Fetal Breathing Activity Research Articles

Effects of regular and decaffeinated coffee on fetal breathing and heart rate

The effects of maternal consumption of regular or decaffeinated coffee on the fetus were determined in eight pregnant women at 32 to 36 weeks of gestation. This was a single-blind crossover study in which two cups of caffeinated or decaffeinated coffee were consumed after an overnight fast. The total maternal caffeine ingested was 454 +/- 4 mg for regular coffee and 12 +/- 0.4 mg for decaffeinated coffee. Maternal consumption of regular coffee was associated with a twofold increase in the incidence of fetal breathing activity and a significant fall in baseline fetal heart rate. Decaffeinated coffee also increased the incidence of fetal breathing activity and produced a slight reduction in fetal heart rate. These results indicate that maternal consumption of regular and decaffeinated coffee can stimulate fetal breathing. Moreover, these results suggest that caffeinated coffee can produce baseline shifts in fetal heart rate.

Method for processing of fetal breathing epoch analysis: studies in the primate

An automated method for detecting fetal breathing and an analytic technique for providing significant data reduction that take the episodic nature of fetal breathing activity into account are described. The aim of the new technique, called epoch analysis, is to derive parameters of breathing and apnea that both summarize the activity and permit examination of its relationship to changes that occur naturally during day and night and with fetal maturation. The discussion covers: the acquisition of data from pregnant baboons; the breath detection process, for which a program was written; the recognition of breathing; computer recognition of artifacts; epoch characterization; validation of the methods of breath detection and epoch characterization; and application of the method. It is found that the technique has a broad capacity for data reduction and provides summaries of the activity that are amenable to analysis with standard statistical techniques.

Value of Observation of Fetal Breathing Activity in Antenatal Assessment of High-Risk Pregnancy

Value of Observation of Fetal Breathing Activity in Antenatal Assessment of High-Risk Pregnancy

Effects of regular and decaffeinated coffee on fetal breathing and heart rate

The effects of maternal consumption of regular or decaffeinated coffee on the fetus were determined in eight pregnant women at 32 to 36 weeks of gestation. This was a single-blind crossover study in which two cups of caffeinated or decaffeinated coffee were consumed after an overnight fast. The total maternal caffeine ingested was 454 ± 4 mg for regular coffee and 12 ± 0.4 mg for decaffeinated coffee. Maternal consumption of regular coffee was associated with a twofold increase in the incidence of fetal breathing activity and a significant fall in baseline fetal heart rate. Decaffeinated coffee also increased the incidence of fetal breathing activity and produced a slight reduction in fetal heart rate. These results indicate that maternal consumption of regular and decaffeinated coffee can stimulate fetal breathing. Moreover, these results suggest that caffeinated coffee can produce baseline shifts in fetal heart rate. (Am J Obstet Gynecol 1989;160:1043-7.)

Value of observation of fetal breathing activity in antenatal assessment of high-risk pregnancy

While observation of fetal breathing movements has been used in fetal assessment, quantitative parameters (percent time spent in breathing [incidence], breath rate, or breath rate variability) have not been adequately evaluated as predictive tools. We examined 283 patients with high-risk pregnancies between 32 and 42 weeks' gestation and correlated their fetal breathing movement parameters with the rates of perinatal mortality, intrapartum fetal distress, neonatal acidosis, low 5-minute Apgar score, and intrauterine growth retardation. Fetal breathing data from standardized 60-minute biophysical tests were analyzed and compared with our institutional standards. Parameter values greater than 2 SD from the means of a previously studied normal population were considered abnormal. Whereas no individual parameter was a highly accurate predictor of adverse outcome, a fetal breathing movement incidence of less than 5% provided the best cutoff for diagnostic accuracy. Seventy percent of fetuses with 30 minutes of apnea had normal outcomes, whereas abnormally high breath rates (greater than 60 breaths/min) and low breath rates (less than 33 breaths/min) occurred with equal frequency among normal and pathologic fetuses. Breath interval variability was of no benefit in detecting fetuses with poor outcomes. Observation of fetal breathing movement incidence appeared to be most effective in pregnancies complicated by chronic hypertension and least effective in those with preeclampsia.

