Fig. 1.1
Cardiac output in pregnancy. Increase in cardiac output, stroke volume , and heart rate from the nonpregnant state throughout pregnancy (From Gabbe [17]. Reprinted with permission from Elsevier)
The CO in twin gestations incrementally increases an additional 20% greater than that of singleton pregnancies [8]. Robson et al. showed that by 5 weeks’ gestation, CO has already risen by more than 10%. At 12 weeks, the rise in output is 34–39% above nongravid levels, accounting for about 75% of the total increase in CO during pregnancy. There is no literature consensus as to the exact gestation when CO peaks, but most studies point to a range between 25 and 30 weeks [18].
The data on whether the CO continues to increase in the third trimester are very divergent, with equal numbers of good longitudinal studies showing a mild decrease, a slight increase, or no change [14].
These study discrepancies are not explained by differences in investigative techniques , position of the women during measurements, or study design. This apparent discrepancy appears to be explained by the small number of individuals in each study and the probability that the course of CO during the third trimester is determined by factors specific to the individual [14].
Desai and coworkers reported that CO in the third trimester is significantly correlated with fetal birthweight and maternal height and weight [19].
Increases in CO are mostly directed to the uterus, placenta, and breasts . The uterus receives 2–3% of CO in the first trimester as well as in the nongravid state. The breasts receive 1%. CO going to the kidneys (20%), skin (10%), brain (10%), and coronary arteries (5%) remains at similar nonpregnant percentages. However, because of the overall increase in CO, this results in an increase in absolute blood flow of about 50% [15]. At term, the uterus receives 17% (450–650 mL/min) and the breasts 2%, mostly at the expense of a reduction of the fraction of the CO going to the splanchnic bed and skeletal muscle. The absolute blood flow to the liver is not changed, but the overall percentage of CO is significantly decreased.
CO is the product of SV and HR (CO = SV × HR). Both are increased during pregnancy and contribute to the overall rise in CO. Maternal HR initially rises at 5 weeks’ gestation and peaks at 32 weeks’ gestation at 15–20 beats above the nongravid rate, an increase of 17%. The SV starts to rise by 8 weeks’ gestation reaching its maximum at about 20 weeks, which is 20–30% above nonpregnant values. In the third trimester, it is primarily variations in the SV that determine whether CO increases, decreases, or remains stable, as described earlier.
Maternal position influences CO in pregnancy. One study in 10 normal gravid women in the third trimester, using pulmonary artery catheterization, CO was noted to be highest in the knee–chest position and lateral recumbent position at 6.6–6.9 L/min. CO decreased by 2.2–5.4 L/min in the standing position. The decrease in CO in the supine position compared with the lateral recumbent position is 10–30%. In both the standing and the supine positions, decreased CO results from a fall in SV secondary to decreased blood return to the heart. The enlarged uterus compresses the inferior vena cava in the supine position, reducing venous return. However, this effect is not observed before 24 weeks. Importantly, in late pregnancy, the inferior vena cava is completely occluded in the supine position, with venous return from the lower extremities occurring through the dilated paravertebral collateral circulation [16].
Most supine women are not hypotensive or symptomatic because of the compensated rise in systemic vascular resistance (SVR) , despite decreased CO. However, 5–10% of gravidas experience supine hypotension with symptoms of dizziness, lightheadedness, nausea, and occasional syncope. The women who are symptomatic have a greater decrease in CO and blood pressure (BP) and a greater increase in HR when in the supine position than do asymptomatic women [20]. It has been proposed that the determination of whether women become symptomatic depends on the development of an adequate paravertebral collateral circulation. Interestingly, with engagement of the fetal head, less of an effect on CO is seen [16].
Maintaining a normal BP in the supine position may be lost during epidural or spinal anesthesia because of the inability to increase SVR. The clinical significance of the effects of maternal position on CO are especially important when the gravida is clinically hypotensive or in the setting of a category II or III fetal heart rate tracing . The observation of decreased birthweight and placental infarctions in working women who stand for prolonged periods may be associated with findings of a decreased CO in the standing position.
