Hypertensive Disorders of Pregnancy

Hypertensive Disorders of Pregnancy

Judith H. Poole

Hypertension is a common medical complication of pregnancy and a leading cause of maternal morbidity and mortality. The woman may present with hypertension that predates her pregnancy or be diagnosed for the first time after the pregnancy is established. Regardless of when the diagnosis is made, it is important for the healthcare provider to recognize that the hypertensive disorders of pregnancy are part of a spectrum of diagnoses. This spectrum of diagnoses is categorized by the gestational age at the onset of hypertension and the presence of proteinuria. This chapter will discuss the current terminology for the diagnosis of hypertension during pregnancy, common risk factors, pathophysiology, and management. Assessment of maternal-fetal status and implications for the perinatal nurse are included.


Terminology used to describe the hypertensive disorders of pregnancy has suffered from imprecise usage, causing confusion for healthcare providers caring for women with hypertensive complications during pregnancy, childbirth, and postpartum. The National High Blood Pressure Education Program Working Group Report on High Blood Pressure in Pregnancy, published through the National Institutes of Health and the National Heart, Lung, and Blood Institute, outlines current accepted terminology for the hypertensive disorders of pregnancy (National High Blood Pressure Education Program [NHBPEP], 2000; NHBPEP Working Group, 2000). See Table 5-1 for the current classification of hypertension in pregnancy. The American College of Obstetricians and Gynecologists (ACOG) published a practice bulletin in 2002, reaffirmed in 2008, on the diagnosis and management of preeclampsia endorsing the new classification scheme. Clinically, there are two basic types of hypertension during pregnancy: chronic hypertension and gestational hypertension. The distinction is based on the gestational age at onset of the disease and the presence of proteinuria.


Chronic hypertension is hypertension present and observable before the pregnancy, diagnosed before 20 weeks’ gestation, or hypertension continuing beyond the 12th week post partum (ACOG, 2012; NHBPEP, 2000; NHBPEP Working Group, 2000). Hypertension is defined as a systolic blood pressure equal to or greater than 140 mm Hg or a diastolic blood pressure equal to or greater than 90 mm Hg (ACOG, 2012; NHBPEP, 2000; NHBPEP Working Group, 2000). Hypertension is diagnosed when either value is above the defined values; elevation of both systolic and diastolic pressures is not necessary for the diagnosis. The severity of hypertension is determined by the higher value, even if the other value is within normal parameters.


Gestational hypertension is the onset of hypertension, generally after the 20th week of gestation, in a previously normotensive woman, appearing as a marker of a pregnancy-specific vasospastic condition (Roberts & Funai, 2008). Gestational hypertension in clinical practice is a retrospective diagnosis. If hypertension is first diagnosed during pregnancy, is transient, does not progress into preeclampsia, and the woman is normotensive by 12 weeks postpartum, the diagnosis is gestational hypertension; if the blood pressure elevation persists, then the diagnosis is chronic hypertension (NHBPEP, 2000; NHBPEP Working Group, 2000). These two types of hypertension (chronic hypertension and gestational hypertension) may occur independently or simultaneously.


Type of Hypertension

Diagnostic Criteria


Gestational hypertension

  • New onset of hypertension, generally after 20 weeks of gestation

  • Hypertension defined as:

    ○ SBP ≥140 mm Hg, OR

    ○ DBP ≥90 mm Hg

  • Absence of proteinuria

  • Replaces pregnancy-induced hypertension

  • A retrospective diagnosis

  • BP normalizes to prepregnancy values by 12 weeks’ postpartum

  • Think oxygenation and perfusion


  • Gestational hypertension plus gestational proteinuria in a previously normotensive woman before 20 weeks of gestation

  • Gestational proteinuria defined as

    ○ >300 mg on random specimen

    ○ ≥1+ on dipstick

  • In absence of proteinuria, suspect if any of the following are present:

    ○ Headache

    ○ Blurred vision

    ○ Abdominal pain

    ○ Abnormal laboratory tests

Severe preeclampsia

  • Diagnosis of preeclampsia plus at least one of the following:

    ○ SBP ≥160 mm Hg

    ○ DBP ≥110 mm Hg

    ○ Proteinuria >2 g/24 hr

    ○ Serum creatinine >1.2 mg/dL

    ○ Platelets <100,000

    ○ ↑ LD (hemolysis)

    ○ ↑ ALT or AST

    ○ Persistent headache or cerebral/visual disturbances

    ○ Persistent epigastric pain

  • One of sickest patients on unit

  • At increased risk for complications

  • Additional criteria for diagnosis may include:

