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 3 – Activation of coagulation factors during pregnancy. F: factor. Adapted from Bremme et al., 2003. 12 Contact surface Collagen Activated F XII Tissue/cellular defect F XII F XI F VIII F VIIIa F VIIa F VII F IX F X F Va F V F Xa Prothrombin I Thrombin Fibrinogen Fibrin meshwork F X F III (thromboplastin tissue) Platelet factor 3 Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ Ca 2+ F IXa F XIa F XIIIa Fibrin polymers Fibrin monomers F XIII F XIIa Intrinsic pathway Extrinsic pathway Figure 4 – Respiratory changes during pregnancy. ERV: expiratory reserve volume; FRC: functional residual capacity; IC: inspiratory capacity; RV: residual volume; TPC: total pulmonary capacity; VC: vital capacity. Adapted from Hegewald and Crapo, 2011. 16 Pulmonary volume compartment Not pregnant Pregnant (28–40 weeks) IC VC TPC ERV FRC RV contrary, undergoes a significant reduction, possibly due to relaxation of smooth muscle tone secondary to hormonal action. This reduction serves to decrease work of breathing. With hyperventilation, an increase in PaO 2 occurs, and the hemoglobin dissociation curve shifts to the right. Normal blood gases in pregnant women should have a pH between 7.40 and 7.47, PaCO 2 between 30 and 32, and a slight increase in PaO 2 . Respiratory alkalosis is partially offset by increased renal excretion of bicarbonate, which maintains serum levels of HCO 3 between 18 and 21 mEq/L (a baseline deficit of 3 to 4 mEq/L). The decrease in pulmonary FRC and the increase in oxygen consumption reduce the maternal oxygen reserve, which, in the event of respiratory failure, represents a state of alert for adopting early measures of respiratory or ventilatory support, in order to avoid harm to the fetus or the mother. 16 The mechanism behind dyspnea during normal pregnancy is not completely clear. Hyperventilation induced by progesterone is probably at least partially responsible, perhaps due to the elevation of ventilation above the level necessary to meet the increased metabolic demand. 2.1.4. Structural Vascular Changes Hormonal changes during pregnancy may alter the structure of the vascular, resulting in weakening of the arterial walls. Estrogen influences abnormal collagen deposition inside the middle layer of the large and medium arteries. Circulating elastase may provoke a rupture of the elastic lamina and weakening of the middle layer of vessel walls. In addition to this, relaxin, an insulin-like growth factor hormone (detected in the plasma), causes a redction in the synthesis of collagen and predisposes pregnant women to artery dissection. 17 2.1.5. Key Points Knowledge regarding physiological modifications related to the pregnancy and postpartum period is fundamental to clinical practice for management of pregnancy and risk stratification of women with heart disease. 857