2 What hematologic changes accompany pregnancy?

Table 59-2 summarizes the hematologic changes of pregnancy. Plasma volume increases from 40 to 70 ml/kg near term, and blood volume increases by 1000 to 1500 ml. The relative anemia of pregnancy is caused by a relatively slower rise in red blood cell mass compared to plasma volume. Maternal anemia, usually the result of iron deficiency, occurs when the hemoglobin falls below 10 g or the hematocrit is <30%.

TABLE 59-2 Hematologic Changes of Pregnancy

PTT, Partial thromboplastin time; PT, prothrombin time.

Pregnancy is associated with an increase in platelet activation and consumption and most coagulation factors. Because of this, parturients are hypercoagulable and at risk for thrombotic events (such as deep vein thrombosis and pulmonary embolism). The increase in platelet consumption is compensated for by an increase in platelet production; therefore, the platelet count is usually normal. Thrombocytopenia can occur in 0.9% of normal patients, although it is often associated with preeclampsia or hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. The prothrombin time and partial thromboplastin times are shortened.

3 What pulmonary and respiratory changes occur with pregnancy?

Table 59-3 summarizes the respiratory changes of pregnancy. Pregnancy leads to capillary engorgement and edema of the respiratory tract. The mucosa also becomes friable, which may lead to bleeding with manipulation or trauma. These changes in the airway and the enlarged breasts of the pregnant patient make laryngoscopy difficult. Adding to the problem, the increased oxygen consumption and decreased functional residual capacity (FRC) make the laboring patient more prone to hypoxia and rapid desaturation during apneic periods.

TABLE 59-3 Respiratory Changes at Term in Pregnancy

FEV₁, Forced expiratory volume in 1 second.

4 What is a normal arterial blood gas in a pregnant patient?

See Table 59-4.

5 What gastrointestinal changes occur during pregnancy?

The upward displacement of the stomach by the expanding uterus shifts the gastroesophageal junction. This decreases the tone of the lower esophageal sphincter and predisposes the pregnant patient to reflux. The gravid uterus also increases intragastric pressure. These in combination make the parturient prone to regurgitation and aspiration. Gastric motility and emptying time can be prolonged, and the pregnant patient is always considered to have a full stomach. Standard preoperative aspiration prophylaxis includes metoclopramide, an H₂-blocker, and a nonparticulate antacid.

6 What renal changes are associated with pregnancy?

Renal plasma flow, glomerular filtration rate, and creatinine clearance increase by the fourth month of gestation. Blood urea nitrogen (BUN) and creatinine are decreased; normal values in pregnancy are 6 to 9 and 0.4 to 0.6 mg/dl, respectively. Glucosuria up to 10 g/dl and proteinuria up to 300 mg/dl are not abnormal. Anatomically the renal calyces, pelves, and ureters dilate beginning around 12 weeks’ gestation. Urinary stasis contributes to the frequency of urinary tract infections seen in pregnancy.

7 What changes occur in the central nervous system of pregnant patients?

Progesterone in both the plasma and cerebrospinal fluid increases tenfold to twentyfold in late pregnancy. Progesterone is sedating and potentiates the effects of volatile anesthetics. Pregnant patients are also more sensitive to local anesthetics.

8 What hepatic alterations occur with pregnancy?

Liver size, blood flow, and liver morphology do not change during pregnancy. Lactate dehydrogenase, serum bilirubin, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase (of placental origin) increase with pregnancy. Gallbladder emptying is slowed during pregnancy, and the bile tends to be concentrated, predisposing the pregnant patient to gallstone formation.

9 What pregnancy-related changes occur to plasma proteins?

Plasma albumin concentrations decrease during pregnancy. Free fractions of protein-bound drugs increase with decreasing albumin levels. Total protein levels also decrease, as does maternal colloid osmotic pressure (by approximately 5 mm Hg). Plasma cholinesterase concentrations decrease by about 25% before delivery and 33% by day 3 after delivery but are probably not clinically significant.

10 What is the uterine blood flow at term?

Uterine blood flow is approximately 50 to 190 ml/min before pregnancy and reaches approximately 10% of maternal cardiac output (600 to 700 ml/min) at term. This places the pregnant patient at particular risk for hemorrhage in cases of uterine rupture, uterine atony, placenta previa, or placental abruption.

11 What is aortocaval compression syndrome? How is it treated?

Aortocaval compression is caused by the gravid uterus compressing the inferior vena cava and the aorta and manifests principally as hypotension and tachycardia. Aortic compression may lead to decreases in uterine and placental blood flow, resulting in nonreassuring fetal heart rate (FHR) changes. Aortocaval compression is prevented by uterine displacement (lateral position or a wedge under the right hip) to increase venous return. Symptoms may be treated with intravenous fluid administration, supplemental oxygen, and the use of appropriate vasopressor.

