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Mean amniotic fluid volume increases from 250 to 800 mL between 16 and 32 weeks and decreases to 500 mL at term.
Fetal urine production ranges from 400 to 1200 mL/day and is the primary source of amniotic fluid.
The fetal umbilical circulation receives approximately 40% of fetal combined ventricular output (300 mL/mg/min).
Umbilical blood flow is 70 to 130 mL/min after 30 weeks’ gestation.
Fetal cardiac output is constant over a heart rate range of 120 to 180 beats/min.
The fetus exists in a state of aerobic metabolism, with arterial P o 2 values in the 20 to 25 mm Hg range.
Glucose, amino acids, and lactate are the major substrates for fetal oxidative metabolism.
Approximately 20% of the fetal oxygen consumption of 8 mL/kg/min is required in the acquisition of new tissue.
By week 12 of gestation, thyrotropin-releasing hormone is present in the fetal hypothalamus.
Fetal activity periods in late gestation are often termed active or reactive and quiet or nonreactive.
The relationship between flow and perfusion pressure is linear in the umbilical circulation.
Relative to the uteroplacental bed, the fetoplacental circulation is resistant to vasoconstrictive effects of infused pressor agents, and umbilical blood flow is preserved unless cardiac output decreases. Umbilical blood flow is maintained over a relatively wide range of oxygen tensions.
Mean amniotic fluid volume (AFV) increases from 250 to 800 mL between 16 and 32 weeks of gestation and then declines to about 500 mL at 42 weeks ( Fig. E2.1 ).
AFV is maintained by a balance of fetal fluid production (lung, liquid, and urine) and fluid resorption (fetal swallowing and flow across the amniotic and/or chorionic membranes to the fetus or maternal uterus).
Lung fluid likely serves to maintain lung expansion and facilitate pulmonary growth.
Lung fluid must decrease at parturition for the transition to respiratory ventilation. The absence of this process explains the increased incidence of transient tachypnea of the newborn in infants delivered by cesarean section in the absence of labor.
Fetal urine is the primary source of amniotic fluid, and outputs at term vary from 400 to 1200 mL/day. Fetal swallowing is believed to be a major route of amniotic fluid resorption.
Nutrients are utilized by the fetus for two primary purposes: oxidation for energy and tissue accretion. Under normal conditions, glucose is an important substrate for fetal oxidative metabolism.
Lactate also is a substrate for fetal oxygen consumption. Thus, the combined substrates—glucose, amino acids, and lactate—essentially provide the approximately 87 kcal/kg required daily by the growing fetus.
Because many of the necessary enzymes for conversion of carbohydrate to lipid are present in the fetus, fat acquisition reflects glucose utilization in addition to placental fatty acid uptake.
Growth hormone appears to have little role in regulating fetal growth.
The increase in insulin-like growth factor-1 (IGF-1) levels directly correlates with increase in fetal size, and a reduction in IGF-1 levels is associated with growth restriction.
A role for insulin in fetal growth is suggested from the increases in body weight and in heart and liver weights in infants of diabetic mothers.
As in the adult, β-adrenergic receptor activation increases fetal insulin secretion, whereas β-adrenergic activation inhibits insulin secretion. Fetal glucagon secretion also is modulated by the β-adrenergic system. However, the fetal glycemic response to glucagon is blunted, probably caused by a relative reduction in hepatic glucagon receptors.
Corticosteroids are essential for fetal growth and maturation, and levels in the fetus rise near parturition in step with maturation of fetal organs, such as the lung, liver, kidneys, and thymus, and with slowing of fetal growth. Exogenous maternal steroid administration during pregnancy also has the potential to diminish fetal growth.
The fetal thyroid also is not important for overall fetal growth but is important for central nervous system development.
Growth factors and cytokines exert their functions locally, promoting proliferation and differentiation through their autocrine and/or paracrine mode of actions.
Epidermal growth factor (EGF) is involved in embryonal implantation, it stimulates syncytiotrophoblast differentiation in vitro, and it modulates production and secretion of human chorionic gonadotropin and human placental lactogen.
Imprinted genes play a particularly important role in controlling fetal growth.
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