Effect of prolonged hypoxemia on fetal heart rate accelerations and decelerations in sheep

Experiments were conducted in 10 chronically catheterized fetal sheep to determine the effect of 24 hours of hypoxemia in the absence of progressive acidemia on fetal heart rate accelerations and decelerations. Fetal hypoxemia was produced by mechanically restricting uterine blood flow with a vascular clamp placed around the maternal common internal iliac artery. Fetal arterial oxygen tension decreased from 22.3 +/- 1.8 to 17.8 +/- 1.5 mm Hg at 2 hours and remained low for the 24-hour experimental period. Fetal pH decreased from 7.34 +/- 0.01 to 7.20 +/- 0.05 at 2 hours and returned to normal values by 12 hours. No significant change was observed in the number or characteristics of fetal heart rate accelerations or decelerations during the 24-hour control period. There was a significant increase in the number of accelerations from 48 +/- 4 to 63 +/- 4 per hour at 8 hours of hypoxemia followed by a return to control values by 12 hours. There was no significant change in the mean amplitude or duration of accelerations. There was a significant increase in the number of decelerations per hour with an associated increase in the mean amplitude but a decrease in the mean duration of decelerations during the first 16 hours of hypoxemia. We conclude that prolonged hypoxemia in fetal sheep leads to an initial increase in the number of both accelerations and decelerations in fetal heart rate followed by a return to normal patterns indistinguishable from those of the normoexemic fetus.     

Effects of hypoglycaemia on fetal heart activity and umbilical artery Doppler velocity waveforms in pregnant women with insulin-dependent diabetes mellitus

Objective To study the effect of induced hypoglycaemia on fetal wellbeing as indicated by fetal heart rate and umbilical artery flow velocity waveforms.
Design A prospective experimental investigation.
Setting High risk pregnancy unit and diabetes research unit at Karolinska Institutet, Danderyd Hospital, a university affiliated hospital.
Participants Ten women with insulin-dependent diabetes mellitus in the third trimester of pregnancy.
Interventions The fetal heart rate, the blood flow velocity waveforms in the umbilical artery and the maternal catecholamine levels were investigated during a 150–minute hyperinsulinaemic hypoglycaemic clamp with induction and maintenance of an arterial blood glucose level of about 2.2 mmol/l.
Main outcome measures 1. Fetal: changes of fetal heart rate pattern and pulsatility index of the umbilical artery flow velocity waveforms. 2. Maternal: levels of plasma adrenaline and plasma noradrenaline.
Results Maternal hypoglycaemia was associated with an increase in frequency and amplitude of fetal heart rate accelerations, a slight decrease in the pulsatility index of the umbilical artery and a rise in the maternal catecholamine levels.
Conclusions We speculate that the increased number of fetal heart rate accelerations reflects an increased sympathico-adrenal activity during the hypoglycaemic clamp. No potentially harmful effects on the fetus were observed in the fetal heart rate or in the umbilical artery Doppler waveform analysis during hypoglycaemia.     

Supine position in labor and associated fetal heart rate changes

Presented is an investigation of the relationship of fetal heart rate (FHR) deceleration and position of the patient in labor. In a group of 902 laboring patients, 126 (14%) demonstrated late decelerations. Of the 126, 24 (19%) patients demonstrated late decelerations in the supine position only. These occurred during uterine contractions and were associated with reduced femoral arterial blood pressure and amplitude of the capillary pulse of the big toe. A drop in capillary blood pH of the fetal scalp could also be demonstrated. These effects reproducibly appeared and disappeared when supine and lateral positions were alternated. These data would suggest that maternal aortic compression by the pregnant uterus plays a role in the etiology of fetal stress as expressed by changes in fetal heart rate and acid base balance. This effect can be evaluated and monitored simply by recording the pulse pressure of the big toe and femoral arterial pressure. These atraumatic procedures can be applied to any patient.     

