eMedicine Specialties > Obstetrics and Gynecology > Medical Problems in Pregnancy

Hypertension and Pregnancy

Author: Paul Gibson, MD, Assistant Professor, Departments of Medicine and Obstetrics and Gynecology, Division of General Internal Medicine, University of Calgary
Coauthor(s): Michael P Carson, MD, Associate Professor, Departments of Medicine and Obstetrics and Gynecology, Drexel University College of Medicine; Chief, Division of Internal Medicine, Director, Obstetric Medicine Service, St Peter's University Hospital
Contributor Information and Disclosures

Updated: Dec 13, 2007



Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified into 4 categories, as recommended by the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy: 1) chronic hypertension, 2) preeclampsia-eclampsia, 3) preeclampsia superimposed on chronic hypertension, and 4) gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy). This terminology is preferred over the older but widely used term PIH (pregnancy-induced hypertension) because it is more precise.

Chronic hypertension is defined as blood pressure exceeding 140/90 mm Hg before pregnancy or before 20 weeks' gestation. When hypertension is first identified during a woman's pregnancy and she is at less than 20 weeks' gestation, blood pressure elevations usually represent chronic hypertension. In contrast, new onset of elevated blood pressure readings after 20 weeks' gestation mandates the consideration and exclusion of preeclampsia. Preeclampsia occurs in approximately 5% of all pregnancies, 10% of first pregnancies, and 20-25% of women with a history of chronic hypertension. Hypertensive disorders in pregnancy may cause maternal and fetal morbidity and remain a leading source of maternal mortality.


Chronic hypertension

Chronic hypertension is a primary disorder in 90-95% of cases. Secondary causes are briefly discussed in Causes.


Although the exact pathophysiologic mechanism is not clearly understood, preeclampsia is primarily a disorder of endothelial function with associated vasospasm. In some cases, pathology demonstrates evidence of placental insufficiency with associated abnormalities such as diffuse placental thrombosis, an inflammatory placental decidual vasculopathy, and/or abnormal trophoblastic invasion of the endometrium. This suggests that abnormal placental development or placental damage from diffuse microthrombosis may be central to the development of this disorder.

Evidence also indicates that an altered maternal immune response to fetal/placental tissue may contribute to the development of preeclampsia. The widespread endothelial dysfunction may manifest in a pregnant woman as dysfunction of multiple organ systems, including the central nervous, hepatic, pulmonary, renal, and hematological systems. Endothelial damage leads to pathologic capillary leak that can manifest in the mother as rapid weight gain, nondependent edema (face or hands), pulmonary edema, and/or hemoconcentration. When the placenta is diseased, it can affect the fetus via decreased utero-placental blood flow. This decrease in perfusion can manifest clinically as nonreassuring fetal heart rate testing, low scores on a biophysical profile, oligohydramnios, and as fetal growth restriction in severe cases.

Hypertension occurring in preeclampsia is due primarily to vasospasm, with arterial constriction and relatively reduced intravascular volume compared to normal pregnancy. The vasculature of normal pregnant women typically demonstrates decreased responsiveness to vasoactive peptides such as angiotensin-II and epinephrine. Women who develop preeclampsia show a hyperresponsiveness to these hormones, an alteration that may be seen even before the hypertension becomes apparent. In addition, their blood pressures are labile and the normal circadian blood pressure rhythms may be blunted or reversed.

Transient hypertension

Transient hypertension refers to hypertension occurring in late pregnancy without any other features of preeclampsia, with normalization of the blood pressure postpartum. The pathophysiology of transient hypertension is unknown, but it may be a harbinger of chronic hypertension later in life.


United States

Chronic hypertension occurs in up to 22% of women of childbearing age, with the prevalence varying according to age, race, and body mass index. Using population-based data, approximately 1% of pregnancies are complicated by chronic hypertension, 5-6% by gestational hypertension (without proteinuria), and 1-2% by preeclampsia.