Patterns of fetal breathing activity in the human fetus at 24 to 28 weeks of gestation

Continuous 24-hour observations of fetal breathing were performed in 20 normal, pregnant women between 24 and 28 weeks' gestation by real-time ultrasound. Fetuses made breathing movements approximately 14% of the time. No change in breathing activity after a maternal meal was observed, but a significant increase in the incidence of fetal breathing activity was noted overnight. Fetuses at 24 to 28 weeks' gestation breathed at a rate of 44 breaths per minute, and the longest period of apnea noted was 14 minutes. These data suggest that the pattern and incidence of fetal breathing at 24 to 28 weeks' gestation are different from those of fetuses observed in the last 10 weeks of pregnancy. A maturational process in the control of fetal breathing may explain these observations.

Human fetal breathing response to intravenous glucose is directly related to gestational age

This prospective longitudinal study examined human fetal breathing activity over the second half of pregnancy both in the fasting state and after intravenous glucose administration. There was a linear relationship between gestational age and percent time spent breathing after glucose between 19 and 38 weeks' gestation. However, no such correlation could be demonstrated between gestational age and fetal breathing activity in the fasting state.

FETAL BREATHING MOVEMENTS ARE NOT A RELIABLE PREDICTOR OF CONTINUED LUNG DEVELOPMENT IN PREGNANCIES COMPLICATED BY OLIGOHYDRAMNIOS

Fetal breathing activity was monitored by ultrasonography in 14 patients with oligohydramnios (4 with fetal anuria and 10 with premature rupture of the membranes). 45 patients with intact membranes, with normal amniotic fluid volume, and matched for gestational age were the controls. Fetal breathing movements were seen in all 8 patients who died in the perinatal period with a necropsy diagnosis of lung hypoplasia. While patients with premature rupture of the membranes (irrespective of outcome) spent the same or less time breathing than controls, fetuses with renal anomalies, oligohydramnios, and lung hypoplasia spent more time breathing than controls. The observation of fetal breathing activity is not helpful in identifying patients with oligohydramnios at risk of lung hypoplasia.

The effects of long- and short-term maternal caffeine ingestion on human fetal breathing and body movements in term gestations

The possible effects of long- and short-term maternal ingestion of caffeine during normal human pregnancy on the breathing and body movements of third-trimester fetuses were studied in 14 patients, selected by a dietary questionnaire, and divided into two equal groups: high consumers (greater than 500 mg/day) (group 1) and low consumers (less than 250 mg/day) (group 2). All mothers followed a standard study protocol and underwent overnight fasting; studies began with a 30-minute control period, followed by oral administration of 200 mg caffeine, and a 180-minute subsequent observation period with continued maternal fasting. Blood samples for glucose and caffeine were obtained every 30 minutes and continuous recording of fetal breathing and body movements were entered on a microcomputer for off-line analysis. The two groups were similar for all obstetric outcome features. Plasma glucose levels were similar and constant in both groups whereas caffeine levels increased significantly at 60 minutes after administration; mean plasma caffeine levels were significantly higher in group 1 than in group 2 at all intervals. Fetal breathing rates and body movement incidences were similar in both groups before and after caffeine administration. Fetal breathing movement incidence decreased significantly in group 2 but was sustained at baseline levels in group 1 throughout the study. High long-term ingestion of caffeine during pregnancy is associated with higher maternal plasma caffeine levels and fetal breathing activity when compared with low caffeine ingestion. Short-term administration of 200 mg caffeine does not appear to have a significant physiologic impact on these activities.

Restoration of lung liquid volume following its acute alteration in fetal sheep.

