Pregnancy causes the heart to increase in size, a result of both greater blood volume and increased stretch and force of contraction. These changes, coupled with the elevation of the diaphragm from the expanding uterus, cause several changes in the physical examination and in cardiac studies.

Changes in heart sounds include accentuation of the first heart sound with exaggerated splitting of the mitral and tricuspid components ( Box 2.1 ). The second heart sound changes little, although the aortic-pulmonic interval tends to vary less with respiration during the third trimester, a finding without clinical significance. A fourth heart sound may be heard in 16% of pregnant women, although typically it disappears at term. A grade II systolic ejection murmur is commonly heard at the left sternal border ; the murmur is considered a benign flow murmur, attributable to cardiac enlargement from increased intravascular volume, which causes dilation of the tricuspid annulus and mild tricuspid regurgitation. Elevation of the diaphragm by the growing uterus may shift the mediastinum anteriorly. Evidence of cephalad cardiac displacement varies by study with minimal change in position seen from magnetic resonance imaging and up to 6 cm cranial shift seen on transthoracic echocardiography. No change in hand position for cardiopulmonary resuscitation is recommended for pregnant women compared with nonpregnant women.

Echocardiography demonstrates left ventricular (LV) hypertrophy by 12 weeks’ gestation with a 23% increase in LV mass from the first to the third trimester and an overall 50% increase in mass at term. This eccentric hypertrophy results from an increase in the size of the preexisting cardiomyocytes, resembling the changes that occur from repeated, strenuous exercise. Left atrial diameter increases during pregnancy with maximum diameter in the third trimester. The annular diameters of the mitral, tricuspid, and pulmonic valves increase; 94% of term pregnant women exhibit tricuspid and pulmonic regurgitation, and 27% exhibit mitral regurgitation. The aortic annulus does not dilate from normal pregnancy-induced physiologic changes.

The electrocardiogram typically changes, especially during the third trimester. Heart rate steadily increases during the first and second trimesters, and both the PR interval and the uncorrected QT interval are shortened. This has clinical implications for women with long QT syndrome (see Chapter 41 ). The QRS axis shifts to the right during the first trimester but may shift to the left during the third trimester. Depressed ST segments and isoelectric low-voltage T waves in the left-sided precordial and limb leads are common.

To accurately determine central hemodynamic values and/or changes during pregnancy, patient position should be considered to minimize the impact of aortocaval compression. Comparisons must be made with an appropriate control, such as prepregnancy values or a matched group of nonpregnant women. If control measurements are made postpartum, a sufficient interval must elapse for parameters to have returned to prepregnancy values; this may take weeks to months. There is significant heterogeneity in cardiac output measurement using different noninvasive devices; these differences should be taken into account when caring for individual patients. There may also be diurnal variation in cardiac output, cardiac index, and heart rate measurements, with the highest measurements occurring in the afternoon.

Cardiac output begins to increase by 5 weeks’ gestation and is 35% to 40% above baseline by the end of the first trimester. It continues increasing throughout the second trimester to approximately 50% greater than nonpregnant values ( Figs. 2.1 and 2.2 ). Cardiac output does not change further during the third trimester. Some studies have reported a decrease in cardiac output during the third trimester; however, typically this is with measurements made in the supine position and thus likely reflects vena caval compression rather than a true gestational decline.

Central Hemodynamic Changes at Term Gestation .

Changes are relative to the nonpregnant state. CO , Cardiac output; CVP , central venous pressure; EF , ejection fraction; HR , heart rate; LVEDV , left ventricular end-diastolic volume; LVESV , left ventricular end-systolic volume; LVSWI , left ventricular stroke work index; NC , no change; PADP , pulmonary artery diastolic pressure; PCWP , pulmonary capillary wedge pressure; SV , stroke volume; SVR , systemic vascular resistance.

Data from Conklin KA. Maternal physiological adaptations during gestation, labor, and puerperium. Semin Anesth . 1991;10:221–234.

Cardiac Output During Pregnancy, Labor, and the Puerperium .

Values during pregnancy are measured at the end of the first, second, and third trimesters. Values during labor are measured between contractions. For each measurement, the relative contributions of heart rate ( HR ) and stroke volume ( SV ) to the change in cardiac output are illustrated.

The initial increase in cardiac output results from an increase in heart rate. Heart rate increases 15% to 25% above baseline by the end of the first trimester and remains relatively stable for the remainder of the pregnancy. Cardiac output continues to increase through the second trimester owing to an increase in stroke volume. Stroke volume increases by approximately 20% during the first trimester and by 25% to 30% above baseline during the second trimester. The increased stroke volume correlates with increasing estrogen levels. Stroke volume index decreases over the course of pregnancy, while cardiac index remains slightly increased from prepregnancy values.

LV end-diastolic volume increases during pregnancy, whereas end-systolic volume remains unchanged, resulting in a larger ejection fraction. Central venous, pulmonary artery diastolic, and pulmonary capillary wedge pressures are within the normal nonpregnant range. The apparent discrepancy between LV filling pressure and end-diastolic volume is explained by both hypertrophy and dilation, with the dilated ventricle accommodating a greater volume without an increase in pressure.

Myocardial contractility increases, as demonstrated by a higher velocity of LV circumferential fiber shortening. Tissue Doppler imaging, which is relatively independent of preload, has been used to assess diastolic function. A mild degree of diastolic dysfunction may be seen during the third trimester compared with earlier in pregnancy and nonpregnant controls.