  • Hypertensive disorders in pregnancy are among the leading causes of maternal mortality, along with thromboembolism, hemorrhage and nonobstetric injuries. Between 1991 and 1999, pregnancy-induced hypertension caused 15.7% of maternal deaths in the United States.
  • While maternal diastolic blood pressure (DBP) greater than 110 mm Hg is associated with an increased risk for placental abruption and fetal growth restriction, superimposed preeclamptic disorders cause most of the morbidity due to chronic hypertension during pregnancy. Severe maternal complications include eclamptic seizures, intracerebral hemorrhage, pulmonary edema due to capillary leak or myocardial dysfunction, acute renal failure due to vasospasm, proteinuria greater than 4-5 g/d, hepatic swelling with or without liver dysfunction, and disseminated intravascular coagulation and/or consumptive coagulopathy (rare). Consumptive coagulopathy usually is associated with placental abruption and is uncommon as a primary manifestation of preeclampsia.
  • Fetal complications include abruptio placentae, intrauterine growth restriction, premature delivery, and intrauterine fetal death.


Black women have higher rates of preeclampsia complicating their pregnancies compared to other racial groups, mainly because they have a greater prevalence of underlying chronic hypertension. Among women aged 30-39 years, chronic hypertension is present in 22.3% of black people, 4.6% of white people, and 6.2% of Mexican Americans. Hispanic women generally have blood pressure levels that are the same as or lower than those of non-Hispanic white women.


Preeclampsia is more common at the extremes of maternal age (<18 y or >35 y). The increased prevalence of chronic hypertension and other comorbid medical illnesses in women older than 35 years may explain the increased frequency of preeclampsia among older gravidas.



Determining whether elevated blood pressure identified during pregnancy is due to chronic hypertension or to preeclampsia is a challenge. Clinical characteristics obtained via history, physical examination, and certain laboratory investigations may be used to help clarify the diagnosis.

  • Gestational age
    • Hypertension prior to 20 weeks' gestation is almost always due to chronic hypertension; preeclampsia is rare prior to the third trimester.
    • New-onset or worsening hypertension after 20 weeks' gestation should lead to a careful evaluation for manifestations of preeclampsia.
    • The diagnosis of severe hypertension or preeclampsia in the first or early second trimester necessitates exclusion of gestational trophoblastic disease and/or molar pregnancy.
    • Women diagnosed with severe or early preeclampsia (in the second trimester or early third trimester) have a higher prevalence of thrombophilias. Studies are ongoing to evaluate whether administering anticoagulants in subsequent pregnancies decreases the risk of recurrent preeclampsia.
  • Maternal personal risk factors for preeclampsia
    • First pregnancy
    • New partner/paternity
    • Age younger than 18 years or older than 35 years
    • History of preeclampsia
    • Family history of preeclampsia in a first-degree relative
    • Black race
    • Obesity (BMI ³ 35)
    • Interpregnancy interval less than 2 years or more than 10 years
  • Maternal medical risk factors for preeclampsia
    • Chronic hypertension, especially secondary causes of chronic hypertension such as hypercortisolism, hyperaldosteronism, pheochromocytoma, or renal artery stenosis
    • Preexisting diabetes (type 1 or type 2), especially with microvascular disease
    • Renal disease
    • Systemic lupus erythematosus
    • Obesity
    • Thrombophilia
  • Placental/fetal risk factors for preeclampsia
    • Multiple gestations
    • Hydrops fetalis
    • Gestational trophoblastic disease
    • Triploidy
  • Symptoms of preeclampsia
    • Visual disturbances typical of preeclampsia are scintillations and scotomata. These disturbances are presumed to be due to cerebral vasospasm.
    • Headache is of new onset and may be described as frontal, throbbing, or similar to a migraine headache.
    • Epigastric pain is due to hepatic swelling and inflammation, with stretch of the liver capsule. Pain may be of sudden onset, is typically constant, and may be moderate-to-severe in intensity.
    • While mild lower extremity edema is common in normal pregnancy, rapidly increasing or nondependent edema may be a signal of developing preeclampsia. Edema is no longer included among the criteria for diagnosis of preeclampsia.
    • Rapid weight gain is a result of edema due to capillary leak as well as renal sodium and fluid retention.