1. The experiments were aimed at determining the means by which lung liquid volume is controlled in fetal sheep. Six unanaesthetized chronically catheterized fetuses between 121 and 144 days of gestation were used in experiments in which lung liquid volume was acutely reduced or increased. 2. The effects on lung liquid volume, secretion and flow in the trachea were continuously monitored until the original volume was restored. Tracheal pressure, breathing activity, electrocortical activity and laryngeal adductor muscle activity were also monitored. 3. Following a mean reduction in lung liquid volume of 54.1% (40.0 +/- 4.3 ml) there was a reduction in tracheal pressure of 1.91 +/- 0.26 mmHg. There was no change in the rate of lung liquid secretion and there was a near cessation in its rate of efflux from the trachea. Influx of liquid from the upper airway was rarely seen. 4. 5 h after its reduction, lung liquid volume had returned to control values. Tracheal pressure and the rate of liquid flow in the trachea returned to control values over 7-8 h. 5. In the hour following the reduction in lung liquid volume the incidence and amplitude of fetal inspiratory muscle electromyogram (e.m.g.) activity were reduced by 19% and 28% respectively. There was no change in laryngeal adductor muscle activity or in the duration of fetal sleep states. 6. When lung liquid volume was increased by 25.4 +/- 3.1 ml tracheal pressure increased by 2.01 +/- 0.17 mmHg. Although there was no change in the rate of liquid secretion there was a rapid efflux of liquid from the trachea principally during epochs of fetal breathing activity thus returning lung liquid volume to its control value. 7. Following the increase in lung liquid volume there were no changes in the incidence or amplitude of fetal inspiratory muscle activity, the activity of laryngeal adductor muscles or in the duration of sleep states. 8. It is concluded that following its alteration in fetal sheep lung liquid volume is restored by passive means. There was no evidence of volume-receptive neural reflexes being activated in defence of lung liquid volume.

Fetal breathing, sleep state, and cardiovascular responses to graded hypoxia in sheep.

Graded isocapnic hypoxemia was produced in unanesthetized fetal sheep by varying the inspired O2 concentration (21, 12, 10.5, and 9%) of the ewe. This produced corresponding mean preductal arterial O2 tension (PaO2) values of 25.2 +/- 1.1 (control), 20.1 +/- 1.0 (mild hypoxia), 17.8 +/- 0.9 (moderate hypoxia), and 16.8 +/- 1.4 Torr (severe hypoxia). These were associated with mean arterial O2 contents (CaO2) of 7.18 +/- 0.44, 5.19 +/- 0.34, 4.24 +/- 0.33, and 3.27 +/- 0.20 ml/dl, respectively. The most severe hypoxia was associated with metabolic acidosis and fetal bradycardia. Hypoxia did not reduce significantly the incidence of low-voltage electrocortical activity. The incidence of breathing and rapid eye movements was not affected by mild hypoxia; however, the incidence of both was significantly reduced during moderate and severe hypoxia. It is concluded that 1) acute reductions in the mean PaO2 of 5.9 +/- 0.6 Torr and CaO2 of 2.00 +/- 0.23 ml/dl are critical in that greater reductions inhibit fetal eye and breathing activity and 2) hypoxia probably inhibits eye and breathing movements by altering sleep state.

Maternal dietary substrates and human fetal biophysical activity: I. The effects of tryptophan and glucose on fetal breathing movements

To study the effects of l-tryptophan and glucose on fetal breathing activity, we examined 40 women with normal term pregnancies, randomly assigned to four equal groups who either continued fasting (group C), received 1 gm of oral tryptophan (group T), received 100 gm of oral glucose (group G), or received both substrates (group T + G). Studies lasted 210 minutes, during which fetal breathing movements were observed with real-time ultrasonography and entered and analyzed for incidence, rate, and variability on a microcomputer. Plasma glucose and tryptophan levels were determined every 30 minutes. The incidence of fetal breathing movements declined in group C and rose significantly in the other groups. Breathing rates were unchanged in groups C and T but rose significantly in groups G and T + G during peak breathing intervals. Breath interval variability did not change significantly in any study group. Maternal administration of tryptophan is associated with an alteration in fetal breathing activity but to a lesser degree than that observed after maternal glucose loading.

