Influence of Body Position

Venous return is further compromised with changes in body position, particularly if the pregnant patient is supine. As a result, cardiac output can be diminished by as much as 25% to 30%. The effects of changes in body position are most obvious in the latter half of pregnancy when the fetal size and gravid uterus can effectively tamponade the vena cava. This phenomenon is exaggerated in women with poorly developed venous collaterals. With compression of the vena cava in the supine position, these women exhibit signs of severe hypoperfusion (hypotension and bradycardia), a phenomenon described as the supine hypotensive syndrome of pregnancy. Symptoms quickly resolve after the patient is repositioned to the left lateral recumbent position.⁴ Cardiac output can decrease by 30% to 40% in patients with this syndrome. This vasovagal phenomenon underscores the influence of maternal body position on the hemodynamic alterations occurring in pregnancy.

Hemodynamic changes associated with a decrease in preload and, subsequently, a reduced cardiac output are less pronounced when the gravid uterus is minimally compressing the vena cava. This is optimally achieved by maintaining the pregnant woman with more than 20 weeks gestation in the full left lateral position whenever she is recumbent. Alternatives to this position, less optimal than the left lateral position but preferable to the supine position, are a left lateral tilt to 15 degrees or manual displacement of the gravid uterus. The latter maneuver of left uterine displacement can be performed by manually moving the uterus away from the midline to the left side when the patient is supine. This maneuver is particularly useful when performing cardiac compressions in a pregnant patient. In the supine position, the gravid uterus, which accounts for as much as 10% of the cardiac output, hinders successful resuscitation because of its adverse effects on intrathoracic pressure and venous return. Although hemodynamics are optimized in the left lateral position, it is difficult to achieve optimal chest compressions with the patient tilted all the way into the left lateral decubitus position. Acceptable alternatives are to perform cardiac compressions with the patient supine but with concurrent manual displacement of the uterus to the other side; it is also satisfactory to place a wedge under the right hip of the patient.^5,6

Oxygen Consumption and Ventricular Performance

As cardiac output progressively increases, maternal oxygen consumption also increases. However, the increase in cardiac output is seen earlier than the rise in maternal oxygen consumption. Accordingly, the arteriovenous oxygen difference actually narrows early in pregnancy. The arteriovenous oxygen difference widens at the end of gestation. By term, there is a 20% increase in maternal oxygen consumption, mostly as a result of the increase in metabolic needs of the fetus. The increase in oxygen consumption is also a result of the increased work of ventilation during pregnancy, the increase in myocardial oxygen demand, and the increase in renal oxygen consumption. Oxygen extraction also gradually increases throughout gestation. The increase in cardiac output is probably the result of a combination of factors including increased uterine blood flow, increased maternal circulating blood volume (and hence ventricular preload), and possibly estrogen- and prolactin-induced augmentation of myocardial contractility. Ventricular dynamics are improved during pregnancy as a direct result of the action of steroid hormones on the pregnant myocardium. In animal models, estrogens have been shown to increase cardiac output and decrease peripheral vascular resistance.⁷ Echocardiographic studies performed in healthy pregnant women have demonstrated a decrease in the pre-ejection period of left ventricular systole but an increase in the left ventricular end-diastolic dimension.^8–10 It may be that a combination of improved myocardial contractility and increased ventricular diastolic area may be responsible for increases in cardiac output during normal pregnancy.¹¹

Hemodynamic Changes during Labor and Delivery

Although cardiac output remains relatively constant in the latter half of pregnancy, there is a significant increase during active labor and immediately after delivery. With each uterine contraction, cardiac output dramatically increases as an additional 300 to 500 mL of maternal blood volume from the uterus is returned to the heart. Cardiac output can rise to 50% greater than normal when the pregnant woman is pushing in the second stage of labor. The amount of blood returned to the heart is accentuated in the supine position. When the pregnant patient is supine, uterine contractions can cause a 25% increase in cardiac output, a 15% decrease in maternal heart rate, and a 30% to 35% increase in stroke volume. In the lateral recumbent position, the hemodynamic changes associated with uterine contractions are less pronounced; cardiac output and stroke volume may rise by only 6% to 7%, and there may be only a small change in maternal heart rate. Cardiac output may be preferentially diverted to the heart if there is partial obstruction of the abdominal aorta by the uterus during contraction.

