Professional Documents
Culture Documents
Samuel Thomas Bauer, MD, and Kirsten Lawrence Cleary, MD, MSCE
158 0146-0005/09/$-see front matter © 2009 Elsevier Inc. All rights reserved.
doi:10.1053/j.semperi.2009.02.008
Cardiopulmonary complications of PE 159
Table 1 Comparison of Cardiopulmonary Morbidity in Patients With HELLP Syndrome and in Patients With Severe Pre-Eclampsia
Without HELLP Syndrome3
Class I Class II Class III Severe P
Complication HELLP HELLP HELLP Pre-Eclampsia Value
Congestive heart failure 7 4 8 3 0.365
Pulmonary edema/effusion 11 5 10 7 0.149
Acute lung injury/ARDS 12 3 4 2 0.004
Continuous positive airway pressure/mechanical ventilation 14 7 4 4 0.004
Cardiopulmonary arrest 1 1 1 1 *
Any cardiopulmonary event 26 (12.3%) 13 (4.3%) 23 (8.3%) 12 (6.2%) 0.008
*P value not reported because of insufficient data.
During normal pregnancy, plasma and red cell volumes searchers measure capillary leak by measuring the interstitial
increase by approximately 42% and 24%, respectively. The fluid from subcutaneous tissue in the thorax and ankle by
total blood volume of an average size woman will increase implanted wicks and interstitial fluid hydrostatic pressure.9
from approximately 3500 mL in the nonpregnant state to Pulmonary artery catheter research in pregnancy consists
near 5000 mL toward the end of the third trimester of preg- of retrospective data: case reports, small series, or reviews.
nancy.4 When compared to normal nonpregnant subjects, No randomized trials support their routine use in women
patients with pre-eclampsia demonstrate increased vascular with severe pre-eclampsia. Most of the reports primarily de-
resistance, decreased circulatory volume, and decreased pe- scribe hemodynamic parameters and fluid status of pre-
ripheral perfusion. Plasma volume reduction and hemocon- eclampsia and do not mention particular complications.
centration remains a hallmark of pre-eclampsia and occurs in Given the known complications of pulmonary artery cathe-
proportion to the severity of the disease process.5 In the ters, including cardiac arrhythmias, pneumothorax, hemo-
1980s, Rafferty and Berkowitz studied 3 patients with severe thorax, neurologic injury, and pulmonary hemorrhage, we
pre-eclampsia using thermodilution tip pulmonary artery do not recommend invasive monitoring for routine clinical
catheters during cesarean section under general endotracheal cases. However, invasive hemodynamic monitoring may
anesthesia. The left ventricular stroke work indexes (LVSWI) of prove beneficial in women with pre-eclampsia and severe
these patients were higher than those of normal nonpregnant cardiac disease, severe renal disease, refractory hypertension,
women, but there was no evidence of myocardial depression in oliguria, or pulmonary edema.10,11 Pulmonary artery cathe-
either cardiac index or the LVSWI-pulmonary capillary wedge ters aided in clinical management decisions in 93% of cases of
pressure relationship. Pulmonary arteriolar resistance was severe pre-eclampsia complicated by renal failure or pulmo-
found to be within or below the normal nonpregnant range, nary edema in a small, retrospective series of 17 women with
suggesting that the pulmonary vasculature is not involved in a eclampsia. The pulmonary artery catheter was considered
primary vasospastic process in severe pre-eclampsia. At deliv- subjectively helpful if the initial readings (central venous
ery, a rise in cardiac index and mean pulmonary capillary wedge pressure and pulmonary capillary wedge pressure) clarified
pressure occurred. The pulmonary capillary wedge pressure patients’ fluid status and helped guide decision-making.
