Pregnancy Induced Hypertension Case Study

H O LY A N G E L U N I V E R S I T Y
College of Nursing
In Partial Fulfilment of Requirements for RLE 104
“ PREGNANCY INDUCED HYPERTENSION”

A Book-Based Case Study
Presented To:
Teacher’s Full Name MAN, RN
Submitted By:
Gueco, Daryl C.
GROUP 2 of N-407
September 29, 2010

Pregnancy-Induced Hypertension: A Case Study 2
TABLE OF CONTENTS
INTRODUCTION
BRIEF DESCRIPTION OF THE DISEASE 3
REASONS FOR CHOOSING THE CASE 5
STATISTICS 6
STUDENT NURSE-CENTRED OBJECTIVES 7
DIAGNOSTIC & LABRATORY PROCEDURES 8
PHYSICAL ASSESSMENT 16
ANATOMY & PHYSIOLOGY 29
PATHOPHYSIOLOGY
SYNTHESIS OF THE DISEASE 44
DEFINITION OF THE DISEASE 46
PREDISPOSING & PRECIPITATING FACTORS 47
SIGNS AND SYMPTOMS WITH RATIONALE 48
MEDICAL MANAGEMENT
IVF 50
PHARMACOTHERAPY 52
DIET 61
NURSING CARE PLAN 62
DISCHARGE PLANNING 72
LEARNING DERIVED 73
REFERENCES
N407
“W e learn more by looking for the answer to a question
and not finding it than we do from learning the answer itself .”

~Lloyd Alexander, American Author, 1924
In the field of nursing, one encounters a wide-array of various diseases and conditions. In
order to give adequate and holistic care to individuals, it is necessary that nurses be equipped
with the proper knowledge and skills for dealing with different health states. It is only through
continuous learning that nurses acquire the necessary skill. A case study is a means of continuing
such learning. In doing a case study, the students delve into the question, “what is this disease
condition?” Student nurses learn actively and will be able to handle patients and experience what
it means to care for a patient with that particular condition. They learn, from continuous
interaction with the patients along side with inquires into books and informative journals of the
disease process, it symptoms, and corresponding treatments.
Pregnancy-induced hypertension is one of the conditions which student-nurses encounter
during their exposure at the clinical setting. The disease comprises of complexities of the
anatomical concepts that surveys a thorough description to understand its manifestations and
formulate interventions. It is interesting on our part to learn its definition, causes, and proper
management. The student-nurses chose the case to be able to have an insight about the
condition.
Brief Description
Pregnancy induced hypertension (PIH) is a condition in which vasospasms occurs
during pregnancy. In this condition signs of hypertension, proteinuria and edema develop in
N407
pregnant and postpartum women. Despite years of research and studies investigating the disease,
the cause of the disorder is still seemingly idiopathic. Originally, this condition has been called
the toxemia of pregnancy because researchers depicted and hypothesized that a toxin of some
kind being produces by a woman in response to the foreign protein of the growing fetus, the
toxin leading to the symptoms. Still, despite the efforts in finding an explanation to the cause of
pregnancy induced hypertension, no such toxin has ever identified.
Pregnancy –induced hypertension is an alarming condition which can affect both the
welfare of the mother and the child. Women who develop high blood pressure in pregnancy
appear to have an elevated risk high blood pressure and stoke in later life. Women with a history
of high blood pressure in pregnancy, known as gestational hypertension, were more likely than
women with no history to develop high blood pressure in later years. In terms of the welfare of
the child in-utero, the fetus may be placed in distress due to the presence of the condition, and
complications from high blood pressure such as convulsions can cause dire consequences. The
case of pre-eclampsia, the condition can strike without warning causing blood pressure to risk to
dangerously high levels. Pre-eclampsia may progress to eclampsia in which high blood pressure
and convulsions could be fatal to the mother or child. Pre-eclampsia is a leading cause of
maternal death. It strikes about five percent of first time mothers and one to two percent of
mothers during subsequent pregnancies.
Classification of Hypertensive Diseases in Pregnancy
Chronic Hypertension is defined as blood pressure >140/90 at <20 weeks of gestation.
Pregnancy Induced Hypertension is defined as a sustained blood pressure increase to 140/90 at

>20 weeks gestation.
N407
Superimposed Pregnancy-Induced Hypertension is defined as coexistence of chronic

hypertension and pregnancy-induced hypertension.
Clinical Manifestations of Severe Disease in Patients with PIH
Blood pressure >160-180 mm Hg systolic or >110 mm Hg diastolic
Proteinuria >5 g/24 h or > 1+ on dipstick (normal <300 mg/24 h)
Elevated serum creatinine
Generalized seizures (eclampsia)
Pulmonary edema
Oliguria <500 mL/24 hours
Microangiopathic hemolysis
Thrombocytopenia
Hepatocellular dysfunction (elevated alanine toxemia preeclampsia, aminotransferase, aspartase

aminotransferase)
Intrauterine growth restriction or oligohydramnios
Symptoms suggesting significant end-organ involvement: headache, visual disturbances, or