Maternal dietary substrates and human fetal biophysical activity

Abstract To study the effects of l-tryptophan and glucose on fetal breathing activity, we examined 40 women with normal term pregnancies, randomly assigned to four equal groups who either continued fasting (group C), received 1 gm of oral tryptophan (group T), received 100 gm of oral glucose (group G), or received both substrates (group T + G). Studies lasted 210 minutes, during which fetal breathing movements were observed with real-time ultrasonography and entered and analyzed for incidence, rate, and variability on a microcomputer. Plasma glucose and tryptophan levels were determined every 30 minutes. The incidence of fetal breathing movements declined in group C and rose significantly in the other groups. Breathing rates were unchanged in groups C and T but rose significantly in groups G and T + G during peak breathing intervals. Breath interval variability did not change significantly in any study group. Maternal administration of tryptophan is associated with an alteration in fetal breathing activity but to a lesser degree than that observed after maternal glucose loading.

Stimulation of fetal breathing activity by beta-adrenergic mechanisms.

Experiments were done on chronically prepared fetal lambs, 125-135 days gestation, to test the effects of various catecholamines on fetal breathing (FB) as well as the influence of isoproterenol on the fetal respiratory response to hypoxemia. Bolus injections of epinephrine, norepinephrine, and isoproterenol (5-20 micrograms) were administered via the lingual artery or femoral or jugular vein during periods of FB activity or apnea. The effects of epinephrine and norepinephrine on FB were variable and not statistically significant. Isoproterenol produced a significant increase in FB, frequency of breathing, and mean inspiratory effort, when infused during rapid-eye-movement (REM) sleep but it failed to induce FB during non-rapid-eye-movement (NREM) sleep. The positive response during REM sleep was absent following pretreatment with 3-5 mg propranolol and after bilateral section of the sinus nerves. The effect of hypoxia on FB was tested before and during constant infusion of isoproterenol (1 microgram/min iv). A reduction of the fetal arterial PO2 by 3-10 Torr produced the characteristic depression of FB in either situation. These results indicate that the fetal carotid body chemoreceptors can reflexly stimulate FB under certain circumstances but that their effectiveness is limited by more powerful inhibitory mechanisms such as those operative during NREM sleep and hypoxemia.

Fetal breathing movements and lung hypoplasia: Preliminary human observations

Hypoplasia of the fetal lung is found in association with long-standing oligohydramnios. In animal models, interference with fetal breathing activity has led to lung hypoplasia. It has been suggested that lung hypoplasia associated with oligohydramnios is due to inhibition of fetal breathing. Observations of seven patients with prolonged oligohydramnios, three of whom had lung hypoplasia, indicate that fetal breathing does occur in these cases and that it is unlikely that lung hypoplasia is merely the result of absent fetal breathing activity. In fact, when compared to the four patients with oligohydramnios and presumably normal lungs, the three patients with oligohydramnios and lung hypoplasia spent more time breathing and did so at higher rates.

Intrauterine fetal activity in at term and prolonged pregnancies.

Fetal body movements and breathing movements were recorded with a real time ultrasound scanner in 26 fetuses. There were two recording periods of 25 min each, before and half and hour after maternal IV administration of 50 gr glucose. Six fetuses were at 280 days of gestation (Group A), twelve fetuses were at 294 days of gestation (group B), eight fetuses at 294 days gestation were classified as stage I postmature (group C). The incidence of fetal body movements was not significantly different in the three groups. Maternal glucose administration had no significant influence on fetal body movements in any group. On the other hand fetal breathing activity was significantly increased in all three groups after maternal glucose administration. Breathing activity was significantly greater in group A when compared to group C in both recording periods, and when compared to group B in the period which followed maternal glucose administration. It is concluded that fetal breathing activity is reduced in prolonged pregnancies.

Intrauterine hypercarbia and lamb lung surfactant synthesis

Prenatal asphyxia resulting in hypoxia, hypercabia and amniotic fluid aspiration reduces the synthesis of the pulmonary surfactant. Using 135-day fetal lambs we studied the in utero effects of hyper-carbic acidosis alone on fetal breathing activity, excised lung pressure-volume relationships and lamellar body (LB) surfactant disaturated phosphatidylcholine (DSPC) pool size and specific activity for [ 14C]palmiatet. Fetal PA CO 2 levels > 125 mm Hg for 30 min were associated with pH values < 7.0 and very vigorous breathing activity. Analysis 22 h after the period of hypercarbic acidosis demonstrated no differences in pressure-volume relationships or the quantity of lamellar body surfactant DSPC. The specific activity of lamellar body DSPC also was not different although total label (dpm) per gram dry weight was higher and label was detected in the lavage fluid earlier in the acidotic lambs than controls. We conclude from these data that hypercarbic acidosis does not influence the synthesis or function of the pulmonary surfactant as assessed in this system. From these results and prior work from our laboratory we can infer that hypoxia remains the most probable cause for reduced surfactant synthesis in the asphyxiated fetus.

