perfusion; this results in an increase in cardiac output and a relatively small decrease in mid-gestational blood pressure. Venous blood pressure rises in the lower limbs due to mechanical and hydrostatic pressure in the pelvis, causing edema in the lower limbs. Because of these cardiovascular changes, it is possible to have reduced exercise tolerance and dyspnea.
Physiological changes in circulation during pregnancy are marked and variable (Gabbe et al., 1991; Hytten and Chamberlain, 1991). Plasma volume increases progressively to 50 percent by 30-34 weeks of gestation. Importantly, plasma volume expansion is correlated with clinical performance and birth weight. Poor plasma volume expansion is associated with a poorly growing fetus and poor reproductive performance. The increases in maternal plasma volume account for a significant portion of the increase in total body water during pregnancy.
Red blood cell mass also increases about 18 percent by term without iron supplementation and 30 percent with iron supplementation. Minute ventilation increases 30-40 percent by late pregnancy due to increased tidal volume. Oxygen consumption increases only 15-20 percent, resulting in an increase in alveolar and arterial PAO2 (partial pressure of oxygen) and a fall in PACO2 (partial pressure of carbon dioxide) levels (Gabbe et al., 1991).
Renal plasma flow increases 70 percent over pregravid levels by 16 weeks of gestation and is maintained until late pregnancy when it falls slightly (Gabbe et al., 1991). Glomerular filtration rate (GFR) increases early in pregnancy, up to 50 percent by term. As a result of the increased GFR, serum levels of urea and creatinine decline. Plasma osmolarity declines early in pregnancy due to a reduction in serum sodium and associated anions. There is a net accumulation of approximately 900-1,000 meq of sodium in the fetus, placenta, and intravascular and interstitial fluids. There is a large increase in tubular sodium reabsorption during pregnancy, promoted by increased aldosterone, estrogen, and deoxycorticosterone. Plasma renin activity, renin substrate, and angiotensin levels increase five-to tenfold above the pregravid values. The adaptations in maternal renal physiology during gestation are among the primary mechanisms accounting for the increase in plasma volume and hence total body water during gestation.
The plasma concentration of corticosteroid-binding globulin (CBG) increases significantly, reflecting increased hepatic synthesis (Gabbe et al., 1991). Estrogen-induced increases in CBG lead to an elevated plasma cortisol concentration, with a three-fold increase occurring by the end of the