The increase in cardiac output during pregnancy results in increased perfusion to the uterus, kidneys, and extremities. Uterine blood flow increases to meet the demands of the developing fetus from a baseline value of approximately 50 mL/min (prepregnancy) to a level at term of 700 to 900 mL/min. During the second half of pregnancy, the proportion of cardiac output distributed to the uterine circulation increases from 5% to 12%. Approximately 90% of this flow perfuses the intervillous space, with the balance perfusing the myometrium. At term, skin blood flow is approximately three to four times the nonpregnant level, resulting in higher skin temperature. Renal plasma flow is increased by 80% at 16 to 26 weeks’ gestation but is only 50% above the prepregnancy baseline at term.

The US Department of Health and Human Services recommends that pregnant women have at least 150 minutes of moderate-intensity aerobic activity every week, and the American College of Obstetricians and Gynecologists recommends 20 to 30 minutes per day ; however, most women do not achieve this goal. Pregnant women are less active, with only half as many meeting guidelines for vigorous activity compared with nonpregnant women. For every two women who exercise before pregnancy, one will not do so during pregnancy. Failure to exercise increases the risk for greater gestational weight gain. Exercise is safe for the fetus ; in a study of 45 women, exercise on a treadmill of moderate intensity (40% to 59% of heart rate reserve) did not affect fetal heart or umbilical artery Doppler indices.

During exercise, maximal oxygen consumption is greater in pregnancy, especially during cardiovascular exercise. The rate of increase in minute ventilation is greater with exercise during pregnancy. Cardiac output is also greater, primarily from increased stroke volume and oxygen delivery to the fetus.

Positioning, gestational age, and parity affect blood pressure measurements. Brachial sphygmomanometry yields the highest measurements in the supine position and the lowest measurements in the lateral position, especially with the cuff on the nondependent arm. Blood pressure increases with maternal age, and for a given age, nulliparous women have a slightly higher mean pressure than parous women, although with extended interpregnancy intervals that effect is lost. Systolic, diastolic, and mean blood pressure decrease during mid-pregnancy and return toward baseline as the pregnancy approaches term. Diastolic blood pressure decreases more than systolic blood pressure, with early- to mid-gestational decreases of approximately 20%.

The changes in blood pressure are consistent with changes in systemic vascular resistance (SVR), which decreases during early gestation, reaches its nadir (35% decline) at 20 weeks’ gestation, and increases toward prepregnancy baseline during late gestation. Unlike blood pressure, however, SVR remains approximately 20% below the nonpregnant level at term. A postulated explanation for the decreased SVR is the low-resistance uteroplacental vascular bed as well as systemic maternal vasodilation caused by prostacyclin, estrogen, and progesterone. Other contributions may come from elevation in systemic levels of nitric oxide, prostacyclin, endothelium-derived hyperpolarizing factor, progesterone, and relaxin. The trend toward lower blood pressure often persists beyond pregnancy. A longitudinal study of 2304 initially normotensive women over 20 years showed that nulliparous women who subsequently delivered one or more infants maintained a blood pressure that was 1 to 2 mm Hg lower than women who did not have children. This finding demonstrates that pregnancy may create long-lasting vascular changes. Advanced maternal age has been associated with higher median SVR during pregnancy, and pregnant women who smoke have demonstrated a lower SVR compared with nonsmoking parturients.

The extent of compression of the aorta and inferior vena cava by the gravid uterus depends on positioning and gestational age. At term, partial vena caval compression occurs when the woman is in the lateral position, as documented by angiography. This finding is consistent with the 75% elevation above baseline of femoral venous and lower inferior vena caval pressures. Despite caval compression, collateral circulation maintains venous return, as reflected by right ventricular filling pressure, which is unaltered in the lateral position. Intraabdominal pressure is often elevated in term pregnant patients regardless of BMI but is significantly lower in the lateral position compared with supine.

In the supine position, significant and sometimes complete compression of the inferior vena cava is evident at term. Blood returns from the lower extremities through the intraosseous, vertebral, paravertebral, and epidural veins. However, this collateral venous return is less than would occur through the inferior vena cava, resulting in a decrease in right atrial pressure. Compression of the inferior vena cava occurs as early as 13 to 16 weeks’ gestation and is evident from the 50% increase in femoral venous pressure observed when these women assume the supine position ( Fig. 2.3 ). By term, femoral venous and lower inferior vena caval pressures are approximately 2.5 times the nonpregnant measurements in the supine position. Vena cava volume at term is significantly higher with 30-degree left lateral tilt compared with the supine position, whereas there is no difference between women in the supine position and those tilted left at 15 degrees. A minority of women have the highest inferior vena cava volume with 30-degree right lateral tilt.

Femoral and Antecubital Venous Pressures in the Supine Position Throughout Normal Pregnancy and the Puerperium.

Modified from McLennan CE. Antecubital and femoral venous pressure in normal and toxemic pregnancy. Am J Obstet Gynecol . 1943;45:568–591.

In the supine position, the aorta may be compressed by the term gravid uterus. This compression could account for lower pressure in the femoral versus the brachial artery in the supine position. Angiographic studies in supine pregnant women showed partial obstruction of the aorta at the level of the lumbar lordosis and enhanced compression during periods of maternal hypotension. Conversely, a comparison of magnetic resonance images of healthy women at term in the supine position compared with nonpregnant women showed no difference in aortic volume at the level of the mid- to upper lumbar vertebra.