Maternal and fetal effects of low-dosage bupivacaine paracervical block

Vasoconstriction of the uterine arteries, hypertonus of the uterus, and the direct toxic effects of a local anesthetic on the fetus or a combination of the above have been presented as etiological factors of fetal bradycardia following paracervical block. The reduce fetal side-effects a superficial and lowdosage technique of PCB have been advocated. We have studied the effects of 25 mg of bupivacaine PCB using the above technique on fetal heart rate pattern (FHR), fetal acid-base balance, uterine activity, placental blood flow and maternal and fetal plasma levels of bupivacaine in 38 patients. The analgesic effect of a single 25 mg of bupivacaine PCB was good in 76%, moderate in 12% and poor in 12% of the cases. No changes in maternal heart rate or in blood pressure were noted. Fetal bradycardia defined as a decrease of mean fetal heart rate of at least 20 bpm or an absolute rate less than 100 bpm and a duration greater than two minutes occurred in 12% of the cases. The mean amplitude of the baseline fetal heart rate variability decreased significantly after PCB and a silent pattern (an amplitude less than 5 bpm) was observed in 20% of the cases. The most frequent (27%) pathological finding in our study was the disappearance of FHR accelerations after PCB. Similarly early and late decelerations of FHR occurred more often after PCB than during the control period before the block. The fetal pH from scalp blood samples did not, on average, decrease after PCB, but did so in cases with fetal bradycardia. Intervillous blood flow as measured by the 133Xe washout method did not change when measured before and after PCB. In addition in three cases with fetal bradycardia the changes in the intervillous blood flow were minimal. No significant changes in the mean uterine tone, amplitude and frequency of contractions were observed after PCB. However, an obvious uterine hypertonus was observed after PCB was observed in three cases of fetal bradycardia but not in two other cases of bradycardia or in the 8 cases of silent FHR pattern. Mean maternal bupivacaine concentration 20 minutes after PCB was 0.14 +/- 0.06 microgram/ml and 0.07 +/- 0.04 microgram/ml at birth. Simultaneous fetal and umbilical venous and arterial concentrations were correspondingly 0.04 +/- 0.02 microgram/ml, 0.03 +/- 0.01 microgram/ml and 0.03 +/- 0.01 microgram/ml, and they were significantly lower than respective maternal concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)     

Heart rate variation and movement incidence in growth-retarded fetuses: the significance of antenatal late heart rate decelerations

In 37 intrauterine growth-retarded fetuses, combined 1-hour recordings of fetal heart rate and body movements were made within 24 hours of elective cesarean section. Fetal body movements were recorded simultaneously by use of real-time ultrasound. The study group was divided into two subgroups, according to the presence (n = 29) or absence (n = 8) of antepartum late heart rate decelerations. Correlations were made with umbilical blood gas values obtained immediately after cesarean section. Baseline heart rate variation was reduced below the normal range in 88% of the intrauterine growth-retarded fetuses with decelerations but in only 37% of the group without decelerations. A reduction in fetal heart rate accelerations and body movements and an increase in mean heart rate also were observed only in the group with decelerations. Late heart rate decelerations were associated with low PO2 values in both umbilical artery and vein. It is concluded that in intrauterine growth-retarded fetuses reduced heart rate variation and movement incidence correlate with the presence of late heart rate decelerations before birth and with hypoxemia at birth.     

Combined (stressed and non-stressed) antenatal fetal heart rate monitoring.

Acceleration patterns of the fetal heart rate, or a normal heart rate during spontaneous contractions, were used as a short weekly screening test to evaluate fetal well-being in 1102 high-risk pregnancies. When accelerations or contractions were absent during the initial screening, oxytocin was administered to stimulate uterine contractions. The mean duration of the antenatal monitoring was 18.5 min when the initial antenatal monitoring was normal, but 38.8 min when the initial results were uncertain. Oxytocin was administered to 38% of patients. This reduced the number of occasions where the diagnosis was uncertain from 46.6% to 12%. Patients with uncertain antenatal fetal monitoring had significantly more late decelerations during labor as well as newborns with low Apgar scores when compared to those with normal antenatal monitoring. Patients with abnormal antenatal monitoring (positive stress test) had significantly more low 5-min Apgar scores, late decelerations during labor and growth-retarded infants than the patients with normal antenatal fetal monitoring. Only 1 intrauterine death occurred within 7 days of a normal antenatal heart rate recording. No preventable fetal deaths occurred when antenatal monitoring demonstrated an acceleration pattern of the fetal heart rate.     

