Both the intravascular and extravascular fluid volumes increase substantially during pregnancy. Much of the average 12.5 kg weight gain during pregnancy is attributed to the increase in the intravascular and extravascular fluid volumes. Significant increases in maternal blood volume occur, with plasma volume increasing 55% from 40 mL/kg to 70 mL/kg and red blood cell volume increasing approximately 17% from 25 mL/kg to 30 mL/kg (1,2) (Fig. 1-1). This increase in volume begins in the first few weeks of gestation, rises sharply in the second trimester, peaks early in the third trimester and decreases slightly by term (1). The rise in plasma volume is likely achieved by a decreased osmotic threshold for thirst and alterations in arginine vasopressin metabolism (3). A large portion of the increased blood volume perfuses the gravid uterus and 300 to 500 mL of blood may be forced back into the maternal circulation with contractions during labor (2,4). Blood volume returns to prepregnancy values at approximately 7 to 14 days postpartum (2).

Increased red blood cell production is stimulated by a rise in erythropoietin by the second month of gestation (5). The disproportionate increase in plasma volume to red blood cell volume results in the “physiologic anemia of pregnancy” and a normal hemoglobin concentration of 11.6 gm/dL (6). Maternal anemia is present when the hemoglobin and hematocrit fall to less than 11 g/dL or 33% respectively, the most likely cause of which is iron deficiency.

The increase in blood volume during pregnancy prepares the parturient for normal blood loss at delivery. Blood loss is usually less than 500 mL for vaginal delivery and 1,000 mL for cesarean delivery. Hemodynamic changes due to blood loss are usually not observed until the blood loss is greater than 1,500 mL and transfusion is rarely required unless blood loss exceeds this amount. Blood volume decreases to 125% of prepregnancy levels in the first postpartum week and by the sixth to ninth postpartum week there is a more gradual decline in the blood volume to 110% of the prepregnancy level. The hemoglobin and hematocrit also decrease during the initial postpartum period and then gradually increase to prepregnancy levels by the sixth postpartum week.

Cardiac output begins to increase around 10 weeks’ gestation (7). Serial assessment of maternal cardiac output by impedance cardiography and echocardiography demonstrates that changes in cardiac output start early in gestation with an increase of 35% to 40% by the end of first trimester. The cardiac output continues to increase during pregnancy until 34 weeks when it reaches 50% above prepregnant values and remains stable until term (8,9) (Fig. 1-3). During this time, the percentage of cardiac output devoted to uterine blood flow increases from 5% to 11% (8).

The increase in cardiac output is due to increases in heart rate and stroke volume. The initial increase in cardiac output is due to an increase in the heart rate which starts to occur as early as the fifth week of gestation. The heart rate rises steadily during pregnancy and is elevated approximately 10 to 20 bpm above baseline at term (Fig. 1-4). The hormonal changes and release of estrogens results in an early increase in stroke volume of approximately 20% as early as the fifth to eighth week of gestation. The stroke volume continues to increase by 25% to 30% from the first to third trimester of gestation.

During parturition, further demands are placed on the heart. Additional increases in cardiac output occur during labor and delivery as a result of elevated heart rate and stroke volume
(10,11). Cardiac output further increases 15% during the latent phase of labor, 30% during the active phase, and 45% during the expulsive stage of labor compared to prelabor values (11). Every uterine contraction results in an increase in cardiac output by an additional 10% to 25% (12). Immediately following cesarean delivery, cardiac index increases by 40% and systemic vascular resistance index (SVRI) decreases by 39%. However, the mean arterial pressure is maintained. These changes persist for approximately 10 minutes but may be present for up to 30 minutes after delivery, and return to baseline values by 2 to 5 days postpartum (13). Hemodynamic changes at delivery are similar regardless of mode of delivery (13,14). While this substantial increase in cardiac work is well tolerated by most parturients, those with cardiac disease who are unable to increase cardiac output by meeting the large demands are often at highest risk for complications immediately postpartum.

Systemic vascular resistance decreases from approximately 1,530 dyn s/cm⁵ to 1,210 dyn s/cm⁵ during pregnancy by several mechanisms (7). The production of prostacyclin, a potent vasodilator, is increased during pregnancy (15). Progesterone also has a vasodilator effect on vascular smooth muscle. The low resistance placental circulation is in parallel with the systemic circulation. The sum of two resistances in parallel is less than either alone, which serves to decrease the afterload. The physiologic anemia of pregnancy results in a change in rheology resulting in decreased blood viscosity and improved blood flow, which also decreases afterload (16). Pulmonary vascular resistance (PVR) is also reduced by approximately 30% during pregnancy, presumably by similar mechanisms (7,17). This may have important implications in a patient with a shunt due to a congenital cardiac lesion as the balance between SVR and PVR may be disrupted during pregnancy.