epigastric or right-upper quadrant pain
REASONS FOR CHOOSING THE CASE
The student nurses have chosen this study because of different reasons such as, it is a
very common disease at the obstetric ward as well as the delivery room. There are a lot of cases
of pre-eclampsia, the topic is interesting and most especially, for us to learn more about the
disease and in return, we will gain more knowledge about the study.
N407
STATISTICS
Pregnancy induced hypertension is a condition which effects many women in the world.
This is true even for those expecting mothers in the Philippines. Studies of preeclampsia report
about 5 percent of nulliparous women develop preeclampsia and 40 to 50 percent of these
women develop severe disease worldwide. In the Philippines, according to Department of
Health, Maternal Mortality Rate (MMR) is 162 out of 10,000 live births (Family Planning
Survey 2006). Maternal deaths account for 14% of deaths among women. For the past five years
all of the causes of maternal deaths exhibited an upward trend. Preeclampsia showed an
increasing trend of 6.89%; 20%; 40%; and 100%. Ten women die every day in the Philippines
from pregnancy and childbirth related causes but for every mother who dies, roughly 20 more
suffer serious disease and disability. The UNFPA office in the Philippines declared that family
planning can help prevent maternal deaths by 35%.
N407
STUDENT NURSE-CENTRED OBJECTIVES
G E N E R A L
O B J E C T I V E S

After the completion of this book-based case study, the student nurses will be able to:
 Know and understand the disease process and concept of pregnancy-induced

hypertension.
S P E C I F I C
O B J E C T I V E S

After the completion of this book-based study on pregnancy-induced hypertension, the student
nurses will be able to:
Cognitive
 Review the proper physical assessment (IPPA) and expected findings in a woman with pregnancy
induced hypertension.
 Understand the disease process: the causes, effects, management, treatment, and possible
preventions.
 Determine the pathophysiology of the condition with their rationale for occurrence of each
manifestation.
 Determine why certain management and medications are given and provided for the condition.
 Understand how and why certain diagnostic tests are done for the condition.
 Review the concepts about the anatomy and physiology with regards to the condition.
Psychomotor
 Identify the appropriate health teachings in which to provide to future patients with the said
condition.
Affective
 Share the learning acquired to co-student-nurses to increase awareness and help them if ever they
will encounter patient with the same condition.
N407
DIAGNOSTIC & LABRATORY PROCEDURES
COMPLETE BLOOD COUNT
Diagnostic Procedure Indications or Purpose Possible Results Normal Values
HGB (g/dL) To measure the total May be elevated due 120-160 g/dl
amount of hemoglobin in to hemoconcentration
the blood. of blood.
HCT (%) To aid diagnosis of May be elevated due 36.0 – 47.0

abnormal states of to hemoconcentration
hydration, polycythemia of blood.
and anemia and aids in
calculation of
erythrocyte indices.
Platelet Count To evaluate platelet Thrombocytocpenia 150 – 400

production or decreased platelet
(x10 9/L) states are often found
in PIH
WBC (x10 9/L) To determine for WBC and differential 4.8 – 10.8
presence of for further counts may be
tests such as WBC elevated depending
differential infection and upon the presence of
also for determination infection for the
count individual case of the
patient.
Differential Count: To provide a numeric WBC and differential 55-65%

estimate of the client’s counts may be
Segmenters (%) immune status. elevated depending
upon the presence of
N407
infection for the

individual case of the
patient.
Lymphocytes (%) To check for immune WBC and differential 25-35%

responses counts may be
elevated depending
infection for the
patient.
Eosinophils (%) To determine presence of WBC and differential 2-4%

multicellular parasites counts may be
and certain infections elevated depending
infection for the
patient.
Monocytes (%) To determine presence of WBC and differential 2-6%

Chronic inflammatory counts may be
disease, Parasitic elevated depending
infection, Viral infection upon the presence of
infection for the
patient.
N407
COMPLETE BLOOD COUNT
NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER PROCEDURE
Before the Procedure
 Explain the procedure to the pt. and why it is indicated
 Inform the patient that fluid and food restriction is not required
 Inform the patient that a blood sample will be taken.
 Tell the patient that he may experience transient discomfort from the needle puncture
 Fill up laboratory request form properly and send it to the laboratory technician during
the collection of sample/specimen.
During the Procedure
 Inform the patient that pain may be felt through prick in the needle
 Instruct the patient to calm down to avoid uneasiness.
After the Procedure
 Apply brief pressure to prevent bleeding
 Apply warm compress if Hematoma will develop at the venipuncture site.
N407
BLOOD CHEMISTRY
Diagnostic Procedure Indications or Purpose Possible Findings Normal Values
Creatinine This test measures the Often normal but 0.5-1.69 mg/dl
amount of creatinine in may be increased in
the blood. It is used to cases of severe
preeclampsia.
diagnose impaired renal
function and assess
glomerular filtration.
To check for water Normal in PIH, but 137-145 mmo/l

Sodium (Na+)
balance. may differ due to
comorbid existing
conditions for the
patient
Potassium (K+) Normal in PIH, but 3.6-5.0 mmo/l

To measure acid base
balance and normal may differ due to
muscle activity. comorbid existing
conditions for the
patient
Tests for the presence of Usually below 5

