Chapter 30 Obstetrics
Physiologic changes in pregnant women
1. How do the maternal intravascular fluid, plasma, and erythrocyte volumes change during pregnancy?
2. How does the coagulation status change during pregnancy?
3. What is the average maternal blood loss during the vaginal delivery of a newborn? What is the average maternal blood loss during cesarean delivery?
4. How does the maternal cardiac output change from nonpregnant levels?
5. In an uncomplicated pregnancy, what changes occur in blood pressure, systemic vascular resistance, and central venous pressure?
6. What is the supine hypotension syndrome? What symptoms accompany the syndrome?
7. What compensatory mechanisms do most women have that prevents them from experiencing supine hypotension syndrome and how can maternal hypotension be minimized?
8. What are some aspects of the upper airway that undergo physiologic change in pregnancy? What are the clinical implications of these changes?
9. How is minute ventilation changed during pregnancy from nonpregnant levels? How does the resting maternal PaCO2 change as a result of the change in minute ventilation?
10. How do the binding characteristics of hemoglobin change during pregnancy?
11. What are the changes in maternal lung volumes that occur with pregnancy? What are the anesthetic implications of these changes?
12. How does maternal PaO2 change during pregnancy?
13. What are the gastrointestinal changes in pregnancy that render the woman vulnerable to regurgitation of gastric contents? What clinical implication does this have?
14. How do the epidural and subarachnoid spaces change in pregnancy? How is the sensitivity to local anesthetics different in the pregnant versus nonpregnant patient? How are the dosing requirements for neuraxial anesthesia affected by these changes?
15. How do renal blood flow and glomerular filtration rate change in pregnancy? At what gestational month of pregnancy is this change at a maximum? How does this affect the normal upper limits of creatinine and blood urea nitrogen in pregnant patients?
16. Does hepatic blood flow change during pregnancy? How are plasma protein concentrations and plasma cholinesterase activity altered by pregnancy?
Physiology of uteroplacental circulation
17. How are maternal and fetal blood delivered to the placenta?
18. What is uterine blood flow (UBF) at term?
19. What are the determinants of UBF?
20. What factors affect the transfer of oxygen between the mother and fetus?
21. What factors affect placental exchange of drugs and other substances? What is the most reliable way to minimize fetal transfer of a drug?
22. What common drugs used in anesthesia have limited ability to cross the placenta? Which readily cross the placenta?
Anatomy of labor pain
27. In the first stage of labor, describe the associated sensory levels and where the end organ afferent nerve impulses are initiated.
28. In the second stage of labor, describe the associated sensory levels and where the end organ afferent nerve impulses are initiated.
29. For each stage of labor, describe which analgesic techniques benefit the pregnant woman and why.
Methods of labor analgesia
Nonpharmacologic Techniques and Systemic Medications
30. Describe the different nonpharmacologic techniques used for labor and the efficacy of each.
31. List the different systemic medications used for labor analgesia and their active metabolites, if any.
33. How is remifentanil used as a labor analgesic and what are the indications for its use?
34. Are benzodiazepines used in pregnancy and if so, when?
35. When is ketamine used in labor and delivery and what additional benefits does it provide for pain control?
Neuraxial Analgesia and Neuraxial Techniques
36. List the different types of neuraxial analgesia?
37. When would you use each type of neuraxial analgesia for labor pain?
38. Should laboring women remain “nothing per oral (NPO)” after placement of an epidural or combined spinal and epidural (CSE)?
39. What is a walking epidural and what are the associated risks?
40. What drugs are used or being evaluated as adjuvant neuraxial drugs for labor analgesia?
41. Name the tissue layers and ligaments encountered when placing an epidural and in what order the anesthesiologist encounters each.
42. The American Society of Anesthesiologists (ASA) recommendations regarding aseptic technique for placement of neuraxial block include what specific precautions?
43. What are the interspaces where the neuraxial block for labor analgesia is placed and what are the risks of placing the neuraxial block higher or lower than this range of interspaces?
