the amniotic sac in late gestation (Ross and Brace, 2001). The two major inflow sources are fetal urine and lung liquid secretions. The two major outflows are fetal swallowing and intra-membranous absorption. Brace and Wolf (1989) reported on a series of 705 published amniotic fluid volumes derived from either direct collection or dye dilution techniques. At 8 weeks of gestation, amniotic volume increases at a rate of 10 mL per week, and at 13 weeks the rate increases to 25 mL per week. The maximal increase in amniotic fluid of 60 mL per week occurs at 21 weeks’ gestation. The weekly volume increment then decreases and reaches zero at 33 weeks’ gestation (i.e., the time at which maximal volume is reached).
There is wide variation in the amount of amniotic fluid in a normal pregnancy. Decreased amniotic fluid (i.e., oligohydramnios) occurs in approximately 8.2 percent of pregnancies, and increased amniotic fluid (i.e., polyhydramnios) occurs in approximately 1.6 percent of pregnancies (Ross and Brace, 2001). Oligohydramnios may occur as a consequence of fetal renal obstruction or dysplasia and may be associated with fetal growth restriction. Polyhydramnios is associated with various fetal structural anomalies such as congenital esophageal atresia, fetal anemia, congenital infections, and maternal diabetes. Given the wide range of normal amniotic fluid volume at term, this compartment may affect maternal GWG by as much as 1 kg.
Understanding the unique physiologic, metabolic, and endocrine milieu of the pregnant woman is crucial to understanding the mechanisms underlying GWG. The pregnant woman undergoes dramatic physiologic changes in anticipation and in support of fetal growth. Changes in many of the obligatory components of GWG (for example, TBW) are directly related to the alterations in maternal physiology that must occur for a healthy fetus and placenta to grow and develop. When the evidence permitted, the committee considered how physiological changes impact GWG and neonatal outcome. As with other information in the chapter, the findings summarized here provide a foundation for understanding the physiological predictors of GWG and identifying ways to intervene.
In early pregnancy, cardiac output increases about 30-50 percent as a result of an increase in heart rate—primarily stroke volume—and remains elevated until term (Hytten and Chamberlain, 1991). As pregnancy progresses, blood flow increases to the uterus, kidney, skin, and probably the alimentary tract. Arterial blood pressure may decrease in mid-pregnancy as a result of increased peripheral vasodilatation and in order to maintain