    ○ Oliguria defined as <500 mL/24 hr

    ○ Pulmonary edema

    ○ Impaired liver function of unclear etiology

    ○ IUGR

    ○ Oligohydramnios

    ○ Grand mal seizures (eclampsia)

HELLP syndrome

  • Diagnosis based on presence of:

    ○ Hemolysis

    ○ Elevated liver enzymes

    ○ Low platelets

  • Hemolysis

    ○ Abnormal peripheral smear

    ○ LD >600 U/L

    ○ Total bilirubin ≥1.2 mg/dL

  • Elevated liver enzymes

    ○ Serum aspartate aminotransferase >70 U/L

    ○ LD >600 U/L

  • Low platelets <150,000

  • Form of severe preeclampsia

  • Laboratory diagnosis

  • Impairs oxygenation and perfusion

  • Severity of disease, morbidity/mortality, and recovery related to platelet levels

    ○ <150,000 but >100,000

    ○ <100,000 but >50,000

    ○ <50,000


  • Diagnosis of preeclampsia

  • Occurrence of seizures

  • No other possible etiology for seizure

  • Critically ill patient

  • At risk for cerebral hemorrhage, aspiration, or death

  • Foley’s Rule of 13:

    ○ 13% mortality

    ○ 13% abruption

    ○ 13% seize after MgSO4 therapy

    ○ 13% seize >48 hr postpartum

Chronic hypertension

  • Hypertension defined as:

    ○ SBP ≥140 mm Hg, OR

    ○ DBP ≥90 mm Hg

  • Hypertension

    ○ Present and observable before pregnancy

    ○ Diagnosed before 20 weeks’ gestation

    ○ Persists beyond 12 weeks’ postpartum

  • Diagnosis may not be known prior to pregnancy

  • Places pregnancy at increased risk for abruption

Superimposed preeclampsia

  • Diagnosis based on presence of one or more of the following in the woman with chronic hypertension:

    ○ New onset of proteinuria

    ○ Hypertension and proteinuria before 20th week of gestation

    ○ Sudden ↑ in proteinuria

    ○ Sudden ↑ BP (previously well controlled)

    ○ ↑ ALT or AST to abnormal levels

    ○ Thrombocytopenia

  • Prognosis worse for woman and fetus

  • Mandates close observation

  • Timing of birth indicated by overall assessment of maternal-fetal well-being rather than fixed end point

ALT, alanine aminotransferase; AST, aspartate aminotransferase; DBP, diastolic blood pressure; IUGR, intrauterine growth restriction; LD, lactate dehydrogenase; SBP, systolic blood pressure; U/L, Units per liter.

Adapted from American College of Obstetricians and Gynecologists. (2002) . Diagnosis and Management of Preeclampsia and Eclampsia (Practice Bulletin No. 33; Reaffirmed 2008). Washington, DC: Author. Retrieved from http://mail.ny.acog.org/website/SMIPodcast/DiagnosisMgt.pdf; National High Blood Pressure Education Program. (2000) . National High Blood Pressure Education Program Working Group Report on High Blood Pressure in Pregnancy (NIH Publication No. 00-3029). Bethesda, MD: National Institute of Health; National Heart, Lung, and Blood Institute; and National High Blood Pressure Education Program; National High Blood Pressure Education Program Working Group. (2000) . Report of the National High Blood Pressure Education Program Working Group on high blood pressure in pregnancy. American Journal of Obstetrics and Gynecology, 183(1), S1-S22. doi:10.1067/mob.2000.107928

Once gestational hypertension is present, hypertension is further classified according to the maternal organ systems affected. The practitioner must keep in mind that hypertension during pregnancy represents a continuum of disease processes. Hypertension may be the first sign, but the underlying pathophysiology can involve all major organ systems.


Preeclampsia is characterized by renal involvement, as evidenced by the onset of proteinuria. It must be remembered that preeclampsia is a pregnancy-specific syndrome of reduced organ perfusion, including the utero-placental-fetal unit, secondary to cyclic vasospasms and activation of the coagulation cascade (NHBPEP, 2000; NHBPEP Working Group, 2000). The disease process is said to be mild or severe on the basis of maternal or fetal findings. If signs and symptoms of preeclampsia or eclampsia occur in women with chronic hypertension, the diagnosis of superimposed preeclampsia or eclampsia is made.


