Activated protein , along with the cofactors protein Siand factor V, functions as an anticoagulant by neutralizing the procoagulants factor Va and factor VIlla. During pregnancy, resistance to activated protein C grows progressively and is related to a concomitant drop in free protein S levels and greater factor VIII concentrations. Between the irst and third trimesters, activated protein C levels decline from 2.4 to 1.9 V/mL, and free protein S concentrations diminish from 0.4 to 0.16 V/ mL (Cunningham, 2015; Walker, 1997). Antithrombin levels decrease by 13 percent between midpregnancy and term and fall 30 percent from this baseline until 12 hours after delivery. By 72 hours after delivery, there is a return to baseline Games, 2014).
Normal pregnancy promotes platelet changes. In one study, the average platelet count declined slightly during pregnancy to 213,OOO/1L compared with 250,000/1L in nonpregnant controls (Boehlen, 2000). hrombocytopenia deined as below the 2.5th percentile corresponded to a platelet count of 116,OOO/1L. Lower platelet concentrations are partially due to hemodilution. Also, platelet consumption is likely augmented and creates a greater proportion of younger and therefore larger platelets (Han, 2014; Valera, 2010). Further, levels of several markers of platelet activation rise with gestational age but drop postpartum (Robb, 2010). Because of splenic enlargement, there may be an element of "hypersplenism," in which platelets are prematurely destroyed (Kenny, 2014).
By the end of normal pregnancy, the spleen enlarges by up to 50 percent compared with that in the irst trimester (Maymon, 2007). Moreover, Gayer and coworkers (2012) found that splenic size was 68-percent greater compared with that of nonpregnant controls. he cause of this splenomegaly is unknown, but it might follow the increased blood volume and/or the hemodynamic changes of pregnancy.
Changes in cardiac function become apparent during the irst 8 weeks of pregnancy (Hibbard, 2014). Cardiac output is increased as early as the ifth week and reflects a reduced systemic vascular resistance and an increased heart rate. Compared with prepregnancy measurements, brachial systolic blood pressure, diastolic blood pressure, and central systolic blood pressure are all signiicantly lower 6 to 7 weeks from the last menstrual period (Mahendru, 2012). he resting pulse rate rises approximately 10 beats/min during pregnancy. Nelson and associates (2015) found that for both normal and overweight women, heart rate increased signiicantly between 12 and 16 weeks' and between 32 and 36 weeks' gestation. Between weeks 10 and 20, plasma volume expansion begins, and preload rises. his augmented preload results in signiicantly larger left atrial volumes and ejection fractions (Cong, 2015).
Ventricular performance during pregnancy is inluenced by both the decrease in systemic vascular resistance and changes in pulsatile arterial low. Multiple factors contribute to this overall altered hemodynamic function, which allows the physiological demands of the fetus to be met while maintaining maternal cardiovascular integrity (Hibbard, 2014). hese changes during the last half of pregnancy and efects of maternal posture are summarized in Figure 4-7.
As the diaphragm becomes progressively elevated, the heart is displaced to the left and upward and is rotated on its long axis. As a result, the apex is moved somewhat laterally from its usual position and produces a larger cardiac silhouette in chest radiographs. Furthermore, gravidas normally have some degree of benign pericardial efusion, which may enlarge the