Acute effects of maternal smoking on fetal heart beat intervals

The purpose of this study was to analyse the acute effects of maternal cigarette smoking on the fetal heart beat intervals and their variability during the last trimester of a normal gestation. The fetal heart beat intervals were monitored continuously by abdominal electrocardiography for 60 min before and 60 min after smoking in 10 pregnant women. The mean intervals, their long-term variability (SD) and short-term variability (standard deviation of interval differences (SDID], calculated for 30-sec periods, showed a steady state before smoking. During the control period, the mean beat interval was negatively correlated with daily cigarette consumption and the short-term variability was positively correlated with the maternal plasma nicotine level. After smoking, the mean beat interval and the short-term variability decreased transiently, the values of both these parameters being positively correlated with the maternal nicotine values before smoking. The acute response of fetal heart beat intervals and their variability to one cigarette is distinct but transient, and the results suggest that the effects are modified by the chronic smoking habits of the women.     

Acute effects of maternal smoking on fetal blood flow

Thirty healthy pregnant women were studied to assess the immediate cardiovascular responses of the fetus to the smoking of one cigarette. The fetal blood flow was measured in the aorta and in the umbilical vein by combining real-time ultrasonography and the pulsed Doppler technique. Following maternal smoking, a significant increase was found in the maternal heart rate and also in the blood pressure. In the fetus, a significant transient increase in the aortic and the umbilical blood flow was measured, as characterized by the increase in the fetal heart rate, the mean and maximum blood velocity, and the vessel diameter. Thus, maternal smoking induced acute circulatory changes in the fetus similar to those found in adults. Furthermore, the study demonstrated the feasibility of the method to evaluate non-invasively the immediate effect of a given stress stimulus on the cardiovascular system of the human fetus.     

Acute effects of maternal smoking on fetal hemodynamics.

OBJECTIVE: To investigate acute effects of cigarette smoking on fetal hemodynamics. METHOD: Sixty seven women between 32nd to 40th weeks of gestation were evaluated. Maternal blood pressure and heart rate, fetal heart rate (FHR) tracing, umbilical and fetal middle cerebral arterial (MCA) color Doppler measurements were evaluated. Pre- and postsmoking results were compared with paired t-test. RESULTS: Maternal heart rate significantly increased after smoking. Baseline FHR and FHR variability remained unchanged. The number of participants who had a reactive NST was 60 in 67 before smoking (89.5%) and decreased to 47 after smoking (70.1%) (p=0.009). There were no significant changes between maximum and minimum flow velocities, pulsatility index (PI), resistance index (RI) and systolic/diastolic flow ratio (S/D) of umbilical and middle cerebral arteries. CONCLUSION: The nicotine load of a single cigarette may be inadequate to cause a detectable decrease in utero-placental blood flow; however, smoking prior to the FHR recording may alter the FHR reactivity.     

Acute effect of maternal smoking on the human fetal blood flow

Summary. The immediate effect of maternal smoking of one cigarette on blood flow in the descending thoracic aorta and umbilical vein was studied in 19 fetuses at between 29 and 39 weeks gestation. Blood flow was measured with a combined real-time ultrasound and Doppler ultrasound technique immediately before smoking and immediately after cessation of smoke inhalation. The measured flow changes immediately after maternal smoking were insignificant and suggest that the haemodynamic and chemical effects of smoking in the mother do not produce immediate alterations in the blood flow in the fetal thoracic aorta or in the umbilical vein.     

Acute effects of maternal cigarette smoking on fetal heart rate and fetal body movements felt by the mother.

Acute effects of maternal cigarette smoking on fetal heart rate (FHR) and fetal body movements felt by the mother (FM) were studied in 51 pregnant volunteers. Thirty four were chronic smokers (6 or more cigarettes per day, with an average of 14 cigarettes/day) and 17 were sporadic smokers (1 to 5 cigarettes per day, with an averaged of 3 cigarettes/day). In both groups the number of FM, fetal reactivity and short-term FHR variability decreased significantly in the 20 minutes following cigarette smoking; a sustained FHR rise of 10 or more beats/min was also found after the cigarette in more than 50% of the cases in the 2 groups. No statistically significant differences were found among the 2 groups when the post-cigarette data were compared. We conclude that maternal cigarette smoking produces important acute effects upon FM and FHR regardless the average daily number of cigarettes smoked by the mother.     