Indomethacin-induced fetal breathing: mechanism and site of action.

The mechanism and site of action of indomethacin-induced fetal breathing (FB) was investigated in 26 chronically prepared fetal lambs. Indomethacin, which preferentially blocks prostaglandin production, was infused into the fetal circulation in two stages, 60 mg in 10 min and 60 mg over 7 h. Indomethacin stimulated sleep-state independent FB that was greatly reduced or abolished by infusions of prostaglandin E2 (PGE2). Infusions of nordihydroguaiaretic acid, which preferentially blocks the synthesis of leukotrienes, had no consistent effect on either fetal sleep or breathing activity when administered alone or after indomethacin. This suggests that the characteristic FB induced by indomethacin is due to inhibition of prostaglandin synthesis (PGE2) and not due to an overproduction of leukotrienes. The indomethacin effect on FB was observed in all fetuses tested including those deprived of peripheral chemoreceptor function, vagotomy, decortication, or spinal cord section at the T1 level. Complete constriction of the ductus arteriosus for many hours had no effect on FB. We conclude that inhibition of PGE2 synthesis stimulates FB by a central mechanism other than the cortex.

FETAL BREATHING MOVEMENTS AND LUNG HYPOPLASIA: PRELIMINARY HUMAN OBSERVATIONS

Hypoplasia of the fetal lungs (L.H.) is found in association with long standing oligohydramnios. In the animal model, interference with fetal breathing (F.B.) activity by phrenectomy or curarization has led to lung hypoplasia. It has been suggested that L.H. associated with oligohydramnios is due to inhibition of F.B.Four patients with oligohydramnios (2 intact membranes, 2 prolonged rupture) were studied in a total of eleven 60-minute sessions from 27-38 weeks. F.B. and other fetal movements (OFM) were recorded using linear array sonography. For each patient study session a gestational, age matched control with normal amniotic fluid volume was studied. Three of the four study subjects had fetal lung hypoplasia. F.B. was observed in all four cases. For the 2 cases with intact membranes (Renal Agenesis and Polycystic Kidneys) F.B. was seen during 0.25±0.048 S.D. [L.H.] of the 60 min observation (control 0.06±0.02). With ruptured membranes F.B. was seen (0.02±0.05 and 0.069 [L.H.] of the time with control of 0.19±0.024). No difference in other OFM was noted.From these preliminary observations we conclude that FB does occur in cases of oligohydramnios associated with lung hypoplasia. It is therefore unlikely that lung hypoplasia is merely the result of absent FB.

Absence or impaired response of fetal breathing to intravenous glucose is associated with pulmonary hypoplasia in congenital myotonic dystrophy

Two fetuses of a patient affected with myotonic dystrophy were studied ultrasonically from 28 to 34 weeks' gestation. After a 1-hour observation period, an intravenous injection of 25 gm of 50% glucose solution was given to the mother. Fetal breathing movements were 0% during the control period and increased to only 10% at 90 minutes after the injection of glucose; the episode lasted approximately 30 minutes. The infants, who were delivered at 33 and 35 weeks, had generalized hypotonia, normal arterial cord blood gases, and died shortly after birth from pulmonary insufficiency, in spite of maximum ventilatory support. Postmortem pulmonary hypoplasia was confirmed by a lung weight/body weight ratio of less than 0.019. We postulate that fetal breathing activity and its response to the injection of glucose may be a potential clinical test by which normal fetuses can be differentiated from fetuses affected by neuromuscular disorders, including myotonic dystrophy.