; 95% CI 0.10, 0.43; P = .001), coiling index (r = 0.15; 95% CI 0, 0.33; P = .05), and vessel length index (r = 0.30; 95% CI 0.13, 0.46; P < .001). Statistically significant negative linear correlations were found between the umbilical venous partial pressure of carbon dioxide (PCO2) and cord length (r = -0.34, 95% CI -0.49, -0.17; P < .001), number of vascular coils (r = -0.30, 95% CI -0.46, -0.13; P < .001), coiling index (r = -0.17, 95% CI -0.34, 0; P = .03), and vessel length index (r = -0.34, 95% CI -0.49, -0.17; P < .001). The umbilical artery pH was related to vessel length index and to the number of umbilical vascular coils (r = 0.17, 95% CI 0.03, 0.36; P = .04 and r = 0.17, 95% CI 0.02, 0.35; P = .047, respectively). No relation was found between umbilical cord indices and intrapartum FHR decelerations, meconium staining of the amniotic fluid, or mode of delivery. Placental weight also correlated with umbilical cord length and vessel length index (95% CI 0.15, 0.46; P < .001 and 95% CI 0.05, 0.38; P = .01, respectively), but not with the number of umbilical cord coils or the coiling index. CONCLUSION: Umbilical venous pH and PCO2 and umbilical artery pH are related to umbilical cord morphology. Associated variations in placental morphology or placental blood flow affecting maternal-fetal gas exchange may explain these findings.     

Fetal branch pulmonary arterial vascular impedance during the second half of pregnancy

OBJECTIVE: Our purpose was to establish normal physiologic parameters in the fetal proximal and distal branch pulmonary arterial vascular impedance during the second half of pregnancy and to analyze relationships between proximal and distal pulmonary arterial blood velocity waveforms. STUDY DESIGN: In this cross-sectional study 100 uncomplicated singleton pregnancies were studied by pulsed color Doppler techniques between 18 and 41 weeks of gestation (median 30 weeks). Both right and left proximal (immediately after the bifurcation of the main pulmonary artery) and distal (beyond the first bifurcation of the branch pulmonary artery) pulmonary artery blood velocity waveforms were recorded and pulsatility index values were calculated. Peak systolic velocities and time-to-peak-velocity intervals were measured. Time-to-peak-velocity intervals were also analyzed at the level of aortic and pulmonary valves and at the ductus arteriosus. Right and left pulmonary artery diameters and right lung length were measured. RESULTS: In both right and left proximal and distal pulmonary arteries pulsatility index values decreased (p < 0.0001) and the peak systolic velocities (p < 0.003) and time-to-peak-velocity intervals (p < 0.0001) increased during the second half of pregnancy. In the proximal pulmonary arteries the pulsatility index values decreased linearly until 34 to 35 weeks of gestation and in the distal pulmonary arteries until 31 weeks of gestation. Thereafter they remained unchanged. In pulmonary arteries time-to-peak-velocity intervals were shorter (p < 0.01) than at the pulmonary valve level. There were no significant differences between the right or left pulmonary arteries in the pulsatility index values, peak systolic velocities, time-to-peak-velocity intervals, or pulmonary artery diameters. In the proximal pulmonary arteries the pulsatility index values (p < 0.02) and peak systolic velocities (p < 0.0001) were higher and time-to-peak-velocity intervals (p < 0.0001) were longer than in the distal pulmonary arteries. There was a 2.5-fold increase in pulmonary artery diameters and right lung length. CONCLUSIONS: Fetal branch pulmonary arterial vascular impedance decreases significantly during the second half of pregnancy. The linear decrease in vascular impedance during the second trimester and in the beginning of the third trimester may be related to the growth of the lung and the increase in the number of resistance vessels. During the latter part of the third trimester pulmonary vascular impedance does not decrease further.     

