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Many women experience low blood pressure, defined as below 90/60, while they’re expecting a baby. This is not usually a problem, doesn’t normally require medication, and will start returning to its previous level during the third trimester. Your doctor will monitor your blood pressure throughout the pregnancy. Low blood pressure during pregnancy happens because your body secretes hormones, and progesterone in particular, which help to relax the walls of your blood vessels and increase the flow of blood to you and your baby. Occasionally, low blood pressure may be indicative of some other problem. It may be the result of an ectopic pregnancy, in which a fertilised egg becomes implanted outside your uterus. And if it’s very low, it may cause falls, or shock, in which your brain and other vital organs don’t get enough blood to work properly. Low blood pressure has a variety of symptoms. If you experience any of these, you should mention them to your doctor.
Can low blood pressure harm your baby?We know a lot less about the effects of low blood pressure on babies than the effects of high pressure. Some research suggests that it may lead to stillbirth and low birth weight, but this correlation is difficult to establish because there are so many other variables and risk factors involved during pregnancy. In the vast majority of cases, low blood pressure at this time is nothing to worry about. Is there anything you can do to deal with low blood pressure when you’re pregnant?Although medication is not normally needed when this happens, there are some simple changes you can make that may reduce the likelihood of its happening. Take it easy. Try to slow down, avoid making sudden movements, and don’t stand up too quickly. If you do feel faint or dizzy, lie down on your left side, which may help to increase the blood flow to your heart. Drink lots of water. As well as preventing dehydration, this increases your blood volume, and thus your blood pressure. Eat a healthy diet. Your doctor may also recommend that you increase your salt intake, though it’s important not to overdo this. References: www.bounty.com/pregnancy-and-birth/pregnancy/pregnancy-other-conditions/low-blood-pressure-in-pregnancy www.healthline.com/health/pregnancy/low-blood-pressure-during-pregnancy#risks www.medicalnewstoday.com/articles/320303.php AbstractLow blood pressure during pregnancy has been associated with poor perinatal outcomes. However, whether this association is causal or is due to confounding has never been carefully assessed. The authors used data from the Collaborative Perinatal Project, a large prospective cohort study in 12 hospitals in the United States from 1959 to 1966. A total of 28,095 subjects were included. At first glance, it appeared that the lower the baseline blood pressure during pregnancy, the higher the incidence of very premature birth (<34 weeks) and severe small for gestational age (<5th percentile) in a consistent dose-response pattern. However, women with low blood pressure were generally younger, shorter, lighter, leaner, poorer, and more often a minority, and they gained less weight. After the authors controlled for these factors, low blood pressure was not associated with preterm birth (adjusted relative risks ranging from 0.86 to 0.93, p > 0.05) or small for gestational age (relative risks ranging from 0.45 to 2.0). Therefore, the association between low blood pressure during pregnancy and poor perinatal outcomes is largely due to confounding by other risk factors. Low blood pressure by itself does not increase risk of poor perinatal outcomes at a population level. However, this conclusion may not apply to individual patients who also have a compromised plasma volume expansion or pathologic homeostasis. While hypertension in pregnancy has been extensively studied, little attention has been paid to the other end of the spectrum, namely low blood pressure during pregnancy. Friedman and Neff (1) demonstrated that approximately 10 percent of pregnant women had a maximum diastolic blood pressure (DBP) of 60 mmHg or lower. More importantly, low systolic blood pressure and low DBP were associated with a higher risk of low birth weight, fetal death, and defective intelligence quotient scores at age 4 years in a consistent dose-response pattern. However, no further analysis was conducted. These findings have been cited repeatedly in the literature and were consistent with more recent data (2). Because blood pressure declines in early pregnancy and rises later, maximum blood pressure can be influenced by the level of baseline blood pressure, the degree of rise in late gestation, and the gestational age at delivery, in addition to other factors. Further, from the point of view of prevention, baseline and rise in blood pressure appear to be more useful than the maximum blood pressure. The purpose of this study is to look at this issue in-depth and answer the following specific questions: 1) Is low baseline DBP in early pregnancy associated with poor perinatal outcomes? 