Obstetrics and Gynecology - A.M. Gromova 2000

Changes in the Woman's Body During Pregnancy
The Cardiovascular System During Pregnancy

The Development of a new feto-placental Circulation system alongside the existing circulatory loops, combined with the progressive proliferation of the vascular network in the Mammary Glands and Uterus driven by Sex Hormones—alongside the arteriolar dilatory effect of progesterone and human chorionic gonadotropin, levels of which begin to rise from the 7th day of Pregnancy due to the excretory activity of the fetus and Placenta—results in an increased vascular capacity and a natural drop in total peripheral vascular resistance. This reduction is profound enough that it could potentially lead to a marked drop in Blood pressure. However, in early pregnancy, blood pressure tends to decrease only slightly (by 5-15 mm Hg), and after 28 weeks, it even gradually rises back to pre-pregnancy levels. This is due to hemodynamic changes aimed at intensifying Cardiac Activity and thereby maintaining perfusion pressure in various Organs (especially the uteroplacental circulation) at a level adequate for the body's growing needs as pregnancy progresses.

As a result of the relative underfilling of the Blood Vessels, universal compensatory mechanisms are triggered to match the circulating blood volume (BV) with the expanding vascular capacity (see Section 5.4.). The resulting hypervolemia increases venous return to The Heart and, in accordance with the Frank-Starling law, enhances myocardial contractility. Cardiac Output reliably increases by 30-40%, a value determined by heart rate, stroke volume, and total peripheral vascular resistance. These parameters undergo dynamic changes throughout the course of pregnancy.

In early pregnancy, the heart rate increases by 5-7 beats per minute and remains stable throughout the entire gestation period. It is this elevation in heart rate that drives the increase in cardiac output During the first trimester.

During the second trimester, cardiac output increases primarily due to a rise in stroke volume, supported by an intensive venous return to the heart (driven by expanded BV and reduced cardiac afterload resulting from a progressive drop in total peripheral resistance).

The rise in total peripheral vascular resistance observed in the third trimester leads to a slight decrease in stroke volume. Nevertheless, against the backdrop of an elevated heart rate, cardiac output remains increased. The combined dynamic shifts in total peripheral resistance and cardiac output characteristic of this stage bring the pregnant woman's blood pressure in the third trimester back to the levels seen in healthy non-pregnant women.

Consequently, throughout pregnancy, the heart operates under an increased workload, gradually adapting to these conditions. As a compensatory response, chamber dilation—particularly of the left ventricle—and myocardial fiber hypertrophy develop, which collectively enhance overall cardiac functional capacity.

In late pregnancy, positional changes occur due to the enlarged uterus and high standing of the Diaphragm. This causes the heart to shift into a horizontal position with an anterior tilt along its axis. The borders of the heart expand accordingly, and the apex beat shifts laterally. The kinking of the cardiac vessels may give rise to soft heart murmurs, predominantly systolic, most commonly auscultated at the apex and occasionally over the pulmonary artery. On the ECG, cardiac rotation manifests as a leftward shift of the electrical axis, a slight increase in the amplitude of the S wave in lead I, combined with T-wave inversion in lead III. These auscultatory and electrocardiographic changes are functional in nature, diminish with deep breathing, and completely disappear after childbirth.