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Pre-eclampsia is diagnosed when a pregnant woman develops high blood pressure (two separate readings taken at least 6 hours apart of 140/90 or more) and 300 mg of protein in a 24 hour urine sample (proteinuria). Swelling or edema(especially in the hands and face)was originally considered an important sign for a diagnoses of pre-eclampsia, but in current medical practice only hypertension and proteinuria are necessary for a diagnoses.

Some women develop high blood pressure without the proteinuria, this is called Gestational Hypertension or, Pregnancy Induced Hypertension (PIH). Both Preeclampsia and PIH are very serious conditions and require careful monitoring of mother and baby.


Pre-eclampsia is much more common in the first pregnancy (3-5% of births) and usually becomes evident in the third trimester (and virtually always after the 20th week of pregnancy). It is also more common in women who have preexisting hypertension, diabetes,renal disease, and family history of pre-eclampsia. It is also more common in women with a multiple gestation (twins, triplets and more).

Pre-eclampsia may also occur in the immediate post-partum period or up to 6-8 weeks post-partum. This is referred to as "post partum pre-eclampsia".


Pre-eclampsia is thought to be caused by inflammatory mediators secreted by the placenta and acting on the vascular endothelium. If severe, it progresses to fulminant pre-eclampsia, with headaches and visual disturbances, and further to HELLP syndrome and eclampsia. These are life-threatening conditions for both the developing fetus and the mother.


There are many theories on the pathogenesis of preeclampsia, although the exact cause is not known. Most involve abnormal development of the placenta, which leads to a distressed placenta that secretes factors into the maternal blood. These factors damage the maternal blood vessels, leading to high blood pressure and protein in the urine. In normal placenta the decidual spiral arteries are invaded by extravillous trophoblasts which makes the arteies eventually open into trophoblastic cavities called lacunae (though they are initially kept plugged by the trophoblasts). The invading trophoblasts replace some of the smooth muscles and endothelium of these arteries near the implantation site. This is supposed to help the spiral arteries to widen into thin and funnel like near their opening into the lacunae. This establishes a high capacity and low resistance circulation. The maternal blood in the lacunar network bath the chorionic villi lined by syncytiotrophoblast, supplying oxygen and nutrients to, and removing metabolic wastes from, the fetal circulation which is not in direct contact with the maternal blood. In case of preeclampsia the spiral arteries are insufficiently invaded by trophoblasts. They remain narrow and the smooth mucle layer (tunica media) around the arteries become hyperplastic. This leads to insufficient maternal perfusion of the placenta in preeclampsia. One of the factors, released into blood from the placenta, that has been speculated (by Karumanchi et al) to be a mediator of the "toxemia", is a soluble splice variant isoform of the VEGF receptor 1 (sFlt 1).


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Hemodynamic monitoring high-risk obstetrics patients, II: pregnancy-induced hypertension and preeclampsia - Cardiovascular Medicine
From Critical Care Nurse, 10/1/03 by Elizabeth J. Bridges

Critical care nurses are called upon to assist with the care of critically ill obstetrics patients. Some of the most complex care is required for patients with pregnancy-induced hypertension or preeclampsia. This article provides an overview of the pathological changes and expected hemodynamic changes associated with pregnancy-induced hypertension. A previous article (1) addressed the changes expected during a normal pregnancy and the changes associated with cardiovascular disease or hemorrhage. The clinical manifestations and medical and nursing management are summarized in a case study.

Expected Hemodynamic Changes in Pregnancy

Interpreting the pathophysiological changes that occur with pregnancy-induced hypertension requires a review of the hemodynamic changes expected during pregnancy, particularly during the third trimester. In summary (Table 1), increases in systolic and diastolic blood pressure of up to 10% of baseline are expected. (2-4) These increases in blood pressure reflect an increase in stroke volume and cardiac output, despite a decrease in systemic vascular resistance (SVR). Additionally, despite the marked increase in blood volume (as indicated by an increase in left ventricular end-diastolic volume) and pulmonary blood flow, pulmonary artery pressure and pulmonary artery wedge pressure (PAWP) remain at baseline levels throughout pregnancy. (6,15,16) Recognition of these expected changes is important. In patients with preeclampsia, SVR may increase dramatically, with a resultant decrease in cardiac output, or a hyperdynamic profile (high cardiac output and low SVR) may persist. (8,17-19) Additionally, remembering that pulmonary artery pressure and PAWP generally remain at baseline levels throughout pregnancy is useful in the differential diagnosis of refractory oliguria that may accompany preeclampsia. (20,21)

Hemodynamic Alterations Associated With Pregnancy-Induced Hypertension, Preeclampsia, and Eclampsia