Prostanoid production in umbilical vessels and its relation to glucose tolerance and umbilical artery flow resistance

OBJECTIVE: To study prostanoid synthesis in umbilical vessels relative to maternal glucose tolerance and umbilical artery blood flow resistance. STUDY DESIGN: Umbilical artery pulsatility index was determined by Doppler velocimetry in 21 women with diabetes or impaired glucose tolerance and 10 healthy women. Segments from the umbilical artery and vein were incubated and prostacyclin (PGI2) and thromboxane (TxA2) metabolites determined. Statistical analyses with the Mann-Whitney U test, Kruskal-Wallis test, Wilcoxon signed-ranks matched-pairs test, contingency table analysis, Fisher's exact test, and simple linear regression analysis were used and a two-tailed P value of < 0.05 considered statistically significant. RESULTS: No significant difference in PGI2 or TxA2 production was found in umbilical vessels between the women with diabetes/impaired glucose tolerance and controls, but the PGI2/TxA2 ratio in the vein was significantly lower in the diabetes/impaired glucose tolerance group. The umbilical artery pulsatility index was positively correlated to the PGI2/TxA2 ratio in cord vessel segments and to cord plasma TxA2 concentration. The cord plasma TxA2 concentration was significantly higher in cases with a high umbilical artery pulsatility index. The prostanoid production was not correlated to maternal HbA1c or cord plasma C-peptide concentrations. CONCLUSIONS: In association with diabetes, an increased 'peroxide vascular tone' and an enhanced 'endoperoxide shift' between platelets and vascular endothelium may explain the unexpected positive correlation found between the umbilical artery pulsatility index and the vascular PGI2/TxA2 synthesis ratio.     

Dexamethasone and fetal heart rate variation

OBJECTIVE: To determine the effect of maternal administration of dexamethasone on fetal heart rate and its variation. DESIGN: Retrospective analysis of computerised data derived from cases studied over three years. SETTING: High risk pregnancy unit, John Radcliffe Hospital, Oxford. SUBJECTS: Twenty-eight pregnant women, at 27 to 32 weeks of gestation, to whom dexamethasone was given to accelerate pulmonary maturation in the expectation of preterm delivery. METHODS: Dexamethasone (two doses of 12 mg intramuscularly, 12 h apart) was given on 51 occasions at weekly intervals (one to four occasions per patient). Complete data were available for cardiotocograph analysis from computerised measurement of fetal heart rate variables for two days before and four days after dexamethasone and, in 19 women, measurements of umbilical arterial flow velocity waveforms before and after dexamethasone. RESULTS: In 10 pregnancies without fetal distress there was a highly significant (P < 0.01) transient rise in short term fetal heart rate variation after dexamethasone administration, from means (SE) 6.4 (0.28) to 9.8 (0.4) ms. In 18 pregnancies with subsequent delivery for fetal distress (abnormal fetal heart rate pattern) and high umbilical arterial resistance index [mean 0.93 (0.06 SE)], the rise in short term fetal heart rate variation was less (P < 0.01), from mean (SE) 5.4 (0.26) to 6.1 (0.48) ms. In a further case of discordant twin pregnancy, the larger twin continued to respond to dexamethasone administrations with a rise in fetal heart rate variation for five weeks; the smaller twin, with maintained tachycardia and reduced umbilical arterial end-diastolic flow velocity, failed to respond after the first two weeks. CONCLUSION: The results show that maternal dexamethasone administration normally causes a rise in fetal heart rate variation for up to a day. This rise is reduced in pre-eclampsia or intrauterine growth retardation, associated with a reduction in umbilical flow, perhaps because of a consequential lower concentration of steroid in the fetus. The results contrast with those for betamethasone which has been reported to reduce fetal heart rate variation.     

Fetal heart rate patterns in postasphyxiated fetal lambs with brain damage

OBJECTIVE: We previously showed that in asphyxiated fetal lambs the duration of hypotension correlated well with the severity of histologic damage to the brain, whereas the duration of bradycardia did not. This study compares fetal heart rate patterns with the degree of histologic damage to the brain. STUDY DESIGN: Twelve chronically instrumented near-term fetal lambs were subjected to asphyxia by umbilical cord occlusion until fetal arterial pH was <6. 9 and base excess was <-20 mEq/L. An additional 4 fetuses served as sham-asphyxia controls. Fetal heart rate (from electrocardiogram), arterial blood pressure, fetal breathing movements, and electrocorticogram were continuously monitored before, during, and for 72 hours after asphyxia. Fetal brain histologic features were categorized as mild (group 1, n = 5), moderate (group 2, n = 4), and severe (group 3, n = 3). Long-term fetal heart rate variability expressed as amplitude range was assessed visually every 5 minutes from 30 minutes before asphyxia until 2 hours of recovery and at 6, 12, 24, 48, and 72 hours of recovery. RESULTS: Long-term fetal heart rate variability amplitude decreased from 32 +/- 17 beats/min (mean +/- SEM) preocclusion to 4 +/- 13 beats/min at the end of occlusion (P <.001) without significant differences among the 3 groups. During 10 to 45 minutes of recovery, the long-term variability of group 1 was significantly greater than that of groups 2 and 3. At 24 to 72 hours of recovery, the long-term variability of groups 1 and 2 was significantly higher than that of group 3, which was almost 0. The "checkmark" and sinusoidal fetal heart rate patterns were observed during the recovery period in groups 2 and 3. CONCLUSIONS: Decreased long-term fetal heart rate variability and the "checkmark" and sinusoidal fetal heart rate patterns were indicators of the severity of asphyxial histologic damage in the fetal brain.     

Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations

It was our objective to compare computerized fetal heart rate analysis with blood flow velocity waveform analysis of the arterial and venous fetal circulation in intrauterine growth retardation. We report five illustrative cases with longitudinal observations of fetal Doppler findings and fetal heart rate between 23 and 32 weeks of gestation. Blood flow waveforms were recorded from the umbilical artery, middle cerebral artery, descending aorta, ductus venosus and inferior vena cava. Fetal heart rate was analyzed by a computer system according to the Dawes-Redman criteria. The time sequence of deterioration is described individually for each fetus. An abrupt increase in pulsatility of ductus venosus waveforms with loss of forward flow velocity during atrial contraction preceded abnormally low short-term variation of fetal heart rate. With advanced gestational age and concomitant maternal disease, we observed severe alterations of flow velocity waveforms within 12 h of normal Doppler measurements, which is in contrast to findings in the second trimester, in which severely abnormal venous waveforms were observed over a period of several weeks before intrauterine death occurred. In a fetus with terminally low short-term variation, normal venous waveforms indicated fetal well-being despite an abnormal cardiotocogram (CTG). We challenge the current concept that the CTG is the best available parameter to determine the optimal time for elective delivery of premature growth-retarded fetuses. Deterioration in ductus venosus blood flow seems to precede an abnormal CTG and thus heralds the need for delivery.     

The relationship between umbilical artery Doppler findings, fetal biophysical score and placental inflammation in cases of premature rupture of membranes

BACKGROUND: To assess the relationship between placental inflammation, umbilical artery Doppler waveforms and fetal biophysical profile score, umbilical artery Doppler studies and fetal biophysical evaluations were performed in 24 preterm pregnants with premature rupture of membranes (PPROM). SUBJECTS: After delivery, the placentas were microscopically examined and two subgroups were formed including noninflamed or inflamed placentas. RESULTS: In the first group, which includes 14 cases with no histological signs of placental inflammation, we found increased systolic/diastolic ratio only in one patient, whereas in the second group including ten cases with microscopically proven inflammation, nine were found to have increased systolic/diastolic ratios (p < 0.05). Mean systolic/diastolic ratio in the first and the second groups were 2.74 +/- 0.18 and 4.64 +/- 0.93 respectively (p < 0.001). Mean biophysical profile score was 9 +/- 1.04 in the first group and 7 +/- 1.05 in the second group (p < 0.001). CONCLUSION: Abnormal biophysical profile scores along with increased arterial systolic/diastolic ratios have been shown to be the markers of impending clinical infection.     

Pooling of clodronate urinary excretion data: a new pharmacokinetic method to study drugs with highly variable gastrointestinal absorption

OBJECTIVE: Our purpose was to study effects of vibroacoustic stimuli on electrocortical activity and heart rate changes in fetal sheep in utero. STUDY DESIGN: Seven chronically instrumented near-term fetal sheep were repeatedly stimulated by an electronic artificial larynx for 32 seconds during periods of rapid-eye-movement and non-rapid-eye-movement sleep. Responses to vibroacoustic stimulation were obtained by spectral analysis of the electrocorticogram (fast Fourier transform) and by assessment of changes in fetal heart rate and fetal heart rate variability. RESULTS: During non-rapid-eye-movement sleep vibroacoustic stimulation led to electrocorticogram desynchronization that consisted of a marked reduction of delta and theta band power (p < 0.05). A concomitant fetal heart rate decrease and fetal heart rate variability increase were also noted (p < 0.05). During rapid-eye-movement sleep vibroacoustic stimulation induced a significant increase in alpha and beta band power (p < 0.05) and a slight deviation in basal fetal heart rate and fetal heart rate variability (p < 0.05). CONCLUSION: Vibroacoustic stimulation of fetal sheep provokes reproducible changes in fetal electrocortical activity and heart rate patterns. These changes, which are not easily identifiable in gross polygraphic assessments of the fetal behavioral state, are indicative of fetal arousal.     

