During normal pregnancy, plasma ANP and BNP levels are maintained in the nonpregnant range despite greater plasma volume (Yurteri-Kaplan, 2012). In one study, median BNP levels were stable across pregnancy with values <20 pg/mL (Resnik, 2005). BNP levels are increased in severe preeclamp sia, and this may be caused by cardiac strain from increased afterload (Afshani, 2013). It would appear that ANP-induced ume expansion and in the elevated plasma aldosterone concen trations characteristic of normal pregnancy.
Elevated prostaglandin production during pregnancy is thought to have a central role in control of vascular tone, blood pressure, and sodium balance. Renal medullary prostaglandin E2 synthesis is markedly elevated during late pregnancy and is presumed to be natriuretic. Levels of prostacyclin (PGI2), the principal prostaglandin of endothelium, also rise during late pregnancy. PGI2 regulates blood pressure and platelet function. It helps maintain vasodilation during pregnancy, and its deiciency is associated with pathological vasoconstriction (Shah, 2015). Thus, the ratio of PGI2 to thromboxane in maternal urine and blood is considered important in preeclampsia pathogenesis (Majed, 2012).
Several endothelins are generated in pregnancy. Endothelin-1 is a potent vasoconstrictor produced in endothelial and vascular smooth muscle cells and regulates local vasomotor tone (George, 2011; Lankhorst, 2016). Its production is stimulated by angiotensin II, arginine vasopressin, and thrombin. Endothelins, in turn, stimulate secretion of ANP, aldosterone, and catecholamines. Vascular sensitivity to endothelin-1 is not altered during normal pregnancy. Pathologically elevated levels may playia role in preeclampsia (Saleh, 2016).
This potent vasodilator is released by endothelial cells and may modiy vascular resistance during pregnancy. Moreover, nitric oxide is an important mediator of placental vascular tone and development (Krause, 2011; Kulandavelu, 2013). Abnormal nitric oxide synthesis has been linked to preeclampsia development (Laskowska, 2015; Vignini, 2016).
Of anatomic changes, the diaphragm rises approximately 4 cm during pregnancy (Fig. 4-11). he subcostal angle widens appreciably as the transverse diameter of the thoracic cage lengthens approximately 2 cm. The thoracic circumference increases about 6 cm, but not suiciently to prevent reduced residual lung volumes created by the elevated diaphragm. Even so, diaphragmatic excursion is greater in pregnant than in nonpregnant women.