Physical Examination and Cardiac Studies

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 shifts the heart anteriorly and to the left. The point of maximal cardiac impulse is displaced cephalad to the fourth intercostal space and left to at least the midclavicular line.

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. 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.

Central Hemodynamics

To accurately determine central hemodynamic values and/or changes during pregnancy, measurements should be made with the patient in a resting position with left uterine displacement to minimize vena caval 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 24 weeks or more. There is significant heterogeneity in cardiac output measurement using different noninvasive devices; these differences should be taken into account when caring for individual patients.

Cardiac output begins to increase by five 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; SV, stroke volume; HR, heart rate; LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; EF, ejection fraction; LVSWI, left ventricular stroke work index; PCWP, pulmonary capillary wedge pressure; PADP, pulmonary artery diastolic pressure; CVP, central venous pressure; SVR, systemic vascular resistance; NC, no change.

(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. The 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.

Left ventricular 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 left ventricular 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 higher velocity of left ventricular circumferential fiber shortening ( Fig. 2.3 ). 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.

Left ventricular function in late phase of third-trimester normotensive pregnant patients. LVSWI, left ventricular stroke work index; PCWP, pulmonary capillary wedge pressure.

(Modified from Clark SL, Cotton DB, Lee W, et al. Central hemodynamic assessment of cardiac function. Am J Obstet Gynecol. 1989;161:439–442.)

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 U.S. 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 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.

Blood Pressure and Systemic Vascular Resistance

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 upper arm. Blood pressure increases with maternal age, and for a given age, nulliparous women have a higher mean pressure than parous women. 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, 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, systemic vascular resistance remains approximately 20% below the nonpregnant level at term. A postulated explanation for the decreased systemic vascular resistance is the low-resistance uteroplacental vascular bed as well as systemic maternal vasodilation caused by prostacyclin, estrogen, and progesterone. The 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 systemic vascular resistance during pregnancy, and pregnant women who smoke have demonstrated a lower systemic vascular resistance compared with nonsmoking parturients.

Aortocaval Compression

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 cava pressures. Despite caval compression, collateral circulation maintains venous return, as reflected by the right ventricular filling pressure, which is unaltered in the lateral position. Intra-abdominal 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. 2.4 ). 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 a 30-degree lateral tilt compared with the supine position, whereas there is no difference between women in the supine position and those tilted 15 degrees.

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 has also been shown to result in aortocaval compression, with a decrease in cardiac output of 10%. Flexing the legs rotates the uterus to compress against the vena cava. Short intervals in the sitting position, such as occurs during epidural catheter placement, have no 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 systemic vascular resistance 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.

Hemodynamic Changes during Labor and the Puerperium

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 alterations in 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 loss of the low-resistance placental circulation. 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. Other anatomic and functional changes of the heart are also fully reversible.

Anatomy

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 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.

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.

Airflow Mechanics

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 function 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 (FVC), 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 the 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. Harirah et al. found that peak expiratory flow rate declined throughout gestation in all positions and that flow rates in the supine position were lower than those during standing and sitting. The mean rate of decline was 0.65 L/min per week, and PEF rate remained below normal at 6 weeks postpartum. By contrast, Grindheim et al. reported that PEF rate increased throughout pregnancy starting at an average of 6.7 L/s in the early second trimester and peaking at 7.2 L/s at term ( Fig. 2.5 ). These authors also reported that the FVC increased by 100 mL after 14 to 16 weeks’ gestation, with the change being greater in parous than in primigravid women.

Changes in airflow mechanics during pregnancy. The magnitude of the increase in flow rates is small. The forced expiratory volume in one second (FEV ₁ ) is within the normal range of predictive values for nonpregnant individuals. FVC, forced vital capacity; PEF, peak expiratory flow.

(Based on data from Grindheim G, Toska K, Estensen ME, Rosseland LA. Changes in pulmonary function during pregnancy: a longitudinal study. BJOG. 2012;119:94–101.)

Lung Volumes and Capacities

Lung volumes can be measured using body plethysmography or by 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. 2.6 ). 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% reduction in expiratory reserve volume (200 to 300 mL) and a 15% reduction in residual volume (200 to 400 mL). 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.

Ventilation and Blood Gases

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 to 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 less than 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.

TABLE 2.4

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