2) Does low blood pressure cause poor perinatal outcomes, or does it merely reflect other risk factors? 3) How might a rise in DBP in late pregnancy modify the effect of baseline DBP on fetal growth? MATERIALS AND METHODSWe used data from the Collaborative Perinatal Project. Details of the study have been described elsewhere (3). Briefly, women who attended prenatal care at 12 hospitals from 1959 to 1966 were invited to participate in this prospective observational study. At entry, detailed demographic, socioeconomic, and behavioral information was collected by in-person interview. A medical history was obtained, and a physical examination was also given. Women were interviewed, and physical findings were recorded in all following prenatal visits. Detailed findings in labor/delivery and postpartum were also collected. Blood pressure was recorded at entry, during each prenatal visit, during labor and delivery, and postpartum. Either Korotkoff phase 4 (muffling) or phase 5 (disappearance) was used for DBP (1). A validation study in which the information on blood pressure was checked against that in the original medical records showed remarkable accuracy (1). In that study, the authors selected 772 recordings suspected of error because of wide deviations from the sequence of blood pressures recorded in that patient during the course of pregnancy. The percent error for these blood pressure readings was 1.8 percent. Furthermore, since assessment of blood pressure has not changed substantially in the last 40 years, the current data are suitable and reliable for the purpose of our study. A total of 58,760 pregnancies were included in the Project. We restricted our analyses to singleton pregnancies with a first prenatal visit before 25 weeks, at least three prenatal visits, and birth between 25 and 45 weeks inclusive. Since it is well established that high blood pressure during pregnancy causes poor perinatal outcomes, we limited our analysis to women with baseline DBP less than 80 mmHg. A total of 28,095 subjects were eligible. The baseline DBP is defined as the average of all the DBP measures from 15 to 24 weeks of gestation (83 percent of subjects had at least two measures). Rise in DBP was calculated by subtracting the baseline DBP from the highest DBP, defined as the last antepartum DBP within 3 weeks from delivery (85 percent were less than 2 weeks). Since blood pressure progressively rises in the second half of pregnancy and intrapartum blood pressure is affected by other factors, we considered the last antepartum DBP to be more likely to reflect true DBP and, therefore, preferable to the actual highest recording. Postpartum blood pressure was defined as blood pressure at least 5 weeks after delivery. Mean arterial pressure (MAP) was calculated as: DBP + (systolic blood pressure − DBP)/3. Main outcomes include preterm births less than 34 weeks (based on the last menstrual period) and severe small for gestational age (SGA) less than the 5th percentile (4). To reduce potential misclassification owing to erroneous gestational age, infants with birth weights of 3,100 g or more were considered to have a gestational age of 34 weeks or more (4). Univariate analysis was conducted first. Analysis of covariance and χ2 test were used for continuous and categorical variables, respectively. We used multiple logistic regression for preterm birth and SGA to adjust for potential confounders. Appropriate transformation of the variables was made before they were incorporated into the statistical models. RESULTSFigure 1 illustrates that at a baseline DBP value of less than 80 mmHg, the lower the baseline DBP the higher the incidence of very premature birth among women with a rise in DBP of less than 15 mmHg (χ2 test, p < 0.001). Similarly, incidence of severe SGA increased with decreasing baseline DBP. However, this trend was reversed among those with excessive rise in DBP. The