The influence of the maternal heart rate on the uterine artery pulsatility index in the pregnant ewe

We investigated the influence of the maternal heart rate on the uterine artery pulsatility index in pregnant ewes. We used an external pacemaker to alter the heart rate of 5 pregnant ewes at 16-17 weeks of pregnancy and examined the effect of changes in the maternal heart rate on the uterine artery flow velocity waveforms and the pulsatility index, as determined by Doppler velocimetry. The uterine artery pulsatility index showed a significant negative correlation with the maternal heart rate. There were no significant changes in other hemodynamic parameters. The maternal heart rate had a significant influence on the uterine artery pulsatility index.     

Doppler ultrasonography of canine maternal and fetal arteries during normal gestation

Two-dimensional ultrasonography was used in combination with colour-flow imaging and pulsed wave Doppler ultrasonography to study the maternal circulation and the development of fetal vascularization in six Beagles during normal gestation. For the first time, the development of the circulation was demonstrated in the bitch and her fetuses intra vitam. The bloodstream was examined in small uteroplacental arteries, the umbilical artery, the fetal aorta and the common carotid artery. The duration of the study was from week 3 after insemination until birth. Relatively large vessels were detected by cross-sectional ultrasonography, and small vessels were detected by colour-flow imaging. In pulsed wave Doppler ultrasonography, the blood flow was measured and described using the parameters of systolic peak velocity, diastolic peak velocity, end-diastolic velocity, pulsatility index, resistance index, A:B ratio (systolic peak velocity:end-diastolic velocity) and S:D parameter (systolic peak velocity:diastolic peak velocity). The development of the measured parameters is typical and similar to that in humans. The systolic peak velocity of the canine maternal uteroplacental arteries shows important differences in comparison with humans. The pulsatility index, resistance index and A:B ratio decrease in nearly all vessels. Only the fetal common carotid artery has constant pulsatility and resistance indices during gestation. For the first time, the quality and quantity of the normal blood flow have been monitored during the whole of gestation. A normal circulation is fundamental for supplying the fetus adequately with oxygen and nutrients and thus for physiological development. These ultrasonographic results are the basis for further clinical studies.     

Analysis of risk factors influencing imminent distress in growth-retarded fetuses undergoing oxygen test

We previously demonstrated a prognostic significance of maternal oxygen test in predicting imminent fetal distress. The purpose of this study was to investigate eventual other factors related to the length of the time interval elapsing between the Doppler diagnosis of brain sparing effect and abnormal fetal heart rate patterns. To this end we considered 101 growth-retarded fetuses free of structural and chromosomal abnormalities with a ratio between the pulsatility indices of umbilical and middle cerebral artery above the 95th centile in presence of a normal fetal heart rate pattern. The factors, other than the oxygen test, analyzed for a potential influence on this time interval were gestational age, presence of hypertension or preeclampsia, amniotic fluid index, severity of growth retardation (centile of the ultrasonographic estimated fetal weight) and 9 different Doppler indices calculated from extra- and intracardiac districts. Statistical actuarial methods were used to determine the effect of these prognostic factors on the duration of this time interval. The occurrence of abnormal fetal heart rate patterns (antepartum late heart rate decelerations) was used as censoring variable. The time interval between the entry in the study and delivery ranged from 1 to 39 days. Indications for delivery were fetal distress in 53 fetuses (52.4%) and different maternal or fetal complications in the remaining 48 fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)     

The hemodynamic effects of maternal hypo- and hyperoxygenation in healthy term pregnancies