Acute effects of smoking on fetal heart-rate variability

Summary. Smoking a standard filter cigarette caused an acute decrease both in the interval index and the differential index of fetal heart-rate variability in eight healthy pregnant women at term. The maximum effect occurred 5–10 min after smoking and the indices returned to the presmoking level in 20 min. We suggest that smoking has a dual effect on the fetus: one being narcotic, leading to a lowered interval index, and the other hypoxic, leading to a lowered differential index.     

Acute effects of maternal ethanol infusion on fetal cardiac performance

In adult animals and man, both acute and chronic ethanol intake is associated with depression of myocardial performance. Accordingly, the cardiac effects of maternal ethanol infusions, in a manner comparable to common obstetric practice for inhibition of premature labor, were evaluated in six chronically instrumented fetal sheep. Fetal and ewe arterial Po₂, Pco₂, and pH values remained within normal limits with infusion rates of 15 c.c. per kilogram of 10 per cent ethanol over two hours (blood ethanol = 110 mg. per cent) and 15 c.c. per kilogram over one hour (blood ethanol = 210 mg. per cent). Fetal instrument evaluation (for 14 to 30 days after operation) provided data concerning pressures and cardiac dimensions which allowed analysis of left ventricular performance. Ethanol produced a significant depression of the extent (p < 0.01) and velocity (p < 0.001) of left ventricular myocardial fiber shortening as well as in the mean rate of left ventricular circumferential fiber shortening (p < 0.01). These indices of cardiac contractility were depressed in the absence of changes in end diastolic diameter, left atrial pressure, and systemic arterial pressure. Thus, the practice of inhibition of premature labor with ethanol might contribute to depressed myocardial performance in the neonatal period.     

Chronic effects of maternal smoking on pulse waves in the fetal aorta

Objective.?In order to evaluate the impact of maternal smoking on arterial stiffness in utero, pulse wave characteristics in the fetal aorta were investigated. A prospective clinical study was made of 34 smoking and 34 non-smoking healthy volunteers with uncomplicated pregnancies at 31–40 weeks of gestation.

Methods.?The mechanical properties of the fetal thoracic aorta were assessed by an ultrasonic phase-locking echo-tracking system. For each fetus with a smoking mother, a non-smoking control matched for gestational and maternal age was monitored. Women with later appearing pregnancy complications were excluded. Pulse wave velocity (PWV), maximum diameter in systole (Ds), end-diastolic diameter (Dd), pulse amplitude (ΔD), and maximum incremental velocity (MIV) in the fetal aorta were measured and analyzed in relation to maternal smoking and gestational age.

Results.?Results were computed on fetuses of 32 smokers and 30 non-smokers. PWV increased with gestational age in smokers (corr. coeff. 0.49, p < 0.006) but not in non-smokers (corr. coeff. ?0.12). MIV did not change in smokers (corr. coeff. ?0.15) but increased in non-smokers (corr. coeff. 0.40, p < 0.03). Differences in regression lines between the groups regarding PWV and MIV were significant (p < 0.02 for both).

Conclusions.?Maternal smoking seems to promote the stiffening of the fetal aorta during gestation.     