12 What are the most important physiologic changes during labor?

During active labor cardiac output increases by 40% above prelabor values. Immediately after delivery cardiac output sharply increases, reaching 75% of prelabor values. This is mainly caused by autotransfusion during uterine contractions, particularly after delivery of the placenta. Hyperventilation is common during active labor and may contribute to the preexisting respiratory alkalosis leading to uterine vasoconstriction and decreased placental perfusion, hypoxemia, and fetal distress. Regional anesthesia has been shown to decrease circulating maternal catecholamine levels and may attenuate the hemodynamic changes, hyperventilation, and stress response associated with active labor.

13 How quickly do the physiologic alterations of pregnancy return to normal after delivery?

Cardiac output rises immediately after delivery because of autotransfusion of 500 to 750 ml of blood from the uterus. Patients with pulmonary hypertension and stenotic valvular lesions are at a particular risk at this time. Cardiac output returns to slightly above prepregnancy values about 2 to 4 weeks after delivery.

FRC and residual volume rapidly return to normal. Many of the pulmonary changes caused by mechanical compression by the gravid uterus resolve quickly. Alveolar ventilation returns to baseline by 4 weeks postpartum, and there is a rise in maternal PCO₂ as the progesterone levels decrease.

The dilutional anemia of pregnancy resolves, and the hematocrit returns to normal within 4 weeks secondary to a postpartum diuresis.

Serum creatinine, glomerular filtration rate, and BUN return to normal levels in less than 3 weeks.

Mechanical effects of the gravid uterus on the gastrointestinal system resolve about 2 to 3 days after delivery; however, gastric emptying may be delayed for several weeks as serum progesterone levels slowly decrease.

14 Discuss the pathways involved in labor pain

Pain during the first stage of labor is caused by uterine contractions and cervical dilation. This visceral pain is transmitted via sympathetic fibers entering the dorsal horn of the spinal cord at T10–L1. As labor progresses and the fetal head descends into the pelvis and during stage 2, pain is transmitted from the pelvic floor, lower vagina, and perineum via the pudendal nerve, entering the spinal cord at S2–S4.

15 What are the three stages of labor?

Stage 1. Cervical dilation and effacement. It begins with the onset of regular, painful contractions and ends when dilation of the cervix is complete (or 10 cm). The latent phase is characterized by slow cervical dilation and effacement. The active phase is defined as the period of progressive cervical dilation, which usually begins around 4 to 5 cm.

Stage 2. The second stage ends with delivery of the neonate.

Stage 3. The third stage ends with delivery of the placenta.

16 Describe the anatomy of the placenta and umbilical cord

The maternal side of the placenta is made up of a basal plate. Within the basal plate are spiral arteries, which are divisions from the uterine arteries, and veins. The fetal side is the chorionic plate, made up of villi surrounded by chorion. The space where these two surfaces meet is the intervillous space. The villi contain divisions from two umbilical arteries, which carry blood to the placenta, and divisions from the single umbilical vein, which carries the nutrient-rich blood back to the fetal circulation.

17 What factors influence uteroplacental perfusion?

Aortocaval compression: When lying supine, the gravid uterus compresses the abdominal aorta, decreasing uteroplacental perfusion (UPP).

Hypotension: A fall in maternal mean arterial pressure >25 mm Hg decreases uterine blood flow.

Increased uterine vascular resistance: Increases in uterine vascular resistance occur during contractions and parturition. Other causes include intravenous ketamine (>1.5 mg/kg), oxytocin administration, and conditions such as preeclampsia and abruptio placentae.

Maternal hypoxia, hypercarbia, and hypocarbia: These are associated with decreased UPP.

Catecholamines: Increased maternal catecholamine levels (e.g., laboring patients) decrease UPP.

18 How should hypotension associated with spinal anesthesia be treated in a cesarean section or laboring patient?

Historically ephedrine had been the preferred agent for treating hypotension associated with regional anesthesia during pregnancy because it was thought that other agents decreased uteroplacental blood flow, whereas ephedrine did not. Recent studies show that doses of ephedrine large enough to maintain homeostasis after induction of spinal anesthesia may be detrimental to the fetus. Problems observed with ephedrine are related to the β-agonist activity that causes increased fetal metabolism and include dose-dependent fetal metabolic acidosis, tachycardia, and abnormal FHR variability. Phenylephrine, a pure α-agonist, is as effective as ephedrine in restoring and maintaining maternal blood pressure. Phenylephrine does not appear to cause fetal acidosis even in large doses. However, it is important to note that all of these studies were done in healthy parturients at term undergoing cesarean section. It is reasonable to infer that ephedrine would cause similar metabolic derangements in laboring patients and those with high-risk pregnancies. The routine use of prophylactic ephedrine to prevent any adverse effects of maternal hypotension following spinal anesthesia for cesarean delivery is also not supported by systematic reviews of the literature.