HELLP syndrome is a clinical and laboratory diagnosis characterized by hepatic involvement as evidenced by Hemolysis, Elevated Liver enzymes, and Low Platelet count. HELLP syndrome is not part of the current classification system but is a reflection of disease progression to severe preeclampsia.


Eclampsia is characterized by the onset of seizure activity or coma in the woman diagnosed with preeclampsia with no history of preexisting neurologic pathology or other identifiable cause (NHBPEP, 2000; NHBPEP Working Group, 2000).


Hypertensive disorders of pregnancy are one of the most common medical complications during pregnancy, labor, birth, and the postpartum period. Between 2000 and 2009, the rate of chronic hypertension complicating pregnancy increased 67% from a rate of 7.6 per 1,000 births to a rate of 12.7. In contrast, the rate for gestational hypertension has increased slightly from 39.4 per 1,000 births in 2008 to a rate of 41.2 in 2009 (Martin et al., 2011). A diagnosis of hypertension complicating pregnancy challenges the care provider, who must weigh the risk, benefits, and alternatives of treatment related to maternal, fetal, and neonatal well-being. Everyone caring for the woman during her pregnancy must be aware of the significance of the disease process, current diagnostic criteria, and management recommendations. Prompt recognition of the disease process and monitoring for potential complications decreases the risk of significant morbidity for the woman and her baby.

Preeclampsia is a significant contributor to maternal and perinatal morbidity and mortality, complicating approximately 5% to 8% of all pregnancies not terminating in first-trimester abortions (Han & Norwitz, 2011). In 2009, hypertension, both chronic and pregnancy related, complicated 221,403 (5.36%) of the 4.13 million pregnancies in the United States (Martin et al., 2011).

Maternal race influences the rate of gestational hypertension complicating pregnancy, with the highest rates seen for non-Hispanic black women (50.2/1,000 live births). The rate for non-Hispanic white women is 46.1 per 1,000 live births, and for Hispanic women the rate is 28.9 per 1,000 live births. Non-Hispanic black women also have higher rates for chronic hypertension (25.7/1,000) when compared to non-Hispanic white (12.3/1,000) and Hispanic (6.8/1,000) women. Maternal age distributions demonstrate women older than 30 years of age have the highest rates of hypertension for all reported races (Martin et al., 2011).


In the United States, pregnancy-associated hypertension is a leading cause of maternal death. Final mortality data for 2007 reported a total of 548 maternal deaths, producing a rate of 12.7 deaths per 100,000 live births (Xu, Kochanek, Murphy, & Tejada-Vera, 2010). The overall rate of maternal death from preeclampsia or eclampsia was 8.4 per 100,000 live births, which was one of the leading specific causes of death identified. There is a large disparity among rates of maternal death by race. African American women are more likely to die of preeclampsia. The overall maternal death rate for African American women was 26.5 per 100,000 live births in 2007, compared with 10.0 for white women and 21.7 for all other races. Of those maternal deaths from preeclampsia or eclampsia, the maternal mortality rate was 6.6 for whites, 17.3 for African Americans, and 14.6 for all other races (Xu et al., 2010).

In 2003, the Department of Health and Human Services and the Centers for Disease Control and Prevention (CDC) published data from the Pregnancy Mortality Surveillance System reporting pregnancy-related mortality from 1991 to 1999 (Chang et al., 2003). This publication examined the pregnancy-related mortality
by pregnancy outcome. Hypertension remained a leading cause of maternal death, accounting for 15.7% of all maternal deaths from 1991 to 1999. For women who had hypertension as the cause of death, 19.3% gave birth to a living infant and 20% had a stillbirth; for 11.8%, the pregnancy outcome was unknown (Chang et al., 2003). The cause-specific, pregnancyrelated mortality ratio was three to four times higher for African American women diagnosed with a hypertensive disorder (Chang et al., 2003).

The significance of preeclampsia as a contributor to maternal morbidity and mortality has recently been addressed in the Sentinel Event Alert Preventing Maternal Death published by The Joint Commission (TJC, 2010). In the alert, TJC identified the leading causes of maternal death: hemorrhage, hypertensive disorders, pulmonary embolism, amniotic fluid embolism, infection, and preexisting chronic conditions. Of those maternal deaths related to hypertension, TJC identified two commonly preventable errors. The failure to adequately control blood pressure in the hypertensive woman and the failure to adequately diagnose and treat pulmonary edema in women with preeclampsia contribute to preventable maternal mortality (TJC, 2010).

