Fetal heart rate responses to maternal exercise

The fetal heart rate responses to mild, moderate, and strenuous maternal exercise were studied in 45 healthy subjects. In the majority of cases, the fetal heart rate increased during and after maternal exercise. Fetal bradycardia was recorded in five fetuses; this appears to be a sporadic event. There was no correlation between the individual fetal heart responses, gestational age, exercise intensity, and maternal circulating catecholamines.     

Fetal circulatory responses to maternal blood loss

We examined the fetal circulatory responses to maternal blood loss in pregnant women during the third trimester. Seven healthy women with placenta previa and singleton pregnancies underwent phlebotomies in an autologous donation program. Four hundred milliliters of blood was collected within 15 min at 34 and 35 weeks of gestation. Continuous electric recordings of fetal heart rate were performed during the first blood collection, and the maternal uterine artery (UtA), umbilical artery (UmA) and fetal middle cerebral artery (MCA) Doppler velocity waveforms were recorded before, immediately after and 24 h after the second collection in each patient. The average fetal heart rate, maternal UtA and UmA pulsatility indices did not change measurably during or after maternal blood collections. However, the average fetal MCA pulsatility index decreased significantly 24 h after maternal blood loss. The observation of a decrease in fetal MCA pulsatility index may indicate delayed fetal asphyxia following mild maternal hemorrhage.     

Fetal vascular responses to maternal nicardipine administration in the hypertensive ewe

Calcium channel blockers such as nicardipine act as arterial vasodilators and are effective in the treatment of hypertension. Although they are also effective tocolytic agents, fetal effects have not been fully studied. Fifteen chronically catheterized near-term ewes were studied. Maternal and fetal cardiorespiratory parameters were measured in the control period and again 15 minutes after maternal venous infusion of angiotensin II. Nicardipine 20 micrograms/kg/min was given over 2 minutes and maternal and fetal cardiorespiratory parameters and fetal blood flow were measured 5.30 and 60 minutes later. Nicardipine reversed maternal hypertension and produced transient tachycardia. Fetuses responded initially with transient bradycardia and then developed hypercapnia and acidemia (p less than 0.03) by 60 minutes after nicardipine. Fetal placental blood flow decreased and vascular resistance increased by 5 minutes after nicardipine but returned toward control values after 30 minutes. Unexpectedly we observed the death of five fetuses by 65 minutes after nicardipine. We conclude that the administration of nicardipine in the hypertensive ewe results in significant alterations of fetal cardiorespiratory status and placental function that may lead to acidemia.     

Fetal and maternal endocrine responses to experimental intrauterine infection in rhesus monkeys

OBJECTIVE: Our purpose was to describe the temporal and quantitative relationships among intrauterine infection, fetal-placental steroid biosynthesis, and preterm labor in a nonhuman primate model. STUDY DESIGN: On approximately day 130 of gestation (term 167 days) chronically instrumented rhesus monkeys (Macaca mulatta) were infected with 10⁶ colony-forming units of group B streptococci either by intraamniotic (n = 4) or choriodecidual (n = 2) inoculation. As controls, four additional chronically instrumented noninfected monkeys were followed up to spontaneous parturition. Amniotic fluid and maternal and fetal arterial blood were serially sampled in all monkeys (both before and after infection) for progesterone, estrone, estradiol, dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, and cortisol by specific radioimmunoassays, and uterine activity was continuously recorded. RESULTS: Spontaneous parturition was preceded by gradual and significant increases in the plasma concentrations of fetal dehydroepiandrosterone, dehydroepiandrosterone sulfate, and androstenedione and fetal and maternal levels of estrone, estradiol, and progesterone but not by changes in cortisol. In contrast, infection-associated parturition (either intraamniotic or choriodecidual) was characterized by abrupt increases in fetal dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, progesterone, and cortisol but not by increases in maternal or fetal estrone or estradiol. Infection-associated steroid changes occurred concurrently with or after increases in uterine activity. CONCLUSION: Infection-associated preterm parturition is associated with dramatic increases in fetal adrenal steroid biosynthesis but not by corresponding increases in placental estrogen biosynthesis. This suggests that fetal stress is accompanied by placental dysfunction and that infection-associated parturition is not dependent on the increased estrogen biosynthesis observed in spontaneous parturition. (Am J Obstet Gynecol 1996;174:1725-33.)     