striking and consistent pattern prompted us to ask who these subjects with low baseline DBP were. Table 1 indicates that these women were generally younger, shorter, lighter, leaner, poorer, and more often minority and that they gained less weight. These are well-known risk factors for poor perinatal outcomes. After we had controlled for race, socioeconomic status, prepregnancy body mass index, and smoking during pregnancy, low blood pressure was no longer associated with very preterm birth. The adjusted relative risks were 1.0 (reference), 0.93 (95 percent confidence interval: 0.83, 1.05), 0.86 (95 percent confidence interval: 0.71, 1.03), and 0.88 (95 percent confidence interval: 0.55, 1.42) for baseline DBPs of 70–79, 60–69, 50–59, and less than 50 mmHg, respectively. Likewise, low blood pressure was not associated with severe SGA (figure 2). We reran the logistic regression for severe SGA without net weight gain. The results were similar. Figure 2 further suggests that rise in DBP in late pregnancy does not seem to influence the risk of SGA in most women. However, women with relatively high baseline and excessive rise in DBP had twice the risk of having a baby with severe SGA. FIGURE 1. Incidence of very premature birth (<34 weeks) and severe small for gestational age (SGA) (<5th percentile) in association with baseline diastolic blood pressure and rise in late pregnancy, Collaborative Perinatal Project, 1959–1966. FIGURE 2. Adjusted relative risks and 95% confidence intervals (CI) for severe small for gestational age by diastolic blood pressure in pregnancy (logistic regression, adjusting for maternal height, prepregnancy body mass index, smoking, and net maternal weight gain), Collaborative Perinatal Project, 1959–1966. TABLE 1. Characteristics of women with a low diastolic blood pressure at the baseline, Collaborative Perinatal Project, 1959–1966
* 1 inch = 2.54 cm; 1 pound = 0.454 kg. † Net weight gain = overall weight gain − birth weight − placental weight. ‡ Mean arterial pressure (MAP) = diastolic pressure + (systolic pressure − diastolic pressure)/3. Analysis of variance and chi-square test were used to test the significance of differences among levels of baseline diastolic pressure for continuous and categorical variables, respectively. All tests were statistically significant (p < 0.05). TABLE 1. Characteristics of women with a low diastolic blood pressure at the baseline, Collaborative Perinatal Project, 1959–1966
* 1 inch = 2.54 cm; 1 pound = 0.454 kg. † Net weight gain = overall weight gain − birth weight − placental weight. ‡ Mean arterial pressure (MAP) = diastolic pressure + (systolic pressure − diastolic pressure)/3. Analysis of variance and chi-square test were used to test the significance of differences among levels of baseline diastolic pressure for continuous and categorical variables, respectively. All tests were statistically significant (p < 0.05). DISCUSSIONOur study indicates that the association between low blood pressure during pregnancy and poor perinatal outcomes is due to confounding by other risk factors. After multiple factors are adjusted for, low DBP in early pregnancy is no longer associated with poor perinatal outcomes. Literature on this association is not only scarce but is also inconsistent. Steer (2) found from his database of more than 22,000 term births that the incidence of having a small-for-gestational age baby (<10th percentile) was 3.7, 2.6, 3.2, and 6.9 percent for a maternal maximum DBP of 60 or less, 61–70, 71–89, and 90 or more mmHg, respectively. Ng and Walters (5) compared 134 patients with a blood pressure of 110/70 mmHg or less at all antenatal visits with 134 patients with a blood pressure of greater than 110/70 mmHg on at least three antenatal visits. Incidence of preterm birth, low birth weight, significant meconium staining of the amniotic fluid, and maternal postpartum complications was about twice as high in the former group as in the latter. However, the hypotensive group was significantly younger (26 vs. 28 years) and weighed much less at the first prenatal visit (56.5 vs. 64.7 kg). No confounders were controlled in their analysis. Accurate blood pressure measurement is difficult to achieve. In the best conducted study so far, Churchill et al. (6) used ambulatory blood pressure monitors on 209 low-risk, nulliparous women. Twenty-four-hour recordings of blood pressure were obtained at around 18, 28, and 36 weeks' gestation. After adjustment for maternal