was higher in the postpartum period than before delivery, po- Catheter placement was not helpful if the initial readings
tentially representing an increase in circulating blood volume.6 were unobtainable, inconsistent, or not used to influence or
Benedetti et al. substantiated these findings when they noted an determine decision-making.12
increase in LVSWI and hyperdynamic ventricular function in 10
patients with severe pre-eclampsia and pulmonary artery cath-
eters during labor.7 Table 2 Hemodynamic Findings in Severe Pre-Eclampsia8
Cotton and colleagues later performed right-heart cathe-
terization in 45 women with severe pre-eclampsia or eclamp- Cardiac output is variable
sia. Most patients had high-normal or elevated systemic vas- Mean arterial pressure is elevated; systemic vascular
resistance is normal (early) or elevated (late)
cular resistance indexes, hyperdynamic left ventricular
Central venous pressure is usually low to normal and does
function, normal or increased pulmonary capillary wedge not correlate with pulmonary capillary wedge pressure
pressure, and low central venous pressure (Table 2).8 Pulmonary hypertension and pulmonary vascular
In the setting of chronic hypertension with superimposed resistance are not present, but low pulmonary artery
pre-eclampsia, systemic vascular resistance and left heart fill- pressure may occur in the presence of hypovolemia
ing pressures are increased. This leads to a decrease in cardiac Pulmonary capillary wedge pressure may be low, normal,
output and an increase in pulmonary vascular hydrostatic or high
pressure, which culminates in the development of pulmo- Oliguria may not reflect volume depletion
nary edema. An additional feature that may predispose to the Ventricular function is usually hyperdynamic but may be
development of pulmonary edema in the setting of pre- depressed in the presence of marked elevation in
eclampsia is an increase in capillary leak and capillary fluid systemic vascular resistance
Colloid oncotic pressure is usually low
extravasation secondary to vascular endothelial damage. Re-
160 S.T. Bauer and K.L. Cleary
If pulmonary edema remains refractory to initial manage- Pulmonary edema is a clinical diagnosis characterized by
ment or is accompanied by persistent oliguria, insertion of a worsening dyspnea and orthopnea along with signs of respi-
pulmonary artery catheter and transfer to an intensive care ratory compromise (tachypnea, auditory crackles and rales,
unit where mechanical ventilatory support could be pro- and hypoxemia). Arterial blood gas and chest X-ray may
vided may be considered.13 assist in the diagnosis. On postanterior and lateral chest X-ray
films, the early signs of pulmonary edema (interstitial edema)
are Kerley B lines, which are horizontal lines seen laterally in
Pulmonary Edema the lower zones reaching the lung edge. As the edema
Pulmonary edema is the most common cardiopulmonary progresses, alveolar edema is observed in a “butterfly-like”
complication of pre-eclampsia and refers to an excessive ac- pattern, which is characterized by the central predominance
cumulation of fluid in the pulmonary interstitial and alveolar of shadows with a clear zone at periphery lung lobes. Cardiac
spaces. The development of pulmonary edema is usually enlargement characterizes progression to cardiac failure. Pul-
multifactorial. According to the Starling equation, any factor monary edema may resemble the initial stages of ARDS.19 In
that results in a reduction in colloid osmotic pressure, an select patients, electrocardiography, echocardiography, spi-
increase in capillary permeability, or an increase in intravas- ral computed tomographic imaging, ventilation/perfusion
cular hydrostatic pressure will lead to extravasation of fluid scan, or pulmonary arteriography may be necessary to ex-
from the vasculature and predispose to the development of clude other causes of cardiopulmonary compromise, such as
pulmonary edema.14 The underlying physiological changes pulmonary embolism, pneumonia, and cardiomyopathy.
in the maternal cardiovascular system, including increased Two-dimensional and Doppler echocardiography provide
plasma blood volume, cardiac output, heart rate, and capil- an additional diagnostic modality for patient with pre-
lary permeability and a decrease in plasma colloid osmotic eclampsia complicated by pulmonary edema. Desai and col-
pressure, are exaggerated in pre-eclampsia and predispose leagues diagnosed impaired left ventricular systolic function
women to develop pulmonary edema. Plasma colloid os- in 4 of 16 (25%) patients with pre-eclampsia and pulmonary
motic pressure decreases from around 22 mm Hg at term to edema. In the remaining 12 patients with preserved systolic
16 mm Hg after delivery, in normal pregnancies, and from 18 function, left ventricular diastolic filling abnormalities were
mm Hg at term to 14 mm Hg postpartum in pregnancies demonstrated in a significant proportion compared to con-
complicated by pre-eclampsia. The reduction in postpartum trol hypertensive and normotensive groups.20
colloid osmotic pressure may result from excessive blood Mabie and colleagues evaluated the role of echocardiogra-
loss, fluid shifts secondary to increased capillary permeabil- phy in determining the cause of pulmonary edema in preg-
ity, especially in pregnancies complicated by pre-eclampsia. nancy. Forty-five pregnant or recently postpartum women
Such changes help to explain why 70%-80% of cases of pul- admitted to an obstetrical intensive care unit with pulmonary
monary edema in the setting of pre-eclampsia develop after edema during a 6-year period were followed prospectively.