At term, the left lateral decubitus position is associated with less enhancement of cardiac sympathetic nervous system activity and less suppression of cardiac vagal activity than the supine or right lateral decubitus position. Women who assume the supine position at term gestation experience a 10% to 20% decline in stroke volume and cardiac output, consistent with the decrease in right atrial filling pressure. Blood flow in the upper extremities is normal, whereas uterine blood flow decreases by 20% and lower extremity blood flow decreases by 50%. Perfusion of the uterus is less affected than that of the lower extremities because compression of the vena cava does not obstruct venous outflow via the ovarian veins. The adverse hemodynamic effects of aortocaval compression are reduced once the fetal head is engaged. The sitting position, especially with neck and hip flexion, has also been shown to rotate the uterus against the vena cava, resulting in aortocaval compression with a decrease in cardiac output of 10%. There is no evidence that short intervals in the sitting position, such as occurs during epidural catheter placement, have any clinically significant impact on uteroplacental blood flow.

Some term pregnant women exhibit an increase in brachial artery blood pressure when they assume the supine position, which is caused by higher SVR from compression of the aorta. Up to 15% of women at term experience bradycardia and a substantial decrease in blood pressure when supine, the so-called supine hypotension syndrome . It may take several minutes for the bradycardia and hypotension to develop, and the bradycardia is usually preceded by a period of tachycardia. The syndrome results from a profound decrease in venous return and preload for which the cardiovascular system is not able to compensate.

Cardiac output during labor (but between uterine contractions) increases from prelabor values by approximately 10% in the early first stage, by 25% in the late first stage, and by 40% in the second stage of labor. In the immediate postpartum period, cardiac output may be as much as 75% above predelivery measurements and 150% above prepregnancy baseline. These changes result from an increase in stroke volume caused by greater venous return and increased sympathetic nervous system activity. During labor, uterine contractions displace 300 to 500 mL of blood from the intervillous space through the ovarian venous outflow system into the central circulation (autotransfusion). The postpartum increase in cardiac output results from relief of vena caval compression, diminished lower extremity venous pressure, sustained myometrial contraction, and increased venous return. Cardiac output decreases to just below prelabor values at 24 hours postpartum and returns to prepregnancy levels between 12 and 24 weeks postpartum (see Fig. 2.2 ). Heart rate decreases rapidly after delivery, reaches prepregnancy levels by 2 weeks postpartum, and is slightly below the prepregnancy rate for the next several months.

The thorax undergoes both mechanical and hormonal changes during pregnancy. Relaxin (the hormone responsible for relaxation of the pelvic ligaments) causes relaxation of the ligamentous attachments to the lower ribs. The subcostal angle progressively widens from approximately 69 degrees to 104 degrees. The anteroposterior and transverse diameters of the chest wall each increase by 2 cm, resulting in an increase of 5 to 7 cm in the circumference of the lower rib cage. These changes peak at 37 weeks’ gestation. The subcostal angle remains about 20% wider than the baseline value after delivery. The vertical measurement of the chest cavity decreases by as much as 4 cm as a result of the elevated position of the diaphragm ( Fig. 2.4 ). The timing of return to baseline nonpregnant status is unclear.

Changes in the Geometry of the Ribcage During Pregnancy .

The position of the ribs is depicted for the first (T1), the second (T2), and the third (T3) trimesters of pregnancy.

Reproduced from LoMauro A, Aliverti A. Respiratory physiology in pregnancy and assessment of pulmonary function. Best Pract Res Clin Obstet Gynaecol . 2022;85(Pt A):3–16.

Capillary engorgement of the larynx and the nasal and oropharyngeal mucosa begins early in the first trimester and increases progressively throughout pregnancy. The effect of estrogen on the nasal mucosa may cause symptoms of rhinitis and epistaxis. Nasal breathing commonly becomes difficult, and nasal congestion may contribute to the perceived shortness of breath of pregnancy.

Inspiration in the term pregnant woman is almost totally attributable to diaphragmatic excursion because of greater descent of the diaphragm from its elevated resting position and limitation of thoracic cage expansion because of its expanded resting position ( Table 2.2 ). Both large- and small-airway functions are minimally altered during pregnancy. The shape of flow-volume loops, the absolute flow rates at normal lung volumes, forced expiratory volume in 1 second (FEV ₁ ), the ratio of FEV ₁ to forced vital capacity, and closing capacity are unchanged during pregnancy. There is no significant change in respiratory muscle strength during pregnancy despite the cephalad displacement of the diaphragm. Furthermore, despite the upward displacement of the diaphragm by the gravid uterus, diaphragm excursion actually increases by 2 cm.

The peak expiratory flow (PEF) rate achieved with a maximal effort after a maximal inspiration is often considered a surrogate for FEV ₁ and can be used to monitor asthma therapy. Studies of changes in PEF rate during pregnancy show conflicting results, likely reflecting differences in measurement devices and patient position; however, any changes seen are likely not clinically significant and PEF remains a valid tool during pregnancy. In the postpartum period, Harirah et al. reported significantly decreased PEF at 6 weeks.