44. What is a “test dose” and what does it assess?
45. Can a test dose be used with a CSE?
46. What type of needle is used in placement of spinal analgesia and why?
47. What is a “saddle block” and when is it used during labor and delivery?
Contraindications and complications of neuraxial anesthesia
48. What are the contraindications to neuraxial procedures?
49. Is known infection with human immunodeficiency virus (HIV) a contraindication to epidural placement?
50. List the potential complications of a neuraxial block.
51. What is the occurrence rate of postdural puncture headache (PDPH)? What are the treatment options for PDPH?
52. What is the treatment for systemic local anesthetic toxicity of bupivacaine?
53. What physiologic effects do you expect to see with a high spinal or high epidural?
54. What are the important differences in performing advanced cardiac life support (ACLS) for a pregnant woman compared to a nonpregnant patient?
55. What is the rate of hypotension after neuraxial blockade?
56. What is the first-line pharmacologic treatment of hypotension after a neuraxial block?
57. How does epidural analgesia affect maternal body temperature?
Anesthesia for cesarean delivery
61. What are some benefits of regional anesthesia over general anesthesia for cesarean delivery?
62. What are the benefits of general anesthesia over regional anesthesia for cesarean delivery?
63. What are some advantages and disadvantages of spinal anesthesia for cesarean delivery compared to an epidural block?
64. What dermatome level of spinal anesthesia ensures patient comfort adequate for cesarean delivery? How can this be achieved?
65. What are some advantages and disadvantages of epidural anesthesia for cesarean delivery compared to spinal anesthesia?
66. Which local anesthetics, and corresponding doses, are typically administered to achieve an adequate density and dermatomal level of epidural anesthesia for cesarean delivery?
67. What is the advantage of the administration of morphine into the epidural space for cesarean delivery? What are some of the negative side effects that may accompany this route of morphine administration?
68. What are some indications for general anesthesia for cesarean delivery? What are some benefits of general anesthesia for cesarean delivery?
69. What are the main causes of increased morbidity and mortality associated with general anesthesia during pregnancy?
70. How should difficulty with endotracheal intubation be managed by the anesthesiologist?
71. What is the level of exposure of the fetus to thiopental after the administration of induction doses for general anesthesia? Is there an advantage to using propofol for the induction of general anesthesia?
72. What are some of the advantages and disadvantages of inducing general anesthesia for cesarean delivery with etomidate?
73. What are the effects of using volatile anesthetics for cesarean delivery on the fetus?
74. What neuromuscular agents are typically used for cesarean delivery with general anesthesia? Do they result in neuromuscular blockade of the fetus or relaxation of the uterus?
Abnormal presentations and multiple births
75. What percent of live births are twins and why is the number increasing? What are the complications that develop with multiple gestations?
76. What are the modes of delivery for twin pregnancies? What anesthetic techniques can be used to optimize delivery?
77. Describe external cephalic version and the associated risks.
78. What is a shoulder dystocia? What are the risk factors associated with the development of a shoulder dystocia? What are the risks to the fetus during a shoulder dystocia?
Hypertensive disorders of pregnancy
79. At what gestational age does gestational hypertension present?
80. What is the percent of preeclampsia in the general population? What are the risk factors for developing preeclampsia?
81. What are the criteria for the diagnosis of preeclampsia?
82. What are the criteria for severe preeclampsia?
84. What is the mechanism of preeclampsia?
85. How should patients with preeclampsia be managed for labor? What is the definitive treatment of preeclampsia?
86. How is magnesium sulfate infusion used and why? What are the signs of and treatment of magnesium sulfate toxicity?
87. What are the typical antihypertensive drugs used in preeclampsia?
Hemorrhage in pregnant women
88. What are some causes of hemorrhage in the pregnant patient? When do these typically manifest?
89. What is placenta previa? What are the associated risk factors?
90. If a massive postpartum hemorrhage is not controlled with standard measures (i.e., uterine massage, uterotonics), what invasive options can be considered by the obstetrician?
