Over the course of a normal pregnancy, profound hemodynamic changes occur (). Chief among these changes are increases in blood volume, cardiac output, left ventricular (LV) stroke work, and oxygen consumption. While these changes are well documented, their specific causes are incompletely understood.
Qualitative representation of the hemodynamic changes during pregnancy by week of gestation. Vol, plasma volume; HR, heart rate; SV, stroke volume.
A. First and second trimester
A reduction in peripheral vascular resistance and an increase in plasma volume are seen as early as six weeks of gestation and are associated with activation of the renin-angiotensin-aldosterone system and a mild reduction of plasma atrial natriuretic peptide (ANP) concentration (4
). This fall in vascular resistance is augmented after full placentation, when low placental vascular resistance allows for high uterine blood flow (5
). The blood volume continues to rise over the course of the first two trimesters and reaches a plateau of 140–150% of the pre-pregnancy level at approximately 32 weeks of gestation. Concomitant with this increase in plasma volume and fall in vascular resistance, the cardiac output increases steadily until approximately 25 weeks of gestation. During the earlier stages of pregnancy, this increase is mediated primarily by an increase in the stroke volume. During later stages, an increase in heart rate is primarily responsible for the increase in cardiac output. Systolic and diastolic arterial pressures both fall, but there is a larger proportional fall in the diastolic pressure and consequently an increase in pulse pressure.
B. Third trimester and term
As noted above, the stroke volume rises until approximately 25 weeks and the blood volume reaches a plateau at approximately 32 weeks. The third trimester of pregnancy is characterized by a rapid growth in the size of the fetus, and enlargement of the uterus frequently results in hemodynamically significant compression of the inferior vena cava and a resultant drop in venous return to the heart and in cardiac output. This typically occurs when the patient is in the supine position, and rolling the patient from the supine to the left lateral position has been shown to result in an increase of 25–30% in the stroke volume and cardiac output (5
C. Labor and peripartum
During active labor, further hemodynamic changes occur. The cardiac output typically increases by an additional 50%. Each uterine contraction forces an additional 300–500 ml of venous blood back into the central venous system. In addition, during the second stage of labor, blood pressure and heart rate can increase markedly with pain while Valsalva maneuvers during active labor can result in large fluctuations in central venous pressure. These latter changes can be attenuated by the use of neuraxial blockade and through the use of vacuum- or forceps-assisted vaginal delivery (7
). While caesarian delivery can eliminate the hemodynamic stresses during active labor and can afford control over the timing of delivery, it is often associated with greater blood loss, and consequently greater fluid shifts, than is vaginal delivery. As such, with few exceptions, the recommendation for caesarian delivery is made on obstetric, rather than cardiologic considerations. Immediately after delivery of the placenta, splanchnic vasoconstriction occurs, and approximately 500 ml of blood is diverted from the uteroplacental bed back into the maternal circulation. This “autotransfusion” phenomenon, in conjunction with the release of caval compression, increases central venous pressures, ventricular preload and cardiac output and may offset the effect of peripartum blood loss.
Starting at approximately 48 hours after delivery, a diuresis and natriuresis occur, and the blood volume, peripheral vascular resistance, and cardiac output return to their pre-pregnancy levels over the course of four to 12 weeks (9