TERMINOLOGY

A. Calculation of gestation: 280 days, 40 postmenstrual weeks, or 10 lunar months counted from the first day of the last menstrual period. (Actual duration of gestation from conception to estimated date of delivery is 38 weeks, assuming a 28-day cycle.)

1. First trimester: 0 to 12 weeks.

NORMAL MATERNAL PHYSIOLOGIC CHANGES BY SYSTEMS

A. Alimentary tract and perinatal nutrition (Blackburn, 2013).

1. During pregnancy there is an increased caloric need of 300 kcal/day to support the growing fetus and increased maternal metabolic rate, resulting in a caloric requirement of 2500 kcal/day during pregnancy (Pillitteri, 2010). Pregnant teenagers need an additional 100 to 200 kcal/day. Total recommended weight gain for women with normal body mass index (BMI) is 25 to 35 pounds, and for underweight women a gain of up to 40 pounds may be recommended (American College of Obstetricians and Gynecologists [ACOG], 2013b). Limiting weight gain to 11 to 20 pounds is recommended for obese women (ACOG, 2013b).

2. An inadequate intake of folic acid has been associated with neural tube defects (NTDs) (London et al., 2011). It is likely that the functional mechanism for folate’s effect on NTDs is its epigenetic role in DNA methylation and histones (Ross and Desai, 2012). Routine supplementation of folic acid 0.4 to 0.8 mg is recommended for women of childbearing age or planning a pregnancy to assist in the prevention of NTDs (U.S. Preventive Services Task Force, 2009). Women with a previously affected child should take folic acid 4 mg daily for 4 weeks prior to conception and throughout the first 3 months of gestation (Gregory et al., 2012).

3. Approximately 50% of pregnancies are affected by morning sickness during the first trimester, which is associated with increased levels of human chorionic gonadotropin (hCG) and progesterone (Pillitteri, 2010).

4. The stomach loses tone and has decreased motility and delayed emptying time because of the effects of progesterone.

5. Relaxation of the pyloric sphincter and upward displacement of the diaphragm in combination with increased intra-abdominal pressure from the enlarging uterus can result in gastroesophageal reflux and heartburn.

6. The small bowel has reduced motility and hypertrophy of the duodenal villi to increase absorption of nutrients. Constipation is a problem because of mechanical obstruction from the uterus, reduced motility, and increased water absorption.

7. The gallbladder has decreased muscle tone and motility after 14 weeks as a result of the effects of progesterone. High levels of estrogen may decrease water absorption by the gallbladder’s mucosa, leading to dilute bile with resulting inability to sequester cholesterol. This increase in cholesterol may lead to gallstone formation during the second and third trimesters of pregnancy. Decreased gallbladder tone may also lead to increased retention of bile salts, resulting in pruritus and cholestasis gravidarum. Cholestasis gravidarum has been associated with increased risk of stillbirth and preterm deliveries (Kroumpouzos, 2007).

8. The liver is displaced upward by the enlarging uterus. Estrogen may cause altered production of plasma proteins, bilirubin, serum enzymes, and serum lipids. Alterations in laboratory values such as reduced serum albumin, elevated alkaline phosphatase, and elevated serum cholesterol may mimic liver disease. Serum levels of bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) are unchanged in normal pregnancy and may be used as an indicator of hepatic compromise during pregnancy. During labor, alkaline phosphatase levels may increase further, and AST, ALT, and lactate dehydrogenase levels may increase as a result of stress of labor.

B. Respiratory system (Blackburn, 2013).

1. The increased vascularity and vascular congestion of the upper respiratory tract resulting from increased levels of estrogen causes hypersecretion of mucus from the nasopharynx, resulting in nasal stuffiness, sinus congestion, and epistaxis (nosebleed) during pregnancy (Lowdermilk et al., 2012).

2. Maternal oxygen requirements increase during pregnancy as a result of increased maternal metabolic rate, fetal oxygen requirements, and increased tissue mass (Lowdermilk et al., 2012).

3. The chest wall profile changes. Increased levels of estrogen and relaxin cause relaxation of intercostal ligaments with resulting increased chest expansion and chest circumference and an increase in the subcostal margin angle (Cunningham et al., 2010). The diaphragm is elevated by 4 cm in the third trimester (Lowdermilk et al., 2012).