91. What is abruptio placentae? What are some risk factors for abruptio placentae?
92. What are some risk factors for uterine rupture? What is the incidence of uterine rupture associated with vaginal birth after a previous cesarean delivery?
93. What approximate percent of vaginal deliveries are associated with some amount of retained placenta? What are some options for the anesthetic management of patients with retained placenta?
94. What are some risk factors for uterine atony?
95. What medications are used to manage uterine atony? What are their side effects?
96. Define placenta accreta, increta, and percreta.
97. In a patient with known placenta previa, how does the risk of placenta accreta change with the number of prior cesarean deliveries?
Anesthesia for nonobstetric surgery during pregnancy
100. What are common nonobstetric surgeries that occur during pregnancy?
101. When should nonobstetric surgeries be performed during pregnancy?
102. What anesthetics are teratogenic?
103. How can intrauterine fetal hypoxia and acidosis be prevented?
104. When should fetal heart rate monitoring be done during nonobstetric surgery?
105. What is the usual etiology of premature labor that presents in the pregnant patient after having undergone nonobstetric surgery? How can premature labor be treated?
106. Can laparoscopic surgery be performed safely during the third trimester?
Diagnosis and management of fetal distress
107. Describe the frequency of normal uterine contractions and tachysystole. What is the treatment for tachysystole?
108. What is the normal baseline fetal heart rate (FHR)?
109. Define FHR variability in terms of absent, minimal, moderate, and marked.
110. What is the definition of a FHR acceleration?
111. What are late decelerations indicative of in the fetus?
112. What is a variable deceleration indicative of in the fetus?
113. What was fetal heart rate monitoring designed to assess?
Evaluation of the neonate and neonatal resuscitation
114. Define the values of each Apgar score category.
115. What are normal blood gas values for the umbilical artery and vein?
116. During neonatal evaluation and resuscitation, when is it appropriate to give positive pressure ventilation?
117. What is the dose of epinephrine given for neonatal resuscitation?
118. Should naloxone be given in the delivery room for neonatal resuscitation?
119. In neonates delivered with meconium-stained amniotic fluid, when should suctioning below the cords be instituted?
120. What have been significant advances in the prevention of meconium aspiration syndrome?
Answers*
Physiologic changes in pregnant women
1. During pregnancy the maternal intravascular fluid volume increases from its prepregnancy volume. The increase in intravascular volume begins in the first trimester of pregnancy. By term, the intravascular fluid volume has increased by about 35% above the prepregnancy state. The plasma volume increases by approximately 45% at term. The erythrocyte volume in the pregnant patient increases by approximately 20%. Because the plasma volume increases by over twice as much as the erythrocyte volume, the woman has a relative physiologic anemia. That is, the hematocrit of the pregnant patient is relatively less than her prepregnancy state. This is termed the physiologic anemia of pregnancy. (515, Table 33-1)
2. The pregnant woman at term is in a hypercoagulable state secondary to increases in factors I, VII, VIII, IX, X, and XII, and decreases in factors XI, XIII, and Antithrombin III. This results in an approximately 20% decrease in prothrombin time (PT) and partial thromboplastin time (PTT). Platelet count may remain normal or decrease 10% by term. (515)
3. The average maternal blood loss during vaginal delivery of a newborn is 300 to 500 mL. The average maternal blood loss during the delivery of a newborn by cesarean delivery is 800 to 1000 mL, but blood loss during a cesarean delivery is greatly variable. The increase in intravascular fluid volume and the hypercoagulable state of the mother help to counter the blood losses incurred during this time. The contracted uterus after either type of delivery creates an autotransfusion of approximately 500 mL of blood, which decreases the overall effect of the blood loss on the mother. (515)
4. Maternal cardiac output increases 10% by the tenth week of gestation, and at term pregnancy increases by approximately 40% to 50% of its prepregnancy value. Cardiac output is equal to the product of stroke volume and heart rate. The increase in cardiac output is primarily due to an increase in stroke volume. The increase in heart rate during pregnancy is less and is therefore only a minimal contributor to the increase in cardiac output. Labor is associated with further increases in cardiac output with output above prelabor values by 10% to 25% during the first stage and 40% in the second stage. The greatest increase in cardiac output occurs just after delivery, when it increases by as much as 80% above prelabor values. This is the maximal change in cardiac output in the woman. Cardiac output decreases substantially toward prepregnant values by 2 weeks postpartum. (515, Table 33-1)