Lung volumes can be measured by using body plethysmography or inert gas techniques with slightly differing results. By term, total lung capacity is slightly reduced, whereas tidal volume increases by 45%, with approximately half the change occurring during the first trimester ( Table 2.3 and Fig. 2.5 ). The early change in tidal volume is associated with a transient reduction in inspiratory reserve volume. Residual volume tends to decrease slightly, a change that maintains vital capacity. Inspiratory capacity increases by 15% during the third trimester because of increases in tidal volume and inspiratory reserve volume. There is a corresponding decrease in expiratory reserve volume. The functional residual capacity (FRC) begins to decrease by the fifth month of pregnancy with uterine enlargement and diaphragm elevation and is decreased by 400 to 700 mL to 80% of the prepregnancy value at term. The overall reduction is caused by a 25% (200 to 300 mL) reduction in expiratory reserve volume and a 15% (200 to 400 mL) reduction in residual volume. Assumption of the supine position causes the FRC to decrease further to 70% of the prepregnancy value. The supine FRC can be increased by 10% (approximately 188 mL) by placing the patient in a 30-degree head-up position.

Lung Volumes and Capacities During Pregnancy. ERV , Expiratory reserve volume; FRC , functional residual capacity; IC , inspiratory capacity; IRV , inspiratory reserve volume; RV , residual volume; TLC , total lung capacity; TV , tidal volume; VC , vital capacity.

During pregnancy, respiratory patterns remain relatively unchanged. Minute ventilation increases via an increase in tidal volume from 450 to 600 mL and a small increase in respiratory rate of 1 to 2 breaths/min. This occurs primarily during the first 12 weeks of gestation with a minimal increase thereafter. The ratio of total dead space to tidal volume remains constant during pregnancy, resulting in an increase in alveolar ventilation of 30% to 50% above baseline. The increase in minute ventilation results from hormonal changes and from an increase in CO ₂ production at rest by approximately 30% to 300 mL/min. The former is closely related to the blood level of progesterone, which acts as a direct respiratory stimulant. The progesterone-induced increase in chemosensitivity also results in a steeper slope and a leftward shift of the CO ₂ -ventilatory response curve. This change occurs early in pregnancy and remains constant until delivery.

Dyspnea is a common complaint during pregnancy, affecting up to 75% of women. Contributing factors include increased respiratory drive, decreased Pa co ₂ , increased oxygen consumption from the enlarging uterus and fetus, larger pulmonary blood volume, anemia, and nasal congestion. Dyspnea typically begins in the first or second trimester but improves as the pregnancy progresses. In a study in which 35 women were observed closely during pregnancy and postpartum, dyspnea was not caused by alterations in central ventilatory control or respiratory mechanical factors but rather by the awareness of the increased ventilation. Exercise has no effect on pregnancy-induced changes in ventilation or alveolar gas exchange. The hypoxic ventilatory response is increased during pregnancy to twice the normal level, secondary to elevations in estrogen and progesterone levels. This increase occurs despite blood and cerebrospinal fluid (CSF) alkalosis.

During pregnancy, Pa o ₂ increases to 100 to 105 mm Hg (13.3 to 14.0 kPa) as a result of greater alveolar ventilation and a decline in Pa co ₂ ( Table 2.4 ). As pregnancy progresses, oxygen consumption continues to increase and cardiac output increases to a lesser extent, resulting in a reduced mixed venous oxygen content and increased arteriovenous oxygen difference. After mid-gestation, pregnant women in the supine position frequently have a Pa o ₂ < 100 mm Hg (13.3 kPa). This occurs because the FRC may be less than closing capacity, resulting in closure of small airways during normal tidal volume ventilation. Moving a pregnant woman from the supine to the erect or lateral decubitus position improves arterial oxygenation and reduces the alveolar-to-arterial oxygen gradient. The increased oxygen tension facilitates the transfer of oxygen across the placenta to the fetus.

Pa co ₂ declines to approximately 30 mm Hg (4.0 kPa) by 12 weeks’ gestation but does not change further during the remainder of the pregnancy. Although a gradient exists between the end-tidal CO ₂ tension and Pa co ₂ in nonpregnant women, the two measurements are equivalent during early pregnancy, at term gestation, and in the postpartum period. This is attributable to a reduction in alveolar dead space, which results from an increase in cardiac output and increased basilar atelectasis during pregnancy. The mixed venous P co ₂ is 6 to 8 mm Hg (0.8 to 1.1 kPa) below the nonpregnant level from late in the first trimester until term.

The respiratory alkalosis of pregnancy causes a compensatory increase in renal bicarbonate excretion and a reduction in serum bicarbonate concentration to approximately 20 mEq/L, the base excess by 2 to 3 mEq/L, and the total buffer base by approximately 5 mEq/L. This compensation is incomplete, as demonstrated by the elevation of venous, capillary, and arterial blood pH by 0.02 to 0.06 units (see Table 2.4 ). The decrease in plasmabicarbonate affects the woman’s ability to buffer an acid load while pregnant. The slight respiratory alkalosis would normally shift the oxyhemoglobin saturation curve to the left; however, a concurrent increase in 2,3-bisphosphoglycerate (also known as 2,3-diphosphoglycerate) causes the curve to shift slightly to the right.

Minute ventilation in the unmedicated parturient increases by 70% to 140% in the first stage of labor and by 120% to 200% in the second stage of labor compared with prepregnancy values. Pain, anxiety, and coached breathing techniques all increase minute ventilation. Pa co ₂ may decrease to as low as 10 to 15 mm Hg (1.3 to 2.0 kPa). Oxygen consumption increases above the prelabor value by 40% in the first stage of labor and by 75% in the second stage, secondary to the increased metabolic demands of hyperventilation, uterine activity, and maternal expulsive efforts. The maternal aerobic requirement for oxygen exceeds oxygen consumption during labor, as is evident from the progressive elevation of blood lactate concentration, an index of anaerobic metabolism. Effective neuraxial analgesia prevents these changes during the first stage of labor and mitigates the changes during the second stage of labor.