Arterial Blood Pressure and Systemic Vascular Resistance
Blood Pressure (BP) is the product of CO and resistance (BP = CO × SVR). Even with the large increase in CO, typically the maternal BP is decreased until later in pregnancy because of a decrease in SVR that peaks in midpregnancy, followed by a gradual rise until term. The SVR remains 21% lower than prepregnancy values in pregnancies not affected by gestational hypertension or preeclampsia, even at full term. Progesterone-mediated smooth muscle relaxation is the most obvious cause for the decreased SVR. However, the precise mechanism for the fall in SVR is not well understood. Increased nitric oxide (NO) also contributes to decreased vascular resistance by direct actions and by blunting the vascular responsiveness to vasoconstrictors such as angiotensin II and norepinephrine. During conception, the expression and activity of NO synthase is elevated and the plasma level of cyclic guanosine monophosphate, a second messenger of NO and a mediator of vascular smooth muscle relaxation, is also increased [21]. Consequently, despite the overall increase in the renin–angiotensin–aldosterone system (RAAS), the normal gravida is resistant to the vasoconstrictive effects of angiotensin II. Gant et al. showed that nulliparous women who developed preeclamptic continue to respond to angiotensin II before the appearance of clinical signs of preeclampsia [22].
Initial decreases in BP manifest at 8 weeks’ gestation or earlier paralleling the falling SVR. Current studies did not include preconception BP or frequent first-trimester BP sampling and, therefore, cannot determine the exact time course of hemodynamic alterations. Menstruation causes fluctuations in BP, which is decreased in the luteal phase . Therefore, it seems reasonable that BP drops immediately in early pregnancy. The diastolic BP and the mean arterial pressure [MAP = (2 × diastolic BP + systolic BP)/3] decrease more than the systolic BP (Fig. 1.2).
Fig. 1.2
Blood pressure in pregnancy. Blood pressure trends (sitting and lying) during pregnancy. Postnatal measures performed 6 weeks postpartum (From Gabbe [17]. Reprinted with permission from Elsevier)
The diastolic BP and the MAP reach their peaks at midpregnancy. By term, they both return to prepregnancy levels and rarely exceed prepregnancy or postpartum values. However, some investigators have reported that at term, the BP is greater than in matched nonpregnant controls and believe that in the third trimester, the BP is higher than prepregnant values. These studies are very limited by the absence of preconceptional values for comparison within individual patients .
Positioning and Korotkoff sounds are important when the BP is taken to determine the diastolic BP. BP is lowest in the lateral recumbent position, and the BP of the superior arm in this position is 10–12 mm Hg lower than the inferior arm. Clinically, BP should be taken in the sitting position and the Korotkoff 5 sound should be used. This is the diastolic BP when the sound disappears as opposed to the Korotkoff 4, when there is a muffling of the sound. One study of 250 gravidas showed that the Korotkoff 4 sound could only be identified in 48% of patients, whereas the Korotkoff 5 sound could always be determined. The Korotkoff 4 should only be used when the Korotkoff 5 occurs at 0 mm Hg [23].
When compared with mercury sphygmomanometry during pregnancy, automated BP monitors tended to overestimate the diastolic BP. However, the overall results were similar in normotensive women. Automated monitors appear increasingly inaccurate at higher BPs in women with preeclampsia .
Venous Pressure
Venous pressure in the upper extremities remains unchanged in pregnancy but rises progressively in the lower extremities. Femoral venous pressure increases from values near 10 cmH2O at 10 weeks’ gestation to 25 cmH2O near term [24]. Clinically, the increase in venous pressure, as well as the obstruction of the inferior vena cava by the enlarging uterus, leads to the development of edema, varicose veins, and hemorrhoids, and increases the risk for developing deep venous thrombosis.
Pulmonary System
Upper Respiratory Tract
Pregnancy causes the mucosa of the nasopharynx to become hyperemic and edematous with hypersecretion of mucus due to increased estrogen. Marked nasal stuffiness is the result of these changes; epistaxis is also common. Insertion of nasogastric tubes may cause excessive bleeding if adequate lubrication is not used [25]. Polyposis of the nose and nasal sinuses develop in some individuals, which regress postpartum. Because of these changes, many pregnant women complain of chronic cold symptoms; however, the temptation to use nasal decongestants should be avoided because of the risk for hypertension and rebound congestion.
Mechanical Changes
The anatomic configuration of the thorax changes early in pregnancy, much earlier than can be explained by mechanical pressure from the enlarging uterus. Relaxation of the ligaments between the ribs and sternum may be responsible for these configurations. The subcostal angle increases from 68° to 103°, the transverse diameter of the chest expands by 2 cm, and the chest circumference expands by 5–7 cm. As pregnancy progresses, the diaphragm rises 4 cm; however, diaphragmatic excursion is not impeded and actually increases 1–2 cm. Respiratory muscle function is not affected by pregnancy, and maximal inspiratory and expiratory pressures are unchanged [26].