Bilirubin liver disease or 0.2-1.9 mg/dL
mg/dL
dysfunction through
evaluation of bilirubin
levels in the blood.
N407
AST is usually below 6-34 IU/L

500 IU
Aspartate The aspartate
Aminotransferase (AST) aminotransferase (AST)
test can be used
specifically to check for
liver or heart problems,
or it can be part of
standard medical test
screening.
Alkaline phosphotase 20-140 IU/L
may increase 2 to 3
Alkaline Phosphotase A test which evaluates fold in PIH
the alkaline phosphotase
levels in blood. This is
an enzyme that is
normally present in high
concentrations in
growing bone and in
bile. It is essential for the
deposition of minerals in
the bones and teeth.
N407
BLOOD CHEMISTRY
 Explain the procedure to the pt. and why it is indicated
 Inform the patient that fluid and food restriction is not required
 Inform the patient that a blood sample will be taken.
 Tell the patient that he may experience transient discomfort from the needle puncture
 Fill up laboratory request form properly and send it to the laboratory technician during
the collection of sample/specimen.
 Inform the patient that pain may be felt through prick in the needle
 Instruct the patient to calm down to avoid uneasiness.
After the Procedure
 Apply brief pressure to prevent bleeding
 Apply warm compress if Hematoma will develop at the venipuncture site.
N407
URINALYSIS
Diagnostic Procedure Indications or Purpose Possible Findings Normal Values
Urinalysis For general health Urinalysis reveals Color: Straw

screening to detect renal Proteinuria (positive yellow to
and metabolic disease; albumin levels) and amber.
diagnosis of disease or occasional hyaline
disorders of the kidney casts. Transparency:
or urinary tract; transparent
monitoring patient’s with Sugar: negative
diabetes.
Albumin:
negative
Specific
Gravity: 1.015 –
1.025
Pus cells: 5-
10/HPF
RBC: o-2 HPF
Epithelial cells:
Moderate
N407
URINALYSIS
 Explain to the significant others the test, it’s purpose and how it done.
 Inform the significant others that the test will require urine specimen.
 Provide a clean container for the specimen.
 Label the specimen cup before giving it to the client
 Assist the client in the comfort room
 Instruct the client to take the middle urine
After the Procedure
 The specimen should be delivered to the lab within 1 hour.
 Obtain result and secure it to the chart
Refer result to the physician
N407
PHYSICAL EXAMINATION & ASSESSMENT