Acute effects of nicotine on fetal heart rate variability

Summary. The effects of nicotine on fetal heart rate (FHR) variability were studied in seven women in the second trimester and eight women in the third trimester of pregnancy by giving them nicotine-containing chewinggum. The possible effects of carbon monoxide or some other agents of nicotine-free smoke on FHR variability were tested in eight women in the second and eight in the third trimester of pregnancy by giving them herbal cigarettes to smoke. The gum caused an acute decrease in the interval index of FHR variability in both trimesters, as we have observed previously in association with tobacco smoking, and an acute decrease in the differential index in the second trimester but not in the third trimester. These effects differ from those associated with tobacco smoking, during which the differential index decreased in the third trimester but remained unchanged in the second trimester. In the second trimester the gum elevated the baseline FHR, as did tobacco smoking. In the third trimester, the gum decreased the baseline FHR in contrast to tobacco smoking, which had no effect on it. Smoking a herbal cigarette had no effect on FHR and no depressant effect on FHR variability, as had nicotine. The only fetal response was a transient increase in the interval index 5—10 min after smoking in the second trimester. We conclude that nicotine seems to be responsible for the depressant effect of tobacco smoke on the fetus, as manifested in lowered interval indices. The different responses of the differential index and baseline FHR to tobacco smoking and chewing nicotine-containing gum at different stages of gestation remain unexplained.     

Chronic effects of maternal smoking on pulse waves in the fetal aorta.

OBJECTIVE: In order to evaluate the impact of maternal smoking on arterial stiffness in utero, pulse wave characteristics in the fetal aorta were investigated. A prospective clinical study was made of 34 smoking and 34 non-smoking healthy volunteers with uncomplicated pregnancies at 31-40 weeks of gestation. METHODS: The mechanical properties of the fetal thoracic aorta were assessed by an ultrasonic phase-locking echo-tracking system. For each fetus with a smoking mother, a non-smoking control matched for gestational and maternal age was monitored. Women with later appearing pregnancy complications were excluded. Pulse wave velocity (PWV), maximum diameter in systole (Ds), end-diastolic diameter (Dd), pulse amplitude (DeltaD), and maximum incremental velocity (MIV) in the fetal aorta were measured and analyzed in relation to maternal smoking and gestational age. RESULTS: Results were computed on fetuses of 32 smokers and 30 non-smokers. PWV increased with gestational age in smokers (corr. coeff. 0.49, p < 0.006) but not in non-smokers (corr. coeff. -0.12). MIV did not change in smokers (corr. coeff. -0.15) but increased in non-smokers (corr. coeff. 0.40, p < 0.03). Differences in regression lines between the groups regarding PWV and MIV were significant (p < 0.02 for both). CONCLUSIONS: Maternal smoking seems to promote the stiffening of the fetal aorta during gestation.     

Midtrimester fetal heart rate variability and maternal hemodynamics in association with smoking

Maternal heart rate (MHR), blood pressure (BP), the differential index (DI) describing the short-term component of fetal heart rate (FHR) variability, and the interval index (II) describing the long-term component were measured in eight subjects in the midtrimester before, during, and after the mothers smoked a standard cigarette. The analyses of FHR variability were performed by an "on-line" method with an abdominal fetal electrocardiogram used as a triggering signal and with a sample time of 1 minute. An increase of MHR, FHR, and BP with a concomitant decrease of II was observed. Unlike our findings regarding the third trimester, no significant change of DI was observed. A correlation analysis revealed fetomaternal hemodynamic relationships different from those in the third trimester: There was a negative correlation between DI and FHR (p less than 0.01) and between DI and MHR (p less than 0.01). There was a positive correlation between FHR and MHR (p less than 0.001). Unlike our findings regarding the third trimester, no correlation was found between DI and BP or between II and MHR. We suggest that the midtrimester fetus shows the narcotic effect (decrease of II) of one cigarette, as does the term fetus, but fails to show the hypoxic effect (decrease of DI), which has been observed in the term fetus.     