delivery.15 In 21 patients (47%), echocardiography demonstrated clini-
Sibai described a series of 37 severe preeclamptic or cally unsuspected findings, which altered the long-term
eclamptic patients with pulmonary edema in which the inci- management in 16. Because clinical and roentgenographic
dence of pulmonary edema was significantly higher in older findings do not accurately differentiate patients with respect
patients (P ⬍ 0.0001) and in multigravidas (P ⬍ 0.05). to the presence and type of cardiac dysfunction, we recom-
Eleven (30%) had antepartum pulmonary edema with 10 mend echocardiography to evaluate all pregnant women with
(90%) of the 11 having pre-existing chronic hypertension. pulmonary edema.21
Twenty-six (70%) had postpartum onset of pulmonary Prompt diagnosis of pulmonary edema and intervention
edema with an average onset at 71 hours postpartum.16 In a are critical. The morbidity and mortality associated with pre-
retrospective cohort study of California birth records, Gilbert eclampsia complicated by pulmonary edema have been
and colleagues reviewed 29,842 pregnant women with greatly reduced by accurately assessing cardiovascular func-
chronic hypertension. As compared to nonchronic hyperten- tion and aggressive treatment. The presence of hypertension,
sive patients, pulmonary edema was increased: (OR 5.2; 95% proteinuria, and pulmonary edema satisfies the criteria for
CI 3.9, 6.7).17 severe pre-eclampsia and precludes further conservative
Clinicians have often questioned whether magnesium sul- management. The diagnosis of severe pre-eclampsia requires
fate, administered to preeclamptic women for seizure pro- immediate hospitalization in labor and delivery. Intravenous
phylaxis, leads to pulmonary edema. Yeast and colleagues magnesium sulfate prevents seizures and antihypertensive
measured the effect of intravenous magnesium sulfate ad- medications lower severe levels of hypertension (systolic
ministered for preterm labor or seizure prophylaxis on col- pressure greater than 160 mm Hg and/or diastolic pressure of
loid osmotic pressure and the risk for pulmonary edema in at least 110 mm Hg). Patients with pulmonary edema deliver
294 pregnant women. Only 4 of the 294 women developed within 24-48 hours irrespective of fetal gestational age.22
pulmonary edema, and all 4 had low colloid osmotic pressure Medical therapies to treat pulmonary edema should be
in the setting of severe pre-eclampsia. Magnesium sulfate did optimized to expedite treatment results. Furosemide (Lasix)
not significantly change colloid osmotic pressure and does can be administered intravenously as a single dose of 10-40
not pose a significantly increased risk for developing pulmo- mg over 2 minutes to promote diuresis. Bladder catheteriza-
nary edema.18 tion allows for accurate measurement of urine output. While
Cardiopulmonary complications of PE 161
most patients will respond to initial diuresis therapy, if ade- within 4 days of admission. Of the 4 infants who did not
quate response is not seen within 30-60 minutes, the dose survive intact, 2 suffered perinatal asphyxia, 1 suffered peri-
should be increased to 40-60 mg administered by slow intra- natal asphyxia and cerebral palsy, and 1 suffered perinatal
venous injection to a maximum of 120 mg in 1 hour. Elec- death.