5. The systolic blood pressure of the woman having an uncomplicated pregnancy does not exceed her prepregnancy blood pressure and typically decreases secondary to a 20% reduction in systemic vascular resistance at term. Systolic, mean, and diastolic blood pressure may all decrease 5% to 15% by 20 weeks gestational age and gradually increase toward prepregnant values as the pregnancy progresses towards term. Central venous pressure does not change during pregnancy despite the increased plasma volume because venous capacitance increases. (515-516, Table 33-1)
6. Supine hypotension syndrome, as the name implies, is the decrease in blood pressure seen when the pregnant patient lies in the supine position after midgestation. The supine hypotension syndrome occurs because of a decrease in cardiac output by approximately 10% to 20%. When the pregnant woman is in the supine position, the gravid uterus compresses the inferior vena cava, resulting in decreased venous return and decreased preload for the heart. Symptoms that accompany the hypotension include diaphoresis, nausea, vomiting, and possible changes in cerebration. Symptoms must be present for the patient to be considered susceptible to supine hypotension syndrome. (516, Figure 33-1)
7. Most pregnant women, when lying in the supine position, are able to compensate for the possible decrease in blood pressure that results from the compression of the inferior vena cava by the gravid uterus. One compensatory mechanism includes maintaining venous return by diverting blood flow from the inferior vena cava to the paravertebral venous plexus. The blood then goes to the azygos vein and returns to the heart via the superior vena cava. Dilation of the epidural veins may make unintentional intravascular placement of an epidural catheter more likely. A “test dose” is given before dosing an epidural catheter to decrease the likelihood of an unrecognized intravascular placement before initiating neuraxial blockade.
Another compensatory mechanism is an increase in peripheral sympathetic nervous system activity. This increases peripheral vascular tone and helps to maintain venous return to the heart. Regional anesthesia, however, can interfere with these compensatory mechanisms by causing sympathetic nervous system blockade, rendering the pregnant woman at term more susceptible to decreases in blood pressure. The gravid uterus can also compress the lower abdominal aorta and lead to arterial hypotension in the lower extremities, but maternal symptoms or decreases in systemic blood pressure as measured in the arms are often not reflective of this decrease. The major clinical significance of the aortocaval compression is the decrease in placental and uterine blood flow that results. The decrease in blood flow through the uteroplacental unit leads to a decrease in blood flow to the fetus. The aortocaval compression can be minimized by having the woman lie in the lateral position. Uterine displacement can also be used, typically with displacement being to the left because the inferior vena cava sits just to the right of and anterior to the spine. Left uterine displacement is easily accomplished by table tilt or the placement of a wedge or folded blanket under the right hip, elevating the hip by 10 to 15 cm. (516-517, Figures 33-1 and 33-2)
8. There is significant capillary engorgement of the mucosal layer of the upper airways and increased tissue friability during pregnancy. There is increased risk of obstruction from tissue edema and bleeding with instrumentation of the upper airway. Additional care is needed during suctioning, placement of airways (avoid nasal instrumentation if possible), direct laryngoscopy, and intubation. In addition, because the vocal cords and arytenoids are often edematous, smaller-sized cuffed endotracheal tubes (6.0 to 6.5 mm internal diameter) may be a better selection for intubation of the trachea for these patients. The presence of preeclampsia, upper respiratory tract infections, and active pushing with associated increased venous pressure further exacerbate airway tissue edema, making both intubation and ventilation more challenging. (517)
