Anesthesia for Obstetrics

Physical Examination and Cardiac Studies

The cardiovascular changes of a normal pregnancy are significant. In cardiac auscultation an accentuated first heart sound (S ₁ ) can be heard, with an increased splitting noted from dissociated closure of the tricuspid and mitral valves. A third heart sound (S ₃ ) is often heard in the final trimester, and a fourth heart sound (S ₄ ) can also be heard in some pregnant patients as a result of increased volume and turbulent flow. Neither the S ₃ nor S ₄ heart sounds have clinical significance. In addition, a benign grade 2/6 systolic ejection murmur is typically heard over the left sternal border and is secondary to mild regurgitation at the tricuspid valve from the annular dilation associated with the increased cardiac volume. Table 62.1 details the effects of pregnancy on the electrocardiogram and echocardiography. The elevation of the diaphragm by the growing uterus shifts the heart anteriorly and to the left. Left axis deviation as well as left ventricular hypertrophy are common findings in normal pregnancy. Women who present with chest pain, syncope, high-grade flow murmurs, arrhythmias, or heart failure symptoms such as hypoxia or clinically significant shortness of breath should undergo appropriate diagnostic investigation and referral.

Intravascular Volume

Maternal intravascular fluid volume begins to increase in the first trimester secondary to changes in the renin-angiotensin-aldosterone system promoting sodium absorption and water retention. These changes are likely induced by rising progesterone from the gestational sac. Plasma protein concentrations accordingly decrease with a 25% decrease in albumin and 10% decrease in total protein at term compared with nonpregnant levels. Consequently, colloid osmotic pressure decreases from 27 to 22 mm Hg over the time of gestation. At term, the plasma volume is 50% to 55% above the nonpregnant level. It is thought that the increase in blood volume prepares the parturient for delivery blood loss. Blood volume returns to prepregnancy values approximately 6 to 9 weeks postpartum.

Cardiac Output

By the end of the first trimester, maternal cardiac output typically increases approximately 35% to 40% above prepregnancy values and continues to increase 40% to 50% by the end of the second trimester. Cardiac output remains stable throughout the third trimester. This increased cardiac output is secondary to increases in both stroke volume (25%-30%) and heart rate (15%-25%). Labor further increases cardiac output, which fluctuates with each uterine contraction. Increases above prelabor values of 10% to 25% occur during the first stage and 40% in the second stage. The largest increase in cardiac output occurs immediately after delivery, when cardiac output can increase by 80% to 100% more than prelabor values. This abrupt increase is secondary to the autotransfusion of uteroplacental blood as the evacuated uterus contracts, reduced maternal vascular capacitance from loss of the intervillous space, and diminished lower extremity venous pressure from release of the aortocaval compression. This large fluctuation in cardiac output presents a unique postpartum risk for patients with cardiac disease, especially those whose heart cannot accommodate an increase in cardiac output such as those with fixed valvular stenosis or pulmonary vascular hypertension. Cardiac output returns toward prelabor values within 24 hours postpartum depending on the mode of delivery and degree of blood loss. Cardiac output decreases substantially toward prepregnant values by 2 weeks postpartum, with complete return to nonpregnant levels between 12 and 24 weeks after delivery.

Systemic Vascular Resistance

Although cardiac output and plasma volume increase, systemic blood pressure decreases in an uncomplicated pregnancy secondary to a reduction in systemic vascular resistance. Systemic vascular resistance decreases as a result of the vasodilatory effects of progesterone and prostaglandins as well as the low resistance of the uteroplacental vascular bed. Although affected by positioning and parity, systolic, diastolic, and mean blood pressure may all decrease 5% to 20% by 20 weeks gestational age and then gradually increase toward nonpregnant values by term. Diastolic arterial blood pressure decreases more than systolic arterial blood pressure resulting in a slight increase in pulse pressure. Central venous and pulmonary capillary wedge pressures do not change during pregnancy, despite the increased plasma volume, because venous capacitance increases.

