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Neurologic disorders requiring surgical intervention during pregnancy are not uncommon, and many anesthesiologists eventually encounter a pregnant woman in need of a neurosurgical procedure. The anesthetic management of such patients can be complicated by the physiologic changes that occur during pregnancy. These changes might require adjustments in anesthetic management that would be inappropriate for a nonpregnant patient with the same neurosurgical condition.
Maternal well-being must remain a primary concern, but it is important to recognize that interventions which benefit the mother might have the potential to harm the fetus. Thus, the major challenge in providing anesthesia for neurosurgery performed during pregnancy is to provide an appropriate balance between competing, and sometimes contradictory, clinical goals.
The pregnant woman undergoes a number of physiological adaptations to pregnancy. The earliest of these changes are hormonally driven, while changes that occur later in pregnancy are associated with the mechanical effects of the enlarging uterus, increased metabolic demands of the fetus, and a low resistance placental circulation.
Anesthetic requirements for volatile anesthetics during pregnancy, as measured by minimum alveolar concentration (MAC), are decreased by 30% from the nonpregnant state. , Higher levels of plasma endorphins and progesterone are said to account for this change. Hence, inspired anesthetic concentrations that would be appropriate in the nonpregnant patient could have exaggerated effects during pregnancy. However, the relationship between pregnancy and MAC is complicated by the findings from one study that showed no differences in electroencephalographic measures during sevoflurane anesthesia between pregnant and nonpregnant women. The authors of that study suggested that a decrease in MAC during pregnancy does not correlate with an enhanced hypnotic effect of sevoflurane on the brain. They believe that pregnant women should receive the same dose of volatile agent as a nonpregnant woman in order to prevent intraoperative awareness, and we should reconsider MAC as an indicator of the efficacy of volatile anesthetics.
Local anesthetic requirements for neuraxial anesthesia are decreased by 30–40% during pregnancy. This reduction is in part due to the decreased volume of cerebrospinal fluid (CSF) in the lumbar subarachnoid space secondary to engorgement of the epidural veins. The decrease in local anesthetic requirements precedes the onset of significant epidural venous engorgement, however. In vitro preparations of vagus nerves obtained from pregnant rabbits show increased sensitivity to local anesthetic-induced blockade of nerve conduction. When nerves obtained from nonpregnant rabbits are bathed in a progesterone-containing solution, however, this greater sensitivity is not seen. It is, therefore, suggested that long-term but not short-term exposure to progesterone leads to changes in the neuronal membrane Na + channel that increase its sensitivity to local anesthetics.
In summary, parturients may have decreased anesthetic requirements but despite a 30% reduction in MAC, recent research indicates that it might be prudent to use the same dose of volatile agent as in a nonpregnant woman in order to avoid awareness. However, parturients appear to need reduced doses of neuraxial local anesthetics.
The accumulation of extracellular fluid produces soft tissue edema during pregnancy, particularly in the upper airway where marked mucosal friability can develop. Nasotracheal intubation and the insertion of nasogastric tubes should be avoided unless absolutely necessary because of the risk of significant epistaxis. Laryngeal edema can also reduce the size of the glottic aperture, leading to difficult intubation. Mallampati scores can increase during labor making endotracheal intubation more difficult, and this problem is likely to be worsened in preeclamptic patients. A smaller (6.0–7.0-mm) endotracheal tube is appropriate for most pregnant patients.
By the end of the third trimester, functional residual capacity (FRC) decreases 20% from prepregnant values, whereas closing capacity remains unchanged. The FRC drops further in the supine position, a situation in which closing capacity commonly exceeds FRC. This decrease leads to closure of small airways, increased shunt fraction, and a greater potential for arterial oxygen desaturation. Additionally, because FRC represents the store of oxygen available during a period of apnea, decreases in FRC will lead to the rapid development of hypoxemia when the pregnant patient becomes apneic, as occurs during the induction of general anesthesia. Because oxygen consumption rises by as much as 60% during pregnancy, significant desaturation can occur even when intubation is performed expeditiously. This process was demonstrated in a computer model of pregnancy in which apnea was simulated after 99% denitrogenation. Desaturation to 90% occurred in approximately 5 minutes in the pregnant model, versus 7.5 minutes in the nonpregnant model. Thus, at least 2 minutes of preoxygenation and denitrogenation with a tightly fitting face mask is mandatory before the induction of general anesthesia during pregnancy.
Significant increases in minute ventilation occur as early as the end of the first trimester. At term, minute ventilation increases by 45%, owing to an increase in tidal volume; respiratory rate is essentially unchanged. This most likely results from a progesterone-induced increase in the ventilatory response to carbon dioxide (CO 2 ); there also appears to be an effect due to pregnancy-induced changes in wakefulness. Because the increase in ventilation exceeds the increase in CO 2 production, the normal arterial partial pressure of CO 2 (Paco 2 ) diminishes to approximately 32 mmHg. The greater excretion of renal bicarbonate partially compensates for the hypocarbia, so that pH rises only slightly, to approximately 7.42 to 7.44.
Blood volume increases by 45% during pregnancy, with the majority of this increase occurring by the end of the second trimester. Because plasma volume increases to a greater extent than red blood cell mass, a dilutional anemia commonly occurs. Normal hematocrit at term ranges from 30% to 35% and is often lower in women not receiving supplemental dietary iron.
Significant increases in cardiac output (CO) occur as early as the first trimester. Capeless and Clapp demonstrated a 22% rise in CO by 8 weeks’ gestation, which represents 57% of the total change seen at 24 weeks. Cardiac output rises steadily throughout the second trimester. Maximum increases in CO occur between 28 and 32 weeks’ gestation. At term, cardiac output is approximately 50% above prepregnancy baseline.
Cardiac output can increase by an additional 60% during labor. Part of this increase is caused by the pain and apprehension associated with contractions, an increase that can be blunted with the provision of adequate analgesia. There is a further rise in CO, unaffected by analgesia, from the autotransfusion of 300–500 mL of blood from the uterus into the central circulation with each contraction. Finally, CO increases further in the immediate postpartum period, by as much as 80% above pre-labor values, because of autotransfusion from the rapidly involuting uterus as well as the augmentation of preload after relieving aortocaval compression.
In the supine position after 20 weeks’ gestation, the enlarged uterus can compress the inferior vena cava against the vertebral column. Collateral flow through the epidural venous plexus and paravertebral vessels can partially compensate for decreased caval blood flow, but the net return of blood to the heart can be significantly decreased, leading to reduced CO. This can decrease uterine blood flow (UBF) and impair uteroplacental oxygen delivery. Supine positioning can also produce aortic compression. If this occurs, upper extremity blood pressure might be normal but distal aortic pressure and thus uterine artery perfusion pressure could decrease. The effects of aortocaval compression are magnified in the anesthetized patient when venous return is reduced from sympathetic blockade. Therefore, the supine position must be avoided in pregnant patients undergoing anesthesia after the mid-second trimester. One study evaluated the degree of tilt necessary to minimize aortocaval compression in term, nonlaboring patients prior to cesarean delivery. CO and pulse pressure were highest at 15 degrees of left tilt, equal to full 90 degrees left lateral position.
Ectopic gastrin is produced by the placenta. However, plasma gastrin levels appear to be unchanged during pregnancy, and there appears to be no significant difference in either the volume or the acidity of gastric secretions in pregnancy.
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