Nitrous oxide inhalation: effects on maternal and fetal circulations at term.

OBJECTIVE: To evaluate the hemodynamic effects of nitrous oxide inhalation in normal term pregnancy. METHODS: Twenty healthy term pregnant women were given 30% nitrous oxide in pure oxygen for 2 minutes, and the hemodynamics were assessed by pulsed-wave color Doppler velocimetry of the uterine and internal carotid artery of the mother and the umbilical and middle cerebral artery of the fetus. Each vessel was assessed separately, allowing a 5-minute wash-out period between the inhalations. The measurements were continued for 2 minutes after the inhalation, and the pulsatility index (PI) was determined at 1-minute intervals. The maternal heart rate and blood pressure (BP) were recorded before and after inhalation; fetal well-being was confirmed with cardiotocography. Analysis of variance for repeated measurements and paired-sample t test were used for statistical analysis. RESULTS: A significant decrease in the PI of the maternal internal carotid artery was observed after 2-minutes of inhalation (from 0.83 +/- 0.22 to 0.71 +/- 0.20; P < .001). The uterine artery PI and maternal BP and heart rate were not affected by nitrous oxide. A significant decrease was evident even in the fetal middle cerebral artery PI (from 1.37 +/- 0.27 to 1.22 +/- 0.17; P = .02). The umbilical artery PI remained unchanged. CONCLUSION: Both maternal and fetal central vascular resistance were decreased by 30% nitrous oxide inhalation. So far, no adverse effects to mother or fetus have been demonstrated in clinical practice. However, preterm fetuses are susceptible to intracranial hemorrhage, and the cerebral hyperemia by nitrous oxide might increase the risk of hemorrhage in these fetuses. This hypothesis requires further investigation.

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.

Vaginal and intracervical prostaglandin E2 for cervical ripening: a Doppler study of hemodynamic effects.

The hemodynamic effects of vaginally and intracervically administered prostaglandin E2 gel were evaluated by pulsed wave color Doppler ultrasound. Twenty term pregnant mothers were recruited. Mothers were randomized to receive either vaginal or intracervical prostaglandin E2 gel. The hemodynamics was assessed by repeated color Doppler velocimetry of the uterine artery and fetal umbilical and middle cerebral arteries; analysis of variance was used to test statistical significance. In the uterine artery a statistically significant rise (P < or = 0.001) of the pulsatility index (PI) was observed. A slightly higher rise of the PI was observed after intracervical administration, but the difference between the groups was not statistically significant (P = 0.4). The fetal PI remained unchanged both in the umbilical and cerebral vessels throughout the study. The rise in the uterine artery PI is probably caused by an increase in the uterine tone as prostaglandins of the E series usually cause vasodilation. No detectable fetal effects were evident.