The increase in cardiac output during gestation results in an overall increase in uteroplacental perfusion, renal perfusion, and lower y perfusion. Uterine blood flow increases gradually from 50 mL/min to 700 to 900 mL/min at term with over 90% of the blood flow going to the intervillous space. The remainder of the perfusion goes to the myometrium. At term, the skin blood flow increases by 3- to 4-fold thus resulting in an increase in the skin temperature.

During gestation, the diaphragm is shifted upward by the gravid uterus. The result is a leftward shift in the position of the heart that can produce an enlarged appearance of the cardiac silhouette on chest radiograph (Fig. 1-5) as well as axis changes on the ECG. Echocardiographic studies reveal
left ventricular hypertrophy, demonstrated by increased end-diastolic chamber size and increased left ventricular wall thickness compared to nonpregnant women (18). The increase in cardiac mass is due to increased cardiac myocyte size rather than increased myocyte number (19). The left ventricular mass increases during gestation by 23% by the third trimester. Left ventricular end-diastolic volume also increases during gestation, with no change in the end-systolic volume thus resulting in a larger ejection fraction. When monitoring the hemodynamics, it should be noted that the central venous pressure, pulmonary artery diastolic pressure, and pulmonary capillary pressure are the same and comparable to the values in nonpregnant patients. Asymptomatic pericardial effusion has been reported in some parturients by echocardiographic studies (20).

Normal ECG findings in pregnancy include shortened PR and uncorrected QT interval, a shift in the QRS axis in any direction, a small right QRS axis deviation in the first trimester, a small leftward QRS axis deviation in the third trimester, and transient S–T segment changes. Women with long QT syndrome experience fewer cardiac events during pregnancy but are at increased risk for cardiac events ranging from syncope to sudden death in the 9 months following delivery (21). The most common benign dysrhythmias in pregnancy are premature ectopic atrial and ventricular contractions and sinus tachycardia (22). These normal findings must be differentiated from those indicating heart disease which include: (a) Systolic murmur greater than grade III; (b) any diastolic murmur; (c) severe arrhythmias; and (d) unequivocal cardiac enlargement on radiographic examination (21,22). Regurgitation of the pulmonary and tricuspid valves is observed in 94% of normal pregnant women at term, while regurgitation of the mitral valve is present in
27% (23). Changes in heart sounds are not uncommon during pregnancy with an accentuation of the first heart sound and an exaggerated splitting of the mitral and tricuspid component. There are minimal changes in the second heart sound. In late pregnancy, a third heart sound may be heard as well (24). A murmur resulting from aortic regurgitation is not normally present in the pregnant patient (23), but grade I to II systolic heart murmurs caused by increased blood flow and tricuspid annulus dilation are commonly heard on auscultation of the heart (24).

The maternal blood pressure measurement is affected by position, gestational age, maternal age, and parity. The changes in systemic vascular resistance result in a decrease in the systolic, diastolic, and mean arterial pressure during midgestation followed by a return to baseline by the end of gestation. The decrease in diastolic pressure is more than the systolic pressure with maximum decrease of 20% toward the midgestation (Fig. 1-6). Blood pressure increases with maternal age. Measurement of blood pressure obtained in the dependent left arm in the left lateral position correlates closely with the supine or sitting blood pressure.

Decreased systemic vascular resistance results in part from the blood flow through the developing low resistance bed of the uterine intervillous space. Studies attribute the decrease in vascular tone to α- and β-receptor down-regulation and increased prostacyclin production (25,26,27), resulting in increased renal, uterine, and extremity blood flow. Despite a general decrease in vascular tone, there is greater maternal dependence on the sympathetic nervous system for maintenance of hemodynamic stability during pregnancy. Dependence increases progressively throughout pregnancy and peaks at term (28,29,30). The effects of decreased vascular tone are primarily observed on the venous capacitance system of the lower extremities. These effects counteract the untoward effects of uterine compression of the inferior vena cava on venous return. Parasympathetic deactivation toward term is likely to contribute to increased heart rate and cardiac output at rest (31). Complex hormonal mediation results in depression of baroreflexes during pregnancy, making pregnant women even more susceptible to hypotension (32). In addition, some investigators suggest that an even greater decrease in vagal tone during pregnancy allows for relatively normal sympathetic function (33,34). This helps to explain why few women become severely bradycardic despite the high sympathectomy commonly seen at cesarean delivery. Although pharmacologic sympathectomy in term pregnant women can result in a marked decrease in blood pressure, there are minimal changes in blood pressure in nonpregnant women (28).