Characteristics of maternal heart rate patterns during labor and delivery

OBJECTIVE: To find patterns characteristic of maternal heart rates recorded by an electronic fetal monitor and compare them with concomitant fetal heart rate (FHR) patterns. METHODS: Maternal heart rates and FHRs during active labor and delivery were simultaneously recorded in 26 parturients with singleton pregnancies in vertex presentation. The FHRs were obtained by an external ultrasound transducer or via a spiral scalp electrode and maternal heart rates by a triple-wire cable with electrocardiographic electrodes attached to the chest. Representative tracings of 30-60 minutes duration were selected from all stages of labor and after delivery of the placenta. Quantitative assessments were carried out under guidelines from the National Institute of Child Health and Human Development after blinding the source of these tracings. Patterns were compared by appropriate statistical analyses. RESULTS: Baseline maternal heart rates were significantly lower and their variability significantly higher than FHRs during all stages of labor. Maternal heart rates showed no decelerations; the proportion of tracings with accelerations increased as labor advanced, most of them coinciding with uterine contractions or bearing down efforts. The FHRs had both decelerations and accelerations. However, tracings with only accelerations (and no decelerations) were observed in decreasing frequency as labor advanced. Maternal accelerations had higher amplitudes and longer durations than fetal accelerations, especially in the second stage of labor. CONCLUSION: Maternal heart rate patterns recorded by electronic fetal monitors closely resemble fetal patterns. Baseline "fetal bradycardia," the absence of decelerations in the second stage of labor, and marked accelerations coinciding with uterine contractions may suggest a maternal heart rate rather than an FHR recording.     

Intrapartum fetal heart rate patterns in the prediction of neonatal acidemia

OBJECTIVE: This study was undertaken to correlate changes in the intrapartum electronic fetal heart rate patterns with the development of significant neonatal acidemia. STUDY DESIGN: We identified 488 fetuses at a gestational age of >37 weeks' gestation who had continuous electronic fetal monitoring during labor for the last 2 hours and umbilical artery cord gas analysis performed at delivery. One investigator blinded to the cord gas outcome reviewed all 488 tracings using the National Institute of Child Health and Human Development guidelines for fetal heart rate monitoring. All fetal heart rate tracings with bradycardia were removed from further analysis. The patients were placed in six groups, depending on the absence or presence of normal variability (amplitude >5 beats) during the last hour of monitoring combined with the absence of decelerations or the presence of variable or late decelerations. The relationship between changes in variability and the outcome variables of pH and base deficit in the six groups was assessed with analysis of variance and chi(2) test. Significance was set at the P <.05 level. RESULTS: Patients with normal variability and accelerations, even in the presence of late decelerations or variable decelerations, maintained an umbilical artery pH 7.0 or greater in more than 97% of cases. In the presence of minimal/absent variability (amplitude <5) for at least an hour, the incidence of significant acidemia (pH <7.0) ranged from (12%-31%). CONCLUSION: The most significant intrapartum fetal heart rate parameter to predict the development of significant acidemia is the presence of minimal/absent variability for at least 1 hour as a solitary abnormal finding or in conjunction with late decelerations in the absence of accelerations. Urgent delivery should be considered in these cases after appropriate ancillary testing.     