The effects of maternal caffeine and chocolate intake on fetal heart rate

Objective: The aim of our study was to analyze the effects of caffeine and chocolate (70% cocoa) on fetal heart rate (FHR). Study design: Fifty pregnant women with uncomplicated gestation, matched for age and parity, underwent computerized FHR recording before and after the consumption of caffeine and then, after one week, before and after 70% cocoa chocolate intake. Computerized cardiotocography (cCTG) parameters were expressed as mean and SD. The differences were tested for statistical significance using the paired t-test, with significance at p?<?0.05. Results: The number of uterine contraction peaks, the number of small and large accelerations (10 and 15 beats per minute for 15 seconds), the duration of episodes of high variation and the short-term FHR variation were significantly higher (p?<?0.001) after maternal coffee intake. The number of large accelerations, the duration of episodes of high variation and the short-term FHR variation were significantly higher (p?<?0.001) after maternal consumption of chocolate, whilst no effect of cocoa was found during contractions. Conclusions: Our results suggest that maternal intake of both caffeine and 70% cocoa have a stimulating action on fetal reactivity. This finding is likely due to the pharmacological action of theobromine, a methilxanthine present in coffee and in chocolate. The correlation between maternal caffeine intake and increased uterine contraction peaks is likely due to the effect of caffeine on the uterine muscle.     

Reexamining the effects of gestational age, fetal growth, and maternal smoking on neonatal mortality

BACKGROUND: Low birth weight (<2,500 g) is a strong predictor of infant mortality. Yet low birth weight, in isolation, is uninformative since it is comprised of two intertwined components: preterm delivery and reduced fetal growth. Through nonparametric logistic regression models, we examine the effects of gestational age, fetal growth, and maternal smoking on neonatal mortality. METHODS: We derived data on over 10 million singleton live births delivered at >/= 24 weeks from the 1998-2000 U.S. natality data files. Nonparametric multivariable logistic regression based on generalized additive models was used to examine neonatal mortality (deaths within the first 28 days) in relation to fetal growth (gestational age-specific standardized birth weight), gestational age, and number of cigarettes smoked per day. All analyses were further adjusted for the confounding effects due to maternal age and gravidity. RESULTS: The relationship between standardized birth weight and neonatal mortality is nonlinear; mortality is high at low z-score birth weights, drops precipitously with increasing z-score birth weight, and begins to flatten for heavier infants. Gestational age is also strongly associated with mortality, with patterns similar to those of z-score birth weight. Although the direct effect of smoking on neonatal mortality is weak, its effects (on mortality) appear to be largely mediated through reduced fetal growth and, to a lesser extent, through shortened gestation. In fact, the association between smoking and reduced fetal growth gets stronger as pregnancies approach term. CONCLUSIONS: Our study provides important insights regarding the combined effects of fetal growth, gestational age, and smoking on neonatal mortality. The findings suggest that the effect of maternal smoking on neonatal mortality is largely mediated through reduced fetal growth.     

The association between maternal smoking and fetal hydranencephaly

OBJECTIVE: To evaluate the relationship between maternal smoking and fetal congenital central nervous system malformations. METHODS: Retrospective review of all cases of fetal congenital malformations of the central nervous system (CNS) identified at or shortly after birth over a 10-year period (1986-1995) in a university teaching obstetric department. RESULTS: The total number of CNS abnormalities identified was 79, constituting 0.13% of all deliveries over the period (n = 59,392) and 4.7% of all congenital malformations (n = 1,678). The incidence of smoking mothers was 1.64% over the study period. Four babies had hydranencephaly, 3 of these mothers being smoking teenagers. The odds ratio of having a hydranencephalic fetus in smoking mothers compared to non-smokers was 56 (95% CI 7.41-427) in the group with CNS abnormalities, 136 (95% CI 14.5-1280) in the group including all congenital malformations, and 179 (95% CI 18.6-1719) in the group including all deliveries. CONCLUSION: Maternal smoking did not appear to increase the incidence of fetal congenital CNS abnormalities overall, but might be associated with particular vascular patterns of damage to the developing brain that could predispose to a hydranencephalic malformation.     