  • Physical findings in preeclampsia
    • Blood pressure
      • Blood pressure should be measured in the sitting position, with the cuff at the level of the heart. Inferior vena caval compression by the gravid uterus while the patient is supine can alter readings substantially, leading to an underestimation of the blood pressure. Blood pressures measured in the left lateral position similarly may yield falsely low values if the blood pressure is measured in the higher arm, unless the cuff is carefully maintained at the level of the heart.
      • Women should be allowed to sit quietly for 5-10 minutes before each blood pressure measurement.
      • Korotkoff sounds I (the first sound) and V (the disappearance of sound) should be used to denote the systolic blood pressure (SBP) and DBP, respectively. In about 5% of women, an exaggerated gap exists between the fourth (muffling) and fifth (disappearance) Korotkoff sounds, with the fifth sound approaching zero. In this setting, both the fourth and fifth sounds should be recorded (eg, 120/80/40 with sound I = 120, sound IV = 80, sound V = 40) as the fourth sound will more closely approximate the true DBP.
      • Maternal SBP greater than 160 mm Hg or DBP greater than 110 mm Hg denotes severe disease; depending on the gestational age and maternal status, delivery should be considered for sustained BPs in this range.
      • Many automated blood pressure cuffs provide reasonable estimates of true blood pressure during normal pregnancy (especially those validated for pregnancy) but tend to underestimate blood pressure in preeclamptic women. Only a few automated BP cuffs have been validated in preeclampsia. Manual blood pressure measurement with a mercury sphygmomanometer remains the criterion standard in this setting.
      • Home and ambulatory BP measurements are increasingly being used in the pregnant population. Assuming the BP device is accurate (validated relative to an office measurement) they may provide valuable additional data regarding hypertension severity and control during pregnancy.
    • Retinal vasospasm is a severe manifestation of maternal disease; consider delivery.
    • Retinal edema is known as serous retinal detachment. This can manifest as severely impaired vision if the macula is involved. It generally reflects severe preeclampsia and should lead to prompt consideration of delivery. The condition typically resolves upon completion of pregnancy and resolution of the hypertension and fluid retention.
    • Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular stretch. Consider delivery.
    • Brisk, or hyperactive, reflexes are common during pregnancy. Clonus is a sign of neuromuscular irritability that usually reflects severe preeclampsia.
    • Approximately 30% of pregnant women will have some lower extremity edema as part of their normal pregnancy. A sudden worsening in dependent edema, edema in nondependent areas (such as the face and hands), or rapid weight gain suggest a pathologic process and warrant further evaluation for preeclampsia.
  • Signs suggesting a secondary medical cause of chronic hypertension
    • Centripetal obesity, "buffalo hump," and/or wide purple abdominal striae suggest glucocorticoid excess.
    • A systolic bruit heard over the abdomen or in the flanks suggests renal artery stenosis.
    • Radiofemoral delay or diminished pulses in lower versus upper extremities suggests coarctation of the aorta.
    • Clinical signs may demonstrate hyperthyroidism, hypothyroidism, or growth hormone excess.
  • Signs of end-organ damage from chronic hypertension
    • S4 on cardiac auscultation is not a normal finding in pregnancy. It suggests left ventricular hypertrophy or diastolic dysfunction due to preeclampsia-induced vasospasm.
    • Despite a well-conducted phonocardiographic study of pregnant women that found an S3 to be common in normal pregnancy, the authors' findings at busy obstetric centers have not supported this. In the presence of preeclampsia, any cardiac gallop may be a pathological finding and warrants further evaluation.
    • Diminished distal pulses due to peripheral vascular disease may be identified.
    • Retinal changes of chronic hypertension may be noted.
    • Carotid bruits may reflect atherosclerotic disease due to longstanding hypertension.