4. Respiratory changes during pregnancy include a 30% to 40% increase in tidal volume, a 20% to 30% decrease in expiratory reserve volume, a 20% decrease in residual volume, and a 20% decrease in functional residual capacity (Pillitteri, 2010). Forced expiratory volume does not change in pregnancy and is a reliable indicator of asthma status in pregnant women. Progesterone, estradiol, and prostaglandins increase the sensitivity of the respiratory center to carbon dioxide (Lowdermilk et al., 2012. Maternal PaCO₂ levels decrease to 32 mm Hg and oxygen levels rise to 106 mm Hg early in pregnancy to allow fetal–placental exchange (Pillitteri, 2010). As a result of these cumulative respiratory changes, pregnant women may experience physiologic dyspnea. To prevent the maternal acidosis due to the carbon dioxide levels from the fetus, mild hyperventilation occurs. This hyperventilation may increase to cause a respiratory alkalosis. According to Cunningham et al. (2010), progesterone lowers the threshold and increases chemosensitivity to carbon dioxide; in response to the respiratory alkalosis, plasma bicarbonate levels decrease from 26 to 22 mmol/L, creating a slight increase in blood pH that shifts the oxygen dissociation curve to the left. Although pulmonary function is not impaired, respiratory diseases may be more serious during pregnancy (Cunningham et al., 2010).

C. Skin (Blackburn, 2013).

1. Because of elevated levels of estrogen, spider angiomas are frequently seen on the neck, face, throat, and arms. Palmar erythema is common in two thirds of white women and one third of African American women (Cunningham et al., 2010).

2. Striae gravidarum occur in women with a genetic predisposition to stretching of the skin or connective tissue. Stretching due to the increased activity of adrenocorticosteroids, estrogens, and relaxin may cause separation and rupture of areas of connective tissue of the skin, leading to pink or red streaks on the abdomen, thighs, and breasts (Lowdermilk et al., 2012; Pillitteri, 2010). After pregnancy, striae do not completely resolve; however, they turn a silvery-white color (Pillitteri, 2010).

3. Increased pigmentation is due to increased levels of estrogen, progesterone, and melanocyte-stimulating hormone. This is most marked on the nipples, areolas, perineum, and midline of the lower portion of the abdomen (commonly called the linea nigra).

4. Sun-sensitive hyperpigmentation of the face, called chloasma or melasma and also referred to as the “mask of pregnancy,” results in a dark, blotchy appearance of the face, forehead, and upper lip and occurs in 45% to 70% of women. There is a genetic predisposition to melasma.

5. During gestation a greater percentage of the hair remains in the anagen (growth) phase, which decreases normal hair loss. Hair loss commonly occurs between 2 and 4 months after delivery and is due to an increase in the telogen (resting) phase of hair growth. The hair returns to a normal growth phase within 1 to 5 months (Kroumpouzos, 2012).

6. Changes in secretory glands occur during pregnancy. Sebaceous gland activity changes are variable, with resulting changes in acne unpredictable (Kroumpouzos, 2012). Eccrine sweat gland activity increases as a result of increased thyroid activity, body weight, and metabolic activity and may result in miliaria and dyshidrotic eczema.

7. Changes in the nails are uncommon but may occur beginning in the first trimester. These changes include brittleness, distal separation of the nail bed, subungual hyperkeratosis, whitish discoloration (leukonychia), and transverse grooving (Kroumpouzos, 2012). The cause is unknown.

D. Urinary system (Blackburn, 2013).

1. Structural renal changes begin during the first trimester and are a result of estrogen, progesterone, and prostaglandin E₂ secretion; pressure from the enlarging uterus; and increase in blood volume (Lowdermilk et al., 2012). The kidneys enlarge, the ureters dilate, hyperplasia of the smooth muscle walls of the ureters occurs, and the ureters elongate (Lowdermilk et al., 2012). Hydronephrosis occurs in 80% of pregnant women. Bladder capacity also increases to 1000 mL (Pillitteri, 2010). The consequences of these changes include the following:

a. An increase in asymptomatic bacteriuria that may lead to cystitis and pyelonephritis.

a. Mean 24-hour urine output increases from 1475 to 1919 mL, and the mean number of daily voids increases as well.