Impact of maternal cigarette smoking on fetal growth and body composition

OBJECTIVE: The aim of this study was to determine the impact of maternal cigarette smoking on the fetal accretion of fat and lean body mass. We hypothesized that maternal smoking would result in a reduction in the deposition of lean body mass. STUDY DESIGN: Longitudinal ultrasonographic examinations on 65 singleton fetuses without anomalies of smoking mothers were compared with 36 singleton fetuses without anomalies of nonsmoking mothers. A total of 214 ultrasonographic examinations were performed between 27 and 37 weeks' gestation. All subjects underwent at least 2 ultrasonographic examinations separated by 4 weeks. We compared the slopes of the growth curves for individual morphometric parameters including head circumference, femur length, abdominal circumference, thigh muscle area, thigh fat area, estimated fetal weight and percentage of thigh fat between groups. Analysis was performed with a repeated measures analysis of covariance. Potential covariates included prepregnancy body mass index (in kilograms per square meter), weight gain during pregnancy, maternal age, parity, and fetal sex recorded at birth. Demographic variables are expressed as mean +/- SD; fetal measurements are expressed as mean +/- SE. Both t tests and chi(2) analyses were used to compare groups with respect to demographic variables. P <.05 was accepted for significance. RESULTS: There were no significant differences between groups in maternal prepregnancy weight, maternal height, maternal prepregnancy body mass index, weight gain in pregnancy, parity, or fetal sex. Smokers were younger than nonsmokers (smokers, 23.7 +/- 6.0 years; nonsmokers, 31.8 +/- 6. 0 years; P <.0001), and neonatal weight was reduced among smokers (smokers, 3269 +/- 507 g; nonsmokers, 3519 +/- 411 g; P <.01). There were no differences in the growth rates of head circumference (P =. 79) and femur length (P =.67). Growth rates of abdominal circumference (smokers, 9.0 +/- 0.3 mm/wk; nonsmokers, 10.3 +/- 0.5 mm/wk; P =.01), estimated fetal weight (smokers, 171 +/- 5.4 g/wk; nonsmokers, 193 +/- 8.0 g/wk; P =.008), and muscle area (smokers, 64. 1 +/- 3.8 mm(2)/wk; nonsmokers, 76.4 +/- 5.6 mm(2)/wk; P =.03) were significantly reduced among smokers. There was a reduction in the rate of fat deposition in the thighs of fetuses of smoking mothers (smokers, 38.7 +/- 3.7 mm(2)/wk; nonsmokers, 54.6 +/- 5.4 mm(2)/wk; P =.004); however there was no absolute difference in the amount of fat measured in the thigh between 33 and 37 weeks' gestation. CONCLUSION: We detected reduced fetal growth that selectively affected abdominal circumference and peripheral muscle mass while not affecting head circumference and femur length in fetuses of smoking mothers. The effect of cigarette smoking on fetal fat deposition was less clear. Cigarette smoking appears to have a selective effect within lean body mass compartments, with affected compartments including peripheral fetal muscle. The findings of a reduction in abdominal circumference growth compared with control subjects in combination with no difference in subcutaneous fat content beyond 33 weeks' gestation are potentially explained by a reduction in fetal liver size that may result from maternal smoking.     

Effect of intravenous glucose injection on human maternal and fetal heart rate at term

The effects of maternal intravenous glucose administration (25 gm) on maternal heart rate, fetal heart rate, gross fetal body movements, and fetal heart rate accelerations was measured in 11 healthy pregnant women at 38 to 40 weeks' gestational age. Mean maternal heart rate increased from 78.3 ± 0.8 bpm during the control period to 82.7 ± 0.5 bpm at 30 to 85 minutes following glucose injections (p < 0.01). Mean fetal heart rate rose from 137.8 ± 0.4 bpm to 142.4 ± 0.3 bpm at 50 to 95 minutes following injections (p < 0.001). The incidence of gross fetal body movements and the number, duration, and amplitude of fetal heart rate accelerations did not change following glucose injection. We conclude that maternal glucose administration near term results in a small but significant increase in the mean maternal heart rate and fetal heart rate and no change in the incidence of gross fetal body movements or in fetal heart rate accelerations.