Upon assuming the supine position, up to 15% of pregnant patients near term experience signs of shock, including hypotension, pallor, sweating, nausea, vomiting, and mental status changes. This constellation of symptoms is due to decreased venous return to the right ventricle and has been dubbed “supine-hypotension syndrome” (35). Imaging studies demonstrate complete or nearly complete occlusion of the inferior vena cava by the gravid uterus in the supine position (36,37). Partial compensation is accomplished by blood bypassing the obstructed inferior vena cava and returning to the heart via the paravertebral (epidural) veins emptying into the azygos system. However, the net result of occlusion of the inferior vena cava is decreased cardiac output and decreased organ perfusion in the supine position. Shifting from the supine to the lateral position partially relieves the obstruction of the vena cava (37) (Fig. 1-7). The collateral circulation is adequate enough to maintain right ventricular filling pressures in the lateral position.

Compression of the inferior vena cava is most common in late pregnancy before the fetal presenting part becomes fixed in the pelvis. The pooling of venous blood in the lower extremities results in a tendency toward phlebitis, venous varicosities, and lower extremity edema during pregnancy. Ankle edema, leg varicosities, and hemorrhoids indicate lower extremity venous engorgement. Blood flow to the uterus is proportional to perfusion pressure, i.e., uterine artery minus venous pressure. Compression of the inferior vena cava affects uteroplacental perfusion resulting in an overall decrease in perfusion. Increased uterine venous pressure further decreases uterine blood flow which can compromise fetal well-being. Even when maternal blood pressure is normal, uterine artery perfusion pressure decreases in the supine position because of increases in uterine venous pressure. While typically not associated with maternal symptoms, aortic compression results in increased maternal blood pressure measured in the upper extremity analogous to an aortic cross clamp. Partial occlusion of the aorta by the gravid uterus occurs in the supine position as well (38). At the same time, arterial hypotension is occurring in the lower extremities and uterine arteries. This results in decreased uterine blood flow to the fetus and fetal hypoxia (39). Therefore, even with normal upper extremity maternal blood pressure, uteroplacental perfusion may be decreased in the supine position. In fact, turning the term parturient from the supine to the left lateral position increases intervillous blood flow by 20% and increases fetal oxygen tension by 40% (40,41). Nonreassuring fetal heart rate patterns are more often observed in parturients in the supine position, particularly in the presence of neuraxial or general anesthesia (42).

It is critical during anesthetic management to recognize the importance of aortocaval compression, the effects of which are observed as early as the 20th week of gestation. Drugs causing vasodilation, such as propofol and volatile anesthetics, or techniques resulting in sympathetic blockade, will further decrease venous return to the heart in the presence of vena cava obstruction. The presence of sympathetic blockade reduces or eliminates vasoconstriction in response to decreased venous return thus prevention of aortocaval compression is imperative. The vast majority of women avoid the supine position at night after 30 weeks (43). Therefore, it would do well to heed this natural instinct and avoid the supine position in a gravid patient. Maintaining the patient in lateral position with left uterine displacement (LUD) is essential to prevent aortocaval compression. This can be accomplished by manual displacement of the uterus, where the uterus is lifted and displaced to the left. Other alternatives include tilting the operating or delivery table 15 degrees or using sheets, a foam rubber wedge, or an inflatable bag to elevate the right buttock and back 10 to 15 cm. In the presence of conditions such as polyhydramnios or multiple gestations where the uterus is unusually large, more displacement (up to 30 degrees) may be required to relieve compression of the great vessels (44). Visual assessment of the position of the uterus is often invaluable—when the patient is in the supine position, the uterus should be visibly tilted away from the great vessels in the abdomen. Frequently, when maternal hypotension is present left uterine displacement is inadequate and repositioning the patient should be immediately considered. Occasionally, right uterine displacement or right lateral position may be at least as effective as left uterine displacement. Placement of the mother in LUD is imperative during cesarean delivery because neonates have less frequent and less severe depression of Apgar scores and are less likely to develop acidosis when LUD is employed (45). The Trendelenburg position without LUD is not an effective means to prevent or treat maternal hypotension and in fact, may worsen the maternal vital signs by shifting the uterus back further onto the vena cava and aorta. Maternal bearing down during the second stage of labor may also cause aortocaval compression and potentially decreased uterine perfusion (46). Any gravid patient near term with hypotension should be placed in LUD or the complete lateral position without delay as adequate venous return is essential to the success of any subsequent treatment. The anesthetic significance of the cardiovascular changes in pregnancy is summarized in Table 1-2.