b. The renal plasma flow increases by 75%, with a 25% decrease in the third trimester (Gordon, 2012). The increased renal plasma flow is accompanied by an increase in glomerular filtration rate of 50%, which leads to an increase in creatinine clearance and a decrease in nitrogen levels, as reflected by decreased blood urea nitrogen (BUN) and serum creatinine levels (Pillitteri, 2010).

c. An increased filtration of sodium is balanced by an increased reabsorption of sodium by the renal tubules.

d. The lower renal threshold for glucose excretion negates using urine glucose measurements in the management of diabetes mellitus.

e. Proteinuria of trace to 1 + may occur as a result of an increased load of amino acids. Although this level of proteinuria may not indicate pathology, the pregnant woman with proteinuria and hypertension should be evaluated for preeclampsia (Lowdermilk et al., 2012).

E. Cardiovascular system (Blackburn, 2013; Cunningham et al., 2010).

1. There is an increase in maternal blood volume by 1500 mL or 30% to 50% from the end of the first trimester, peaking at 28 to 32 weeks (Lowdermilk et al., 2012). If plasma volume increases faster than red blood cell (RBC) production, a hemodilutional pseudoanemia may result (Pillitteri, 2010).

2. There is an increase in maternal heart rate, which increases by 10 to 20 beats above the nonpregnant state by the third trimester. Stroke volume increases during the first and second trimesters and then decreases during the third trimester. Pregnancies with multiples have a greater increase in maternal cardiac output.

3. Because the heart is displaced leftward and upward by the enlarging uterus, the cardiac silhouette increases on x-ray films.

4. Altered cardiac sounds in pregnancy include splitting of the first heart sound, an audible S₃ heart sound, systolic flow murmurs (90% of pregnant women), and transient diastolic murmurs (20% of pregnant women).

5. Blood pressure remains at the prepregnancy level in the first trimester and drops during the second trimester at approximately 24 weeks of gestation by 5 to 10 mm Hg systolic and 10 to 15 mm Hg diastolic. It returns to normal prepregnancy levels at the end of pregnancy.

6. Between 20 and 24 weeks of gestation, pressure on and resulting obstruction of the inferior vena cava may occur in the supine position. The resulting 25% fall in cardiac output is called supine hypotension. Positioning the mother in a lateral position or with lateral displacement of the uterus with placement of a wedge under her hip assists in the prevention of supine hypotension.

7. Blood stagnates in the lower extremities because of compression of the pelvic veins and the inferior vena cava, contributing to dependent edema, varicosities of the legs and vulva, and hemorrhoid formation.

F. Breasts (Blackburn, 2013).

1. Early changes in the breasts (beginning by 4 weeks of gestation) include tingling, heaviness, tenderness, and enlargement in response to increased levels of estrogen (Lowdermilk et al., 2012). These symptoms usually subside at the end of the first trimester.

2. The areolas enlarge and darken. Sebaceous glands on the areolae increase activity in preparation for lactation and therefore become more prominent (Kroumpouzos, 2012).

3. Estrogen, progesterone, human placental lactogen (hPL), hCG, prolactin, and luteal and placental hormones cause hyperplasia of the breast tissue and development of lactiferous ducts and lobular alveolar tissue during the second and third trimesters (Lowdermilk et al., 2012; Pillitteri, 2010). Physical examination may reveal palpable milk ducts and excretion of colostrum from the nipples.

4. Colostrum, which is a high-protein precursor of breast milk, may be expressed as early as the fourth month of pregnancy (Pillitteri, 2010).

5. The breast is capable of lactogenesis after 16 weeks. Compared to milk produced after a term delivery, the milk produced after delivery of a preterm infant (i.e., < 34 weeks) has higher protein content; higher antiinfective properties, including secretory immunoglobulin A and lactoferrin; and higher oligosaccharides, fat, sodium, chloride, and iron.

G. Skeletal changes (Gordon, 2012).

1. Compensating for the anteriorly positioned growing uterus, the lower portion of the back curves. This lordosis shifts the center of gravity backward over the lower extremities and causes low back pain, a common complaint in pregnancy.

4. Numbness, tingling, weakness, and aching in the upper extremities are a result of marked lordosis. Symptoms are the result of anterior flexion of the neck in the cervicodorsal region, producing traction on the brachial plexus and ulnar and median nerves (Lowdermilk et al., 2012).