FRC increases after delivery but remains below the prepregnancy volume for 1 to 2 weeks. Although minute ventilation decreases halfway toward nonpregnant values by 72 hours, oxygen consumption, tidal volume, and minute ventilation remain elevated until at least 6 to 8 weeks after delivery. The alveolar and mixed venous P co ₂ values increase slowly after delivery and are still slightly below prepregnancy levels at 6 to 8 weeks postpartum.

Baseline gastric volume in fasting pregnant nonlaboring patients is not significantly different to that in nonpregnant women. The stomach is displaced upward toward the left side of the diaphragm during pregnancy, and its axis is rotated approximately 45 degrees to the right from its normal vertical position. This altered position displaces the intraabdominal segment of the esophagus into the thorax in most women, causing a reduction in tone of the lower esophageal high-pressure zone (LEHPZ), which normally prevents the reflux of gastric contents. Progestins also may contribute to relaxation of the LEHPZ.

Approximately 30% to 50% of women experience gastroesophageal reflux disease (GERD) during pregnancy. The prevalence of GERD is approximately 10% in the first trimester, 40% in the second trimester, and 55% in the third trimester. In the first trimester of pregnancy, basal LEHPZ pressure may not change, but the sphincter is less responsive to physiologic stimuli that usually increase pressure. In the second and third trimesters, LEHPZ pressure gradually decreases to approximately 50% of basal values, reaching a nadir at 36 weeks’ gestation and returning to prepregnancy values at 1 to 4 weeks postpartum ( Table 2.5 ). Risk factors for GERD in pregnancy include gestational age, heartburn antecedent to pregnancy, and multiparity. Gravidity, prepregnancy BMI, and weight gain during pregnancy do not correlate with the occurrence of reflux, whereas maternal age has an inverse correlation.

Gastric emptying is not altered during pregnancy. This has been demonstrated by studies that measured the absorption of orally administered acetaminophen (paracetamol) and by studies that assessed the emptying of a test beverage or meal by radiographic, ultrasonographic, dye dilution, epigastric impedance, and applied potential tomographic techniques. In a study of morbidly obese women at term, no difference was noted between gastric emptying of 300 and 50 mL of water, suggesting that fasting guidelines should not differ for obese versus lean parturients. In fasted pregnant patients who consumed 250 mL of tea with milk, ultrasonographic measurement of the gastric antrum returned to baseline by 90 minutes.

Esophageal peristalsis and intestinal transit are slowed during pregnancy, which has been attributed to the inhibition of gastrointestinal contractile activity by progesterone. However, this inhibition may be an indirect action that results from a negative effect of progesterone on the plasma concentration of motilin, which declines during pregnancy. Up to 40% of women suffer from constipation at some time during their pregnancy. The prevalence of constipation is greatest in the first two trimesters of gestation and declines in the third trimester.

Early work suggested that both basal and maximal gastric acid secretion decline in mid-gestation, reaching a nadir at 20 to 30 weeks’ gestation. Van Thiel et al. demonstrated no difference in basal or peak gastric acid secretion in four pregnant women studied in each trimester and at 1 to 4 weeks postpartum, although a plasma gastrin level significantly lower than postpartum levels was observed during the first trimester. Levels of gastric pH and serum gastrin concentration were compared in 100 women scheduled for elective cesarean delivery and in 100 nonpregnant women undergoing gynecologic surgery. The mean pH was lower in the pregnant group (2.4 versus 3.0), but serum gastrin levels were not different despite the fact that gastrin is secreted by the placenta from 15 weeks’ gestation onward. This may reflect a dilutional effect of increased plasma volume. Other studies have shown that approximately 80% of both pregnant and nonpregnant women have gastric pH ≤ 2.5, approximately 50% have gastric volume ≥ 25 mL, and 40% to 50% exhibit both low pH and gastric volume > 25 mL.

Approximately 80% of pregnant women will experience nausea and vomiting during pregnancy. The symptoms typically start between 4 and 9 weeks’ gestation and may last until 12 to 16 weeks’ gestation. Of these women, 1% to 5% will develop symptoms that persist throughout the pregnancy, known as hyperemesis gravidarum (see Chapter 17 ).

Gastric emptying is slowed during labor, as shown by ultrasonographic imaging, emptying of a test meal, and the rate of absorption of oral acetaminophen. Direct measurements show that the mean gastric volume increases. However, in one study, postpartum gastric volume was found to be no different in parturients who consumed water in labor compared with those who consumed an isotonic sports drink composed of mixed carbohydrates and electrolytes. Gastric acid secretion may decrease during labor because only 25% of parturients who are in labor have a gastric pH ≤ 2.5. Gastric emptying is also delayed during the early postpartum period but returns to prepregnancy levels by 18 hours postpartum. Fasting gastric volume and pH values are similar to nonpregnant patients at 18 hours postpartum. The effects of opioids and neuraxial analgesia on gastric emptying are discussed in Chapters 24 and 28 .