Fetal and maternal hemodynamic responses to exercise in pregnancy assessed by Doppler ultrasonography

It is common for women to undertake vigorous exercise in the late phase of pregnancy. This may have detrimental effects on the blood flow to the uterus and placenta or from the fetus to the placenta. Fifteen pregnant women with no obstetric or medical complications were subjected to a 5-minute exercise period. The maternal heart rate and blood pressure were elevated after exercise. The uteroplacental and umbilical circulations were assessed with Doppler ultrasonography. The ratio of the systolic/diastolic velocity in the uterine artery was elevated, which suggests that uteroplacental vascular resistance increased. The fetal heart rate was elevated after exercise, whereas the systolic/diastolic velocity ratio in the umbilical artery was unaltered. We conclude that moderate maternal exercise causes increased resistance to blood flow in the uterine circulation, whereas the umbilical circulation remains unaltered.     

Fetal and neonatal consequences of antenatal exposure to type 1 angiotensin II receptor-antagonists.

Sartans are selective type 1 angiotensin II receptor-antagonists that are used in the treatment of arterial hypertension. Few reports are available concerning the use of sartans during pregnancy. We report two cases of adverse fetal outcome in hypertensive pregnancies exposed to sartans. In the first case, anamnios and fetal renal failure due to severe tubular dysgenesia led to termination of pregnancy in the 27th week. The second patient presented with hypocalvaria and developed fetal renal failure. The use of sartans during the two last trimesters of pregnancy should be strictly avoided.     

Exercise in pregnancy. II. Fetal responses

Healthy pregnant women underwent a mild exercise study to evaluate the effects of this amount of work on their fetuses. The results indicated that there were no direct correlations between exercise and fetal body or breathing movements at this particular work intensity (2.33 m). We found a relationship between the maternal sympathetic activity as reflected in epinephrine levels and the degree of fetal activity.     

The blood pressure response to infusions of angiotensin II during normal pregnancy: relation to plasma angiotensin II concentration, serum progesterone level, and mean platelet volume.

OBJECTIVE: This study is a survey of the determinants of refractoriness to the pressor effects of angiotensin II during normal pregnancy. STUDY DESIGN: In 25 normal pregnant women, the effective angiotensin II pressor dose was determined 88 times from the twenty-fifth to the thirty-second week of gestation. Immediately before the angiotensin II infusion, blood samples were collected and measured for plasma angiotensin II concentration, serum progesterone level, platelet count, and mean platelet volume. RESULTS: The effective pressor dose had a significantly positive correlation with plasma angiotensin II concentration and serum progesterone level and a negative correlation with mean platelet volume. CONCLUSION: The pregnancy-associated refractoriness to angiotensin II is physiologically determined, at least in part, by the elevated circulating levels of endogenously produced angiotensin II and by the progesterone produced by the placenta, whereas platelet activation attenuates the relative refractoriness during normal pregnancy.     

Fetal responses to external stimuli

The fetus is clearly able to respond to various external stimuli. The nature of the response is related to gestational age, intact neurologic function, and also the behavioral state of the fetus. Of the various modalities described herein, vibroacoustic stimulation utilizing an artificial larynx appears to be clinically useful in both ante- and intrapartum management. The positive predictive value is excellent (greater than 99 per cent). The fetus who responds to the stimulus with an acceptable acceleration is uniformly nonacidotic. Like many other tests of fetal health, vibroacoustic stimulation is less useful in predicting fetuses in distress, as many fail to respond and yet show no signs of compromise. It is evident that there is no single test that is without false-positives; thus accurate assessment of fetal health will depend upon utilization of a variety of biophysical parameters.     

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.     