Hypertension during pregnancy predisposes the woman to potentially lethal complications such as abruptio placentae, disseminated intravascular coagulation (DIC), cerebral hemorrhage, cerebral vascular accident, hepatic failure, and acute renal failure. Leading causes of maternal death from hypertension complicating pregnancy include complications from abruptio placentae, hepatic rupture, and eclampsia (Roberts & Funai, 2008). The risk of stroke is disproportionately high among women diagnosed with either preeclampsia or eclampsia. While rare, there is a fourfold increased risk of stroke in this population either during the pregnancy or later in life (Bushnell & Chireau, 2011).

Maternal hypertension contributes to intrauterine fetal death and perinatal mortality. The main causes of neonatal death are placental insufficiency and abruptio placentae (Roberts & Funai, 2008). Intrauterine growth restriction (IUGR) is common in babies of women with preeclampsia. The exact cause is unknown, but fetal and neonatal consequences of preeclampsia may be related to the changes in the uteroplacental unit. Histologic findings of placentas from pregnancies complicated by preeclampsia are consistent with poor uteroplacental perfusion, which can lead to chronic hypoxemia in the fetus (Roberts, 2004).


Preeclampsia is a subtle and insidious disease process unique to human pregnancy. The signs and symptoms of preeclampsia become apparent relatively late in the course of the disease, usually during the third trimester of pregnancy. However, the underlying pathophysiology may be present as early as 8 weeks of gestation.

Historically, several well-defined risk factors have been identified for the development of preeclampsia (Display 5-1). Although risk factors are identified, the individual predictive values of the risk factors for screening and risk identification purposes have not been verified. Women should not be arbitrarily labeled as low- or high-risk patients based solely on historical risk factors.

Of interest today is the identification of physiologic or biochemical markers that would allow early identification of the woman at risk for the development of preeclampsia. Such markers would permit healthcare providers the opportunity to target close surveillance and timely interventions to the subpopulation of hypertensive women that would best benefit from the interventions. Biomarkers currently being investigated include soluble fms-like tyrosine kinase I (sflt-I), soluble endoglin (sEng), placental growth factor (PlGF), placental protein 13 (PP-13), a disintegrin and metalloprotease 12 (ADAM12), Pentraxin 3 (PTX3), pregnancy-associated plasma protein A (PAPP-A), Visfatin, and adrenomedullin (Grill et al., 2009). Of interest, the identified biomarkers may be more predictive in combination than as an isolated finding.



Early studies examining the use of antiplatelet therapy to prevent preeclampsia failed to demonstrate a significant difference in outcomes between treatment and control groups for most women, including nulliparas. However, a recent review of 59 trials by The Cochrane Collaboration did demonstrate a 17% reduction in the risk of preeclampsia with the use of antiplatelet agents (Duley, Henderson-Smart, Meher, & King, 2007). When stratified for risk level, there was no statistical difference in the relative risk based on maternal risk factors, but there was a significant increase in the absolute risk reduction of preeclampsia for high-risk women. Antiplatelet use was also associated with a reduction in the relative risk for preterm birth (8%), fetal/neonatal deaths (14%), and small-for-gestational-age babies (10%).


Dietary supplementation to reduce the risk or development of preeclampsia includes vitamin, mineral, and antioxidant supplementation. Calcium supplementation has demonstrated a reduction in hypertension; the greatest effect was seen in women with low calcium intake (Hofmeyr, Lawrie, Atallah, & Duley, 2010). Currently, there are no data to support the use of antioxidants (e.g., vitamin C, vitamin E, selenium, lycopene) to reduce the risk of preeclampsia or other complications of pregnancy (Rumbold, Duley, Crowther, & Haslam, 2008). Fish/marine oil supplementation, like other dietary supplementation, has failed to reduce the incidence of preeclampsia in low- and high-risk populations (Makrides, Duley, & Olsen, 2006).

The use of nitric oxide donors (glyceryl trinitrate) or precursors (L-arginine) has also been investigated as a means for reducing the risk of or preventing preeclampsia. While investigations continue, to date there is insufficient evidence to draw reliable conclusions related to effectiveness (Meher & Duley, 2007).


Preeclampsia has been called the “disease of theories.” There is not one established cause. Research is ongoing to identify the pathophysiology. Although the exact mechanism is unknown, preeclampsia is thought to occur because of changes within the maternal cardiovascular, hematologic, and renal systems.