OBJECTIVE: To evaluate the hemodynamic effects of maternal hypo- and hyperoxygenation in normal term pregnancy. METHODS: Ten healthy women between 35-41 weeks' gestation were exposed to 10% oxygen in inspired air for 10 minutes and, after a 5-minute recovery period, to a stepwise increase in oxygenation with 50 and 100% oxygen for 10 minutes. Maternal ventilation, hemodynamics, and oxygenation were assessed noninvasively, and maternal and fetal vascular responses were assessed with pulsed-wave color Doppler velocimetry. Computerized cardiotocography was used for fetal heart rate (FHR) analysis. RESULTS: Substantial maternal hypoxia was achieved and accompanied by a statistically significant rise in the maternal heart rate (from 89 +/- 11 to 104 +/- 16 beats per minute) and systolic blood pressure (from 123 +/- 13 to 131 +/- 13 mmHg). Doppler measurements demonstrated a statistically significant decline in the pulsatility index (PI) of the maternal internal carotid artery (from 1.8 +/- 0.3 to 1.5 +/- 0.4) and an increase in the uterine artery PI (from 0.60 +/- 0.12 to 0.72 +/- 0.13). Baseline FHR, heart rate variability, and Doppler velocimetry in the umbilical artery and the middle cerebral artery showed no statistically significant changes. Hyperoxia did not cause changes in the maternal circulation, but the FHR decreased significantly (from 142 +/- 12 to 133 +/- 11 beats per minute). CONCLUSION: Acute short-term hypoxia modifies the maternal circulation, suggesting redistribution of maternal blood flow, but exerts no detectable effects on the healthy fetus. Maternal hyperoxygenation induces no apparent adverse effects.     

A study for predicting toxemia of pregnancy by the diastolic notch in pulsed Doppler flow velocity waveforms of the uterine arteries--quantitative analysis of the diastolic notch as uterine arterial index (UTAI)

To investigate the ability of measurement of the diastolic notch in Doppler flow velocimetry to predict development of toxemia of pregnancy, analysis of uteroplacental and fetal blood flow waveforms was performed. The waveforms were analyzed by calculating the resistance index (RI) and the pulsatility index (PI) and were investigated whether diastolic notches existed or not. In the prospective study, the uterine arterial index (UTAI; an index introduced to evaluate the degree of diastolic notch quantitatively) was also calculated. RETROSPECTIVE STUDY: The waveforms in the uterine arteries, the umbilical artery and the fetal vessel (inferior vena cava, descending aorta and middle cerebral artery) were measured in 153 pregnant women. PROSPECTIVE STUDY: Uterine artery velocimetry was performed at 16-23 weeks' gestation in 387 pregnant women. RESULT 1: Subjects with a diastolic notch had significantly higher rates of development of toxemia of pregnancy. Indexes of the fetal blood flow waveforms had no significant correlations with the development of toxemia of pregnancy. RESULT 2: UTAI showed an equivalently high negative predictive value (98.1%) and higher positive predictive value (17.6%) than RI (98.2%, 10.2% respectively) and PI (98.7%, 12.7% respectively). CONCLUSION: UTAI measurement was more useful for predicting toxemia of pregnancy than RI or PI.     

Effect of antenatal administration of thyrotrophin releasing hormone on fetal flow velocity waveforms

AIM: To determine whether antenatal administration of thyrotrophin releasing hormone (TRH), to promote lung maturation, alters blood flow through the fetal middle cerebral, umbilical artery, or ductus arteriosus and through the maternal uterine arteries. METHODS: The effect of transplacentally administered TRH on the fetal circulation was prospectively evaluated in 30 patients between 24 and 34 weeks' gestation. TRH (400 micrograms) was given to the mother intravenously either as a bolus or an infusion. Fetal effects were determined by measuring the maximum velocity and pulsatility index (PI) in middle cerebral artery, ductus arteriosus, uterine artery and umbilical artery Doppler waveforms. Measurements were made immediately before, and 10 and 60 minutes after maternal TRH administration. RESULTS: Intravenous injection of TRH had no significant effect on PI in the uterine, umbilical, or middle cerebral artery and the ductus arteriosus within 60 minutes of administration in either group. CONCLUSION: The antenatal use of TRH in conjunction with steroids for fetal lung maturity does not affect utero-placental or fetal haemodynamic variables, as measured by Doppler. These findings, therefore, do not support the suggestion that antenatal intravenous administration of TRH either as bolus or infusion may have immediate adverse vascular effects in the fetus.