V-shaped deceleration differs in the pattern of carotid blood flow from variable deceleration provoked by cord compression

OBJECTIVE: To investigate whether V-shaped decelerations in fetal heart rate tracing are a physiologic response to fetal movements or secondary to cord compression. STUDY DESIGN: Six pregnant sheep and their fetuses (115-125 days of gestation) were surgically instrumented and studied. Fetal electrocardiogram, carotid blood flow, arterial blood pressure and fetal movement were continuously monitored for 24 hours. Following the undisturbed 24 hour recording, these parameters were monitored during umbilical cord compression (n = 6). Differences in these parameters between V-shaped decelerations and decelerations provoked by cord compressions were examined. RESULTS: Elevation of blood pressure and decreased carotid blood flow were observed coincidentally with the initiation of V-shaped decelerations. In cord compression, elevation of both blood pressure and carotid blood flow were followed by a decreased heart rate. V-shaped decelerations exhibited a different alteration of carotid blood flow compared to decelerations caused by umbilical cord compression. CONCLUSION: V-shaped deceleration is a physiologic response secondary mainly to fetal movements and is not caused by cord compression.     

Terbutaline: effects on the fetal heart at term

The aims of this study were to evaluate the cardiac effects of subcutaneous terbutaline on the mother and fetus. Terbutaline was given in 250 or 500 μg doses to term gravidas not in labor. The mean arterial pressure (MAP), pulse, and uterine activity were measured. The fetal heart rate (FHR), accelerations, and decelerations were recorded. There were significant increases in maternal heart rate, FHR, and FHR accelerations, and a decrease in uterine basal activity after 500 μg, but not significantly after 250 μg of terbutaline. MAP was not significantly increased with either dose, although a small mean increase was observed. Terbutaline has a direct effect on the fetal heart apart from the effect of uterine relaxation.     

Poor prognostic value of the basal fetal heart rate as observed during antenatal monitoring

The basal fetal heart rate, accelerations, decelerations and amplitude and frequency of variation were scored in positive stress tests of 146 and in suspicious recordings of 296 patients. Positive tests scored lower for accelerations, decelerations and amplitude and frequency of variation but not for the basal heart rate. When the outcome was poor, as characterized by low 5-min Apgar score and intrauterine growth retardation, it was reflected by all parameters of the fetal heart rate pattern except for the basal heart rate.     

Umbilical artery blood flow velocity waveforms during variable deceleration of the fetal heart rate

Blood flow velocities of the umbilical arteries were measured by Doppler ultrasonography during variable decelerations of the fetal heart rate. The flow velocity waveforms, being normal between uterine contractions, showed either an unchanged flow velocity waveform with an exclusive fetal heart rate effect on end-diastolic velocities or a rapid change to absent and reverse diastolic flow during the decelerations, indicating an abrupt increase in placental resistance with a halt in placental perfusion. Computer-aided reconstruction of the fetal heart rate curve revealed the exact temporal relationship between the reduction of umbilical artery perfusion and deceleration of fetal heart rate. We showed that variable decelerations of fetal heart rate can be observed during only slightly changed umbilical perfusion or can be caused by a halt in placental perfusion, which does not necessarily mean an absence of any movement of the fetal blood column, but is a result of a systolic forward and diastolic reverse flow to the same extent.     

Mechanisms of late decelerations in the fetal heart rate. A study with autonomic blocking agents in fetal lambs.

Fetal heart rate decelerations resembling the late deceleration FHR pattern were produced in fetal sheep by periodic occlusion of the maternal common hypogastric artery for 30-60 sec. Transient fetal hypertension also occurred during the occlusions. Alpha-adrenergic blockade with phentolamine eliminated or markedly reduced the hypertensive response. FHR decelerations still occurred intermittently with some occlusions; however, their character was greatly altered. After parasympathetic blockade with atropine, the decelerations were replaced by periodic FHR accelerations during the occlusions. These accelerations were, in turn, eliminated by the beta-adrenergic blocking agent, propranolol. In the presence of combined parasympathetic, alpha- and beta-adrenergic blockade, the FHR remained essentially constant during the hypogastric artery occlusions in non-acidemic fetuses. FHR decelerations persisted after parasympathetic or total autonomic blockade when the fetuses were significantly hypoxic, as judged by depressed arterial blood pH and base excess values. Beat-to-beat variability of the baseline FHR persisted in the face of severe hypoxia and acidosis. These observations demonstrate that reflex mechanisms are involved importantly in the genesis of late deceleration FHR patterns in the acutely hypoxemic fetus, but that direct depression of myocardial rhythmicity becomes a factor as hypoxic acidosis develops.     

