ABC | Volume 114, Nº5, May 2020

Statement Brazilian Cardiology Society Statement for Management of Pregnancy and Family Planning in Women with Heart Disease – 2020 Arq Bras Cardiol. 2020; 114(5):849-942 Figure 1 – Variation in cardiac output and peripheral vascular resistance (PVR) during and after pregnancy. Adapted from Sanghavi and Rutheford, 2014. 3 Cardiac Output (I/min) PVR (dynes.s –1 .cm –5 ) 7 6.5 5.6 5.8 6.2* 6.1* 5.6 5.5 4.5 3.5 1250 1150 1050 950 850 1229 1129 999* 1081* 1207* 6 5 4 Prepregnancy * p < 0.05 versus previous value Early pregnancy Second Trimester Third Trimester Postpartum approximately 6% reduction in heart rate, and a 27% increase in systolic volume. Compression of the inferior vena cava by the enlarged uterus in the supine position provokes what is known as supine hypotensive syndrome, which may manifest with dizziness and/or syncope. 4 During pregnancy, a reduction occurs in plasma colloid osmotic pressure in approximately 12% to 18% of cases, as a consequence of the drop in circulating albumin concentrations, which are observed in lower levels during week 24 of pregnancy. This decline prompts edema in lower limbs, and it predisposes pregnant and parturient women who have received excessive intravenous crystalloid infusion to pulmonary congestion. 5 The decrease in peripheral vascular resistance during the beginning of pregnancy is not limited to the uterine plexus, and it has a greater magnitude than the concomitant elevation in cardiac output. During the second half of pregnancy, resistance reaches its lowest values, at the moment when cardiac output reaches its maximum values (Figure 1). 6 Arteriolar dilation during pregnancy has been attributed to estrogenic components, prolactin, and increased levels of circulating prostaglandin (PGE2 and PGI2), a substance that is responsible for reducing vascular response to exogenous angiotensin. A decrease in prostaglandin synthesis or an increase in its metabolism may result in increased vascular responsiveness to angiotensin II, a characteristic that has been observed in pregnant women who develop hypertension. Progesterone and its metabolites also appear to participate in modulation of vascular response to angiotensin II during pregnancy. It has recently been demonstrated that alterations in vascular tone during pregnancy may be partly attributed to changes in the synthesis of endothelium-derived vasoactive substances, especially endothelin, which is theoretically capable of mediating prostaglandin synthesis, and to the reduction in nitric oxide, which has been related to vasodilation during pregnancy. 7 It is worth emphasizing that, during pregnancy, the arterial system undergoes remodeling in order to accommodate increased blood volume. Estrogen promotes collagen deposition in the middle layer of the large and medium arteries; circulating elastase favors rupture of the elastic lamina and weakening of the middle layer of vessel walls; and relaxin, an insulin-like growth factor hormone (detected in the plasma), causes a reduction in collagen synthesis. All of these factors explain the predisposition to artery dissection during pregnancy. Systemic arterial pressure (SAP) decreases from the beginning to the middle of pregnancy, 8 particularly at the expense of diastolic pressure, and it subsequently rises to pre‑gestation values as the term approaches (Figure 2). SAP rises during uterine contractions, especially during the second stage of delivery. A clinical picture of orthostatic hypotension may occasionally occur, secondary to reduced venous return when a pregnant woman is in the supine position, with a consequent drop in cardiac output. Considering pulmonary output equal to aortic output in normal adults, changes in pulmonary vascular resistance are parallel to those in systemic vascular resistance. 9 Recent studies have challenged this “dogma,” showing a tendency toward increased arterial pressure in women with body mass index (BMI) > 25 kg/m² and women who were obese prior to gestation. 2 Normal labor is associated with significant hemodynamic alterations, due to anxiety, exertion, pain, uterine contractions, maternal posture (left lateral versus supine), uterine involution, and bleeding. During labor, blood from the uterine sinusoids is released into systemic circulation with each contraction, increasing the preload by about 500 ml of blood, which leads to increased cardiac output and blood pressure. Thus, during the second stage of labor, cardiac output is around 50% higher in relation to pre-delivery, and, during fetal expulsion, it is 60% to 80% higher than pre-gestational levels. This abrupt change in cardiac output is transient. It remains elevated during the immediate postpartum period, and it is not accompanied by variations in arterial pressure. During normal delivery, around 400 ml of blood are lost. In cesarean section, blood loss may be greater, namely, around 800 ml. After the delivery, a sudden increase occurs in venous return, due to “auto transfusion” 855