Upper airway changes begin early in the first trimester and increase progressively throughout the duration of the pregnancy (47). Capillary engorgement of the larynx, nasal, and oropharyngeal mucosa leads to increased mucosal friability and vascularity of the upper airway. Many patients appear to have symptoms of an upper respiratory tract infection as a result of respiratory tract swelling. Furthermore, many patients complain of shortness of breath due to nasal congestion (48). The hormonal influences of pregnancy and, in particular, the effects of estrogen result in an increase in airway connective tissue, increased blood volume, increased total body water, and an increase in interstitial fluid. These factors contribute to hypervascularity and edema of oropharynx, nasopharynx, and respiratory tract. The edematous changes in soft tissue of the airway may be markedly exacerbated by a mild upper respiratory infection, or fluid overload. Increased vascularity and consequent mucosal engorgement can be expected to be even greater in parturients with preeclampsia resulting in difficult endotracheal intubation especially in laboring women (49). All of these changes contribute to an increase in the Mallampati classification of the airway during pregnancy and labor resulting in a compromised airway (50). Manipulation of the airway should be approached with caution since all of these changes have important implications for airway management.

Although an 8 mm cuffed endotracheal tube many be suitable for a nonpregnant adult woman, pregnant women will typically require a smaller endotracheal tube, usually 6.0 to 6.5 mm because of increased vascularity and edema. Consequently, mucosal injury during suctioning, airway placement, and laryngoscopy is more likely, and should such injury occur, there is an increased risk of excessive bleeding. Nasotracheal intubation and placement of nasogastric tubes should be avoided unless absolutely necessary, because of the potential for significant epistaxis.

The thorax also undergoes several important changes during pregnancy. Increases in both the anteroposterior and transverse diameters contribute to a 5 to 7 cm circumferential enlargement of the thoracic cage (47,51). Increased levels of relaxin causes structural changes in the ribcage resulting in relaxation of the ligamentous attachment of the ribs and an ∼50% increase in the subcostal angle (52). Although the diaphragm is elevated by as much as 4 cm, diaphragmatic excursion is increased despite this change. These changes have important implications in the pregnant patient who sustains a penetrating thoracic injury resulting in a concurrent abdominal injury secondary to the elevated diaphragm.

Lung volumes or capacities are not changed substantially during gestation. The total lung capacity is generally preserved or minimally decreased during pregnancy (53,54). Although changes in lung capacity are primarily due to a decrease in the functional residual capacity (15% to 20%) at term, tidal volume increases by nearly 45% during pregnancy. The majority of the increase occurs during the first trimester, and results in a increase in inspiratory reserve volume. In
addition, a decrease in residual volume helps to maintain the vital capacity. By the third trimester, the inspiratory capacity increases resulting from increases in both tidal volume and inspiratory reserve volumes (53,55). Consequently, expiratory reserve volume decreases (53,55).

Decreases in FRC result from elevation of the diaphragm and the enlarging uterus. These changes begin during the 20th week of pregnancy and are decreased 80% of prepregnancy by term (53,55,56). Functional residual capacity is reduced even further when parturients assume a supine position (Fig. 1-8). Vital capacity measurements in the upright position remain essentially unchanged; it also remains unchanged throughout pregnancy largely due to an increase in the inspiratory reserve volume. A measurable decrease in vital capacity occurs in obese parturients. The supine position markedly impairs the respiratory function in late pregnancy. Measurements of closing volume (lung volumes at which small airways begin to close in the dependent zones of the lungs) decrease by 30% to 50% in pregnant patients while they are in the supine position. Since the closing capacity will exceed the FRC, the parturient is at risk for hypoxemia and impaired organ perfusion in the supine position.

Minute ventilation is increased by 30% at the seventh week of pregnancy and approximately 50% at term (57,58,59). Hormonal changes (60) and greater CO₂ production (61) result in increased tidal volume with little change in respiratory rate and are responsible for the increased minute ventilation. Although the ratio of total dead space to tidal volume is unchanged during pregnancy, there is an increase in alveolar ventilation approximately 30% above baseline. Progesterone acts as a direct respiratory stimulant (62) and sensitizes central respiratory centers, increasing the ventilatory response to CO₂ and producing a leftward shift of the CO₂ curve (63). A recent study has shown that the hyperventilation of human pregnancy is the result of pregnancy-induced changes in wakefulness and central chemoreflex drives for breathing, acid–base balance, metabolic rate, and cerebral blood flow (64). Although CO₂ production at rest increases by about 300 mL/min during pregnancy (61), a normal pregnant PaCO₂ is 30 to 32 mm Hg, owing to the hyperventilation. Due to increased urinary excretion of bicarbonate (normal pregnant level 20 mm Hg), however, pH is partially corrected;
normal pH is 7.41 to 7.44 (65). These changes in the arterial blood gas analysis have important implications for anesthetic management. For example, if a pregnant woman’s PaCO₂ is 40 mm Hg, this indicates hypercarbia and the need for further evaluation and treatment.