Pregnancy-induced hypertension is hypertension that develops as a consequence of pregnancy and regresses after delivery. Pregnancy-induced hypertension can be differentiated from chronic hypertension, which appears before 20 weeks' gestation or continues for a long period after delivery. (22) Preeclampsia, which is a type of pregnancy-induced hypertension characterized by progressive hypertension and pathological edema, is clinically defined as a blood pressure greater than 140/90 mm Hg after 20 weeks' gestation plus proteinuria (300 mg/24 hours or greater than 1+ protein on a dipstick sample of urine collected at random). (23) Eclampsia is the occurrence of convulsions or coma unrelated to other cerebral conditions with signs and symptoms of preeclampsia. Preeclampsia and eclampsia may be complicated by the onset of the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count). Patients with HELLP syndrome are a subset of those with severe pregnancy-induced hypertension who are at increased risk for multiple organ system dysfunction. (24,25) Maternal complications associated with HELLP include a coagulopathy (specifically, microangiopathic hemolytic anemia) due to liver failure and thrombocytopenia, acute respiratory distress syndrome, and acute renal failure; all of these may require hemodynamic monitoring to guide therapy.

The hemodynamic profile of a patient with preeclampsia varies depending on the stage of the disease. During the preclinical or latent phase of preeclampsia, the hemodynamic profile is characterized as hyperdynamic, that is, increased cardiac output with normal vascular resistance. (8,17) With the onset of preeclampsia, the hemodynamic profile varies. In one longitudinal study, (17) women in whom preeclampsia developed crossed over from a high-output state to a high-resistance state, with a dramatic decrease in cardiac output (ie, greater than 3 L/min) and an increase in vascular resistance. However, in other studies, (8,18,19) many women had an unchanged profile (high-output or high-resistance states). These differences may be due to variability in treatment among different study populations or to the presence of more than a single hemodynamic profile for preeclampsia. These findings highlight the importance of individualizing the treatment of patients who have preeclampsia.

Hemodynamic monitoring may be required for 3 subsets of patients with preeclampsia, specifically patients with refractory oliguria, pulmonary edema, or refractory hypertension. (20,21,26) In patients with preeclampsia, central venous pressures correlate poorly with PAWP; thus if hemodynamic monitoring is needed, a pulmonary artery catheter is generally required. (27)

Refractory Oliguria

Three different hemodynamic subsets of patients with preeclampsia with persistent oliguria have been described (Table 2). (20,21) Subset 1 (low PAWP, hyperdynamic left ventricular function, and normal or increased SVR) is consistent with intravascular volume depletion. Patients in this subset respond to volume resuscitation. Subset 2, which is characterized by normal or increased PAWP, normal cardiac output, and normal SVR, is thought to be caused by renal arteriospasm. Treatment for patients in this subset is focused on reducing arteriospasm by administration of low-dose dopamine. In subset 3, the hemodynamic profile is consistent with systemic vasoconstriction (increased PAWP, increased SVR, decreased cardiac output). Treatment for patients in this subset is focused on afterload reduction and diuresis to improve ventricular function.

Pulmonary Edema

The risk of pulmonary edema is increased in patients with pregnancy-induced hypertension and preeclampsia because of a decrease in colloid osmotic pressure (COP). (6,28-33) COP, which is approximately 16 to 20 mm Hg in a healthy person lying supine, offsets the pressure (capillary hydrostatic pressure) that forces fluid out of the capillary. If the COP is decreased, net movement of fluid into the interstitium is increased, resulting in pulmonary edema. The risk of pulmonary edema is especially high during the postpartum period when a further decrease in COP occurs. (28,34) The decreased COP is particularly problematic if large volumes of crystalloids are used in resuscitation. (35-37) Other causes of pulmonary edema, including cardiogenic pulmonary edema (eg, iatrogenic volume overload) and alteration in pulmonary capillary permeability must also be ruled out.

Refractory Hypertension

Placement of a pulmonary artery catheter may be useful in treating patients who are refractory to standard hypertensive therapy (eg, hydralazine or labetolol). (21,38) Monitoring via a pulmonary artery catheter may help differentiate the cause of increased blood pressure, such as increased blood pressure due to increased vascular resistance. In patients with increased blood pressure due to increased vascular resistance, when the vascular resistance is decreased, the cardiac output increases without a change in blood pressure. The other less common cause of increased blood pressure is increased cardiac output, which can be diagnosed via pulmonary artery pressure monitoring. (21,26,39)

Other Clinical Concerns in Preeclampsia

Other factors to consider in the care of patients with preeclampsia are that compared with women who have a normal pregnancy, women with severe preeclampsia have decreased oxygen consumption, oxygen delivery, and oxygen extraction ratio. (17,35,39-41) The altered oxygen balance may be particularly important in patients with compromised cardiac output. Additionally, in patients with preeclampsia or eclampsia, the blood volume does not increase as much as in a normal pregnancy, making these patients with complicated preeclampsia less tolerant to peripartum blood loss. (42)

Case Study

The following case study describes the hemodynamic changes and medical and nursing care for a patient with complicated preeclampsia.

