Evaluation of maternal fluid dynamics during tocolytic therapy with ritodrine hydrochloride and magnesium sulfate

• Published in: American journal of obstetrics and gynecology Vol. 167; no. 3; p. 758
• Main Authors: Armson, B A, Samuels, P, Miller, F, Verbalis, J, Main, E K
• Format: Journal Article
• Language: English
• Published: United States 01.09.1992
• Subjects: Arginine Vasopressin - blood; Body Fluids - physiology; Cardiovascular System - drug effects; Colloids - analysis; Female; Hematocrit; Humans; Magnesium Sulfate - therapeutic use; Natriuresis - drug effects; Obstetric Labor, Premature - metabolism; Obstetric Labor, Premature - physiopathology; Obstetric Labor, Premature - therapy; Osmotic Pressure - drug effects; Pregnancy; Ritodrine - therapeutic use; Tocolysis
• ISSN: 0002-9378
• DOI: 10.1016/S0002-9378(11)91585-3

The purpose of the study was to observe and compare the effects of ritodrine hydrochloride and magnesium sulfate on maternal fluid dynamics. Fourteen women in preterm labor were prospectively studied during tocolytic therapy with either ritodrine hydrochloride or magnesium sulfate. The cardiovascular and renal effects of a pretreatment crystalloid infusion were compared with those observed during tocolytic therapy. Profile analysis and repeated measures of variance were used to analyze the data. Ritodrine hydrochloride was associated with decreased colloid osmotic pressure, hematocrit, and serum proteins and increased maternal and fetal heart rates. Arginine vasopressin levels increased during the first 2 hours of therapy, then returned to baseline. Sodium excretion was reduced and there was marked fluid retention. Intravenous magnesium sulfate also resulted in a reduction of colloid osmotic pressure, but hematocrit, serum protein concentration, arginine vasopressin, maternal and fetal heart rates, and mean arterial pressure were minimally affected. Sodium excretion increased to a maximum at 6 to 8 hours of treatment, then returned to baseline. A positive fluid balance was also noted in magnesium sulfate-treated patients but to a lesser degree than with ritodrine. Sodium retention appears to be the primary cause of plasma volume expansion in ritodrine-treated patients, whereas volume expansion during magnesium sulfate therapy is probably related to intravenous overhydration. In the absence of risk factors for pulmonary capillary membrane injury, available evidence supports volume overload as the principal mechanism for pulmonary edema during tocolytic therapy.