Morris and associates (2015) studied measures of vas cular compliance before pregnancy, during pregnancy, and postpartum. Compared with healthy nonpregnant controls, stifness, measured using pulse wave velocity, were observed between the prepregnant and the postpartum time periods.
sibly help explain why the risk of preeclampsia is reduced in subsequent pregnancies.
Antecubital venous pressure remains unchanged during pregnancy. In the supine position, however, femoral venous pressure rises steadily, from approximately 8 mm Hg early in pregnancy to 24 mm Hg at term. Venous blood flow in the legs is retarded during pregnancy except when the lateral recumbent position is assumed (Wright, 1950). his tendency toward blood stagnation in the lower extremities during later pregnancy is attriburable to occlusion of the pelvic veins and inferior vena cava by the enlarged uterus. he elevated venous pressure returns to normal when the pregnant woman lies on her side and immediately after delivery (McLennan, 1943). These alterations contribute to the dependent edema frequently experienced and to the development of varicose veins in the legs and vulva, as well as hemorrhoids. These changes also predispose to deep-vein thrombosis.
In approximately 10 percent of women, supine compression of the great vessels by the uterus causes signiicant arterial hypotension, sometimes referred to as the supine hypotensive syndrome (Kinsella, 1994). Also when supine, uterine arterial pressure-and thus uterine blood flow-is signiicantly lower than that in the brachial artery. Evidence to support whether this directly afects fetal heart rate patterns in uncomplicated low-risk pregnancies is conlicting (Armstrong, 2011; Ibrahim, 2015; Tamas, 2007). Similar changes can also be seen with hemorrhage or with spinal analgesia.
• Renin, Angiotensin II, and Plasma Volume
The renin-angiotensin-aldosterone axis is intimately involved in blood pressure control via sodium and water balance. All components of this system show increased levels in normal pregnancy. Renin is produced by both the maternal kidney and the placenta, and greater amounts of renin substrate (angiotensinogen) are produced by both maternal and fetal liver. Elevated angiotensinogen levels result, in part, from augmented estrogen production during normal pregnancy and are important in irst-trimester blood pressure maintenance (Lumbers, 2014).
Gant and associates (1973) reported that nulliparas who remained normotensive became and stayed refractory to the pressor efects of infused angiotensin II. Conversely, those who ultimately became hypertensive developed, but then lost, this refractoriness. The diminished vascular responsiveness to angiotensin II may be progesterone related. Normally, pregnant women lose their acquired vascular refractoriness to angiotensin II within 15 to 30 minutes after the placenta is delivered.
Large amounts of intramuscular progesterone given during late labor delay this diminishing refractoriness.
At least two species of these-atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)-are secreted by cardiomyocytes in response to chamber-wall stretching. These peptides regulate blood volume by provoking natriuresis, diuresis, and vascular smooth-muscle relaxation. In nonpregnant and pregnant patients, levels of BNP and of amino-terminal pro-brain natriuretic peptide (Nt pro-BNP), as well as newer analytes such as suppressor of tumorigenicity 2 (ST2), may be useful in screening for depressed left ventricular systolic function and determining chronic heart failure prognosis (Ghashghaei, 2016).