trolytes should be monitored closely and repleted as indi- Respiratory support provides the cornerstone to manage-
cated. Morphine sulfate can be administered intravenously as ment of ARDS in pregnancy, especially as respiratory alkalo-
needed both for pain as well as in an attempt to reduce the sis develops. Although a Pao2 of 55 mm Hg and an Sao2 of
adrenergic vasoconstrictor stimuli to the pulmonary arterio- 88% would be tolerated in the general population, adequate
lar and venous beds. As with the management of all parturi- fetal oxygenation requires a Pao2 of ⱖ70 mm Hg, which
ents with pre-eclampsia, sodium and water should be mod- corresponds to a maternal Sao2 of about 95%.24 The broad
estly restricted, and maternal fluid balance should be strictly goals of ventilatory support in a pregnant woman with ARDS
monitored. Oxygen saturation can be monitored using a are no different from the general population, namely, to man-
pulse oximeter, and oxygen supplementation using a non- age blood-gas variables while avoiding ventilator-associated
rebreather facemask can be used to treat maternal hypox- lung injury. Likewise, the clinical criteria for intubating a
emia. In addition to these standard measures, it is appropri- pregnant patient remain the same and include increased
ate to follow the patient’s blood pressure, electrocardiogram, work of breathing, mental status deterioration, hemody-
and fetal heart rate tracing. Afterload reduction using vaso- namic instability, and inability to protect the airway or man-
dilators may be necessary, especially in parturients with age secretions.26
chronic hypertension and superimposed pre-eclampsia. Be- Little literature exists to guide the decisions on the mode of
cause most obstetrical patients have normal left ventricular delivery in patients with ARDS. A small retrospective study
systolic function, inotropic support is rarely necessary.13 suggests that cesarean delivery may improve the maternal
status in ventilated women in late pregnancy that have ARDS
but are clinically stable.24 Other studies have not supported
Acute Respiratory an improvement.21 Pregnant women with ARDS may not
Distress Syndrome tolerate a vaginal delivery due to increased oxygen consump-
tion. Cesarean delivery results in larger and more rapid fluid
ARDS is a form of respiratory failure characterized by acute shifts and blood loss than with vaginal delivery and may
hypoxemia and increased alveolar-capillary permeability re- present a greater physiological stress. Until further data are
sulting from diffuse and ongoing pulmonary inflammation.23 available, the decision for a mode of delivery should be based
Patients experience acute hypoxemic respiratory failure, of- on standard obstetrical indications. Attempts should be made
ten accompanied by dyspnea, tachypnea, cyanosis, and to optimize maternal oxygenation and pain control during
tachycardia. Diffuse bibasilar crackles or wheezing can be vaginal deliveries.27
appreciated on auscultation of the chest. Minimal evidence Although ARDS during pregnancy is uncommon, when it
exists regarding the management of ARDS in pregnancy; does occur, optimum management requires multidisci-
mortality remains high, and few strategies have shown a mor- plinary care from maternal-fetal medicine, critical care med-
tality benefit. The treatment of ARDS in pregnancy is often icine, obstetrical anesthesiology, pulmonology, and neona-
extrapolated from studies performed in the general ARDS tology.
patient population, with consideration given to the normal
physiological changes of pregnancy.
Definitions vary for pregnancy-related ARDS, including Peripartum Cardiomyopathy
ARDS during pregnancy or within 1 week or 1 month post-
partum. Expanding this definition to several weeks postpar- Peripartum cardiomyopathy (PPCM) affects patients late in
tum may be appropriate, as it can take up to 6 weeks post- pregnancy or in the early postpartum period. It is an infre-
delivery for most of the physiological changes of pregnancy quent complication of pre-eclampsia, but a history of pre-
to resolve.24 eclampsia can be found in up to 70% of those who develop
Pre-eclampsia complicated by HELLP syndrome, pulmo- PPCM. The 4 following criteria are needed to meet the defi-
nary edema, and/or cardiopulmonary disease can advance to nition of peripartum cardiomyopathy: (1) development of
pregnancy-related ARDS. In a series of 83 obstetrical patients cardiac failure in the last month of pregnancy or within 5
with ARDS from all causes, the antepartum mortality rate was months of delivery; (2) absence of an identifiable cause for