The hemodynamic changes seen during labor and delivery are influenced by anesthetic and analgesic techniques. The increase in cardiac output is less if caudal anesthesia is used.^12,13 Within the first 20 to 30 minutes after delivery of the fetus and placenta, there is an even greater increase in cardiac output, because blood is no longer diverted to the uteroplacental vascular bed. Approximately 500 mL is redirected to the maternal circulation in the so-called autotransfusion effect of pregnancy. This effect can cause cardiac output to increase by 60% to 80% after aortocaval compression is removed and blood volume is increased. Most of the physiologic changes of pregnancy resolve and revert to normal within several days after delivery. Cardiac output returns to normal within 2 weeks to 3 months after delivery as sodium and water balances normalize.

Blood Volume Changes

The changes in maternal blood volume during pregnancy are dramatic. Plasma volume increases by 30% to 50% by the end of gestation. This value is increased in the multigravida patient compared with primigravidas, but the exact mechanism responsible for this effect is unclear. The increase in blood volume can be as high as 70% with twin pregnancies. An increase of 10% to 15% in blood volume is seen as early as the seventh week of gestation. Blood volume is maximal at 30 to 34 weeks, after which the value plateaus until term.¹⁴ Ventricular filling pressures do not increase despite the large increases in plasma volume.¹⁵ This is most likely the result of concurrent decreases in systemic and pulmonary vascular resistance.

The increase in blood volume is a striking adaptive mechanism that permits additional blood flow to the uterus and other maternal organs, in particular the kidneys. Uterine blood flow increases to 100 mL/min by the end of the first trimester and reaches 1200 mL/min at term. Both sodium and water retention contribute to the increase in plasma volume. Total body water increases by approximately 6.5 to 8 L. Most of this increase is seen in the extracellular space and is preferentially distributed in the lower extremities. The total increase in body water includes approximately 3.5 L of amniotic fluid, placental fluid, and water in the fetus. The maternal blood volume increases by 1 to 2 L. Red blood cell (RBC) mass accounts for only 300 to 400 mL of the increase in total blood volume.

Plasma renin and aldosterone levels are elevated during pregnancy despite expansion of the maternal blood volume. Activation of the renin-angiotensin-aldosterone system may result from the concomitant decrease in peripheral vascular resistance and the increase in vascular capacitance seen as early as the first 6 weeks of pregnancy.² Both estrogens and progesterone increase aldosterone levels, increasing sodium and water retention.¹⁶ At 12 weeks of gestation, atrial natriuretic peptide levels also increase, most likely in response to the increase in plasma volume.

The increase in blood volume is an adaptive mechanism that provides some level of protection for the inevitable blood loss that accompanies delivery of the fetus and placenta. Average blood loss during vaginal delivery is 500 mL; average blood loss during cesarean delivery is approximately 1000 mL. Although providing some degree of protection from peripartum blood loss, the increased plasma volume associated with pregnancy also can lull the clinician into a false sense of security. A pregnant woman can lose up to 35% of her blood volume before the usual signs of hypovolemia and acute hemorrhage are obvious. Although the pregnant woman may appear to have stable vital signs up to this point, the fetus may be severely compromised and deprived of adequate maternal blood flow. Tachycardia, hypotension, and other signs of hemodynamic instability are late manifestations of a significant deficit in maternal blood volume.