Fetal vascular responses to prostacyclin

Prostacyclin is a potent vasodilator produced by both maternal and fetal tissues that dilates the umbilical placental vasculature in vitro. To test the hypothesis that prostacyclin dilates the fetal placental circulation in vivo, we measured blood flow by the radioactive microsphere technique in six unanesthetized near-term ovine fetuses before and during prostacyclin infusion. Fetal mean arterial pressure fell 15% from 35 +/- 3 to 31 +/- 3 mm Hg (p less than 0.05) during prostacyclin infusion, and heart rate increased from 182 +/- 6 to 208 +/- 19 beats/min (p less than 0.05). Placental blood flow changed from 240 +/- 58 to 191 +/- 46 ml.min-1.kg-1 fetal weight (p = 0.07), whereas vascular resistance was unchanged (0.16 +/- 0.04 to 0.18 +/- 0.06 mm Hg.ml-1.min.kg fetal weight). Fetal arterial pH decreased from 7.33 +/- 0.03 to 7.28 +/- 0.02 (p less than 0.05) during prostacyclin infusion, with a significant decrease in base excess from -1.2 +/- 1.4 to -3.1 +/- 1.6 (p less than 0.05) and a trend toward hypercarbia (p = 0.07). We conclude that in vivo administration of prostacyclin to the ovine fetus does not cause fetal placental vasodilation and does cause a significant fetal acidemia. The mechanism for these unexpected observations is likely shunting of blood away from the placenta to other organs in the face of systemic vasodilation.     

Fetal adaptive responses to asphyxia

The fetal environment is thus well suited for normal growth and development with oxygen availability exceeding oxidative needs. With impairments in blood gas exchange this excess oxygen acts as a "margin of safety," providing for the maintenance of oxidative metabolism through increases in fractional O2 extraction, although with resultant fetal hypoxemia. Increases in blood O2 capacity and redistribution of cardiac output in response to this hypoxemia further protect fetal oxygenation. Additional adaptive mechanisms involve a decrease in energy-consuming processes, including growth restriction, decreasing fetal movements, and behavioral state alterations. Although protective in so far as essential metabolic functions are maintained, pathologic change may occur as the "oxygen margin of safety" becomes limited or energy-conserving measures give rise to abnormal growth and development.     

Fetal chylothorax response to maternal dietary treatment

Background: Fetal chylothorax is associated with elevated perinatal mortality. Development of mediastinal shift with significant lung compression before 35 weeks’ gestation needs treatment.Case: A 24-year-old gravida 2, para 0 presented at 26 weeks’ gestation with a fetal pleural effusion with a mediastinal shift and abnormal Doppler velocimetry indices in several vessels. Thoracentesis was successful but 3 days later, the fetal effusion had reaccumulated. Because of fetal position, a pleuro-amniotic shunt was difficult technically, so maternal medical treatment was initiated with a low-fat, high medium-chain triglyceride diet. After initial mild decrease, the estimated volume of the fetal chylothorax remained stable until 36 weeks’ gestation, at which time we delivered by cesarean an infant with good Apgar scores. After aspiration of the remaining thoracic fluid and administration of a similar diet, the infant did well, with normal growth and development.Conclusion: Maternal dietary treatment might help delay the need for thoracentesis in cases of fetal chylothorax.     

Fetal distress secondary to vancomycin-induced maternal hypotension

The rapid administration of intravenous vancomycin may produce fetal distress secondary to maternal hypotension.     

Fetal heart rate response to maternal exercise

Twenty-five pregnant women without complications underwent fetal heart rate evaluation during a program involving exercise at a relative intensity of 61% to 73% of maximal capacity during the course of the pregnancy. Assessment of the influence of gestational age on the fetal heart rate response to exercise and evaluation of the course of fetal heart rate recovery were the main goals of the study. The results of the study confirmed previous findings that fetal heart rate is accelerated after maternal exercise. However, contrary to other studies we found no effect of gestational age on the fetal heart rate response to exercise. Neonatal findings provided further evidence that quantitated maternal exercise up to 70% of maximal capacity does not interfere with normal fetal growth and development.     

Neonatal acute renal failure secondary to maternal exposure to telmisartan, angiotensin II receptor antagonist.

Fetal and neonatal toxic effects of angiotensin II receptor antagonists have been described in animals and humans. Five cases of fetal or neonatal deaths have been reported following maternal use of sartans for hypertension. We report a case of neonatal transient renal failure following telmisartan therapy during pregnancy. This class of antihypertensive drugs should be avoided during pregnancy and breastfeeding.