Lung Volume and Pulmonary Function
The anatomic changes in chest wall configuration and the diaphragm lead to changes in static lung volumes. In a review of studies with at least 15 subjects compared with nonpregnant controls, Crapo found significant changes [25] (Fig. 1.3 and Table 1.1).
Fig. 1.3
Lung volumes in pregnant and nonpregnant women . ERV expiratory reserve, FRC functional residual capacity, IC inspiratory capacity, IRV inspiratory reserve, RV residual volume, TLC total lung capacity, TV tidal volume, VC vital capacity (From Gabbe [27]. Reprinted with permission from Elsevier)
Table 1.1
Lung functions in pregnancy
Lung volumes and capacities in pregnancy | ||
|---|---|---|
Measurement | Definition | Change in pregnancy |
Respiratory race (RR) | Number of breaths per minute | Unchanged |
Vital capacity (VC) | Maximal amount of air that can be forcibly expired after maximal inspiration (IC + ERV) | Unchanged |
Inspiratory capacity (IC) | Maximal amount of air that can be inspired from resting expiratory level (TV + IRV) | Increased 5–10% |
Tidal volume (TV) | Amount of air inspired and expired with a normal breath | Increased 30–40% |
Inspiratory reserve volume (IRV) | Maximal amount of air that can be inspired at end of normal inspiration | Unchanged |
Functional residual capacity (FRC) | Amount of air in lungs at resting expiratory level (ERV + RV) | Decreased 20% |
Expiratory reserve volume (ERV) | Maximal amount of air that can be expired from resting expiratory level | Decreased 15–20% |
Residual volume (RV) | Amount of air in lungs after maximal expiration | Decreased 20–25% |
Total lung capacity (TLC) | Total amount of air in lungs at maximal inspiration (VC + RV) | Decreased 5% |
The elevation of the diaphragm decreases the volume of the lungs in the resting state, thereby reducing total lung capacity and the functional residual capacity (FRC). The FRC can be subdivided into expiratory reserve volume and residual volume, and both decrease.
Spirometric measurements evaluating bronchial flow are unchanged in pregnancy. The forced expiratory volume in 1 second (FEV1) and the ratio of FEV1 to forced vital capacity are both unchanged, implying that airway function remains stable. Additionally, peak expiratory flow rates measured using a peak flow meter seem to be unaltered in pregnancy at rates of 450 ± 16 L/min [28]. Harirah and associates performed a longitudinal study of the peak flow in 38 women from the first trimester until 6 weeks postpartum [29]. They reported that the peak flows had a statistically significant decrease as the pregnancy progressed; however, the amount of the decrease was minimal enough to be of questionable clinical significance. Similarly, a small decrease in the peak flow was noted in the supine position versus the standing or sitting position. Therefore, during gestation, both spirometry and peak flow meters can be used in diagnosing and managing respiratory illnesses, but the clinician should ensure that measurements are performed in the same maternal position [29].
Gas Exchange
Rising progesterone levels drive a state of chronic hyperventilation, as noted by a 30–50% increase in tidal volume by 8 weeks’ gestation. In turn, increased tidal volume results in an overall parallel rise in minute ventilation, regardless of a stable respiratory rate (minute ventilation = tidal volume × respiratory rate). The rise in minute ventilation, combined with a decrease in FRC, leads to a larger than expected increase in alveolar ventilation (50–70%). Chronic mild hyperventilation produces an increase in alveolar oxygen (PaO2) and a decrease in arterial carbon dioxide (PaCO2) from normal levels (Table 1.2).
Table 1.2
Lung volumes in pregnant and non-pregnant women
Blood gas values in third trimester of pregnancy | ||
|---|---|---|
Pregnant | Nonpregnant | |
Pao 2 (mm Hg)a | 101.8 ± 1 | 93.4 ± 2.04 |
Arterial Hgb saturation (%)b | 98.5 ± 0.7% | 98 ± 0.8% |
Paco 2 (mm hg)a | 30.4 ± 0.6 | 40 ± 2.5 |
pHa | 7.43 ± 0.006 | 7.43 ± 0.02 |
Serum bicarbonate (Hco 3) (mmol/L) | 21.7 ± 1.6 | 25.3 ± 1.2 |
Base deficit (mmol/L)a | 3.1 ± 0.2 | 1.06 ± 0.6 |
Alveolar-arterial gradient [P(a-a)o 2 (mm Hg)]a | 16.1 ± 0.9 | 15.7 ± 0.6 |
The drop in the PaCO2 is extremely important because it drives a more favorable carbon dioxide (CO2) gradient between the fetus and mother, facilitating CO2 transfer. The low maternal PaCO2 results in a chronic respiratory alkalosis. The increased excretion of bicarbonate, as a result of partial renal compensation, helps maintain the pH between 7.4 and 7.45 and lowers the serum bicarbonate levels. In early pregnancy, the arterial oxygen (PaO2) increases (106–108 mm Hg) as the PaCO2 decreases; however, by the third trimester, a slight decrease in the PaO2 (101–104 mm Hg) occurs as a result of the expanding uterus. This decrease in the PaO2 late in pregnancy is even more pronounced in the supine position, with a further drop of 5–10 mm Hg and an increase in the alveolar-to-arterial gradient to 26 mm Hg, and up to 25% of women exhibit a PaO2 of less than 90 mm Hg [25, 32].
