Respiratory system

A variety of pregnancy-related changes occur in the respiratory system and may lead to maternal airway complications, which contribute to anesthesia-related maternal mortality risk in the United States. Increased vascularity of the upper airway and nares may result in edema of the upper airway, thus necessitating the use of a smaller tracheal tube. Decreased chest wall compliance may lead to early O₂ desaturation, and decreased functional residual capacity (20%) and increased O₂ demand (60%) may result in rapid O₂ desaturation during apneic episodes.

Physiologic compensatory mechanisms in the mother yield improved fetal oxygenation. The mechanisms include a rightward shift in the maternal oxyhemoglobin dissociation curve (P₅₀ = 30 mm Hg) and a 50% increase in minute ventilation. Progesterone is responsible for increasing the sensitivity of the central respiratory center to CO_2, which would cause a respiratory alkalosis; however, because renal excretion of bicarbonate is increased in pregnant women, a neutral pH is maintained. Pregnant women also have a higher PO₂ concentration, compared with the nonpregnant state.

Cardiovascular system

A myriad of cardiovascular changes occur during pregnancy. For example, maternal cardiac output increases 40% to meet the metabolic demands of both the mother and the fetus. The rise in cardiac output is initially due to an increase in stroke volume and, as pregnancy progresses, is maintained by an increase in heart rate as the stroke volume decreases. Progesterone decreases pulmonary and systemic vascular resistance, yet central venous and pulmonary artery occlusion pressures remain unchanged. Plasma volume increases up to 40% to 50% due to increased aldosterone production. Because red blood cell mass does not increase as much as does the blood volume, a dilutional anemia results.

When the pregnant woman is in the supine position, uterine compression of the inferior vena cava and aorta causes hypotension; however, this can be readily resolved by placing the parturient in a 15-degree left lateral tilt. Compression of the inferior vena cava and fluid retention also produce ankle edema and varicose veins and can enlarge portal-systemic shunts. Electrocardiographic changes (e.g., left-axis deviation, T-wave inversion in lead III) occur, with cardiac enlargement and rotation of the heart cephalad and leftward.

Gastrointestinal system

Pregnant women are more prone to developing symptomatic gastroesophageal reflux because their gastric pH is decreased, resulting from the production of gastrin by the placenta beginning at approximately 15 weeks of gestation and mechanical obstruction by the gravid uterus that delays gastric emptying and increases intragastric pressure. Lower esophageal sphincter competency is compromised when the gravid uterus causes the gastroesophageal junction to shift cephalad and posterior. Additionally, lower esophageal sphincter tone is altered by high progesterone and estrogen levels.

The risk of aspiration of gastric contents during induction of anesthesia is increased not only when the parturient undergoes emergency cesarean section (2% of deliveries in the United States) under general anesthesia, but, in reality, at any time after 18 to 20 weeks of pregnancy if the woman requires general anesthesia for a surgical procedure. Patients with larger intrauterine size (e.g., multiple gestations or polyhydramnios) are at risk even earlier during pregnancy.

Renal function

Elevated intraabdominal pressure and changes in bladder size and shape lead to mechanical obstruction and ureteral reflux, which increases the incidence of ascending urinary tract infection. Glomerular filtration is increased by 50% above nonpregnant values and is responsible for a 40% reduction in blood urea nitrogen and creatinine levels during normal pregnancy. Glucosuria without hyperglycemia is due to a decrease in renal absorption of glucose, whereas protein excretion rises, resulting in proteinuria (up to 300 mg/day).

Hepatic function

Minor changes in hepatic transaminase concentrations (e.g., aspartate aminotransferase [AST], lactate dehydrogenase [LDH]) may occur. Dilution of plasma proteins causes a decrease in the albumin:globulin ratio. Accordingly, the free fraction of albumin-bound medications is increased. Plasma cholinesterase levels are decreased (by dilution), but this does not result in a significant prolongation of succinylcholine-induced neuromuscular blockade.

Hematologic system

Pregnancy causes an activation of platelets, with an increased platelet turnover and shorter half-life. Levels of factors VII, VIII, X, and XII and fibrinogen are increased. The fibrinolytic system is depressed by a relative reduction of antithrombin III, resulting in a hypercoagulable state and rendering pregnant women more susceptible to developing thromboembolic disease.

Neurologic system

Local anesthetic requirements for neuraxial blockade are decreased during pregnancy secondary to reduced volume in the epidural space (epidural vein engorgement), decreased volume of cerebrospinal fluid, increased cerebrospinal fluid pH, and enhanced neural sensitivity to local anesthetic agents. The minimum alveolar concentration of inhalation anesthetics is also reduced 40% because of the hormone changes of pregnancy.

Uterine physiology

Uterine blood flow and placental perfusion are affected by systemic vascular resistance, aortocaval compression, and uterine contraction. Placental blood supply is determined by spiral intervillous arteries, which are maximally dilated (Figure 180-1). They are supplied by arcuate and radial arteries, the ovarian arteries, and uterine arteries. Myometrial tension decreases the caliber of spiral arteries, reducing placental perfusion. Spiral arteries are maximally dilated and sensitive to the effects of α-adrenergic receptor agonists (e.g., phenylephrine). Vasoconstriction can cause dramatic changes in placental blood supply. The surface area and integrity of the placenta are affected by maternal and placental disorders.

Prolonged uterine contraction (hypertonia) can cause fetal asphyxia. Treatment options include fluids, bed rest, O₂ and tocolytic agents (e.g., nitroglycerin and albuterol). After delivery, uterine contraction is potentiated with massage, oxytocin, methylergonovine maleate, and carboprost tromethamine. Approximately 500 mL of blood are added to the maternal circulation with uterine contraction.

Fetal oxygenation

Fetal oxygenation is dependent on placental blood supply, surface area integrity, and fetal cardiac output. Fetal cardiac output is rate dependent. Mechanical compression of the umbilical cord decreases the delivery of O₂ to the fetus. Maternal-fetal O₂ transfer is facilitated by a leftward shifting of the fetal oxyhemoglobin curve. Fetal blood gas concentrations are dependent on placental perfusion and maternal ventilation. Respiratory acidosis occurs with maternal hypoventilation.

Parturition

At 40 weeks of gestation, the fetus is mature and ready for birth. Factors that control the initiation of labor are not clearly understood, but labor results from a production of prostaglandin, which increases oxytocin receptors in uterine myometria. As oxytocin levels increase, rhythmic contractions of the uterus lead to cervical dilation. The cervix is softened prior to the descent of the fetus by an ovarian hormone, relaxin.

Postpartum period

Most of the changes that have occurred in the maternal physiology return to normal within 3 to 4 weeks after parturition but can take up to 8 weeks to return to normal.