Formulas for deriving some hemodynamic parameters are shown in Table 47-3. hese measurements can be indexed for body size by dividing by body surface area (BSA). Normal values for nonpregnant adults are used, but with the caveat that these may not necessarily reflect changes induced by the more "passive" uteroplacental perfusion.
In a landmark investigation, Clark and colleagues (1989) used PAC to obtain cardiovascular measurements in healthy pregnant women and again in these same women when nonpregnant (Chap. 4, p. 62). Because increased blood volume and cardiac output are compensated by decreased vascular resistance and increased pulse rate, ventricular performance remains within the normal range at term.
Cardiac complications are a common indication for ICU admission of pregnant women (Guntupalli, 2015b). Evaluation of cardiac unction is frequently performed using echo cardiography. his technology is indispensable in interrogating cardiac anatomy and especially right-ventricular unction (Krishnan, 2015; hiele, 2015). It is considered in more detail in Chapter 49 (p. 951), and some norml values are listed in the Appendix (p. 1261). A working knowledge of cardiovascular physiology in pregnancy is paramount to understanding the pathophysiology of gestational complications discussed later in this chapter and throughout the book.
TABLE 47-3. Formulas for Deriving Various Cardiopulmonary Parameters
BSA = body surface area (m2); CVP = central venous pressure (mm Hg); DBP = diastolic blood pressure; HR = heart rate (beats/min); MAP = mean systemic arterial pressure (mm Hg); MPAP = mean pulmonary artery pressure (mm Hg); PCWP = pulmonary capillary wedge pressure (mm Hg); SBP = systolic blood pressure.
Critical Care and Trauma 91.7
The incidence of pulmonary edema complicating pregnancy averages 1 in 500 deliveries at tertiary referral centers. The two general causes are: (1) cardiogenic, namely, hydrostatic edema caused by high pulmonary capillary hydraulic pressures, and (2) noncardiogenic, that is, permeability edema caused by capillary endothelial and alveolar epithelial damage. In pregnancy, noncardiogenic pulmonary edema is more common. Taken in toto, studies in gravidas indicate that more than half who develop pulmonary edema have some degree of sepsis syndrome in conjunction with tocolysis, severe preeclampsia, or obstetrical hemorrhage combined with vigorous luid therapy (O'Dwyer, 2014; hornton, 2011).
lthough cardiogenic pulmonary edema is less frequent, common precipitating causes include resuscitation for hemorrhage and vigorous treatment of preterm labor. In one study, the causes in 51 women with pulmonary edema were cardiac failure, tocolytic therapy, iatrogenic luid overload, and preeclampsia (Sciscione, 2003). In another study, more than half of cases were associated with preeclampsia, and the other three causes had equal distribution (Hough, 2007). In still another study of 53 cases, 83 percent were caused by hypertensive disorders, 11 percent cardiac, and 6 percent sepsis (O'Dwyer, 2015). Although used less commonly today, tocolytic therapy with �-mimetic drugs at one time was the cause of up to 40 percent of pulmonary edema cases (DiFederico, 1998; Gandhi, 2014; Jenkins, 2003).