Findings at Admission

A 20-year-old, gravida 2, para 0 woman was admitted at 30 weeks' gestation because of pregnancy-induced hypertension. She was having irregular contractions. She had no history of hypertension or other medical conditions.

Her vital signs were as follows:

Heart rate: 108/min

Blood pressure: 160/110 mm Hg

Respirations: 26/min Temperature: 37.4[degrees]C (99.2[degrees]F)

Arterial oxygen saturation: 94%

Nursing Note All blood pressure measurements should be done with the patient in the same position (blood pressure is highest in the sitting position and lowest in the side-lying position) (43) and by using the same technique (ie, do not compare a measurement obtained via an arterial catheter with a measurement obtained by using an automated blood pressure cuff). (44-46)

The assessment findings were as follows:

Renal system: 4+ proteinuria with a urine output of approximately 12 mL/h

Generalized peripheral edema

Respiratory system: lung sounds clear

Fetal heart tones: heart rate = 140/min, with accelerations and occasional variable decelerations. (Variable decelerations occur in approximately 50% of all fetuses during labor, are usually temporary, and may change with the mother's body position. (47))

Nursing Note Despite clear lung sounds, this patient is at increased risk for pulmonary edema, particularly during the postpartum period. (28,34) Continued close assessment of pulmonary status is warranted. The oliguria may reflect intravascular volume deficit, renal arterial vasospasm, or systemic vasoconstriction. Evaluation of the patient's response to a bolus of fluid and evaluation of her hemodynamic status will aid in the differential diagnosis of the oliguria. (20,21)


The patient was given a 4-g bolus dose of magnesium sulfate and then a maintenance dose of 2 g. Isotonic sodium chloride solution was infused at a rate of 125 mL/h after intravenous administration of a bolus dose of 500 mL. Pitocin was administered to induce labor.

Nursing Note Continued close monitoring of neurological status is warranted Lo detect signs and symptoms of hypoxemia, impending seizure activity, increased intracranial pressure, or toxic effects of magnesium. (48) Calcium gluconate, the antidote for magnesium poisoning, should be kept at the bedside; the usual dose is a 1-g intravenous bolus. (48) Administration of crystalloid solution must be performed with caution because the combination of increased volume resuscitation and decreased COP increases the risk for pulmonary edema. (45-37)

Findings 4 Hours After Initial Treatment

Four hours after treatment, the patient's vital signs were as follows:

Heart rate: 120/min

Blood pressure: 169/104 mm Hg

Respirations: 28/min

Arterial oxygen saturation: 87%, with oxygen given at a rate of 10 L/min

Assessment findings were as follows:

Renal system: urine output 30 to 50 mL/h

Respiratory system: crackles in lower lobes

Fetal heart tones: tracing worsened In deceleration with no variability (indicative of fetal compromise)


The patient was delivered of her infant by cesarean birth. The mother had a catheter inserted in the pulmonary artery because of intraoperative bleeding and pulmonary compromise. Her hemodynamic profile was as follows:

Blood pressure: 173/118 mm Hg, mean 136 mm Hg

Right atrial pressure: 6 mm Hg

Pulmonary artery pressures (systolic/diastolic): 32/18 mm Hg

PAWP: 16 mm Hg

Cardiac output: 12 L/min

SVR: 832 dynes * s * [cm.sup.-5]

COP: 10 mm Hg

The rate of administration of intravenous fluids was decreased to 50 mL/h. The patient was given furosemide (Lasix) 10 mg intravenously and labetolol 10 mg intravenously.


Within 24 hours of delivery, the patient's hemodynamic profile returned to normal.


This patient had the classic signs and symptoms of preeelampsia (hypertension, proteinuria, edema) along with oliguria. (48) The oliguria was initially treated with crystalloids. Four hours later, her condition had deteriorated and was consistent with uncontrolled hypertension and pulmonary edema (bibasilar crackles and decreased arterial oxygen saturation). After placement of the pulmonary artery catheter, the hemodynamic profile reflected a hyperdynamic state (increased cardiac output and decreased SVR). The pulmonary edema most likely was due to decreased COP and was exacerbated by the slight increase in PAWP associated with the crystalloid administration. (Note: pulmonary edema does not generally become apparent until the PAWP exceeds 18 mm Hg.) As in this case, the treatment for preeclampsia is delivery if possible. (47) The pulmonary edema was treated in a standard manner with diuretics and reduction of intravenous fluids.


The opinions and assertions contained herein are the private views of the authors and are not to be construed as the official policy or position of the US government, the Department of Defense, or the Department of the Air Force.


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Elizabeth J. Bridges is Deputy Commander of the 59th Clinical Research Squadron and senior nurse researcher at the 59th Medical Wing, Lackland AFB, San Antonio, Tex.

Shannon Womble, Marlene Wallace, and Jerry McCartney are staff nurses in the surgical intensive care unit of the 59th Medical Wing at Lackland AFB.

COPYRIGHT 2003 American Association of Critical-Care Nurses
COPYRIGHT 2003 Gale Group

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