9. During pregnancy, the minute ventilation increases to about 50% above prepregnancy levels. This change occurs in the first trimester of pregnancy and remains elevated for the duration of the pregnancy. An increase in tidal volume is the main contributor to the increase in minute ventilation seen, with only small increases in respiratory rate from prepregnancy. During the first trimester, as a result of the increase in minute ventilation, the resting maternal PaCO2 decreases from 40 mm Hg to about 30 or 32 mm Hg. Arterial pH, however, remains only slightly alkalotic (7.42 to 7.44) secondary to increased renal excretion of bicarbonate ions. (517, Table 33-1)
10. Maternal hemoglobin has less of an affinity for binding oxygen during pregnancy, which facilitates downloading oxygen to the tissues and the fetus. The hemoglobin dissociation curve is thus shifted to the right with the P-50 increasing from 27 to approximately 30 mm Hg. (517)
11. Maternal lung volumes start to change in the second trimester. This is a result of mechanical compression by the gravid uterus as it enlarges and forces the diaphragm cephalad. This leads to a decrease in the woman’s functional residual capacity by approximately 20% at term. This decrease is a result of approximately equal decreases in both the expiratory reserve volume and residual lung volume. This can result in a functional residual capacity less than closing capacity and increased atelectasis in the supine position. There is no significant change in vital capacity seen during pregnancy. The rates of change in the alveolar concentration of inhaled anesthetics during induction and emergence from anesthesia are both increased secondary to the increase in minute ventilation and decrease in functional residual capacity. Clinically this, along with the decrease in MAC that accompanies pregnancy, leads to a more rapid achievement of an anesthetized state than when the patient is not pregnant. Apnea in the woman rapidly leads to arterial hypoxemia. There are at least two explanations for this. First, a decreased functional residual capacity and subsequent decreased oxygen reserve are contributors. Second, aortocaval compression and decreased venous return leading to decreases in cardiac output may also contribute. The decrease in cardiac output would lead to an increase in overall oxygen extraction and therefore decrease the level of oxygenation of blood returning to the heart. Third, maternal oxygen consumption is increased by 20% at term, with further increases noted during labor. Because of the rapid decrease in maternal PaO2 with apnea or hypoventilation, preoxygenation with 100% O2 for 3 minutes or four maximal breaths over the 30 seconds just prior to the induction of emergent general anesthesia is recommended. (517, Table 33-1)
12. Maternal PaO2 changes during the progression from early gestation to term. Early in gestation, the PaO2 in the mother is slightly increased over prepregnancy values to over 100 mm Hg breathing room air. This is secondary to maternal hyperventilation and subsequent decreased PaCO2 during this time. As the pregnancy progresses, the PaO2 is normal or even slightly decreased. The decrease in PaO2 during the course of pregnancy likely results from airway closure and associated intrapulmonary shunt. (517)
13. There are at least four gastrointestinal changes in pregnancy that render the woman significantly vulnerable to the regurgitation of gastric contents beyond midgestation. The enlarged uterus acts to displace the stomach and pylorus cephalad from its usual position. This repositions the intraabdominal portion of the esophagus into the thorax and leads to relative incompetence of the physiologic gastroesophageal sphincter. The tone of the gastroesophageal sphincter is further reduced by the higher progesterone and estrogen levels of pregnancy. Gastric pressure is increased by the gravid uterus. Gastrin secreted by the placenta stimulates gastric hydrogen ion secretion. The pH of the woman’s gastric fluid is predictably low as a result. Reflux and subsequent esophagitis are common during pregnancy. During labor, gastric emptying is delayed and intragastric fluid volume tends to be increased as a result. (Epidural analgesia alone does not alter gastric emptying.) Anxiety, pain, and the administration of opioids can further decrease gastric emptying. Clinically, this means that the pregnant patient must always be treated as if she has a full stomach. Regardless of what amount of time has elapsed since her last ingestion of solids, she is at increased risk of regurgitation and aspiration of gastric contents. This includes the routine use of nonparticulate antacids, rapid sequence induction, cricoid pressure, and cuffed endotracheal intubation as part of general anesthesia induction sequence in a pregnant woman after approximately 20 weeks gestational age.
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