19 What is the role of intravenous fluid preloading before regional anesthesia for cesarean delivery?

Intravenous crystalloid or colloid preload may prevent hypotension associated with neuraxial anesthesia for cesarean delivery. However, under urgent circumstances block placement should not be delayed to administer a preset volume of fluid.

20 How are drugs and other substances transported across the placenta?

Placental transfer is accomplished by simple diffusion, active transport, bulk flow, facilitated diffusion, and breaks in the chorionic membrane. Anesthetic compounds cross the placenta mostly by simple diffusion. Compounds that are low in molecular weight, small in spatial configuration, poorly ionized, and lipid soluble have high rates of placental transfer. Most anesthetic drugs are highly lipid soluble and have molecular weights <600, and for this reason their rates of placental transfer are high.

21 What methods are used to evaluate fetal well-being during labor?

Measurement of FHR and uterine activity is important. The baseline (FHR) is measured between contractions and is normally 110 to 160 beats/min. Fetal tachycardia (>160) may indicate fever, hypoxia, use of β-sympathomimetic agents, maternal hyperthyroidism, or fetal hypovolemia. Fetal bradycardia (<110) may be caused by hypoxia, complete heart block, β-blockers, local anesthetics, or hypothermia. The beat-to-beat variability is thought to represent an intact neurologic pathway in the fetus. Increased variability is seen with uterine contractions and maternal activity. Decreased variability can be seen with central nervous system depression, hypoxia, acidosis, sleep, narcotic use, vagal blockade, and magnesium therapy for preeclampsia. Absence of beat-to-beat variability, especially in the presence of FHR decelerations or bradycardia, is a particular concern for fetal acidosis.

22 What is the significance of fetal heart rate decelerations?

Early decelerations in FHR are caused by head compressions (vagal stimulation), are uniform in shape, begin near the onset of a uterine contraction with its nadir at the same time as the peak of the contraction, and are benign.

Variable decelerations are caused by umbilical cord compression and are nonuniform in shape. They are abrupt in onset and cessation. The decrease is >15 beats/min. They last longer than 15 seconds but less than 2 minutes. Although they usually do not reflect fetal acidosis, repetitive variable decelerations can lead to fetal hypoxia and acidosis.

Late decelerations are caused by uteroplacental insufficiency. They are uniform in shape. The onset and return to baseline are gradual. They often begin just after the onset of a contraction, with their nadir and recovery after the peak and recovery of the contraction. These decelerations are associated with maternal hypotension, hypertension, diabetes, preeclampsia, or intrauterine growth retardation. These are ominous patterns and indicate that the fetus is unable to maintain normal oxygenation and pH in the face of decreased blood flow.

The treatment for nonreassuring neonatal heart rate changes involves administering oxygen to the mother, maintaining maternal blood pressure, and placing the parturient in the left uterine displacement position (Figure 59-1).

Figure 59-1 Early, variable, and late fetal heart rate (FHR) deceleration during labor.

23 What is the Apgar score?

The Apgar score is the most widely accepted and used system to evaluate the neonate, determine which neonates need resuscitation, and measure the success of resuscitation (Table 59-5). The score evaluates heart rate, respiratory effort, muscle tone, reflex irritability, and color, with heart rate and respiratory effort being the most important criteria. Each variable is given a score of 0 to 2, for a total score of 10. The Apgar score is measured at 1 and 5 minutes and then at 10 and 20 minutes as resuscitative efforts are continued. A score of 0 to 3 indicates a severely depressed neonate, whereas a score of 7 to 10 is considered normal.

24 Describe the management of the pregnant patient undergoing nonobstetric surgery

Nonemergent surgery should be avoided to protect the developing fetus. If a procedure must be done, the second trimester is the safest time, avoiding organogenesis and minimizing the risk of preterm labor. Surgery during pregnancy increases perinatal mortality, and manipulation of the uterus should be minimized to decrease the risk of premature labor. The most common surgical condition during pregnancy is appendicitis, followed by torsion, rupture, or hemorrhage of ovarian cysts and cholecystectomy.

There is no evidence that any drug or technique is preferred over another as long as maternal oxygenation and perfusion are maintained. Nitrous oxide has been associated with deoxyribonucleic acid synthesis inhibition and probably should be avoided in the first trimester. If general anesthesia is chosen, the patient should receive an antacid regimen before rapid-sequence intubation with cricoid pressure. Use uterine displacement to avoid aortocaval compression. Treat hypotension with fluids and an appropriate vasopressor; an oxygen concentration of 100% is advisable to increase fetal oxygenation. When considering regional anesthesia, keep in mind the patient’s altered responsiveness to local anesthetics. Fetal heart tones should be obtained before and after any procedure. Intraoperative FHR monitoring is rarely used before 26 weeks’ gestation. The decision to use intraoperative FHR monitoring depends on maternal and fetal status, the procedure being performed, and the obstetric plan to act on abnormalities that occur. Since patients may be administered opioids, labor may not be recognized. After surgery the patient should be monitored for early onset of labor and tocolysis instituted in its presence.