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 2 – Variation in systemic arterial pressure during the pregnancy-postpartum cycle. Adapted from Sanghavi and Rutheford, 2014. 3 115 105 95 85 75 65 55 45 108 103 105 81 82 63* 68* 69 104* 76 84 71 65* 104* 78 Prepregnancy Early pregnancy Second Trimester Third Trimester Postpartum * p < 0.05 versus previous value of the uterine plexus, decompression in the flow of the inferior vena cava, and reduction in venous system capacity. In addition to this, peripheral vascular resistance is increased by sustained contraction of the uterus, occluding the vessels that open on the maternal placenta surface. The continuous “auto transfusion” that occurs during 24 to 72 hours after delivery represents a high risk of pulmonary congestion in women with heart disease. 10 Cardiovascular effects during delivery are also influenced by the eventual occurrence of infection, hemorrhage, and use of anesthetics drugs. 11 In general, the patterns of alteration in maternal blood volume during labor, the expulsion period, and the postpartum period are described by the following phases: 1. Blood concentration during labor, varying with the degree of uterine activity and maternal dehydration; 2. Reduced blood volume during and immediately after delivery, proportional to blood lose volume; 3. Immediate, transient elevation in blood volume following placental clearance, attributed to fluid inflow into the intravascular territory, due to uterine emptying; 4. Slight elevation in blood volume between the second and third days after delivey, secondary to the transient increase in aldosterone secretion; 5. Reduced plasma volume one week after delivery, in a manner that maternal systolic volume may present a slight drop during this period, returning to normal within a short term. 2.1.2 Modifications in Blood Coagulation During pregnancy, activation occurs in the synthesis of coagulation factors II, VII, VIII, IX, and X and fibrinogen, as well as a reduction of endogenous anticoagulants (especially antithrombin and protein S), all of which are determinants of the state of hypercoagulability, which is characteristic of a healthy pregnancy. 12 These modifications occur progressively after the first trimester of gestation, with shortening of prothrombin, partial thromboplastin, and thrombin times, favoring the weakening of the anticoagulant function. 13 Considering these mechanisms, in conjunction with the mechanical compression of the venous plexus on the lower limbs by the gravid uterus, the characteristic predisposition to thromboembolism during pregnancy is justified. (Figure 3). 2.1.3. Respiratory Changes (Figure 4) Oxygen consumption increases by around 50%, especially during the last 2 trimesters of gestation, and this is not proportional to maternal weight gain. Weight gain during gestation includes not only fetal metabolic activity, but also the weight of amniotic fluid and the increase of fluid in maternal tissues, both of which are considered metabolically inert. During labor, oxygen consumption increases by 250 to 750 ml/min with each contraction. 14 The normal respiratory tract undergoes modifications during pregnancy, which induce respiratory alkalosis, with higher arterial oxygen partial pressure (PaO 2 ) and lower arterial carbon dioxide partial pressure (PaCO 2 ), in comparison with the non-pregnant state. Lower PaCO 2 favors a diffusion gradient that facilitates the fetus’ ability to eliminate products of aerobic metabolism. 3 Increased minute ventilation is accompanied by an increase in tidal volume, without modifying respiratory rate. Maternal hyperventilation is considered to be a protective mechanism for the fetus against the detrimental effects of excessive tissue CO 2 concentration, at the same time that PaO 2 increases to 100 mmHg. Modifications in the chest occur with uterine enlargement and diaphragm elevation. Thoracic circumference increases by around 5 to 7 cm; the substernal angle widens, and vertical diameter decreases. These modifications are accompanied by alterations in the distribution of air throughout the diverse pulmonary compartments. Histological examination of the upper respiratory tract mucosa during pregnancy reveals: hyperemia, glandular hyperactivity, increased phagocytic activity, and increased mucopolysaccharide content. Nasal congestion and epistaxis, which are frequent during gestation, are possibly caused by these changes. 15 Airway and respiratory function is preserved during pregnancy, as reflected by an unchanged forced expiratory volume in one second (FEV1) and an unchanged ratio of FEV1 to forced vital capacity (FVC). 15 The 25% reduction in lung functional residual capacity (FRC) is associated with a similar increase in inspiratory capacity (IC). Consequently, vital capacity (VC) does not show any modifications during pregnancy. The decrease in FRC to 300 ml during pregnancy is not accompanied by increased airway resistance, which, on the 856