Oxygen delivery (DO₂)—the amount of oxygen that is pumped from the left ventricle throughout the body via the arterial system—increases during pregnancy to meet increased demands. Specifically, DO₂ increases secondary to increased maternal cardiac output that occurs during normal pregnancy, labor, and delivery. Oxygen consumption (VO₂)—the amount of oxygen that is consumed by the body—is also increased during pregnancy to meet generalized demands, including those associated with growing fetal, placental, and maternal needs. Normal DO₂ and VO₂ prior to pregnancy, approximately 1,000 mL/minute and 250 mL/minute respectively, increase 20 to 40 percent during pregnancy. The increase in DO₂ over non-pregnant values supplies the growing fetus and placenta, which individually consume approximately 6.6 mL/kg/minute and 3.0 mL/kg/minute of O₂, respectively.⁴ A more thorough discussion of hemodynamic and oxygen transport concepts may be found in Chapter 4 of this text.

To accommodate the increase in maternal cardiac output in pregnancy, maternal uterine vascular beds dilate to maximum expansion, increasing perfusion and therefore gas exchange with the placenta. In fact, the internal lumen of the uterine artery doubles in size without thickening of the vessel wall.⁷ The expansion provides a dilated vasculature that accommodates larger volumes of blood and oxygen to the uterus and further to the placental membrane barrier. To fill the expanded vasculature, uteroplacental blood flow increases during pregnancy from a baseline volume of less than 50 mL/minute to 750 to 1000 mL/minute at term.⁷ It is important to note, however, that despite the increase in volume of blood flow, the uterine arteries lose auto-regulation capability during pregnancy, which may limit the maintenance of maternal blood pressure during periods of diminished flow. Since uterine blood flow is dependent upon uterine perfusion, the quantity of uterine blood flow dictates the quantity of oxygen delivered to the fetus.⁸ Normal maternal cardiac output and blood pressure are therefore vital for the maintenance of uterine perfusion, placental blood flow and fetal oxygenation. To maintain constant oxygen delivery during periods of decreased uterine perfusion pressures (e.g., post epidural anesthesia with vasodilation of maternal vasculature), the fetus is able to increase the oxygen extraction. However, the ability for a fetus to accomplish this feat assumes the fetus is at term, healthy, and that the uterine perfusion (maternal cardiac output) is at maximum volume prior to the decrease.⁸ When these conditions cannot be met in pregnancies of women with reduced cardiac output or decreased DO₂, the fetus is less likely to tolerate episodes of reduced blood flow and is at a greater risk for deterioration and compromise.

Once labor begins, maternal, fetal and placental demands for oxygen dramatically increase, not only from the physical “work” of labor but also from catecholamine release related to maternal pain, anxiety and other psychosocial factors. Maternal VO₂ increases approximately 86 percent (between 35 and 140 percent) during the course of labor compared to pre-labor values.⁴ In patients without anesthesia or analgesia, second-stage VO₂ may elevate 200 to 300 percent over third trimester values. Therefore, for patients with marginal oxygen delivery, the use of effective analgesia and anesthesia during labor and delivery is essential.

Labor is defined as progressive maternal cervical effacement and dilation associated with intermittent regular uterine contractions. The establishment of progressive cervical dilation from repetitive uterine contractions relies in part on the effectiveness of intermittent pressure transferred to the fetal presenting part that is applied to the maternal cervix. The uterine myometrium produces this pressure by coordinated shortening and relaxing of muscle fibers to thin the lower uterine segment and dilate the cervix. This synchronized “work” of the uterus is dependent upon multiple maternal and fetal physiologic factors, some of which are yet to be realized. Effective myometrial activity is dependent upon adequate calcium stores, functioning calcium channels, normal uterine perfusion pressures, normal pH balance, absence of metabolic acidosis, absence of over-stretched muscle fibers, adequate glycogen stores, the availability of oxygen to maintain aerobic metabolism, and similar physiologic steady states.^9,10 Additionally, the movement of calcium through channels may be further dependent on maternal lipid concentrations. An elevated concentration of serum lipids may be a factor in the increased incidence of dysfunctional labor reported in obese women.⁹

Each uterine contraction during labor expresses 300 to 500 mL of blood from the uterine vessels into the maternal systemic circulation.¹¹ This transient increase in blood volume slightly decreases the maternal heart
rate; increases mean arterial pressure, central venous pressure, pulmonary artery pressures, and left ventricular filling pressures; and increases cardiac output by approximately 20 to 30 percent.^12,13 These changes may significantly alter maternal cardiovascular profiles during contractions; thus, assessment and measurement of non-invasive and, if utilized, invasive hemodynamic and pulmonary parameters should be performed between contractions when the uterus is at rest.

Oxygen transport and maternal pH status have been shown to affect uterine activity associated with both spontaneous and induced labor. Acute hypoxemia and/or disruption of maternal oxygen transport below a critical threshold can lead to uterine contractions, progressive cervical dilation, and delivery of the fetus at any gestational age.¹¹ In contrast, chronic hypoxemia in some situations may work in an opposite manner to down-regulate precursors responsible for uterine contractions.⁹ This may help explain why a number of critically ill pregnant women continue their pregnancies for several days and/or weeks prior to the onset of labor, whereas other women exhibit uterine contractions around the time they become physiologically unstable. It is important to note that there are critical levels of maternal hypoxemia beyond which a pregnancy cannot be successfully maintained. The end result may include fetal death, spontaneous uterine expulsion of the pregnancy, or both.

Quenby and colleagues studied the effect of myometrial pH and lactate levels both in vitro and in vivo to determine their effects on uterine contractions.¹⁰ The researchers hypothesized that during a contraction the myometrium may become locally hypoxic from the loss of oxygenated vascular blood that is “squeezed” from the uterine vessels. Consequently, if the time between contractions does not permit re-establishment of vascular flow, the smooth muscle is unable to maintain aerobic metabolism; subsequently, pH values decrease and lactate levels increase. The group further found that when myometrial tissue had a low pH it was more likely to be associated with ineffective contractions compared to myometrium with a normal pH.¹⁰ From these observations, Quenby and colleagues speculated that dysfunctional labor in both critically ill and normal women may be the result of either inadequate uterine rest or tachysystole.¹⁰ It is also important to note from the same study that myometrial pH had an almost identical effect on spontaneous labor contractions versus induced labor contractions. Conditions common in patients with significant complications or critical illness that are known to negatively affect uterine activity are listed in Table 12-3.

Once a woman has been identified as a candidate for induction of labor, further analysis of her ability to tolerate labor should be considered and specific plans made for labor management, delivery, and postpartum care. The same extensive cardiopulmonary alterations of pregnancy, labor, and birth that normal pregnant women experience and generally tolerate without problems, may have deleterious effects on patients who have complications prior to the process. Patients who are at risk for oxygen transport deterioration will be maximally challenged during the second
stage of labor and immediately postpartum—two instances that produce the most dramatic changes in fluid shifts, intra-cardiac pressures, cardiac output, oxygen demand, and pulmonary capillary permeability. These normal changes of pregnancy make the critically ill parturient and her fetus more vulnerable to decreases in maternal cardiac output and oxygen delivery.¹⁴

Induction of labor to achieve a vaginal delivery is a goal for many pregnant women with significant complications or critical illness. Vaginal delivery requires less oxygen and metabolic demand when compared to Cesarean delivery and carries a lower risk for pulmonary embolism and surgical site infection. Additionally, more blood may be lost during Cesarean versus vaginal delivery, thereby decreasing the patient’s oxygen carrying capacity and increasing her risk for inadequate DO₂

Stay updated, free articles. Join our Telegram channel

Join