A simultaneous but smaller increase in oxygen uptake and consumption occurs as the minute ventilation increases. Most investigators have found maternal oxygen consumption to be 20–40% above nonpregnant levels. This increase is a result of the oxygen requirements of the fetus, the placenta, and the increased oxygen requirement of maternal organs. With exercise or during labor, an even greater rise in both minute ventilation and oxygen consumption takes place [25]. Oxygen consumption can triple during contractions. Increased oxygen consumption and decreased FRC results in a lowering of the maternal oxygen reserve. Therefore, pregnant women are more susceptible to the effects of apnea, for example, during intubation when a more rapid onset of hypoxia, hypercapnia, and respiratory acidosis is seen.
Gastrointestinal System
Appetite
The appetite of most women increases throughout pregnancy. At the end of the first trimester, food intake increases by about 200 kcal/day, in the absence of nausea. An additional 300 kcal/day is recommended, but the majority of gravidas compensate for this by decreasing their activity. Depending on the population being studied, energy requirements vary. More active women and teenagers show a greater increase in the need for calories. Cultural folklore about dietary cravings and aversions during gestation abound. These may be the result of an individual’s perception of which foods aggravate or ameliorate symptoms such as nausea and heartburn. Some women experience a decrease in taste thus producing an increased desire for highly seasoned food. Bizarre cravings for strange foods, Pica , are relatively common among gravidas. Women with anemia or poor weight gain should be evaluated for a history of pica. Pica examples include the consumption of clay, starch, toothpaste, and ice [33].
Mouth
The pH and the production of saliva remain unchanged during gestation. Ptyalism, considered an unusual complication of pregnancy, usually occurs in women suffering from nausea. Women with ptyalism may secrete 1–2 L of saliva per day. Many experts believe that ptyalism actually represents an inability of the nauseated woman to swallow normal amounts of saliva as opposed to a true increase in the saliva production. Decreasing the ingestion of starchy foods may help to lower the amount of saliva. There is no evidence to support that pregnancy produces or accelerates dental caries. The gums, however, swell and may bleed after tooth brushing, thus causing “gingivitis of pregnancy”. Tumorous gingivitis may occur occasionally, presenting as a violaceous pedunculated lesion at the gum line that may bleed profusely. This is called epulis gravidarum or pyogenic granulomas. These lesions consist of granulation tissue and an inflammatory infiltrate [33].
Stomach
The tone and motility of the stomach are decreased because of the smooth muscle–relaxing effects of progesterone and estrogen. The scientific evidence regarding delayed gastric emptying, however, is inconclusive [34]. Macfie et al. studied acetaminophen absorption as an indirect measure of gastric emptying. But they were unable to demonstrate a delay in gastric emptying when comparing 15 nonpregnant controls with 15 women in each trimester [34]. Additionally, a recent study showed no delay in gastric emptying in parturients at term who ingested 300 mL of water following an overnight fast [35]. However, an increased delay was seen in labor, with the etiology being ascribed to the pain and stress of parturition.
A decrease in peptic ulcer disease is observed in pregnancy. However, gastroesophageal reflux and dyspepsia increases by 30–50% [36]. This may be explained, in part, by physiological changes of the stomach and lower esophagus. Gestational hormones causing esophageal dysmotility play a role in gastroesophageal reflux disease. Other factors include gastric compression from the enlarged uterus and a decrease in the pressure of the gastroesophageal sphincter. Progesterone causes the decrease in the tone of the gastroesophageal sphincter, while estrogen may be attributed to increased reflux of stomach acids into the esophagus. This may be the predominant cause of reflux symptoms. The decreased incidence of peptic ulcer disease, in theory, includes increased placental histaminase synthesis with lower maternal histamine levels, increased gastric mucin production leading to protection of the gastric mucosa, reduced gastric acid secretion, and enhanced immunologic tolerance of Helicobacter pylori, the infectious agent that causes peptic ulcer disease [36].
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