5. Although serum calcium levels decrease during pregnancy, serum ionized calcium levels are unchanged. The National Institutes of Health (2013) recommends 1300 mg of calcium for women 14 to 18 years of age and 1000 mg of calcium for women 19 to 50 years of age during pregnancy and lactation.

6. Bone turnover is low in the first trimester and then increases in the third trimester when peak fetal calcium transfer occurs; however, osteoporosis is not associated with pregnancy bone turnover.

H. Hematologic changes (Blackburn, 2013; Gordon, 2012).

1. Plasma volume is increased 15% by the end of the first trimester, undergoes a rapid expansion during the second trimester, peaks at 32 to 34 weeks, and then plateaus near term. Plasma volume at or near term is 40% to 45% (~ 1500 mL) above prepregnant levels (Cunningham et al., 2010).

2. The white blood cell (WBC) count rises progressively during pregnancy and labor. Prepregnancy levels range from 5000 to 12,000 cells/microliter (mcL) and increases up to 25,000 cells/mcL in labor and the early postpartum period.

3. The RBC count rises up to 33% during the first trimester, with an average increase of 30% to 35% throughout pregnancy. The increase in plasma volume changes the ratio of RBCs to plasma, causing a drop in hematocrit. This “physiologic anemia of pregnancy” reaches the lowest levels at 30 to 34 weeks; then as the hematocrit begins to rise, a closer to normal ratio of RBCs to plasma results in a higher hematocrit near term.

4. Iron requirements are increased by 800 mg in pregnancy, with total fetal requirements of 350 to 400 mg of iron (Pillitteri, 2010). Fetal iron requirements are greatest during the third trimester. Serum ferritin levels fall until 30 to 32 weeks, with the greatest decrease between 12 and 25 weeks.

5. Pregnancy has been called a “hypercoagulable state.” The platelet count decreases slightly, but remains within the normal range. Fibrinogen is increased by 50% to 80%, and factors VII through X increase (Pillitteri, 2010). Bleeding and clotting times remain normal. The incidence of thromboembolism increases five- to six-fold and is greatest during the postpartum period (Pettker and Lockwood, 2012).

6. Pregnancy is known to result in altered immunologic function so that the “foreign fetus” is accommodated. Therefore, a decrease in cellular immunity may account for improvement of certain autoimmune diseases in pregnancy and an increased susceptibility to infection. The humoral immune system characterized by antibody-mediated immunity remains intact.

I. Endocrine and Metabolic Changes (Blackburn, 2013).

1. Thyroid: The thyroid enlarges during pregnancy; however, there is little transplacental transfer of the hormones triiodothyronine (T₃) and thyroxine (T₄). Thyroid-binding globulin (TBG) increases during the first trimester owing to the effects estrogen has on the liver. TBG plateaus by 20 weeks and results in increases in total T₄ and total T₃ levels (Mestman, 2012). hCG has thyrotropic activity and can activate thyroid-stimulating hormone (TSH) receptors and also increase secretion of T₄ (Blackburn, 2013). Serum portions of T₃ and T₄ are normal unless a maternal iodine deficiency is present or there are abnormalities of the thyroid gland (Mestman, 2012). Increased hCG levels are associated with decreased TSH levels in early pregnancy. There is a transient decrease in TSH during the first trimester, with a return to normal levels by the second trimester. Fetal thyroid function appears to be independent of maternal thyroid function.

2. Carbohydrate metabolism (Cunningham et al., 2010):

a. Characterized by mild fasting hypoglycemia, postprandial hyperglycemia, and hyperinsulinemia.

ANTEPARTUM CARE

A. Initial antepartum visit.

1. A thorough obstetric history is obtained:

a. Gravidity (G), indicating the number of pregnancies, and parity (P), indicating the number of births. The obstetric history is often written as “G_ P _ _ _ _”. Four-number parity is often used, which includes the number of elective and spontaneous abortions and the number of living children.

(1) G indicates the number of times the woman has been pregnant, including this pregnancy.

(1) African Americans: sickle cell anemia.

e. History of pregnancy loss or neonatal death (Blackburn, 2013).

f. Exposure to teratogens (Blackburn, 2013).

g. History of current pregnancy.

h. Review of systems.

2. Perform a complete physical examination, including a complete pelvic examination.

3. Initial laboratory work (Table 1-1), including genetic screening blood work such as screens for ethnically linked disorders.

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