the following physical assessment guide has been created to create a full picture of what a nurse
may find in the course of assessment of a patient with pregnancy induced hypertension. The
findings are hypothetical and based on the signs and symptoms lifted from authors such as
Pilliteri and Black. The actual signs and symptoms of the disease may vary from case to case.
Assessment of the Central Nervous System
Tissues are capable of regulating their own blood flow; this process is known as autoregulation.
Cerebral perfusion is maintained by autoregulation at a constant level of about 55 mL/min/100 g
at a wide range of blood pressures (Fig 19-1). However, blood pressure may rise to levels at
which autoregulation cannot function. When this occurs, the endothelial tight junctions open,
causing plasma and red blood cells to leak into the extravascular space. This may result in
petechial hemorrhage or gross intracranial hemorrhage. The upper limit of autoregulation varies
from one person to another; eg, chronic hypertension may cause medial hypertrophy of the
cerebral vessels, resulting in a shift of the curve to the right (Fig 19-1). This explains the paradox
of 2 patients with equally severe hypertension who have markedly different clinical
presentations. The young primigravida whose blood pressure is normally 110/70 mm Hg may
convulse with a blood pressure of 180/120 mm Hg, while a chronic hypertensive may be
asymptomatic or have only a headache at the same pressure.
The mechanism of the cerebral damage in eclampsia is unclear. The pathologic findings are
similar to those of hypertensive encephalopathy. These abnormalities include fibrinoid necrosis
and thrombosis of arterioles, microinfarcts, and petechial hemorrhages. In both hypertensive
encephalopathy and eclampsia, the lesions are widely distributed throughout the brain, but the
brainstem is more severely affected in the former, while the cortex is more severely affected in
N407
the latter. Other differences in the two conditions are that eclampsia may be seen in the absence
of hypertension and that retinal hemorrhages and infarcts are rare in eclampsia. Two theories
have been proposed to explain the pathogenesis of hypertensive encephalopathy, vasospasm, and
forced dilation. In the first, vasospasm causes local ischemia, arteriolar necrosis, and disruption
of the blood-brain barrier. According to the second, as blood pressure rises above the limit of
autoregulation, cerebral vasodilation occurs. Initially, some vessel segments dilate, and some
remain constricted. Overdistention of the dilated segments results in necrosis of the medial
muscle fibers and damage to the vessel wall. It is possible that both mechanisms are operant.
The presence of cerebral edema in preeclampsia-eclampsia is controversial. One set of
researchers stated that cerebral edema was not present in eclamptic patients when autopsy was
performed within 1 hour of death and that such edema was a late postmortem change. In contrast,
some others found generalized cerebral edema in some autopsy specimens and confirmed
increased intracranial pressure in eclamptics with prolonged coma (> 6 hours). Early studies of
cerebrospinal fluid opening pressure showed elevated pressures; however, more recent studies
have failed to confirm this.
Head computed tomographic (CT) scans in women with eclampsia have shown abnormalities in
about one-third. By using fourth-generation equipment and with a short interval from seizure to
CT scan, abnormalities may be detected in half the patients. The main findings are focal
hypodensities in the white matter in the posterior half of the cerebral hemispheres with
occasional lesions in the gray matter, temporal lobes, and brainstem. One researcher suggested
that these areas of radiographic hypodensity represented petechial hemorrhages accompanied by
N407
local edema. Subarachnoid or intraventricular hemorrhages may be seen in the most severe
cases.
Magnetic resonance imaging (MRI) is more sensitive at demonstrating abnormalities than CT
scan, but it is not as widely available. T2-weighed MRI scans show high signal in the cortical
and subcortical white matter. Most of the abnormalities lie in the occipital and parietal areas in
watershed areas where the anterior, middle, and posterior circulations meet. Basal ganglia and
brainstem abnormalities occur in more critically ill patients.
Cerebral angiography has been performed in a few patients with eclampsia, revealing diffuse
arterial vasoconstriction.
Electroencephalograms (EEGs) show nonspecific abnormalities in about 75% of patients after
eclamptic seizures. The pattern is usually a diffuse slowing of activity (theta or delta waves),
sometimes with focal slow activity and occasional paroxysmal spike activity. These
abnormalities may be seen in other conditions, such as hypoxia, renal disease, polycythemia,
hypocalcemia, and water intoxication. The electroencephalographic pattern is unaffected by
magnesium sulfate. It gradually returns to normal 6-8 weeks postpartum. Uncomplicated
eclampsia causes no permanent neurologic deficit.
Assessment of the Eyes
Both serous retinal detachment and cortical blindness may occur.
Assessment of the Pulmonary System
Pulmonary edema may occur with severe preeclampsia or eclampsia. It may be cardiogenic or
noncardiogenic and usually occurs postpartum. In some cases it may be related to excessive fluid
N407
administration or to delayed mobilization of extravascular fluid. It may also be related to
decreased plasma colloid oncotic pressure from proteinuria, use of crystalloids to replace blood
loss, and decreased hepatic synthesis of albumin. Pulmonary edema is particularly common in
patients with underlying chronic hypertension and hypertensive heart disease, which may be
manifested by systolic dysfunction, diastolic dysfunction, or both. Aspiration of gastric contents
is one of the most dreaded complications of eclamptic seizures. This may result in death because
of asphyxia from particulate matter plugging major airways or in chemical pneumonitis from
aspirated gastric acid. Aspiration may cause various types of pneumonia, ranging from patchy
pneumonitis to full-blown adult respiratory distress syndrome.
Assessment of the Cardiovascular System
Plasma volume is reduced in patients with preeclampsia. Normal physiologic volume expansion