Aortocaval Compression

Aortocaval compression by the gravid uterus as a result of supine positioning is associated with a decrease in systemic blood pressure. Although the inferior vena cava is compressed in nearly all term parturients, supine hypotension syndrome (also known as aortocaval compression syndrome) is experienced by only 8% to 10% of women. Supine hypotension syndrome is defined as a decrease in mean arterial pressure of more than 15 mm Hg with an increase in heart rate of more than 20 beats/min and is often associated with diaphoresis, nausea, vomiting, and changes in mentation. At term, the inferior vena cava can be almost completely occluded in the supine position with the return of blood from the lower extremities through the epidural, azygos, and vertebral veins that become engorged ( Fig. 62.1 A ). Also, significant aortoiliac artery compression occurs in 15% to 20% of pregnant women. Inferior vena caval compression in the supine position causes a decrease in both stroke volume and cardiac output of 10% to 20% in comparison to the upright position (see Fig. 62.1 B ), and may exacerbate venous stasis in the legs and thereby result in ankle edema, varices, and increased risk for lower extremity deep venous thrombosis.

Most pregnant women have compensatory adaptations that reduce supine hypotension symptoms despite aortocaval compression. One compensatory response is a reflexive increase in peripheral sympathetic nervous system activity. This increase in sympathetic activity results in increased systemic vascular resistance and permits arterial blood pressure to be maintained despite the reduced cardiac output. Consequently, the reduced sympathetic tone from neuraxial or general anesthetic techniques impairs the compensatory increase in vascular resistance and exacerbates the impact of hypotension from supine positioning.

Therefore in general, supine positioning is avoided during use of neuraxial techniques for labor analgesia and cesarean deliveries. Reducing the compression of the inferior vena cava and abdominal aorta with left tilt may mitigate the degree of hypotension and help maintain uterine and fetal blood flow. This is accomplished by positioning the patient laterally or by elevating the right hip 10 to 15 cm (with a historical goal of 15 degree left-tilt) with a blanket, wedge, or table tilt.

The practice of left uterine displacement has been challenged recently. In a magnetic resonance imaging (MRI) study of healthy pregnant volunteers, the volume of the inferior vena cava did not differ significantly between the supine position and the 15 degree left-tilt position but when the patients were tilted to the 30 degree left-tilt position, the inferior vena cava volume did increase. Additionally, healthy women undergoing elective cesarean delivery under spinal anesthesia and a phenylephrine infusion were randomized to supine or 15 degree left-tilt position and no difference was found on neonatal acid-base status; however, the supine patients had lower cardiac output and required more phenylephrine. Further studies are needed to investigate who benefits from left uterine displacement and the amount required to achieve the greatest benefit without hindering the surgical procedure. In the meantime, left uterine displacement should continue to be utilized during induction of neuraxial analgesia/anesthesia and during episodes of maternal hypotension or fetal compromise.

The Upper Airway

Capillary engorgement with increased tissue friability and edema of the mucosal lining of the oropharynx, larynx, and trachea begins early in the first trimester. As a result, an increased risk for bleeding exists during manipulation of the upper airway, in addition to an increased risk of difficult mask ventilation and intubation of the trachea. Suctioning of the airway and placement of devices should be performed gently to prevent bleeding and nasal instrumentation should be avoided. Furthermore, there is increased risk for airway obstruction during mask ventilation and both laryngoscopy and tracheal intubation are more difficult. Also, after extubation, the airway may be compromised as a result of edema, with subsequent risk for airway obstruction in the immediate recovery period.

Consequently, attempts at laryngoscopy should be minimized and experts recommend a cuffed endotracheal tube with a smaller diameter (6.0-7.0 mm internal diameter) should be placed to minimize the chances of difficult placement secondary to airway edema. Airway edema can be more severe in patients with coexisting preeclampsia, in upper respiratory tract infections, and after active pushing as a result of associated increased venous pressure. In addition, pregnancy-associated weight gain and increase in breast tissue, particularly in women of short stature or with coexisting obesity, can make insertion of a laryngoscope difficult. A patient’s position should always be optimized and back-up airway instrumentation available before attempts are made at intubation of the trachea. The Obstetric Anaesthetists’ Association and Difficult Airway Society guidelines for the management of difficult and failed intubation in obstetrics recommends a videolaryngoscope should be immediately available for all obstetric general anesthetics.