  • Chronic hypertension
    • Chronic hypertension may be either essential (90%) or secondary to some identifiable underlying disorder, such as renal parenchymal disease (eg, polycystic kidneys, glomerular or interstitial disease), renal vascular disease (eg, renal artery stenosis, fibromuscular dysplasia), endocrine disorders (eg, adrenocorticosteroid or mineralocorticoid excess, pheochromocytoma, hyperthyroidism or hypothyroidism, growth hormone excess, hyperparathyroidism), coarctation of the aorta, or oral contraceptive use.
    • About 20-25% of women with chronic hypertension develop preeclampsia during pregnancy.
  • Preeclampsia
    • The exact cause is not known.
    • The widespread endothelial dysfunction manifests primarily with maternal effects and has the potential to cause dysfunction of multiple organ systems, including the brain and the hepatic, pulmonary, renal, and hematological systems. The endothelial damage leads to pathologic capillary leak that can manifest in the mother as rapid weight gain, edema of the face or hands, pulmonary edema, and/or hemoconcentration resulting in hemoglobin greater than 12 g/dL or creatinine greater than 0.8 mg/dL. Renal biopsy may show glomerular endotheliosis that is associated with proteinuria greater than 300 mg in 24 hours.
    • Effects on the placenta include in situ thrombosis and decidual vasculopathy that can affect the fetus via decreased utero-placental blood flow. This decrease in flow can manifest clinically as nonreassuring fetal heart rate testing, low score on a biophysical profile, oligohydramnios, and fetal growth restriction in severe cases.

More on Hypertension and Pregnancy

Overview: Hypertension and Pregnancy
Differential Diagnoses & Workup: Hypertension and Pregnancy
Treatment & Medication: Hypertension and Pregnancy
Follow-up: Hypertension and Pregnancy
Multimedia: Hypertension and Pregnancy


  1. Aali BS, Nejad SS. Nifedipine or hydralazine as a first-line agent to control hypertension in severe preeclampsia. Acta Obstet Gynecol Scand. Jan 2002;81(1):25-30. [Medline].

  2. Brown MA, Buddle ML, Farrell T, Davis GK. Efficacy and safety of nifedipine tablets for the acute treatment of severe hypertension in pregnancy. Am J Obstet Gynecol. Oct 2002;187(4):1046-50. [Medline].

  3. Caritis S, Sibai B, Hauth J, et al. Low-dose aspirin to prevent preeclampsia in women at high risk. National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units. N Engl J Med. Mar 12 1998;338(11):701-5. [Medline].

  4. Chappell LC, Seed PT, Briley AL, et al. Effect of antioxidants on the occurrence of pre-eclampsia in women at increased risk: a randomised trial. Lancet. Sep 4 1999;354(9181):810-6. [Medline].

  5. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. May 21 2003;289(19):2560-72. [Medline].

  6. Coomarasamy A, Honest H, Papaioannou S, et al. Aspirin for prevention of preeclampsia in women with historical risk factors: a systematic review. Obstet Gynecol. Jun 2003;101(6):1319-32. [Medline].

  7. Duley L, Henderson-Smart DJ. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev. 2002;CD001449. [Medline].

  8. Hermida RC, Ayala DE. Prognostic value of office and ambulatory blood pressure measurements in pregnancy. Hypertension. Sep 2002;40(3):298-303. [Medline].

  9. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of. Sixth Report. Arch Intern Med. Nov 24 1997;157(21):2413-46. [Medline].

  10. Knuist M, Bonsel GJ, Zondervan HA, Treffers PE. Low sodium diet and pregnancy-induced hypertension: a multi-centre randomised controlled trial. Br J Obstet Gynaecol. Apr 1998;105(4):430-4. [Medline].

  11. Kosmas IP, Tatsioni A, Ioannidis JP. Association of Leiden mutation in factor V gene with hypertension in pregnancy and pre-eclampsia: a meta-analysis. J Hypertens. Jul 2003;21(7):1221-8. [Medline].

  12. Kupferminc MJ, Eldor A, Steinman N, et al. Increased frequency of genetic thrombophilia in women with complications of pregnancy. N Engl J Med. Jan 7 1999;340(1):9-13. [Medline].

  13. Kupferminc MJ, Fait G, Many A, et al. Severe preeclampsia and high frequency of genetic thrombophilic mutations. Obstet Gynecol. Jul 2000;96(1):45-9. [Medline].

  14. Levine RJ, Hauth JC, Curet LB, et al. Trial of calcium to prevent preeclampsia. N Engl J Med. Jul 10 1997;337(2):69-76. [Medline].

  15. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. Jul 27 1995;333(4):201-5. [Medline].

  16. Magee LA, Cham C, Waterman EJ, et al. Hydralazine for treatment of severe hypertension in pregnancy: meta-analysis. BMJ. Oct 25 2003;327(7421):955-60. [Medline].

  17. Magpie Trial Collaboration Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. Jun 1 2002;359(9321):1877-90. [Medline].