Maternal plasma volume expansion begins as early as 6 weeks’ gestation and continues until it reaches a net increase of approximately 50% by 34 weeks’ gestation ( Table 2.6 ; Fig. 2.6 ). After 34 weeks’ gestation, the plasma volume stabilizes or decreases slightly. Red blood cell volume decreases during the first 8 weeks of pregnancy, increases to the prepregnancy level by 16 weeks, and undergoes a further rise to 30% above the prepregnancy level at term. The red blood cell volume increases in response to elevated erythropoietin concentration and the erythropoietic effects of progesterone, prolactin, and placental lactogen. The increase in plasma volume exceeds the increase in red blood cell volume, resulting in the physiologic anemia of pregnancy . Hemoglobin concentration (hematocrit), which typically ranges from 12.0 to 15.8 g/dL (35.4% to 44.4%) in nonpregnant woman, decreases to 11.6 to 13.9 g/dL (31% to 41%) in the first trimester, 9.7 to 14.8 g/dL (30% to 39%) in the second trimester, and 9.5 to 15.0 g/dL (28% to 40%) in the third trimester ( Fig. 2.7 ). Women who do not receive iron supplements during pregnancy have greater decreases in hemoglobin concentration and hematocrit. Iron deficiency anemia in pregnancy is defined by a hemoglobin concentration < 10.5 g/dL in the second and third trimesters.

Blood Volume During Pregnancy and the Puerperium .

Values during pregnancy measured at the end of the first, second, and third trimesters. Postpartum values measured after a vaginal delivery. The values for red blood cell volume ( RBC ) and plasma volume ( Plasma ) do not represent the actual percentage of change in these parameters but rather reflect the relative contribution of each to the change in blood volume. The asterisk indicates that RBC volume is below the prepregnancy volume at the end of the first trimester.

The Decrease in Both Hemoglobin Concentration and Hematocrit During Pregnancy Underlies the Physiologic Anemia of Pregnancy .

The decrease is greater for hematocrit, and the greatest decreases occur during the third trimester.

Data from Abbassi-Ghanavati M, Greer LG, Cunningham FG. Pregnancy and laboratory studies: a reference table for clinicians. Obstet Gynecol . 2009;114:1326–1331.

The increase in plasma volume results from fetal and maternal hormone production, and several systems may play a role. The maternal concentrations of estrogen and progesterone increase nearly 100-fold during pregnancy. Estrogens increase plasma renin activity, enhancing renal sodium absorption and water retention via the renin-angiotensin-aldosterone system. Fetal adrenal production of the estrogen precursor dehydroepiandrosterone may be the underlying control mechanism. Progesterone also enhances aldosterone production. These changes result in marked increases in plasma renin activity and aldosterone level as well as in retention of approximately 900 mEq of sodium and 7000 mL of total body water. The concentration of plasma adrenomedullin, a potent vasodilating peptide, increases during pregnancy and correlates significantly with blood volume.

Blood volume is positively correlated with the size of the fetus in singleton pregnancies and is greater in multiple gestations. The physiologic hypervolemia facilitates delivery of nutrients to the fetus, protects the mother from hypotension, and reduces the risks associated with hemorrhage at delivery. The decrease in blood viscosity associated with the lower hematocrit decreases resistance to blood flow, which may be an essential component of maintaining the patency of the uteroplacental vascular bed.

Circulating blood volume may be overestimated with increasing BMI, and a pragmatic approach to estimating blood volume is based on maternal BMI category in a “mL/kg” calculation. For a parturient with a BMI of 18.5 to 24.9 kg/m ² the estimated circulating blood volume is 95 mL/kg, and for patients with a BMI of 25 to 29.9, 30 to 39.9, and more than 40 kg/m ² the estimated circulating blood volumes are 85, 75, and 70 mL/kg, respectively.

Plasma albumin concentration decreases from a nonpregnant range of 4.1 to 5.3 g/dL to ranges of 3.1 to 5.1 g/dL in the first trimester, 2.6 to 4.5 g/dL in the second trimester, and 2.3 to 4.2 g/dL in the third trimester ( Table 2.7 ). The globulin level decreases by 10% in the first trimester and then increases throughout the remainder of pregnancy to 10% above the prepregnancy value at term. The albumin-globulin ratio decreases during pregnancy from 1.4 to 0.9, and the total plasma protein concentration decreases from 7.8 to 7.0 g/dL. Maternal colloid osmotic pressure decreases by approximately 5 mm Hg during pregnancy. The plasma cholinesterase activity decreases by approximately 25% during the first trimester and remains at that level until the end of pregnancy.

Pregnancy is associated with enhanced platelet turnover, clotting, and fibrinolysis ( Box 2.2 ). Thus, pregnancy represents a state of accelerated but compensated intravascular coagulation.

Increases in platelet factor 4 and beta-thromboglobulin signal elevated platelet activation, and the progressive increase in platelet distribution width and platelet volume are consistent with greater platelet consumption during pregnancy. Platelet aggregation in response to collagen, epinephrine (adrenaline), adenosine diphosphate, and arachidonic acid is increased. Some investigators have noted a decrease in platelet count, whereas others have noted no change, suggesting that increased platelet production compensates for greater activation. The platelet count usually decreases during the third trimester, with an estimated 8% of pregnant women having a platelet count < 150,000/mm ³ and 0.9% of pregnant women having a platelet count < 100,000/mm ³ . The most common causes of thrombocytopenia are gestational thrombocytopenia , hypertensive disorders of pregnancy, and idiopathic thrombocytopenia. The decrease in platelet count in the third trimester is caused by increased destruction and hemodilution. Gestational thrombocytopenia is likely an exaggerated normal response.

