During pregnancy, maternal oxygen requirements and metabolism steadily increase and the cardiovascular system must adapt to meet these increased demands. Cardiac output escalates throughout pregnancy, due to increased stroke volume and elevated heart rate. Central venous and pulmonary artery occlusion pressures are unchanged. During labor, uterine contractions cause a cyclical increase in cardiac preload, further augmenting cardiac output. Systemic vascular resistance and mean arterial pressure decrease early in pregnancy and return to baseline at term.

In the supine position, the gravid uterus readily compresses the inferior vena cava. The aorta is affected to a lesser extent. This aortocaval compression impedes venous return and can lead to decreased cardiac output, hypotension, and decreased uterine perfusion. This syndrome, called the supine hypotensive syndrome, may occur as early as 20 weeks gestation and is exacerbated by conditions that increase uterine size – such as macrosomia (large fetus) and multiple gestation. The lateral decubitus, knee-chest, and left uterine displacement positions help to avoid the detrimental effects of aortocaval compression.

Some women may develop gestational hypertension (systolic bp >140 mmHg or diastolic >90 mmHg), pre-eclampsia (hypertension + proteinuria), or eclampsia (pre-eclampsia + seizures). The definitive therapy for pre-eclampsia is delivery of the fetus.

Tidal volume increases during pregnancy. Respiratory rate is also increased, but less profoundly. The increased minute ventilation leads to a compensated respiratory alkalosis, a fact that is especially important to remember when initiating mechanical ventilation.

A number of physiologic changes place the obstetric patient at increased risk for airway complications including failed endotracheal intubation and pulmonary aspiration. Increased oxygen consumption and decreased functional residual capacity (FRC) lead to rapid development of hypoxemia during periods of apnea. Parturients are at an increased risk for difficult and failed intubation because the airway becomes less favorable during pregnancy and even labor. At term, mucosal engorgement frequently afflicts the upper and lower airway, mandating gentle laryngoscopy, smaller endotracheal tubes, and avoidance of nasal airways. In the supine position, the enlarged breasts of pregnant females at term are upwardly displaced and may impede laryngoscopy. Laryngoscopes with short handles are more easily utilized in this setting.

Gastrointestinal anatomic and physiologic changes increase the risk of aspiration, demanding “full stomach” precautions in laboring women. If the parturient loses the ability to protect her airway (e.g., high spinal block, overzealous hypnotic administration), endotracheal intubation is advisable.

The parturient is more sensitive to both inhalational and local anesthetics, an effect that has been attributed to increased progesterone. Endogenous endorphins may also play a role in mediating this effect, especially during the peripartum period. The minimal alveolar concentration (MAC) for volatile anesthetics declines throughout pregnancy. Hormonally-mediated changes may also increase neuronal sensitivity to local anesthetic agents. In addition, the gravid uterus causes distention of epidural veins which is thought to decrease dose requirements for neuraxial blockade.

Total blood volume increases significantly (≈45 %) during pregnancy. Dilutional anemia occurs because plasma volume increases more so than red cell mass. The blood loss associated with a typical vaginal delivery (500 cc) or cesarean section (1000 cc) is usually well tolerated as a result of these changes. Other notable hematologic changes include leukocystosis, increased serum clotting factors, and an occasional mild decrease in platelet count. Parturients become relatively hypercoagulable, which is advantageous during acute obstetric blood loss. Unfortunately, the hypercoagulable state predisposes these patients to deep venous thrombosis, pulmonary emboli, and other thromboembolic events.

A small number of parturients (≈0.5 %) may develop a worsening thrombocytopenia (i.e. low platelet count), liver dysfunction, hemolysis, and anemia – termed HELLP syndrome . This is a life-threatening obstetric complication which usually appears late in pregnancy or even after delivery. The treatment for HELLP is delivery of the fetus.

