Hemodynamic change throughout pregnancy by trimester compared with baseline values.
These hemodynamic changes are closely related to changes in the blood volume and blood constituents. Increases in estrogen lead to elevated levels of renin, thereby activating the renin–angiotensin–aldosterone system and enhancing water retention [2]. Progesterone and prolactin have erythropoietic effects leading to increased red blood cell volume by the end of the third trimester. Plasma volume, however, increases more than red blood cell volume creating a physiologic anemia. During the first trimester, red blood cell volume decreases while plasma volume increases. By the 16th week of gestation, red blood cell volume returns to pre-pregnancy levels and subsequently peaks at 30% above baseline by the end of the third trimester. Blood volume increases throughout pregnancy, resulting in a level that is 45% above baseline by the end of the third trimester [2]. Additionally, pregnancy is associated with mild leukocytosis, thrombocytopenia, and a procoagulant state due to increased Factors I, VII, VIII, IX, X, and XII [3].
The respiratory system undergoes several changes during pregnancy. Capillary engorgement within the nose, larynx, and oropharynx leads to edema. This, combined with mucosal friability, can complicate direct laryngoscopy and contribute to difficult airway management. Thoracic anatomic changes include increased subcostal angle and increased antero–posterior and transverse diameters. These changes result in cephalad movement of the diaphragm and decreased functional residual capacity [4]. Other notable changes in ventilation include decreased expiratory reserve volume, residual volume, and functional residual capacity with an increased inspiratory reserve volume [4]. The basal oxygen consumption is increased up to 20%, as is alveolar ventilation [4–5]. Increased respiratory rate and slightly increased tidal volume lead to increased minute ventilation. With this increased minute ventilation, arterial carbon dioxide decreases (∼32 mmHg), whereas arterial oxygen tension increases (∼106 mmHg). However, arterial buffer concentrations compensate to maintain arterial pH near normal values [5]. Given these changes, parturients are at high risk for hypoxemia during periods of apnea or hypoventilation, even if brief.
Gastrointestinal system changes also occur. Increased estrogen and progesterone cause relaxation of the lower esophageal sphincter [6]. Gastric secretions are also more acidic in the pregnant patient. While gastric emptying time is thought to remain unchanged, total gastrointestinal time is prolonged [7]. Given these changes, parturients are considered at increased risk of aspiration after 12 weeks of gestation.
2. Discuss how pregnancy may alter anesthetic management in terms of medication selection
The anesthetic care of a pregnant patient during non-obstetric surgery poses a distinct set of challenges. While this unique situation requires that maternal health be considered first, the well-being of the fetus must also be considered.
Foremost on most pregnant patients’ minds is how anesthetic medicines will affect the fetus, particularly the possibility of teratogenic effects. To date, only five medications are considered teratogens: thalidomide, isotretinoin, warfarin, valproic acid, and folate antagonists [8]. None of these are anesthetic medications. Most anesthetic agents, including the intravenous induction agents, opioids, and local anesthetics, have been designated by the FDA as either class B or C (Table 15.1). Both of these classes indicate that there are not any human studies, and further suggest that there is either (1) no evidence of risks in animal studies (class B), or (2) animal studies have shown adverse effects on the fetus but the benefits of the medication outweigh the risks (class C) [9].
FDA medication classification for pregnant patients.
| Classification | Definition |
|---|---|
| Pregnancy class A | Adequate and well controlled (AWC) studies have failed to demonstrate harm to the fetus in the first trimester and in later trimesters. |
| Pregnancy class B | Animal studies have failed to demonstrate a risk to the fetus and there are no AWC studies in humans, AND the benefits of use may be acceptable despite potential risk. OR animal studies have not been conducted and there are no AWC studies in humans. |
| Pregnancy class C | Animal studies have shown an adverse effect on the fetus, there are no AWC studies in humans, AND the benefits from use may be acceptable despite the potential risk. OR animal studies have not been conducted and there are no AWC studies in humans. |
| Pregnancy class D | There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, BUT the potential benefits from use may be acceptable despite potential risks. |
| Pregnancy class X | Studies in animals or humans have demonstrated fetal abnormalities OR there is positive evidence of fetal risk based on adverse reaction reports from investigational or marketing experience, or both, AND the risk of use clearly outweighs any possible benefit. |
Although specifically avoiding general anesthesia (GA) in the presented case is a reasonable and possibly superior option, a brief discussion of GA in the pregnant patient is warranted. The MAC for volatile anesthetics may be decreased up to 40% [10]. This is theorized to be the result of the sedating effects of chronic exposure to progesterone. Based on retrospective epidemiological studies, it was once thought that operating room personnel had an increased risk of miscarriage, compared with those not exposed to halogenated agents. However, more rigorous and better designed studies have not confirmed this [11]. The major concerns to the fetus regarding GA are based on a retrospective registry study that looked at births after exposure to GA in Sweden. While the incidence of congenital abnormality or stillborn birth was not increased, significant associations were made with decreased birth weight and increased death in the first seven days after delivery; although maternal morbidity was given as a likely explanation for these findings. Furthermore, the risks to the fetus were not linked to any particular type of anesthetic agent or technique. A more recent and still evolving concern involves the neuronal response of the developing brain to halogenated agents. Agents that block NMDA receptors or enhance GABA (volatile agents, ketamine, benzodiazepines, barbiturates) have been shown to induce widespread neuronal apoptosis in rodents in utero [12–13]. Learning disabilities and deviant behavior have been associated with fetal and early childhood exposure to anesthetic gases [14–15]. The potential adverse effect of exposure to GA combined with the ethical impossibility of ever conducting prospective, randomized human studies, combine to make RA the preferred modality when feasible.
In addition to inhalational anesthetic agents, benzodiazepines and nitrous oxide (N2O) also create discussion when caring for pregnant patients. Benzodiazepines in pregnancy are commonly avoided. This practice evolved following a retrospective study noting an association between the chronic use of diazepam for depression in the first six weeks of gestation and the development of cleft palate [16]. Although prospective studies failed to reproduce these findings, many clinicians avoid the benzodiazepines altogether in pregnancy in the absence of a compelling need. Notably, the one-time use of a short-acting benzodiazepine was never implicated. Similarly, although N2O has never been found to be teratogenic in humans, many clinicians are hesitant to use N2O for non-obstetric surgery in parturients. Nitrous oxide is known to rapidly cross the placenta and in non-human mammals has been determined to be teratogenic. In terms of pathogenesis, N2O oxidizes vitamin B12, a coenzyme for methionine synthase. This results in decreased tetrahydrofolate, a cofactor required for DNA synthesis. However, pretreatment with folinic acid does not prevent congenital abnormalities in rats exposed to N2O, even though folinic acid bypasses methionine synthase in DNA synthesis. This suggests that other mechanisms, not completely understood, contribute to the teratogenicity [17].
The increased progesterone levels associated with pregnancy alter the pharmacokinetics of LAs. The hormonal changes appear to increase the potency of LAs and because of this a lower dosage should be considered in the pregnant patient [18].
For the patient presented in this chapter, an upper extremity brachial plexus block – supraclavicular, infraclavicular, or axillary – would be the anesthesia of choice. It would avoid the potential problems associated with GA, and could require less intravenous sedation than if the procedure were to be performed under monitored anesthesia care, with the surgeon administering LA in the field.
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