age, height, weight, cigarette smoking, alcohol intake, ethnic origin, gestational age, and pregnancy hypertension syndromes, maternal mean 24-hour DBP at 28 weeks' gestation was inversely associated with birth weight. A 1-mmHg decrease in DBP was associated with 13.5-g increase in birth weight (95 percent confidence interval: 0.6, 26.4). This association persisted at 36 weeks' gestation. Despite the inconsistent findings on whether low blood pressure in midpregnancy is actually beneficial to fetal growth, careful analyses suggest that low blood pressure at least does not impose an additional risk to fetal growth. Paradoxically, such an epidemiologic observation seems contradictory to limited evidence from clinical studies. For instance, Grünberger et al. (7) followed 70 pregnant women with a blood pressure of 110/65 mmHg or less, 36 percent of whom had a history of miscarriage. Placental perfusion at 28 weeks' gestation and onward was measured by radioisotopes. More than 80 percent of the patients were considered to have uteroplacental underperfusion. Thirty patients reported only slight discomfort (i.e., fatigue and occasional dizziness), while the other 40 women had severe dizziness, nausea, headache, and the propensity to collapse. The latter were then given mineralocorticoids intramuscularly. Blood pressure was able to be raised to above 110/65 mmHg in 27 patients. Overall, placental perfusion rate improved significantly after treatment. Compared with the untreated women, those who were treated had a lower incidence of preterm birth (5 vs. 20 percent, p = 0.06), moderate-to-severe neonatal dystrophy (5 vs. 60 percent, p < 0.001), and substantially higher mean birth weight (3,308 g vs. 2,800 g; no test was performed). These findings were confirmed in a prospective study by the same authors (8), which involved 60 women with hypotension in pregnancy. Half of the women were treated and compared with the other, untreated half. Placental blood flow was significantly higher in the treated group, as was the birth weight (by 600 g). However, the authors did not mention in either study whether these patients had preexisting homeostatic, renal, or endocrinologic disorders or whether the low blood pressure developed during pregnancy. Such a distinction might determine the possible mechanism(s) of how blood pressure may affect fetal growth. A more recent study examined changes in MAP induced by a transition from a lying to a standing position in 53 and 41 normal singleton women in early (12–18 weeks) and late pregnancy (34–40 weeks), respectively (9). A linear relation was observed between the change in MAP and birth weight in late pregnancy; i.e., the greater drop in MAP, the lower the birth weight (r = 0.57, p < 0.001). However, this relation was not found in early pregnancy. Further, there was no relation between blood pressure at rest and birth weight among all the women. These findings indicate that it is the orthostatic hypotension rather than low blood pressure per se that is associated with poor fetal growth. In a normal pregnancy, systemic vascular resistance drops substantially (10). Despite an marked increase in cardiac output, overall MAP declines significantly in early gestation. Lower baseline MAP might be caused by greater loss of vascular tone and reactivity, by vascular underfill due to insufficient plasma volume expansion, or by both. Table 1 shows that despite large differences in baseline MAP, the difference in postpartum MAP, which reflects nonpregnant MAP, was much smaller among these women. (Some of the postpartum difference might be accounted for by difference in weight and body mass.) Among women who had a baseline DBP of less than 50 mmHg, MAP dropped approximately 20 mmHg compared with a 6-mmHg drop in women whose baseline DBP was 70–79 mmHg. Furthermore, those who had a lower baseline MAP tended to have a substantially greater rise in MAP in late pregnancy (14, 10, 6, and 2 mmHg for women with a baseline DBP of less than 50, 50–59, 60–69, and 70–79 mmHg, respectively). These findings suggest that lower baseline blood pressure in midpregnancy is more likely because of greater vascular relaxation rather than because of blood underfill. On the other hand, failure to drop in vascular tone in early pregnancy coupled with greater rise in blood pressure in late pregnancy, more likely due to vasospasm rather than to greater volume expansion, restricts fetal growth. Given the limited knowledge about low blood pressure in