What is fetal distress?

Fetal distress is a widely used but poorly defined term. This confusion of definition compounds the difficulty of making an accurate diagnosis and initiating appropriate treatment. The fetus reacts at the onset of asphyxia with a remarkable series of responses, primarily a complexly regulated redistribution of blood flow that serves to limit the deleterious effects of oxygen limitation in vital organs. This enables the fetus to survive asphyxia intact unless the insult is profound or prolonged. The most common asphyxial stresses imposed on the fetus during labor are insufficiency of uterine blood flow, or insufficiency of umbilical blood flow, and occasionally decrease in uterine arterial oxygenation. Each of these stresses produces characteristic fetal heart rate patterns: late decelerations, variable decelerations, or prolonged bradycardia. There is strong evidence that the presence of normal fetal heart rate variability represents normal central nervous system integrity, including adequate oxygenation. A decrease or loss of variability in the presence of these patterns is a sign that the physiologic compensations are overwhelmed as a result of the severity of asphyxia. Knowledge of the fetal responses to asphyxia, together with the known evolution of fetal heart rate patterns during asphyxia, should allow a more accurate definition of the onset of unacceptable asphyxia, and more rational management and timing of intervention.     

Acceleration of the fetal heart rate.

Acceleration of the fetal heart rate during contractions was usually followed by deceleration, and evidence is presented to show that it results from increased sympathetic drive and may be associated with fetal tissue hypoxia. However, the presence of accelerations are not serious and merely warn the obstetrician of the possibility of the occurrence of subsequent decelerations. The mechanism thought most likely to produce accelerations is uterine compression of the umbilical vein during contractions.     

Fetal heart rate patterns in the small-for-gestational-age human fetus

A total of 24 pregnant women with growth-retarded fetuses were studied to examine the distribution of fetal heart rate accelerations between 30 and 40 weeks' gestation, as compared with those of fetuses of normal growth that were matched for gestational age and length of fetal heart rate tracings. Growth-retarded fetuses had significantly lower PO2 levels in the umbilical artery at birth (3 mm Hg less) than did healthy fetuses (p less than 0.05), but without metabolic acidosis. There was a larger proportion of small amplitude (less than 10 beats/min) and a smaller proportion of large amplitude (greater than 20 beats/min) fetal heart rate accelerations in the small-for-gestational-age fetuses than in the fetuses of normal growth. Although the number of accelerations was significantly reduced (50% less) in growth-retarded fetuses compared with healthy fetuses, there was no significant difference in the mean basal fetal heart rate and the mean number of decelerations between the two groups. Currently used definition of an acceleration as greater than or equal to 15 beats/min for greater than or equal to 15 seconds was applicable only in fetuses of normal growth. We hypothesized that a decrease in absolute acceleration frequency might be a useful index to detect the chronically hypoxemic fetus before severe metabolic acidosis and irreversible damage occurred.     

Fetal and maternal endocrine responses to prolonged reductions in uterine blood flow in pregnant sheep

To examine the effects of sustained (48-hour) hypoxemia on fetal and maternal adrenocorticotropic hormone concentrations and on maternal progesterone, uterine blood flow was reduced in eight sheep at day 128 of pregnancy by means of an adjustable Teflon clamp placed around the maternal common internal iliac artery. Control measurements were made in four animals in which the vascular clamp was not adjusted. Fetal PaO2 fell from 20.6 +/- 1.1 mm Hg (mean +/- SEM) to 16.6 +/- 0.6 mm Hg within 1 hour after application of the clamp and remained suppressed during 48 hours. There was a transient acidemia at 1 to 2 hours that had corrected by 8 hours. Fetal adrenocorticotropic hormone levels rose from 24 +/- 6 to 1320 +/- 205 pg/ml at 2 hours but decreased by 16 hours. Measured by high-pressure liquid chromatography, more than 95% of immunoreactivity corresponded to adrenocorticotropic hormone1-39. Fetal cortisol levels rose by 6 hours and remained elevated through 48 hours. Maternal adrenocorticotropic hormone, cortisol, and progesterone levels were unchanged during the study period. We conclude that fetal hypoxemia-acidemia after restriction of uterine blood flow provokes fetal adrenocorticotropic hormone release, but the elevation in adrenocorticotropic hormone is not sustained. However, the level of fetal cortisol rises progressively, consistent with fetal adrenal activation.     

