Noninvasive detection of the morphologic and hemodynamic changes during normal pregnancy

Abstract

Summary:To characterize the morphologic and hemodynamic changes during normal pregnancy, serial echocardiogruphic measurements (n = 2 lo) of left ventricular (LV) dimensions and mass (M-mode), volumes and ejection fraction (two-dimensional), stroke volume, and cardiac output (Doppler: aortic, apical, and suprasternal) were performed in 15 patients (mean age 30 years) beginning as early as 12 weeks of gestation, at 2-week intervals through delivery, and up to 12 weeks postpartum. Left atrial size increased from 3.4f0.4 (SD) to 3.8f0.4 cm near temi, decreasing to 3.4 f 0.5 cm postpartum (p = 0.006 overall). LV mass changes correlated with increases in body weight. No consistent significant changes in LV volumes and ejection fraction were observed. LV outflow tract cross-sectional area increased significantly from 3.0k0.2 cm2 at baseline to 3.550.3 cm2 near term, decreasing to 3.2f0.3 cm2 postpartum (p<0.002 for both). Heart rate increased from 70 f 7 to 77 f 10 beats/min near term decreasing to baseline postpartum (p<0.02 for both). Accordingly, cardiac output increased significantly, as detected from both the apical and suprasternal positions averaging tiom 4.7 k 0.6 to 6.5 5 1.5 I/min near term, returning to 4.3 f 0.6 I/min postpartum (p<0.0005 for both). Thus, in normal pregnancy, left atrial size increases significantly without significant changes in LV dimensions, volumes, and eject.ion fraction. Increased LV mass is related to increased body weight. Cardiac output changes result from increased heart rate and an increase in LV outflow area, which contributes to increased stroke volume. Doppler echocardiography permits accurate detection and timing of the morphologic and hemodynamic changes during normal pregnancy.

Maternal cardiovascular changes during pregnancy and postpartum in mice

“…In humans, the decrease in hematocrit is due to the dilutional effect of a greater increase in plasma volume than in red blood cell volume during pregnancy (27). Cardiac afterload decreases during pregnancy in humans and rats due to increases in aortic distensibility and left ventricular and/or aortic diameters (24,39,45) and decreased end-systolic blood pressure (19,32). Increased preload or decreased afterload increase peak aortic blood velocity and peak aortic acceleration in nonpregnant humans (4).…”

Cardiac structure and function in normal pregnancy

“…SV rises by about 20-30% in pregnancy, but there is significant disagreement about the time course of SV changes during pregnancy (supplementary table S2, http://links. lww.com/COOG/A1) [2,4,5,12,[16][17][18]20,21,23,25,[28][29][30][31][32][33][34][35]. SV can be calculated from the product of aortic Doppler flow velocity time integral and cross-sectional area (CSA) of the left ventricle outflow tract (LVOT), where slight differences in LVOT diameter will have a great impact on measurement error.…”

“…The increase in HR starts in the first trimester, peaks at 15-25% higher in the third trimester and returns to preconception levels within the first 10 postpartum days [2,[4][5][6][7][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33].…”

Doppler Echocardiographic Assessment of Pregnant Women with Chronic Arterial Hypertension

“…In addition, the physiological changes characteristic of pregnancy can also increase cardiac output as early as the sixth gestational week 1,2 . Assuming that chronic hypertensive pregnant women have a left ventricle adapted to work in a regimen of higher blood pressure and that pregnancy reduces blood pressure levels, we can conclude that the left ventricle behaves hyperdynamically in the CAH group 20 . The increase in blood volume activating the Frank Starling mechanism, the increase in ventricular mass, the reduction in afterload, and the stimulation of the sympathetic autonomic nervous system could justify the improvement in cardiac performance reflected in the increased systolic volume and cardiac output.…”