does not occur, possibly because of generalized vasoconstriction, capillary leak, or some other
factor. Because the cause of the reduced volume is unknown, management is controversial. One
theory is that the decreased volume is a primary event causing a chronic shocklike state.
Hypertension is thought to be the result of release of a pressor substance from the hypoperfused
uterus or of compensatory secretion of catecholamines. Proponents of this theory advocate
avoidance of diuretics and use of volume expanders. Another theory is that decreased volume is
secondary to vasoconstriction. Proponents of this theory advocate the use of vasodilators and
warn that volume expanders may aggravate hypertension or cause pulmonary edema.
Studies using the Swan-Ganz catheter have demonstrated a spectrum of hemodynamic findings
in preeclampsia ranging from a low-output, high-resistance state to a high-output, low-resistance
state. One study found a low wedge pressure, low cardiac output, and high systemic vascular
N407
resistance in untreated nulliparous preeclamptic women, while patients who received various
therapies and were usually referred, a wide range of hemodynamics was found. The conclusion
was that the untreated preeclamptic patient was significantly volume-depleted and that the wide
spectrum of hemodynamic findings in the treated group resulted from prior therapy and the
presence of other variables such as labor, multiparity, and preexisting hypertension.
In another study of a heterogeneous population of pretreated and nonpretreated patients, a
generally consistent profile emerged. Preeclampsia was in general a high cardiac output state
associated with an inappropriately high peripheral resistance. Although the systemic vascular
resistance was within the normal range for pregnancy, it was still inappropriately high for the
elevated cardiac output. The failure of the circulation to dilate in the setting of increasing cardiac
output appeared to be a characteristic feature of preeclampsia. The normal wedge and central
venous pressures found in their study suggested venoconstriction with central relocation of
intravascular volume if the generally accepted reports of decreased plasma volume in
preeclampsia are correct. They postulated splanchnic venoconstriction as the mechanism of this
volume shift.
Normal pregnant women are resistant to the vasoconstrictor effects of angiotensin II. Pregnant
women require about 21/2 times the amount of angiotensin II required by nonpregnant women to
raise the diastolic blood pressure 20 mm Hg. Patients who will develop superimposed
preeclampsia lose their refractoriness to angiotensin II many weeks before hypertension
develops. These patients may be identified as early as 18-24 weeks' gestation by infusion of
angiotensin II.
N407
Normal pregnant women lose their refractoriness to angiotensin II after treatment with
prostaglandin synthetase inhibitors such as aspirin or indomethacin; this suggests that
prostaglandin is involved in mediating vascular reactivity to angiotensin II in pregnancy.
Refractoriness to angiotensin II can be restored in patients with preeclampsia by the
administration of theophylline, a phosphodiesterase inhibitor that increases intracellular levels of
cAMP. Therefore, prostaglandins synthesized in the arteriole may modulate vascular reactivity to
angiotensin II by altering the intracellular level of cAMP in vascular smooth muscle.
Assessment of the Liver
The spectrum of liver disease in preeclampsia is broad, ranging from subclinical involvement
with the only manifestation being fibrin deposition along the hepatic sinusoids to rupture of the
liver. Within these extremes lie the HELLP syndrome (hemolysis, elevated liver enzymes, and
low platelets) and hepatic infarction.
Assessment of the Kidneys
The characteristic lesion of preeclampsia, glomeruloendotheliosis, is a swelling of the
glomerular capillary endothelium that causes decreased glomerular perfusion and glomerular
filtration rate. Fibrin split products have been found on the basement membrane by some
observers, who have suggested that intravascular coagulation may be secondary to
thromboplastin released from the placenta. However, the fibrin split products are found
infrequently and only in small amounts. Other investigators have detected IgM, IgG, and
complement in the glomeruli of some patients and have suggested an immunologic mechanism.
Serial renal biopsies have shown that the lesion is totally reversible over about 6 weeks.
N407
Assessment of the Blood
Most patients with preeclampsia-eclampsia have normal clotting studies. In some, a spectrum of
abnormalities may be found, ranging from isolated thrombocytopenia to microangiopathic
hemolytic anemia to disseminated intravascular coagulation (DIC). Thrombocytopenia is the
most common abnormality; a count of less than 150,000/uL is found in 15-20% of patients.
Fibrinogen levels are actually elevated in preeclamptic women as compared with normotensive
patients. Low fibrinogen levels in preeclampsia-eclampsia are usually associated with abruptio
placentae or fetal demise. Elevated fibrin split products are seen in 20% of patients (usually in
the range of 10-40 uL/mL). Microangiopathic hemolytic anemia without other signs of DIC may
be seen in about 5% of patients, and evidence of DIC is also present in about 5%. In the past,
DIC was thought to be the cause of preeclampsia; now it is regarded as a sequela of the disease.
The HELLP syndrome describes patients with hemolytic anemia, elevated liver enzymes, and
low platelet count. Criteria for the diagnosis at the authors' institution are schistocytes on the
peripheral blood smear, lactic dehydrogenase > 600 U/L, total bilirubin > 1.2 mg/dL, aspartate
aminotransferase > 70 U/L, and platelet count < 100,000/mm3. This syndrome is present in about
10% of patients with severe preeclampsia-eclampsia. It is frequently seen in Caucasian patients
with delay in diagnosis or delivery and in patients with abruptio placentae. The syndrome may
occur remote from term (eg, at 31 weeks) and with no elevation of blood pressure. The syndrome
is frequently misdiagnosed as hepatitis, gallbladder disease, idiopathic thrombocytopenic
purpura, or thrombotic thrombocytopenic purpura. Most hematologic abnormalities return to
normal within 2-3 days after delivery, but thrombocytopenia may persist for a week.
