Cardiovascular system

During the first two trimesters of pregnancy, maternal circulating blood volume increases 40% (3500 cm³ expands to 5000 cm³) with the largest expansion occurring during the second trimester (Fig. 20.2). The functions of pregnancy-induced hypervolumia are to meet the demands of the enlarged uterus with its greatly hypertrophied vascular system, to provide nutrients to the growing placenta and fetus, to protect both mother and fetus from impaired venous return in certain postures, and to ensure that the mother does not suffer any adverse effects from the obligatory blood loss at delivery.

The increase in plasma volume results from a combination of a modest (10 mOsm/kg) decrease in plasma osmolality and from water retention through enhanced activity of the renin–angiotensin system. Placental estrogen increases hepatic production of angiotensinogen, and estrogen and progesterone together increase renal production of the proteolytic enzyme, renin. Renin cleaves angiotensinogen to form angiotensin I, which converts into angiotensin II (AII) in the lung and elsewhere. The increased amounts of AII act on the zona glomerulosa of the adrenal gland to increase aldosterone production. Aldosterone promotes volume expansion through sodium and water retention. Oxygen-carrying capacity must be maintained in the presence of this increase in circulating blood volume. Iron absorption increases to meet the demand for increased hemoglobin during volume expansion.

A loss of peripheral vascular responsiveness to AII accompanies the increase in circulating blood volume. AII is a potent vasoconstrictor and loss of AII responsivity results in a drop in maternal blood pressure during the early second trimester. This relative hypotension is seen in most pregnant women despite elevated AII levels. Maternal blood pressure slowly rises to prepregnancy levels by the third trimester. Progesterone promotes overall smooth muscle relaxation and is thereby partially responsible for alterations in maternal blood pressure. Production of prostacyclin, the principal endothelial prostaglandin, also increases during pregnancy and has been implicated in the development of angiotensin resistance.

Immediately following delivery of the fetus and placenta, a venous “autotransfusion” from the extremities, pelvis and empty uterus into the right heart occurs. Women with a normal cardiovascular system tolerate this event well but it is a major challenge for women with mitral valve stenosis and Eisenmenger syndrome in whom the increased venous return can result in pulmonary edema and hypoxia.