pregnancy, it is difficult to reconcile the discrepancy between clinical and epidemiologic observations. We can only speculate that since a substantial proportion of pregnant women have a relatively low baseline DBP (19 percent had a baseline DBP of 60 mmHg or lower in our study population), one would assume that most cases are probably physiologic, which may not affect fetal growth. On the other hand, our study showed that several risk factors appear to aggregate in women who were already at high risk for poor fetal growth. If a clinical intervention does improve perinatal outcomes in this group, this might become another option to reduce preterm birth and SGA. Given the scarcity and inconsistency of the literature, more investigations are warranted. To sum up, low blood pressure during pregnancy is a common phenomenon. However, insufficient attention has been paid to the group of women with this condition. Although several studies reported a significant association between low blood pressure during pregnancy and poor perinatal outcomes, our analysis indicates that this association was largely due to confounding. Low blood pressure by itself does not increase the risk of poor perinatal outcomes at a population level. However, this conclusion may not apply to individual patients who also have a compromised plasma volume expansion or pathologic homeostasis. Reprint requests to Dr. Jun Zhang, Epidemiology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Building 6100, Room 7B03, Bethesda, MD 20892 (e-mail: ). The authors are indebted to Dr. Cassandra Henderson for consultation regarding the clinical perspectives. REFERENCES1. Friedman EA, Neff RK. Pregnancy hypertension: a systematic evaluation of clinical diagnostic criteria. Littleton, MA: PSG Publishing Co., 1977. 2. Steer P. Factors influencing relative weights of placenta and newborn infant. (Letter). BMJ 1997 ; 315 : 1542 . 3. Niswander KR, Gordon M, eds. The Collaborative Perinatal Study of the National Institute of Neurological Diseases and Stroke: the women and their pregnancies. Philadelphia, PA: W. B. Saunders, 1972. 4. Zhang J, Harville E. Birth-weight-for-gestational-age patterns by race, sex, and parity in the United States population: the 5th percentile. Paediatr Perinatal Epidemiol 1998 ; 12 : 352 –4. 5. Ng PH, Walters WA. The effects of chronic maternal hypotension during pregnancy. Aust N Z J Obstet Gynaecol 1992 ; 32 : 14 –16. 6. Churchill D, Perry IJ, Beevers DG. Ambulatory blood pressure in pregnancy and fetal growth. Lancet 1997 ; 349 : 7 –10. 7. Grünberger W, Leodolter S, Parschalk O. Maternal hypotension: fetal outcome in treated and untreated cases. Gynecol Obstet Invest 1979 ; 10 : 32 –8. 8. Grünberger W, Parschalk O, Fishchl F. Treatment of hypotension complicating pregnancy improves fetal outcomes. (In German). Med Klin 1981 ; 76 : 257 –60. 9. Hohmann M, Kunzel W. Orthostatic hypotension and birthweight. Arch Gynecol Obstet 1991 ; 248 : 181 –9. 10. Lindheimer MD, ed. Cardiovascular adaptation to normal pregnancy. In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley's hypertensive disorders in pregnancy. 2nd ed. Stamford, CT: Appleton & Lange, 1999:67–166. What does low blood pressure during labor mean?Hypotension during pregnancy is associated with an increased risk of stillbirth (7), as well as pregnancy complications such as preterm birth, intrauterine growth restriction (IUGR), meconium stained fluid, and postpartum hemorrhage (8). The lower the blood pressure, the higher the risk of poor pregnancy outcome.
Can you give birth with low blood pressure?Having low blood pressure during pregnancy is common. Most of the time, this condition won't cause major problems, and blood pressure will return to prepregnancy levels after you give birth. In some cases, however, very low blood pressure can be dangerous for mom and baby.
How is hypotension treated during labor?Hypotension during epidural analgesia is treated with additional intravenous boluses of crystalloid solution and/or administration of small intravenous doses of a vasopressor (e.g., ephedrine, in a dosage of 5 to 10 mg).
Can I get an epidural if I have low blood pressure?You may not be able to get an epidural if you have a bleeding or clotting disorder, current infection, very low blood pressure, are too close to delivery or are unable to cooperate.
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Low blood pressure during labor and delivery
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