  18. Mulrow CD, Chiquette E, Ferrer RL. Management of chronic hypertension during pregnancy. Evidence Report/Technology Assessment No. 14. Aug 2000;AHRQ Publication No. 00-E011.

  19. Onwude JL, Lilford RJ, Hjartardottir H, et al. A randomised double blind placebo controlled trial of fish oil in high risk pregnancy. Br J Obstet Gynaecol. Feb 1995;102(2):95-100. [Medline].

  20. Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN. Recommendations for blood pressure measurement in humans and experimental animals: Part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Hypertension. Jan 2005;45(1):142-61. [Medline].

  21. Powrie RO, Rosene-Montella K. Hypertension and preeclampsia. In: Lee R, Rosene-Montella L, Barbour LA, Garner PR, Keely E, eds. Medical Care of the Pregnant Patient. ed. Philadelphia, Pa: American College of Physicians; 2000:185-208.

  22. Rochat RW, Koonin LM, Atrash HK, Jewett JF. Maternal mortality in the United States: report from the Maternal Mortality Collaborative. Obstet Gynecol. Jul 1988;72(1):91-7. [Medline].

  23. Sibai BM, Mabie WC, Shamsa F, et al. A comparison of no medication versus methyldopa or labetalol in chronic hypertension during pregnancy. Am J Obstet Gynecol. Apr 1990;162(4):960-6; discussion 966-7. [Medline].

  24. Sibai BM, Villar MA, Bray E. Magnesium supplementation during pregnancy: a double-blind randomized controlled clinical trial. Am J Obstet Gynecol. Jul 1989;161(1):115-9. [Medline].

  25. Working Group on High Blood Pressure in Pregnancy. Report of the National High Blood Pressure. Am J Obstet Gynecol. Jul 2000;183(1):S1-S22. [Medline].

  26. Zhang J, Klebanoff MA, Levine RJ, et al. The puzzling association between smoking and hypertension during pregnancy. Am J Obstet Gynecol. Dec 1999;181(6):1407-13. [Medline].

  27. von Dadelszen P, Magee LA. Fall in mean arterial pressure and fetal growth restriction in pregnancy hypertension: an updated metaregression analysis. J Obstet Gynaecol Can. Dec 2002;24(12):941-5. [Medline].

Further Reading


hypertension and pregnancy, pregnancy-induced hypertension, PIH, preeclampsia, hyperpiesis, hyperpiesia, high blood pressure, gestational hypertension, chronic hypertension, preeclampsia-eclampsia, preeclampsia superimposed on chronic hypertension, gestational hypertension, transient hypertension of pregnancy, chronic hypertension in the latter half of pregnancy

Contributor Information and Disclosures


Paul Gibson, MD, Assistant Professor, Departments of Medicine and Obstetrics and Gynecology, Division of General Internal Medicine, University of Calgary
Paul Gibson, MD is a member of the following medical societies: Alberta Medical Association, Canadian Society of Internal Medicine, Royal College of Physicians and Surgeons of Canada, and Society of Obstetric Medicine
Disclosure: Nothing to disclose.


Michael P Carson, MD, Associate Professor, Departments of Medicine and Obstetrics and Gynecology, Drexel University College of Medicine; Chief, Division of Internal Medicine, Director, Obstetric Medicine Service, St Peter's University Hospital
Michael P Carson, MD is a member of the following medical societies: American College of Physicians, Society of General Internal Medicine, and Society of Obstetric Medicine
Disclosure: Nothing to disclose.

Medical Editor

Gerard S Letterie, DO, Associate Clinical Professor, Medical Director of In-vitro Fertilization Lab, Department of Obstetrics and Gynecology, Virginia Mason Medical Center, University of Washington
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Assumption Community Hospital
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

Carl V Smith, MD, The Distinguished Chris J and Marie A Olson Chair of Obstetrics and Gynecology, Professor, Department of Obstetrics and Gynecology, University of Nebraska Medical Center
Carl V Smith, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, American Medical Association, Arkansas Medical Society, Association of Professors of Gynecology and Obstetrics, Central Association of Obstetricians and Gynecologists, Council of University Chairs of Obstetrics and Gynecology, Nebraska Medical Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.


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