23% and the postpartum mortality rate was 50%.25 the cardiac failure; (3) absence of recognizable heart disease
The effect of maternal ARDS on neonatal outcomes is not before the last month of pregnancy; (4) left ventricular sys-
well studied, but high rates of fetal death, spontaneous pre- tolic dysfunction (for example, left ventricular ejection frac-
term labor, and non-reassuring fetal heart rate tracing are tion (EF) below 45%).28 The etiology remains unclear, but
reported. In a series of 10 antepartum patients in the third risks factors include multiple pregnancy, pre-eclampsia,
trimester ventilated for ARDS, only 5 of the neonates sur- multiparity, and advanced maternal age. Pre-eclampsia is as-
vived intact after delivery.24 Spontaneous preterm labor and sociated with peripartum cardiomyopathy; however, peri-
delivery was reported in 6 patients. Fetal heart rate abnor- partum cardiomyopathy is an infrequent complication of
malities were reported in 6 of these pregnancies and occurred pre-eclampsia.29
162 S.T. Bauer and K.L. Cleary
Table 4 Risk of Cardiac Disease After Pre-Eclampsia/Eclampsia With the recognition of hypertensive diseases of pregnan-
in Case-Control Studies49 cies as an etiology for subsequent heart disease later in life,
Odds Ratio Wikstrom and colleagues investigated the question of
Study Weight (%) (Random) 95% CI whether the risk of developing ischemic heart disease in later
Mann46 6.47 3.60 (0.26, 50.70) life increases with severity of hypertensive disease during
Rosenberg47 42.30 1.30 (0.65, 2.60) pregnancy. After a review of 403,550 women in the Swedish
Croft36 32.00 3.60 (1.42, 9.10) Medical Birth Register over a 9-year period with up to 15
Haukkamaa40 19.23 4.80 (1.21, 19.00) years of follow-up, the adjusted incidence rate ratio for later
Total (95% CI) 100.00 2.47 (1.22, 5.01) development of ischemic heart disease was 1.6 (95% CI 1.3,
2.0) when the first pregnancy was complicated by gestational
hypertension without proteinuria, 1.9 (95% CI 1.6, 2.2) for
mild pre-eclampsia, and 2.8 (95% CI 2.2, 3.7) for severe
cases, Jonsdottir and colleagues reviewed the association be-
pre-eclampsia. Women with hypertensive disease in both
tween hypertension in pregnancy, pre-eclampsia, and eclampsia
pregnancies had an RR of 2.8 (95% CI 2.0, 3.9) compared
and death rates from ischemic heart disease. The relative risk of
with women with 2 normal pregnancies.41
dying from ischemic heart disease was significantly higher
In a recent systematic review and meta-analysis,
among eclamptic women (RR 2.61; 95% CI 1.11, 6.12) and
McDonald and colleagues reviewed the existing literature to
those with pre-eclampsia (RR 1.90; 95% CI 1.02, 3.52) than
determine if women with a history of pre-eclampsia/eclamp-
those with hypertension alone. Parous women at the index
sia are at increased risk of long-term cardiovascular sequelae.
pregnancy had a 2-fold higher risk of dying from ischemic
Relative to women with uncomplicated pregnancies, women
heart disease than primigravid women (RR 2.05; 95% CI
with a history of pre-eclampsia/eclampsia had an increased
1.19, 3.55; P ⫽ 0.01).38
risk of subsequent cardiac disease in both the case-control
studies and the cohort studies, as well as an increased risk of
Etiology and Pathophysiology cardiovascular mortality. Women with a history of pre-
Fleming and colleagues have suggested that cardiac troponin eclampsia/eclampsia have approximately double the risk of
levels are elevated in women with pre-eclampsia.39 Fleming early cardiac and cardiovascular mortality (Tables 4 and 5).42
examined troponin I levels in 69 women with pre-eclampsia After a pregnancy complicated by pre-eclampsia, women
or gestational hypertension. There were 43 controls, 20 pa- have an increased risk of vascular disease, including the fol-
tients with gestational hypertension, and 6 patients with pre- lowing: hypertension after 14.1 years (3.70, 95% CI 2.70,
eclampsia. Troponin I levels were significantly higher in the 5.05), ischemic heart disease after 11.7 years (2.16, 95% CI
gestational hypertensive groups compared with controls, 1.86, 2.52), stroke after 10.4 years (1.81, 95% CI 1.45, 2.27),
suggesting that coronary ischemic may be missed in patients and venous thromboembolism after 4.7 years (1.79, 95% CI
with hypertensive disorders in pregnancy, including pre- 1.37, 2.33). Overall mortality after pre-eclampsia was in-
eclampsia. creased after 14.5 years: 1.49 (95% CI 1.05, 2.14).43
Irgens and colleagues demonstrated that mothers have in-
Pre-Eclampsia Impacts creased cardiovascular morbidity and mortality risk after a