Ventilation and Oxygenation

The increased O ₂ demand and carbon dioxide production of the growing placenta and fetus cause minute ventilation to be elevated 45% to 50% more than nonpregnant values in the first trimester and for the remainder of the pregnancy. This larger minute ventilation is attained primarily as a result of a larger tidal volume and a slight increase in respiratory frequency. Maternal Pa CO ₂ decreases from 40 mm Hg to approximately 30 mm Hg during the first trimester as a reflection of the increased minute ventilation. Arterial pH, however, remains only mildly alkalotic (typically 7.42-7.44) because of metabolic compensation with increased renal excretion of bicarbonate ions (HCO ₃ ⁻ is typically 20 or 21 mEq/L at term). Early in gestation, maternal room air PaO ₂ is more than 100 mm Hg because of the presence of hyperventilation and the associated decrease in alveolar CO ₂ . Later, PaO ₂ becomes normal or even slightly decreased in the supine position, most likely reflecting small airway closure with normal tidal volume ventilation and intrapulmonary shunt. Arterial oxygenation can be significantly improved by moving the patient from the supine to the lateral position. With pregnancy, the maternal oxyhemoglobin dissociation curve shifts to the right, with the P50 (partial pressure of O ₂ at which hemoglobin is 50% saturated with oxygen) increasing from 27 to approximately 30 mm Hg at term. The higher P50 in the mother and lower P50 in the fetus means that the fetal blood has higher affinity for O ₂ and offloading of O ₂ across the placenta is facilitated. A comparison of arterial blood gas measurements in pregnant versus nonpregnant patients is summarized in Table 62.3 .

At term, O ₂ consumption is increased by 20% to 35%. During the first stage of labor, O ₂ consumption increases above prelabor values by 40% and during the second stage it is increased by 75%. The pain of labor can result in severe hyperventilation causing Pa CO ₂ to occasionally decrease below 20 mm Hg.

Lung Volumes

During pregnancy, tidal volume increases 20% during the first trimester and increases up to 45% above nonpregnant values at term. The expanding uterus forces the diaphragm cephalad and creates a 20% decrease in functional residual capacity (FRC) by term (see Table 62.2 ). This reduction is comprised of nearly equal reductions in both the expiratory reserve volume (ERV) and residual volume (RV). However, closing capacity (CC) remains unchanged and creates a reduced FRC/CC ratio. This results in more rapid small airway closure with reduced lung volumes, and in the supine position FRC can be less than CC for many small airways, giving rise to atelectasis. Vital capacity does not change with pregnancy. The combination of increased minute ventilation and decreased FRC results in a more rapid rate at which changes in the alveolar concentration of inhaled anesthetics can be achieved. Spirometric measurements of bronchial flow are unchanged in pregnancy.

During induction of general anesthesia, desaturation and subsequent hypoxemia occur more rapidly than in a nonpregnant patient because of decreased O ₂ reserve (secondary to decreased FRC) combined with increased O ₂ uptake (resulting from increased metabolic rate). Preoxygenation before general anesthesia is critical for patient safety to mitigate these physiologic changes and increase apnea time. Preoxygenation with inhalation of 100% O ₂ with a goal of end-tidal oxygen fraction greater than 0.9 is recommended (can usually be obtained with 2-3 minutes of preoxygenation before induction of anesthesia) (see Chapter 44 ). Although the use of high-flow humidified nasal oxygen has been shown to be as effective as conventional preoxygenation in nonpregnant patients, it has not been shown to achieve acceptable preoxygenation levels in term pregnant women. The increased airway edema makes both ventilation and tracheal intubation more difficult and further increases the potential for complications and morbidity of general anesthesia in pregnancy.

Coagulation

Pregnancy is characterized by a hypercoagulable state with a marked increase in factor I (fibrinogen) and factor VII and lesser increases in other coagulation factors ( Table 62.4 ). Factors XI and XIII are decreased, and factors II and V typically remain unchanged. Antithrombin III and protein S are decreased during pregnancy and protein C levels remain unchanged. These changes result in an approximately 20% decrease in prothrombin time (PT) and partial thromboplastin time (PTT) in normal pregnancy. Platelet count may remain normal or slightly decreased (10%) at term as a result of dilution. However, 8% of otherwise healthy women have a platelet count less than 150,000/mm ³ . In the absence of other hematologic abnormalities, the cause is usually gestational thrombocytopenia, from which the platelet count does not usually decrease to less than 70,000/mm ³ . This syndrome is not associated with abnormal bleeding. Gestational thrombocytopenia is due to a combination of hemodilution and more rapid platelet turnover and is a diagnosis of exclusion. Other more consequential diagnoses such as idiopathic thrombocytopenic purpura and hemolysis, elevated liver enzyme, and low platelet count (HELLP) syndrome must be excluded (see section on maternal comorbidities, coagulopathies).