The concentrations of most coagulation factors, including fibrinogen (factor I), proconvertin (factor VII), antihemophilic factor (factor VIII), Christmas factor (factor IX), Stuart-Prower factor (factor X), and Hageman factor (factor XII), increase during pregnancy. The increase in factor VIII is generally more marked in the third trimester. The concentrations of some factors increase by more than 100% (factors VII, VIII, IX, and fibrinogen). Prothrombin (factor II) and serum calcium (factor IV) concentrations do not change, whereas the concentrations of thromboplastin antecedent (factor XI) and fibrin-stabilizing factor (factor XIII) decrease. Proaccelerin (factor V) levels are thought to be stable during pregnancy, although some sources suggest a slight increase. An increase in most factor concentrations, shortening of the prothrombin time and activated partial thromboplastin time, an increase in fibrinopeptide A concentration, and a decrease in antithrombin III concentration suggest activation of the clotting system. Protein S activity decreases steadily during pregnancy, reaching the lowest values at delivery.

Thromboelastrography (TEG) demonstrates evidence of hypercoagulability in pregnancy. These changes (decrease in R and K values, increase in the α angle and maximum amplitude [MA], and decrease in measures of lysis) are observed as early as 10 to 12 weeks’ gestation and are even greater during labor ( Fig. 2.8 ). Compared with samples taken during labor, TEG has demonstrated increased lysis in the postpartum period, possibly caused by the loss of placental expression of plasminogen activator inhibitor-2. In vitro , exogenous oxytocin decreases R and K values, while increasing the α angle. The in vivo effects of exogenous oxytocin are not known. Studies of rotational thromboelastometry during pregnancy also report reference values that show a positive correlation with increasing hypercoagulability and increasing gestational age.

Comparative thromboelastographs in nonpregnant (group I), nonlaboring term pregnant (group II), and laboring (group III) women.

From Steer PL, Krantz HB. Thromboelastrography and sonoclot analysis in the healthy parturient. J Clin Anesth . 1993;5:419–424.

The greater concentration of fibrin degradation products signals increased fibrinolytic activity during gestation. D-dimer values increase across gestation and remain higher than prepregnancy values in the postpartum period. The marked elevation in the plasminogen concentration also is consistent with enhanced fibrinolysis.

Blood loss during normal vaginal delivery and the early puerperium is approximately 600 mL, compared with approximately 1000 mL during and within the first few hours of cesarean delivery. The hematocrit in the immediate postpartum period is lower after cesarean delivery than after vaginal delivery because of the greater blood loss during cesarean delivery. Regardless of the mode of delivery, the normal physiologic changes of pregnancy allow the healthy parturient to compensate for this blood loss. However, blood loss after either vaginal or cesarean delivery is often underestimated, and the discrepancy between actual and estimated blood loss is greater with increasing blood loss (see Chapter 37 ).

Blood volume decreases to 125% of the prepregnancy level during the first postpartum week, followed by a more gradual decline to 110% of the prepregnancy level at 6 to 9 weeks postpartum (see Fig. 2.6 ). The hemoglobin concentration and hematocrit decrease during the first 3 days postpartum, increase gradually during the next 3 days (because of a reduction in plasma volume), and continue to increase to prepregnancy measurements by 3 weeks postpartum.

Albumin and total protein concentrations and colloid osmotic pressure decline after delivery and gradually return to prepregnancy levels by 6 weeks postpartum. Plasma cholinesterase activity decreases below the predelivery level by the first postpartum day and remains at that decreased level during the next week. Globulin concentrations are elevated throughout the first postpartum week.

Beginning with delivery and during the first postpartum day, there is a rapid decrease in the platelet count and in the concentrations of fibrinogen, factor VIII, and plasminogen, and an increase in antifibrinolytic activity. Clotting times remain shortened during the first postpartum day, and viscoelastic testing remains consistent with a hypercoagulable state, although whether systemic fibrinolysis occurs is an area of active research. During the first 3 to 5 days postpartum, increases are noted in the fibrinogen concentration and platelet count, changes that may account for the greater incidence of thrombotic complications during the puerperium. The coagulation profile returns to the nonpregnant state by 2 to 3 weeks postpartum.

The thyroid gland enlarges by 50% to 70% during pregnancy because of follicular hyperplasia and greater vascularity. The estrogen-induced increase in thyroid-binding globulin results in a 50% increase in total triiodothyronine (T ₃ ) and thyroxine (T ₄ ) concentrations during the first trimester, which are maintained until term. The concentrations of free T ₃ and T ₄ do not change. The concentration of thyroid-stimulating hormone decreases during the first trimester but returns to the nonpregnant level shortly thereafter and undergoes no further change during the remainder of pregnancy. The fetal thyroid gland cannot produce thyroid hormone until the end of the first trimester and relies solely on maternal T ₄ production during this critical time of development and organogenesis.

Approximately 4% to 7% of women of childbearing age are either hypothyroid or at risk for hypothyroidism during pregnancy. Only 20% to 30% of affected women demonstrate symptoms of hypothyroidism, likely because some symptoms of hypothyroidism mimic features of pregnancy (e.g., fatigue). In a large study of 502,036 pregnant women, 15% of tested women had gestational hypothyroidism , with 33% of these women demonstrating symptoms. Based on these results, many physicians advocate universal screening, which appears to be cost effective, given the risk for decreased intelligence in the offspring, miscarriage, and postpartum bleeding if hypothyroidism is left untreated.