pregnancy complicated by pre-eclampsia. Women who had
Long-Term Cardiovascular Health pre-eclampsia had a 1.2-fold higher long-term risk of death
Pre-eclampsia and coronary artery disease share common (95% CI 1.02, 1.37) than women who did not have pre-
risk factors for endothelial dysfunction and damage, such as eclampsia. The risk in women with pre-eclampsia and a pre-
hypertension, diabetes, and obesity. The associated maternal term delivery was 2.71-fold higher (1.99-3.68) than in
physiological changes from pre-eclampsia include increased
inflammatory markers, dyslipidemia, insulin resistance, en-
dothelial dysfunction, and oxidative stress and are associated Table 5 Risk of Cardiac Disease After Pre-Eclampsia/Eclampsia
with an increased risk for cardiovascular disease in later life. in Cohort Studies49
A history of pre-eclampsia has been reported to be a risk Relative Risk
factor for several distinct cardiovascular conditions later in Study Weight (%) (Random) 95% CI
life. Haukkamaa and colleagues40 reviewed the history of
Jonsdottir38 8.51 2.12 (1.29, 3.49)
hypertensive pregnancies and conventional risk factors in Hannaford37 16.10 1.65 (1.26, 2.16)
141 relative young parous women with angiographically Irgens44 11.11 2.12 (1.42, 3.16)
documented coronary artery disease and showed that hyper- Smith48 8.39 3.54 (2.14, 5.85)
tension and pre-eclampsia were independent risk factors for Kestenbaum49 11.19 2.53 (1.70, 3.77)
subsequent coronary artery disease, with adjusted odd ratios Wilson50 4.43 1.24 (0.58, 2.68)
of 5.2 (2.6, 11.0; P ⬍ 0.001) and 4.8 (95% CI 1.2, 19; P ⫽ Funai51 13.04 3.07 (2.18, 4.33)
0.03), respectively. Patients with coronary artery disease had Kaaja52 4.78 2.50 (1.20, 5.20)
pre-eclampsia more often in the first or any subsequent preg- Ray53 10.62 2.85 (1.88, 4.32)
nancy than did the control groups (17% vs. 3.0% and 1.8%, Wikstrom41 11.82 2.27 (1.56, 3.32)
Total (95% CI) 100.00 2.33 (1.95, 2.78)
P ⬍ 0.001).
164 S.T. Bauer and K.L. Cleary
women who did not have pre-eclampsia and whose pregnan- 4. Chesley LC: Plasma and red cell volumes during pregnancy. Am J
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5. Hays PM, Cruikshank DP, Dunn LJ: Plasma volume determination in
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Finally, a recent review has demonstrated that women 6. Rafferty TD, Berkowitz RL: Hemodynamics in patients with severe tox-
with severe, very early onset pre-eclampsia have an increased emia during labor and delivery. Am J Obstet Gynecol 138:263-270,
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7. Benedetti TJ, Cotton DB, Read JC, et al: Hemodynamic observations in
early onset severe pre-eclampsia exhibit more cardiovascular severe preeclampsia with a flow-directed pulmonary artery. Am J Ob-
risk factors. Gaugler-Senden and colleagues reviewed 20 stet Gynecol 136:465-470, 1980
women with early onset pre-eclampsia, before 24 weeks’ ges- 8. Cotton DB, Lee W, Huhta JC, et al: Hemodynamic profile of severe
tation. Cardiovascular risk profiles were compared to con- pregnancy-induced hypertension. Am J Obstet Gynecol 158:523-529,
trols. Of the 20 women with history of early onset severe 1988
9. Oian P, Maltau JM, Noddeland H, et al: Transcapillary fluid balance in
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10%, P ⫽ 0.002), as well as increased microalbuminuria (P ⬍ pulmonary artery catheterization in severe preeclampsia and eclamp-
0.05).45 sia. Am J Obstet Gynecol 182:1397-1403, 2000
Women with early onset, recurrent, or severe pre-eclamp- 13. ACOG: Invasive hemodynamic monitoring in obstetrics and gynecol-
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42:199-205, 1993
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women may have unrecognized chronic hypertension, an tol 21:298-306, 1997
inherited thrombophilia, or other genetic or environmental 15. Benedetti TJ, Kates R, Williams V: Hemodynamic observations in se-
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with chronic hypertension: A population-based study. J Reprod Med
Cardiovascular and cardiopulmonary complications due to 52:1046-1051, 2007
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ally. Maternal morbidity and mortality from placental syn- and colloid osmotic pressure changes during magnesium sulfate infu-
dromes, including gestational hypertension and pre-eclamp- sion. Am J Obstet Gynecol 169:1566-1571, 1993
19. Fauci AS, Braunwald E, Kasper DL, et al: Harrison’s Principles of Inter-
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