Assessment of the Endocrine System
N407
The role of the renin-angiotensin-aldosterone system in the regulation of blood pressure during
normal and hypertensive pregnancy has not been clearly defined. In normal pregnancy, estrogen's
effect on the liver markedly increases production of renin substrate. This increases plasma renin
activity, plasma renin concentration, and angiotensin II levels. Plasma aldosterone levels rise
even higher than can be accounted for by the prevailing plasma renin activity. Despite the high
plasma concentration of aldosterone, there is no blood pressure increase or hypokalemia in
normal pregnancy; indeed, blood pressure falls in the midtrimester. This may be due to
counterregulatory factors such as the natriuretic effect of progesterone or activation of
vasodepressor systems such as kinins or prostaglandins.
Interpreting renin, angiotensin, and aldosterone levels in studies of preeclampsia is difficult
because of differences in the definition of preeclampsia (parity, degree of proteinuria, early- or
late-onset disease), differences in taking of blood samples (values may be affected by bed rest,
sodium intake, labor, etc), and differences in assay techniques. In the majority of studies, renin,
angiotensin, and aldosterone are all suppressed in preeclampsia, but they are still above
nonpregnant levels. The available evidence suggests that the renin-angiotensin system is only
secondarily involved in preeclampsia.
Atrial natriuretic peptide (ANP) is a volume regulatory hormone synthesized by cardiac
myocytes, which has potent natriuretic, diuretic, and vasorelaxant properties. ANP secretion is
stimulated by increased atrial pressure and alterations in sodium balance. Elevated
concentrations of ANP accompany pathologic states characterized by fluid overload such as
Cirrhosis, congestive heart failure, and chronic renal failure. However, ANP is elevated in
preeclampsia, a disorder supposedly characterized by hypovolemia. It is even elevated in the
N407
second trimester before the onset of clinical evidence of preeclampsia. The mechanism for the
elevation is unknown. It may be that endothelin or another vasoactive peptide is stimulating
release of ANP. It may also be that the widely accepted concept of central hypovolemia in
preeclampsia is incorrect.
Assessment of the Catecholamines
Urinary and blood catecholamine levels are the same in normotensive pregnant women, women
with preeclampsia, and nonpregnant controls. However, it cannot be ruled out that sympathetic
activity is of pathogenetic importance for initiation or maintenance of hypertension in patients
with preeclampsia. Catecholamine levels increase during labor, presumably owing to stress. The
vascular refractoriness to catecholamines is lacking in preeclampsia, as is the refractoriness to
other endogenous vasopressors such as antidiuretic hormone and angiotensin II.
Assessment of the Prostacyclin
Prostacyclin is a prostaglandin discovered in 1976. It increases intracellular cAMP in smooth
muscle cells and platelets resulting in vasodilator and platelet antiaggregatory effects. Its half-life
is about 3 minutes, breaking down in plasma to 6-keto-PGF1α, which is stable and can be
measured as an indication of prostacyclin levels. These plasma levels are low, indicating that
prostacyclin acts physiologically at the local level rather than as a circulating hormone.
Prostacyclin is made primarily in the endothelial cell from arachidonic acid, catalyzed by the
enzyme cyclooxygenase. Cyclooxygenase can be inhibited by aspirin-like drugs. Mechanical or
chemical perturbation of the endothelial cell membrane stimulates formation and release of
N407
prostacyclin. For example, pulsatile pressure or chemicals such as bradykinin or thrombin
stimulate prostacyclin generation in the vessel wall.
Thromboxane A2 generated by platelets from arachidonic acid via cyclooxygenase induces
vasoconstriction and platelet aggregation. Thus, prostacyclin and thromboxane have opposing
roles in regulating platelet-vessel wall interaction.
Aspirin irreversibly inhibits cyclooxygenase. Cyclooxygenase must be produced continuously by
endothelial cells, because they recover their ability to synthesize prostacyclin within a few hours
after a dose of aspirin. On the other hand, platelets do not have a nucleus and therefore cannot
make fresh cyclooxygenase. Thromboxane synthesis recovers only as new platelets enter the
circulation. Platelet life span is about 1 week. Thus, daily treatment with low-dose aspirin results
in chronic inhibition of thromboxane metabolites and decreased excretion of prostacyclin
metabolites in preeclamptic patients. Low-dose aspirin therapy is aimed at restoring the
presumed thromboxane-prostacyclin imbalance in preeclampsia.
Assessment of the Nitric Oxide
Nitric oxide (NO) is an endogenous vasodilator and inhibitor of platelet aggregation and acts
synergistically with prostacyclin. It is produced by endothelial cells from L-arginine. Synthesis
can be inhibited by arginine analogs such as NG-monomethyl-L-arginine and NG-nitro-L-
arginine. Intravenous injection of one of these inhibitors into rats, rabbits, or guinea pigs causes
an immediate rise in blood pressure that is reversed by L-arginine. This indicates that continual
basal release of NO from endothelial cells keeps the vasculature in a dilated state. NO acts only
in the immediate vicinity of the cell that releases it. Any that escapes into the bloodstream decays
chemically to form nitrite or is immediately inactivated by hemoglobin.
N407
NO plays an important role in several pathologic processes. It is one of the mediators of
hypotension in septic shock. A deficiency of NO contributes to the cause of hypertension and
Atherosclerosis. Currently it is thought that the NO system may be more important than the
prostaglandins in the pathogenesis of preeclampsia. Chronic blockade of the endogenous NO
system produces a model of hypertension and renal damage in pregnant and nonpregnant rats.
Some studies have shown that there is decreased excretion of NO in the urine of pregnant
preeclamptic women, but whether NO plays an important pathophysiologic role in the
development of preeclampsia remains unknown.
Assessment of the Endothelin-1
In addition to the relaxing factors prostacyclin and NO, the vascular endothelium releases
