Pregnant women have a decreased respiratory reserve due to their increased oxygen consumption (15% to 20%) coupled with decreased functional residual capacity (15% to 20%). Thus, they develop hypoxemia and hypercapnia more rapidly than a nonpregnant patient during hypoventilation or apnea. Due to laryngeal edema, engorged and friable oronasopharyngeal
mucosa, weight gain affecting the tissues of the neck, and increased breast size, they also have an increased likelihood of difficult airway management and intubation.

Pregnant women are at increased risk of regurgitation of gastric contents and aspiration pneumonitis due to impaired lower esophageal sphincter tone. Both hormonal and mechanical factors contribute as the pregnancy progresses. There are conflicting data regarding whether pregnant women have slower gastric emptying, increased gastric volume, and/or decreased pH of gastric contents. However, a pregnant patient should be considered at significant risk for aspiration after 18 weeks’ gestation or earlier if symptoms of gastroesophageal reflux exist.

An airway plan for a pregnant patient should include aspiration prophylaxis premedication with at least a nonparticulate antacid (Bicitra); addition of an H2 blocker and/or metoclopramide is at the anesthesiologist’s discretion. Use supplemental oxygen during sedation, and for general anesthetics, plan a full 5-minute preoxygenation, a classic rapid sequence induction, and oral intubation with an endotracheal tube that is one size smaller than usual. If difficult intubation is anticipated, opt for awake oral fiber-optic intubation.

During pregnancy, cardiovascular changes include an increased cardiac output, dilutional anemia, decreased vascular responsiveness, an increased risk of thromboembolism, and, after 20 weeks’ gestation, a risk of aortocaval compression by the gravid uterus leading to supine hypotension syndrome. Even normal physiological compensation for aortocaval compression can be blunted by general and regional anesthetics that interfere with sympathetic nervous system responses to hypotension. The result is a profound decrease in venous return and cardiac output, leading to impressive maternal hypotension and significantly decreased placental perfusion. Uterine blood vessels are maximally dilated at term, leaving no reserve for vascular autoregulation with perfusion pressure changes. Positioning with left uterine displacement by placing a wedge under the right hip, adequate hydration, and judicious use of pressors can help maintain maternal normotension. Ephedrine has long been the initial pharmacologic agent of choice in hypotensive pregnant women. To minimize risk of thromboembolism, thromboprophylaxis including preinduction placement and activation of pneumatic compression stockings is recommended.