1. Pregnancy causes an increase in plasma volume with a lesser increase in red cell volume, which accounts for a reduction in hemoglobin to 11 to 12 g/dL. The increase is 35% to 40% of nonpregnant blood volume.

2. Plasma proteins decline in total concentration (due to the greater plasma volume), but the total amount in circulation increases. Alterations in protein content, especially albumin, may be clinically significant due to the increase in free fractions of protein-bound drugs.

3. Lowered resistance is found in the uterine, renal, and other vascular beds due to hormonal and prostacyclin changes. At term, the heart rate (HR) (92 to 95 beats/min), cardiac output (CO), and blood volume all increase. CO plateaus at 30% to 50% above the normal level at 30 to 34 weeks. Additional increases occur during labor and in the immediate postpartum period. CO decreases to nonpregnant levels by 2 weeks postpartum.

4. Vena caval compression can develop from the second trimester onward and becomes maximal at 36 to 38 weeks. Left uterine displacement should be used during the second and third trimesters regardless of the lack of maternal arterial hypotension.

5. Electrocardiogram (ECG) changes result from a shift in the heart position (left axis deviation). Common changes include the following:

6. Airway edema and friable tissue are due to increased extracellular fluid, reduced colloid oncotic pressure (14%), and vascular engorgement. Edema may be severe in patients who have preeclampsia or have been in the Trendelenburg position for a prolonged period, as well in those receiving tocolytic agents.

7. The diaphragm rises during pregnancy, which is compensated for by an increase in the anteroposterior and transverse diameters of the thoracic cage through flaring of the ribs. From the fifth month, the expiratory reserve volume, residual volume, and functional residual capacity (FRC) are decreased. FRC decreases to 20% of nonpregnant levels. Alveolar ventilation is decreased by 70% at term, mainly from increased tidal volume. Those with preexisting alterations in closing volume (i.e., from smoking, obesity, or scoliosis) may experience early airway closure → hypoxemia as pregnancy progresses. Ventilation returns to normal within 1 to 2 weeks of delivery.

8. Maternal uptake and elimination of inhalation anesthetics is enhanced by the following:

9. Progesterone causes the following:

Gastric reflux and esophagitis develop in 45% to 70% of pregnant women. For all parturients undergoing anesthesia after week 12 of pregnancy, an endotracheal tube is usually recommended to protect the airway, and a rapid sequence induction considered. It is usually necessary for all postpartum women undergoing general anesthesia within 48 hours of delivery, as studies show that 60% will have a gastric volume >25 mL and all have a pH <2.5.

10. MAC is decreased by 32% to 40% in pregnant ewes (possibly due to hormonal changes, increased endogenous opiates, and the sedative activity of progesterone). Lower doses of local anesthetics are needed per segment of epidural or spinal block. There seems to be a greater sensitivity to local anesthetics.

1. The driving force in placental transfer of drugs is the maternal-fetal concentration gradient of free drug. Placental transfer is also determined by molecular size (those <500 d pass easily), lipid solubility, and degree of ionization.

2. Because of the 20% reduction in FRC, the equilibration time between the alveolar and inspired concentrations of inhalation agents is shortened.

3. There is no evidence to suggest that the placenta metabolizes any of the agents commonly used to produce anesthesia or analgesia in pregnant women.

4. When medications were administered during the onset of contractions, a decrease was found in the amount of drug measured in the fetus.

5. Because of the unique pattern of fetal circulation directly through the liver, N₂O or cyclopropane administered during cesarean (C-) section causes newborn depression only if the induction-to-delivery interval exceeded 5 to 10 minutes.

6. During asphyxia and acidosis, a greater proportion of the fetal CO perfuses the fetal brain, heart, and placenta. Therefore, there may be an increased drug uptake in these organs.

7. Any drug that reaches the fetus will be subjected to metabolism and excretion. The fetus can excrete the drug back to the mother once the concentration gradient of the free drug across the placenta has been reversed. Therefore, this may occur even though the total plasma drug concentration in the mother may exceed that in the fetus, because there is lower protein binding in fetal plasma.

8. The newborn is more susceptible than the adult to opioids and local anesthetics.

9. The sequence of toxic manifestations of local anesthetics: convulsions → hypotension → apnea → circulatory collapse.

1. Pain during the first stage of labor is caused by uterine contractions associated with dilation of the cervix and stretching of the lower uterine segment. In early labor, only the lower thoracic dermatomes (T11-12) are affected, but with increased cervical dilation, adjacent dermatomes may be involved and pain referred (T10-L1).

2. Pain in the second stage of labor is due to descent of the fetal presenting part and distention of the vaginal vault and perineum; impulses are carried by pudendal nerves composed of lower sacral fibers (S2-4). Pain has been shown to cause maternal hypertension and reduced uterine blood flow. Analgesia may also eliminate maternal hyperventilation. Hyperventilation may often lead to a decreased fetal arterial oxygen (O₂) tension consequent to the leftward shift of the maternal O₂-hemoglobin dissociation curve.