vasoconstrictor substances. The vasoconstrictor endothelin was discovered in 1988. There are 3
different isopeptides: endothelin 1, 2, and 3. Endothelin-1 is the only endothelin manufactured by
endothelial cells. Endothelins are also synthesized by kidney cells and nervous tissue. There are
widespread endothelin-binding sites including those in the brain, lung, kidney, adrenal, spleen,
intestine, and placenta. It is thought that endothelins act as endogenous agonists of
dihydropyridine-sensitive calcium channels. The most striking property of endothelin-1 is its
long-lasting vasoconstrictor action. It is 10 times more potent than angiotensin II. Endothelin
may play a role in constriction of placental vessels after delivery and may regulate closure of the
ductus arteriosus in the newborn. The mitogenic effects of endothelin-1 may cause vascular wall
hypertrophy in Atherosclerosis and hypertension. Endothelin-1 may play a role in renal
vasoconstriction in acute renal failure. A 3-fold elevation of plasma endothelin 1 and 2 has been
found in women with preeclampsia compared with gestation-matched controls.
N407
One hypothesis is that prostacyclin is an antiplatelet and vasodilator mechanism held in reserve
to reinforce the NO system when endothelial damage occurs. Lack of NO may be a causative
factor in hypertension. Endothelin-1 is released by endothelial cells to constrict the underlying
smooth muscle in an emergency such as laceration. Excess endothelin-1 may also be involved in
the genesis of hypertension.
Assessment of the Placenta
In normal pregnancy, the proliferating trophoblast invades the decidua and the adjacent
myometrium in 2 forms: interstitial and endovascular. The role of the interstitial form is not clear
but it may serve to anchor the placenta. The endovascular trophoblastic cells invade the maternal
spiral arteries, where they replace the endothelium and destroy the medial elastic and muscular
tissue of the arterial wall. The arterial wall is replaced by fibrinoid material. This process is
complete by the end of the first trimester, at which time it extends to the deciduomyometrial
junction. There appears to be a resting phase in the process until 14 to 16 weeks' gestation, when
a second wave of trophoblastic invasion extends down the lumen of the spiral arteries to their
origin from the radial arteries deep in the myometrium. The same process is then repeated, ie,
replacement of the endothelium, destruction of the medial musculoelastic tissue, and fibrinoid
change in the vessel wall. The end result is that the thin-walled, muscular spiral arteries are
converted to saclike, flaccid uteroplacental vessels, which passively dilate to accommodate the
greatly augmented blood flow required in pregnancy.
Preeclampsia develops following a partial failure in the process of placentation. First, not all the
spiral arteries of the placental bed are invaded by trophoblast. Second, in those arteries that are
invaded, the first phase of trophoblastic invasion occurs normally, but the second phase does not
N407
occur, and the myometrial portions of the spiral arteries retain their reactive musculoelastic
walls.
In addition, acute atherosis (a lesion similar to Atherosclerosis) develops in the myometrial
segments of the spiral arteries of patients with preeclampsia. The lesion is characterized by
fibrinoid necrosis of the arterial wall, the presence of lipid and lipophages in the damaged wall,
and a mononuclear cell infiltrate around the damaged vessel. Acute atherosis may progress to
vessel obliteration with corresponding areas of placental infarction.
Thus, in preeclampsia there is an area of vascular resistance in the spiral artery because of
failure of the second wave of trophoblastic invasion. In addition, acute atherosis further
compromises the vascular lumen. Consequently, the fetus is subjected to poor intervillous blood
flow from the time of early gestation; this may result in intrauterine growth retardation or
stillbirth. Antihypertensive therapy may be detrimental because peripheral vasodilatation may
further reduce the already compromised placental blood flow.
Representation of the relationship between cerebral blood flow and mean arterial blood
pressure. Cerebral blood flow normally remains constant at mean arterial pressures of 60-140
mm Hg. In chronically hypertensive patients, medial hypertrophy causes the lower and upper
limits of autoregulation to be shifted to higher blood pressure values. (Modified and reproduced,
with permission, from Donaldson JO: Neurology of Pregnancy. Saunders, 1978.)0
N407
ANATOMY & PHYSIOLOGY
The female reproductive system
consists of the ovaries, uterine
tubes (or fallopian tubes), uterus,
vagina, external genitalia, and
mammary glands. The internal
reproductive organs of the
female are located within the
pelvis, between the urinary
bladder and the rectum. The
uterus and the vagina are in the midline , with an ovary to each side of the organ. The internal
reproductive organs are held in place within the pelvis with ligaments. The most conspicuous is
the brad ligament, which spreads out on both sides of the uterus and to which the ovaries and the
uterine tubes attach.
Ovaries
The two ovaries are small organs suspended in the pelvic
cavity by ligaments. The suspensory ligament extends
from each ovary to the lateral body wall, and the ovarian
ligament attaches the ovary to the superior margin of the uterus. In addition, the ovaries are
attached to the posterior surface of the broad ligament by folds of the peritoneum called the
mesovarium. The ovarian arteries, veins, and nerves transverse the suspensory ligament and enter
the ovary through the mesovarium.
N407
A layer of visceral peritoneum covers the surface of the ovary. The outer part of the ovary is
made up of dense connective tissue and contains the ovarian follicles. Each of the ovarian
follicles contains an oocyte, the female sex cell. Loose connective tissue makes up the inner part
of the ovary, where blood vessels, lymphatic vessels, and nerves are located.
Uterine Tubes
A uterine tube, fallopian tube, or oviduct (named after the italian anatomist, Gabriele Fallopio) is
associated with each ovary. The uterine tubes extend from the area of the ovaries to the uterus.
The open directly into the peritoneal cavity near each ovary and receive an oocyte. The opening