Umbilical artery flow velocity waveforms during acute hypoxemia and the relationship with hemodynamic changes in the fetal lamb

The contributions of the variables of the fetal circulation to changes in the pulsatility index of the umbilical artery flow velocity waveform have not been assessed. Acute fetal hypoxemia was induced by 60 to 90 seconds of total occlusion of the maternal common internal iliac artery in six sheep. Mean fetal PO2 levels decreased from 26.0 to 18.3 mm Hg (p less than 0.01) after occlusion of uterine blood flow. Fetal heart rate decreased from 188 to 121 beats per minute at the end of occlusion (p less than 0.05). Placental vascular resistance did not change during the heart rate deceleration. The pulsatility index increased from 0.86 during the control period to 1.27 at the end of occlusion (p less than 0.05). After fetal parasympathetic blockade with atropine, fetal heart rate and placental vascular resistance did not change during occlusion. The pulsatility index did not change during occlusion after parasympathetic blockade. It is concluded that the changes in the umbilical artery pulsatility index during late decelerations in the fetal heart rate pattern appear to be primarily associated with changes in fetal heart rate and bear no relationship with placental vascular resistance.     

The effect of magnesium sulfate on the behavioral activities of fetal goats

OBJECTIVES: To investigate fetal heart rate accelerations, fetal breathing movements, and fetal electrocortical activities during administration of magnesium sulfate to fetal goats. METHODS: The fetal heart rate accelerations, fetal breathing movements, and fetal electrocortical activities during 6 hours of continuous magnesium sulfate infusion into the fetal jugular vein were examined in 8 chronically instrumented fetal goats at 124-131 days of gestation. Fetal breathing movements were defined as repetitive negative fluctuations of the fetal tracheal pressure. Fetal electrocortical activities were assessed by visual analysis of periods of high-voltage and low-voltage electrocortical activities. RESULTS: Continuous infusion of magnesium sulfate for 6 hours significantly increased the fetal plasma magnesium concentration from 2.8 +/- 1.2 to 8.3 +/- 2.6 mg/dL without significant changes in fetal arterial blood gases. The incidence of fetal heart rate accelerations during magnesium infusion was significantly decreased from that found during the control periods. After 2 hours of infusion, the incidence of fetal breathing movements significantly decreased from 33.9% +/- 20.5% to 1.2% +/- 1.4% and remained at this level during the remaining 4 hours of magnesium infusion. The percentage of time that the fetuses were found to have low-voltage electrocortical activities decreased from 51.6% +/- 9.0% to 40.4% +/- 8.2% after 2 hours of infusion but recovered to 49.9% +/- 12.0% by 6 hours of magnesium infusion. CONCLUSION: We concluded that fetal magnesium sulfate administration affected fetal heart rate accelerations and fetal breathing movements continuously but electrocortical activities only temporarily during 6 hours of observations.     

The relationship between uterine contractions, fetal movements and fetal heart rate patterns in the active phase of labor

The relationship between fetal movements, fetal heart rate and uterine contractions was studied with a computerized system in 18 parturients during the active phase of labor. 80% of FHR accelerations and 39% of uterine contractions were associated with fetal trunk movements. The probability of association was greater in longer movements and larger accelerations. 98% of fetal movements which lasted 10-15 s, 98% of accelerations with an amplitude of 25-30 bpm and 96.4% of accelerations with a duration of 40-50 s were associated with fetal trunk movements.