The obstetric patient is at increased risk for aspiration of gastric contents because of:

Prophylactic measures aimed at reducing the risk of aspiration pneumonitis are generally focused on modifying these risk factors. The most important prophylactic measure is the avoidance of solid food during labor. Other measures should be considered prior to surgery. Many routinely administer oral sodium citrate, a non-particulate antacid. Sodium citrate quickly buffers existing stomach acid, but at the expense of increasing gastric volume and possibly causing nausea. The buffering capacity of sodium citrate is time-limited, and it should therefore not be administered far in advance of surgery. H₂-receptor antagonists or proton-pump inhibitors can be used, but their beneficial effects are likely delayed. Metoclopramide increases gastric emptying and lower esophageal sphincter tone and is advocated by some practitioners. The possibility of extrapyramidal reactions is a major drawback to its routine use.

Renal blood flow and glomerular filtration rate increase markedly during pregnancy. As a result, the obstetric patient’s creatinine should be less than her non-pregnant value. Additionally, total body water increases by ≈ 30 %. Increased glomerular permeability to proteins may lead to a mild proteinuria during pregnancy.

As the gestation progresses, the lumbar spine becomes increasingly lordotic. Lordosis hampers the interlaminar approach for the lumbar spinals and epidurals. Although less feasible with advancing uterine size, good positioning helps to offset the undesirable effects of lordosis. Ligaments tend to become more lax near term as the body prepares for vaginal delivery. Many operators have noted that the ligamentum flavum (see Chap. 13, Regional Anesthesia) has a more spongy texture at term when compared to the non-pregnant state.

By the end of the third trimester, uterine blood flow may represent up to 12 % of cardiac output. Perfusion of the uterus is adversely affected by decreased uterine arterial pressure (hypovolemia, aortic compression), increased uterine venous pressure (vena cava compression), and increased uterine vascular resistance (uterine contractions, severe preeclampsia). Derangement of these variables may adversely affect fetal oxygen delivery.

Exogenous vasoconstrictors can also adversely affect uterine perfusion. Animal data from several decades ago led many to avoid the use of α-agonists (phenylephrine) because of supposed increases in uterine vascular resistance. However, more recent human studies have shown that phenylephrine is superior to ephredrine for the treatment of hypotension following neuraxial block for cesarean section, as evidenced by better hemodynamic control and more favorable umbilical cord gases.

Blood from the maternal uterine spiral arteries bathes fetal villi capillaries within the maternal intervillous spaces of the placenta. Since placental exchange occurs across a membrane, it is dependent on diffusion, bulk flow, and active mechanisms. Oxygen and carbon dioxide diffuse readily across the placenta. Unloading of maternal oxygen is facilitated by a rightward shift in the oxyhemoglobin dissociation curve. Fetal oxygen transfer is further bolstered by fetal hemoglobin’s high affinity for oxygen (leftward shift of the oxyhemoglobin dissociation curve compared to adult hemoglobin).

The goal of intrapartum fetal evaluation is to detect fetal hypoxia such that one can intervene (e.g., change positions, initiate tocolysis, or perform a cesarean section) before irreversible fetal harm occurs. Fetal heart rate, though nonspecific, may be a useful surrogate for fetal oxygen delivery. In one meta-analysis, continuous electronic fetal heart rate monitoring reduced the risk neonatal seizures as compared to intermittent monitoring but did not reduce the intrapartum fetal death rate or reduce the risk of fetal neurologic injury. However, the incidence of operative delivery was higher with continuous electronic fetal heart rate monitoring. With either strategy, the baseline fetal heart rate (FHR) should be between 120 and 160 beats per minute (Fig. 20.1). Abnormalities may include:

Decelerations are a periodic slowing of FHR. Three principal deceleration patterns have been described according to their relationship to uterine contraction: early, late, and variable decelerations (Figs. 20.2, 20.3 and 20.4).

Increased vagal activity due to fetal head compression is believed to cause early decelerations. Early decelerations begin soon after uterine contraction, tend to have a uniform shape, and do not herald fetal hypoxia. Late decelerations represent uteroplacental insufficiency, that is, insufficient fetal oxygen delivery during uterine contraction. Variable decelerations are typically due to umbilical cord compression and have a variable relationship to uterine contraction.

Once the fetus has been delivered, the Apgar Score (Table 20.2) can be used to evaluate its well-being. Named after Virginia Apgar (an anesthesiologist who developed the system in the 1950s), the score is made up of five criteria each on a scale of 0–2. The five scores are then summed to provide a single total Apgar Score of the newborn. The score ranges from 0 to 10, with 7–10 generally considered normal.

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