Normal physiologic adaptations to pregnancy include an increase in plasma volume, vasodilation of the vascular bed, decreased systemic vascular resistance, elevation of cardiac output, and increased prostacyclin production. Physical assessment findings consistent with these changes are dilutional anemia, lower systemic blood pressures and mean arterial pressure (MAP), a slight increase in heart rate, and peripheral edema. In preeclampsia, these normal adaptations are altered. Instead of plasma volume expansion and hemodilution, there is a decrease in circulating plasma volume resulting in hemoconcentration. Women with preeclampsia have inadequate plasma volume expansion, with an average plasma volume 9% below expected values for mild disease and up to 40% below normal with severe disease. Further intravascular volume depletion may occur from endothelial injury and increased capillary permeability. The volume depletion may result in increased blood viscosity, leading to a decrease in maternal organ perfusion, including the uteroplacental unit.

Maternal intravascular volume depletion has been associated with fetal morbidity. The reduction in plasma volume may be more closely related to IUGR than hypertension. The vascular bed demonstrates increased sensitivity to vasoactive substances, resulting in vasoconstriction and increased vascular tone. Vasoconstriction results in increased systemic vascular resistance and hypertension. The hypertension is further aggravated by vasospasms of the arterial bed, the underlying mechanism for observed signs and symptoms of the disease process. The cumulative effect of decreased intravascular volume and vasoconstriction leads to a decreased organ perfusion. As the process worsens, hemolysis may also compromise tissue oxygen delivery.

Vasoconstriction and a further increase in cardiac output above the normal pregnancy elevation result in arterial vasospasms, endothelial damage, and an imbalance in endothelial prostacyclin and thromboxane ratios. Tables 5-2 and 5-3 provide highlights of the pathophysiology of disease progression and multiple organ system involvement.

Of interest is ongoing research examining the relationship of endothelial dysfunction and alterations in the immune response with the development of preeclampsia (Chaiworapongsa et al., 2004; Dechend et al., 2005; González-Quintero et al., 2004; Lévesque, Moutquin, Lindsay, Roy, & Rousseau, 2004; Magnini et al., 2005; NHBPEP Working Group, 2000; Waite, Louie, & Taylor, 2005; Wang, Gu, Zhang, & Lewis, 2004; Yamamoto, Suzuki, Kojima, & Suzumori, 2005). Vascular endothelial cells play a role in the modulation of vascular smooth muscle contractile activity and the coagulation and regulation of blood flow. Receptors within the endothelial cells respond to vasodilators and vasoconstrictors while producing vasoactive substances such as hormones, autacoids, and mitogenic cytokines, including PGI2, nitric oxide, and endothelin. The underlying processes are not fully understood, but women diagnosed with preeclampsia exhibit histologic evidence of increased circulating markers of endothelial activation. Endothelial dysfunction and subsequent increased capillary permeability in turn leads to the pathway of reduced organ perfusion.



Normal Pregnancy

Preeclampsia Alterations

Blood volume


Smaller ↑

Plasma volume


Little or no change

Red cell mass



Cardiac output


Widening pulse pressure


↓ Vascular compliance

Blood pressure

↓ Initially with return to prepregnant values by 3rd trimester


Peripheral vascular resistance

↓ Total peripheral resistance

↑ Resistance

↑ Vascular reactivity

Renal function

↑ Venous capacitance







Creatinine clearance

Serum creatinine

Uric acid

Renin-angiotensin-aldosterone system

Markedly activated and responds appropriately to posture and salt intake

Plasma renin concentration and activity suppressed

Loss of antagonists (vasodilators) to AII

Increased sensitivity to vasoactive substances

Coagulation system


Normal with mild disease

Factors VII, VIII, IX, X

All ↑

Normal initially, then ↓

Increase in ratio of von

Willebrand factor to factor VII, coagulant activity increased leading to consumption of factor VI

Fibrinolytic activity

Platelet count


Bleeding time



AII, angiotensin II; BUN, blood urea nitrogen; GFR, glomerular filtration rate; RPF, renal plasma blood flow.

Adapted from Roberts, J. (1994) . Current perspectives on preeclampsia. Journal of Nurse-Midwifery, 39(2), 70-90. doi:10.1016/0091-2182(94)90015-9

The “two stage model of preeclampsia” is the most recent area of investigation related to the pathophysiology of preeclampsia (Redman & Sargent, 2005; Roberts & Hubel, 2009

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

May 22, 2016 | Posted by in NURSING | Comments Off on Hypertensive Disorders of Pregnancy

Full access? Get Clinical Tree

Get Clinical Tree app for offline access