Mean blood glucose concentration remains within the normal range during pregnancy, although the concentration may be lower in some women during the third trimester compared with nonpregnant individuals. This finding is explained by the greater glucose demand of the fetus and the placenta. The relative hypoglycemic state results in fasting hypoinsulinemia. Pregnant women also exhibit exaggerated starvation ketosis.

Pregnant women are relatively insulin resistant because of hormones such as placental lactogen secreted by the placenta. The blood glucose levels after a carbohydrate load are greater in pregnant women than in nonpregnant women, despite a hyperinsulinemic response. These changes resolve within 24 hours of delivery.

The concentration of corticosteroid-binding globulin (CBG) doubles during gestation as a result of an estrogen-induced enhancement of hepatic synthesis. The elevated CBG value results in a 100% increase in the plasma cortisol concentration at the end of the first trimester and a 200% increase at term. The concentration of unbound, metabolically active cortisol at the end of the third trimester is 2.5 times the nonpregnant level. The increase in free cortisol results from greater production and reduced clearance. An increase in CBG concentration and a decrease in the serum albumin level affect the protein binding of corticosteroids. CBG binding capacity usually saturates at low concentrations of glucocorticoids. Clearance of betamethasone is greater during pregnancy, possibly because the drug is metabolized by placental enzymes.

Sleep disturbances from mechanical and hormonal factors occur commonly during pregnancy. Latency and duration of rapid eye movement (REM) sleep are influenced by changes in progesterone and estrogen concentrations. Pregnant women have more complaints of insomnia and daytime sleepiness. The American Academy of Sleep Medicine defined pregnancy-associated sleep disorder as the occurrence of insomnia or excessive sleepiness that develops in the course of pregnancy. In a cohort study of 189 healthy nulliparous women, Facco et al. reported that sleep duration was shorter in the third trimester (mean 7.0 [SD 1.2] hours) compared with the baseline period between 6 and 20 weeks’ gestation (7.4 [1.2] hours).

Sleep characteristics change as pregnancy progresses. Early pregnancy is characterized by increased total sleep time and decreased stage 3 and 4 non-REM sleep, whereas late pregnancy is characterized by decreased total sleep time, increased waking after sleep onset, and decreased REM sleep. Sleep may be poor for up to 3 months postpartum. Upper airway changes lead to increased airflow resistance and snoring. Although only 4% of nonpregnant women snore, as many as 23% of pregnant women snore by the third trimester. Considerations for screening, diagnosing, and treating sleep apnea during pregnancy were described in a 2023 consensus guideline.

Pregnancy is associated with transient restless legs syndrome , a disorder in which the patient experiences the need to move her legs. The incidence ranges from 15% in the first trimester to 23% in the third trimester.

Cerebral blood flow increases in pregnancy. Nevo et al. measured cerebral blood flow in 210 women at different gestational ages and found that it increased from 44.4 mL/min/100 g during the first trimester to 51.8 mL/min/100 g during the third trimester ( Fig. 2.10 ). The increase was secondary to a decrease in cerebrovascular resistance and an increase in internal carotid artery diameter. Other changes in the brain that occur during pregnancy include (1) an increase in permeability of the blood-brain barrier caused by decreased cerebrovascular resistance with an increase in hydrostatic pressure and (2) an increase in capillary density in the posterior cerebral cortex.

Cerebral Blood Flow During Pregnancy .

Cerebral blood flow increases as pregnancy progresses and is attributable to vasodilation from the hormonal changes of pregnancy. This increase in cerebral blood flow explains the increased risk for complications in patients with intracranial pathology as pregnancy progresses.

Data from Nevo O, Soustiel JF, Thaler I. Maternal cerebral blood flow during normal pregnancy: a cross-sectional study. Am J Obstet Gynecol . 2010;203:475.e1–e6.

Women may experience an elevation in the threshold to pain and discomfort near the end of pregnancy and during labor, though this varies based on factors such as coping capacity. The mechanism, although unclear, may be related to the effects of progesterone and endorphins. Elevated concentrations of endorphins and enkephalins are found in the plasma and CSF of parturients, and opioid antagonists abolish pregnancy-induced analgesia to visceral stimulation in experimental animals.

Anatomic and mechanical changes occur to the vertebral column during pregnancy. The apex of the thoracic curve shifts cephalad from T8 to T6–T7. The volume of epidural fat and the epidural venous plexus enlarge and spinal CSF volume is reduced.

In the lateral position, lumbar epidural pressure is positive in term pregnant women but negative in more than 90% of nonpregnant women. Turning a parturient from the lateral to the supine position increases the epidural pressure. Epidural pressure also increases during labor because of increased diversion of venous blood through the vertebral plexus secondary to either enhanced compression of the inferior vena cava in the supine position or greater intraabdominal pressure during pain and pushing. The epidural pressure returns to the nonpregnant level by 6 to 12 hours postpartum.

Despite compression of the dural sac by the epidural veins, the CSF pressure in pregnant women is the same as in nonpregnant women. Uterine contractions and pushing during labor result in an increase in CSF pressure that is secondary to acute increases in epidural vein distention.

Dependence on the sympathetic nervous system for maintenance of hemodynamic stability increases progressively throughout pregnancy and reaches a peak at term. The dependence on the sympathetic nervous system returns to that of the nonpregnant state by 36 to 48 hours postpartum.