Objective: We sought to determine the effect of magnesium sulfate on fetal heart rate baseline value, variability, and acceleration-deceleration pattern.
Study design: Normal, nonlaboring pregnant patients at >30 weeks' gestation were recruited. Baseline fetal heart rate monitoring for 1 hour was performed. After an 800-kcal meal, patients were randomized to receive either an intravenous loading dose of 6 g of magnesium sulfate in 100 mL of isotonic sodium chloride solution or 100 mL of isotonic sodium chloride solution alone. Subsequently, patients in the magnesium sulfate group received a 2-g/h intravenous infusion for 3 hours at a rate of 125 mL/h. Patients randomized to the sodium chloride solution group received a sodium chloride solution infusion at a similar rate (unlabeled intravenous bags). Maternal blood was drawn at 0, 1, and 3 hours for determination of total and ionized magnesium and calcium, electrolyte, and glucose levels. One hour of fetal heart rate monitoring was repeated at 1 and 3 hours of infusion. Tracings were interpreted without identifiers (of time or group) by using the National Institute of Child Health and Human Development fetal heart rate monitoring guidelines.
Results: Magnesium sulfate administration resulted in decreased fetal heart rate baseline values and variability in the third hour. The fetal heart rate baseline value was 134.4 +/- 6.3 versus 136.6 +/- 6.4 beats/min before infusion (P >.05), 134.4 +/- 7.1 versus 135.1 +/- 6. 6 beats/min in the first hour (P >.05), and 134.6 +/- 7.1 versus 132. 3 +/- 7.6 beats/min in the third hour (P <.05) in the sodium chloride solution group versus the magnesium sulfate group, respectively. Fetal heart rate variability (grades 1-5) was 2.75 +/- 0.33 versus 2.82 +/- 0.29 before infusion (P >.05), 2.81 +/- 0.30 versus 2.84 +/- 0.28 in the first hour (P >.05), and 2.71 +/- 0.52 versus 2.67 +/- 0.36 in the third hour in the sodium chloride solution group versus the magnesium sulfate group, respectively (P <. 05). Magnesium sulfate blocked the positive correlation between gestational age and number of accelerations found in control subjects. No significant decelerations were identified.
Conclusions: Prolonged administration of magnesium sulfate was associated with decreased fetal heart rate baseline values and variability. Given the small magnitude of these changes, the clinical significance of these findings is questionable. Magnesium sulfate inhibition of the increasing number of accelerations with gestational age needs to be considered when fetal well-being is assessed.