Physiologic Anemia of Pregnancy

Accompanying the increase in blood volume is an increase in RBC mass stimulated by increased circulating levels of erythropoietin. The RBC mass increases during the second trimester and continues to increase progressively throughout the pregnancy. However, the increase of 15% to 20% in RBC mass is disproportionate to the 30% to 50% increase in blood volume. As a result, the hematocrit decreases, resulting in the “physiologic hemodilutional anemia” of pregnancy. Hemodilution is most notable during the 30th to 34th gestational weeks. The hemoglobin concentration can decrease by as much as 9%. In the second trimester, the hemoglobin level can decrease to 11 to 12 g/100 mL, compared with the normal nonpregnant value of 13 to 14 g/100 mL. The decrease in blood viscosity associated with the anemia of pregnancy allows for decreased resistance to blood flow and facilitates placental perfusion. The hematocrit decreases until the end of the second trimester but increases later in the pregnancy, when the increase in RBC mass is proportionate to the increase in plasma volume. The hematocrit stabilizes at that point or even increases slightly as term approaches.

The degree of change in RBC mass during pregnancy depends in part on whether iron is supplemented. With the increase in RBC mass, there is a need for additional iron to prevent the development of iron-deficiency anemia. Maternal requirements for iron can increase to 5 to 6 mg/d. The fetus uses iron from maternal stores to prevent fetal anemia, but the presence of significant maternal iron-deficiency anemia has been shown to result in a higher incidence of fetal complications, including preterm labor and late spontaneous abortions.¹⁷

Renal Blood Flow During Pregnancy

Under the influence of circulating hormones, there is a preferential redistribution of blood flow to the uterus, breast, and kidneys during pregnancy. Each kidney increases in length and weight, and the renal pelvis and ureters dilate. The glomerular filtration rate (GFR) increases by 50%, and renal blood flow increases by 25% to 50%. Changes in GFR and renal blood flow occur by the sixth week of gestation. The increase in renal blood flow plateaus early in pregnancy and remains unchanged or decreases slightly as term is approached. Urine flow and sodium excretion are increased and are influenced by position, especially in late pregnancy. Flow rates and the sodium excretion rate are significantly higher in the lateral recumbent position compared with the supine position. Concentrations of serum creatinine and blood urea nitrogen are reduced proportionately to the increase in GFR. Glycosuria may also occur during pregnancy as a result of the increase in GFR and impaired tubular reabsorption of glucose.

Changes in Blood Pressure and Vascular System

Arterial blood pressure decreases as early as the sixth week of pregnancy; the lowest diastolic pressures are recorded during the second trimester. By the eighth week of gestation, diastolic blood pressure decreases by approximately by 10%. Diastolic pressure reaches a nadir at 16 to 24 weeks and is typically 5 to 10 mm Hg less than normal. After the 16th gestational week, blood pressure progressively increases and is back to baseline by term. With the increase in venous return associated with uterine contractions and the additional factors of pain, anxiety, and stress during labor and delivery, an increase in blood pressure usually occurs during this time. The decrease in blood pressure during pregnancy is associated with a significant decrease in peripheral vascular resistance. The decrease in arteriolar tone is influenced by several factors, including hormonal changes that induce vasodilatation and lack of responsiveness to the pressor effect of angiotensin II.¹⁸ There is evidence for blood vessel remodeling in pregnancy, leading to increased venous compliance.^19,20 During pregnancy, circulating levels of numerous endogenous procoagulant and anticoagulant proteins change, leading to a hypercoagulable state. As a consequence, the risk of venous thrombosis increases during pregnancy. The reported incidence is 0.7 cases per 1000 women, and this rate increases threefold to fourfold in the postpartum period.²¹

The treatment of choice for severe hypotension resulting from acute hemorrhage, sepsis, or other critical illness during pregnancy is (ideally) aggressive fluid resuscitation. However, in cases of fluid-unresponsive hypotension, vasopressors must be used to prevent detrimental consequences to both the mother and fetus as a result of inadequate uterine blood flow secondary to hypotension. Most vasopressors increase maternal blood pressure at the expense of fetal blood flow, inducing vasoconstriction of the uterine vessels. There are few human studies of these agents in pregnant women. However, animal studies animals indicate that ephedrine and dopamine increase uterine blood flow to the uteroplacental circulation while at the same time increasing maternal blood pressure.²²