Thromboelastography (TEG) is a hemostatic assay that measures the kinetics of clot formation and breakdown. It can provide information about clotting variables, including platelet function as well as the function of other coagulation factors (see also Chapter 50 ). At term gestation, TEG analysis reflects a hypercoagulable state with decreased time to start of clot formation (R), decreased time to specified clot strength (K), increased rate of clot formation (α), and increased clot strength (MA). Although the timing and degree of change in TEG analysis varies with each parameter, many of the changes begin to occur within the first trimester.

Oxygen Transfer

The delivery of O ₂ from the mother to the fetus depends on a variety of factors, including the ratio of maternal to fetal placental blood flow, the O ₂ partial pressure gradient between the two circulations, the diffusion capacity of the placenta, the respective maternal and fetal hemoglobin concentrations and O ₂ affinities, and the acid-base status of the fetal and maternal blood (Bohr effect). O ₂ delivery to the fetus is facilitated primarily because the fetal oxyhemoglobin dissociation curve is to the left (greater O ₂ affinity) of the maternal oxyhemoglobin dissociation curve (decreased O ₂ affinity). Fetal hemoglobin has a higher O ₂ affinity and lower partial pressure at which it is 50% saturated (P50: 18 mm Hg) compared to maternal hemoglobin (P50: 27 mm Hg). Fetal PaO ₂ is normally 40 mm Hg and never more than 60 mm Hg, even if the mother is breathing 100% O ₂ . Animal studies note that in the face of decreased O ₂ delivery, fetal O ₂ consumption can be maintained with increased O ₂ extraction until the maternal O ₂ delivery is approximately 50% of its normal state. CO ₂ easily crosses the placenta and its transfer from the fetus to the mother is limited by blood flow and not diffusion.

Drug Transfer

Maternal-fetal exchange across the placenta occurs by one of four mechanisms: passive diffusion, facilitated diffusion, transporter-mediated mechanisms, and vesicular transport. Most drugs have molecular weights less than 1000 Daltons and, therefore, cross the placenta by diffusion if the drug is not ionized. The rate of diffusion and peak levels in the fetus depend on maternal-to-fetal concentration gradients, maternal protein binding, molecular weight, lipid solubility, and the degree of drug ionization. The maternal blood concentration of a drug is typically the primary determinant of how much drug will ultimately reach the fetus. Nondepolarizing neuromuscular blocking drugs are ionized, have a high molecular weight, and poor lipid solubility resulting in minimal placental transfer. Succinylcholine has a low molecular weight but is highly ionized and therefore does not readily cross the placenta unless given in large nonclinical doses. Thus during administration of a general anesthetic for cesarean delivery, the fetus or neonate is not paralyzed. Both heparin and glycopyrrolate have minimal placental transfer because they are highly charged. In contrast, placental transfer of volatile anesthetics, benzodiazepines, local anesthetics, and opioids is facilitated by the relatively low molecular weights of these drugs. Dexmedetomidine may cross the placental barrier but is stored within the placenta and transfer to the fetus is reduced. As a general consideration, drugs that readily cross the blood-brain barrier also readily cross the placenta. Therefore most centrally acting general anesthetics cross the placenta and affect the fetus. There is a paucity of evidence on the placental transfer of newer drugs such as liposomal bupivacaine and sugammadex at this time.

Fetal blood is more acidic than maternal blood, and the lower pH creates an environment in which weakly basic drugs, such as local anesthetics and opioids, cross the placenta as nonionized molecules and become ionized in the fetal circulation. Because this newly ionized molecule has more resistance to diffusion back across the placenta, the drug may accumulate in the fetal circulation and reach levels higher than the maternal blood. This process is referred to as “ion trapping.” During fetal distress (fetal acidemia), higher concentrations of these weakly basic drugs can be trapped. High concentrations of local anesthetics in the fetal circulation decrease neonatal neuromuscular tone. Extremely high levels, such as those associated with unintended maternal intravascular local anesthetic injection, result in a variety of fetal effects, including bradycardia, ventricular arrhythmias, acidosis, and severe cardiac depression. Placental transfer and fetal uptake of specific analgesic and anesthetic drugs are detailed later in the sections that discuss methods of labor analgesia and anesthesia for cesarean delivery.