of each uterine tube is surrounded by long, thin processes called fimbriae.
N407
The fimbriae nearly surround the surface of the ovary. As a result, as soon as the oocyte is
ovulated, it comes into contact with the surface of the fimbriae. Cilia on the fimbriae surface
sweep the oocyte into the uterine tube. Fertilization usually occurs in the part of the uterine tube
near the ovary known as the ampulla.
Uterus
The uterus is as big as the size of a medium-sized pear. It is oriented in the pelvic cavity with the
larger, rounded portion directed superiorly. The part of the uterus superior to the entrance of the
fallopian tubes is called the fundus. The main part of the uterus is called the body, and the
narrower part is termed the cervix and is directed inferiorly. Internally, the uterine cavity in the
fundus and uterine body continues through the cervix as the cervical canal, which opens into the
vagina. The cervical canal is lined by mucous glands.
The Uterine wall is composed of three layers: a serous layer or perimetrium of the uterus,
consists of smooth muscle is quite thick and accounts for the bulk of the uterine wall. The inner
most layer of the uterus is called the endometrium. The endometrium consists of simple
columnar epithelium tissues with an underlying connective tissue layer. Simple tubular glands,
called endometrial glands, are formed by folds of the endometrium. The superficial part os the
endometrium is sloughed off during menstruation.
The uterus is supported by the broad ligament and the round ligament. In addition to these
ligaments that support the uterus, much support is provided inferiorly to the uterus by skeletal
muscles of the pelvic floor. If ligaments that support the uterus or the muscles of the pelvic floor
are weakened such as in childbirth, the uterus can extend inferiorly into the vagina, a condition
termed as a prolapsed uterus. Severe cases require surgical correction.
N407
Vagina
The vagina is the female organ of copulation and functions to receive the penis during
intercourse. It also allows menstrual flow and childbirth. The vagina extends from the uterus to
outside the body. The superior portion of the vagina is attached to the sides of the cervix so that a
part of the cervix extends into the vagina.
The wall of the vagina consists of an outer muscular layer and an inner mucous layer. The
muscular layer is smooth muscle and contains many elastic fibers. Thus the vagina can increase
in size to accommodate the penis during intercourse, and it can stretch greatly during childbirth.
The mucous membrane is moist stratified squamous epithelium that forms a protective surface
layer. Lubricating fluid passes through the vaginal epithelium into the vagina.
In young females, the vaginal opening is covered by a thin mucous membrane known as the
hymen. The hymen can completely close the vaginal orifice in which case it must be removed to
allow menstrual flow. More commonly, the hymen is perforated by one or several holes. The
openings of the hymen are usually greatly enlarged during the first sexual intercourse. The
hymen can also be perforated during a variety of activities including strenuous exercise. The
condition of the hymen is therefore not a reliable indicator of virginity.
The External Genitalia
The external female genitalia, also called the vulva, or pudendum, consists of the vestibule and
its surrounding structures. The vestibule is the space into which the vagina and urethra open. The
urethra opens just anterior to the vagina. The vestibule is bordered by a pair of thin, longitudinal
skin folds called the labia minora. A small erectile structure called the clitoris is located in the
N407
anterior margin of the vestibule. The two labia minora unite over the clitoris to form a fold of
skin known as the prepuce.
The clitoris consists of a shaft and a distal glans. Like the glans penis, the clitoris is well supplied
with sensory receptors, and it is made up of erectile tissue. An additional erectile tissue is
located on either side of the vaginal opening.
On each side of the vestibule, between the vaginal opening and the labia minora, are openings of
the greater vestibular glands. These glands produce a lubricating fluid that helps maintin the
moistness of the vestibule.
Lateral to the labia minor are two prominent rounded folds of skin called the labia majora. The
two labia majora unite anteriorly at the elevation of tissue over thepubic symphysis calle dthe
mons pubis. The lateral surfaces of the labia majora and the surface of the mons pubis are
covered with coarse hair. The medial surfaces of the labia minora are covered with numerous
sebaceous and sweat glands. The space between the labia minor is called the pudendal cleft.
Most of the time, the labia minora are in contact with each other across the midline , closing the
pudendal cleft and covering the deeper structures within the vestibule.
The region between the vagina and the anus is the clinical perineum. The skin and muscle of this
region can tear during childbirth. To preven such tearing, an incision called an episiotomy is
sometimes made in the clinical perineum. Traditionally, this clean, straight incision is thought to
result in less injury, and less trouble in healing, and less pain. However, many studies indicate
that there is less injury and pain when no episiotomy is performed.
Mammary Glands
N407
Mammary glands are located inside the breasts of sexually mature female body. They are in
actuality modified sweat glands which are in fact comprised of secretory mammary alveoli and
the appropriate ducts. Mammary glands are considered to be part of the integumentary system
rather than the reproductive system. The glands are associated with the female reproductive
system in part due to their assistance in attracting a mate as well as their role in nourishing a
baby. Size and shape of the female breast are different for every human body and factors such as
race, age, body fat, and pregnancy can make a large difference in these variations.
The release of estrogen during puberty releases hormones that stimulate the growth of the breasts
and the functions of the mammary glands. Pregnant women as well as nursing women
experience hypotrophy of the breasts while it is not uncommon for atrophy of the breasts to
occur after menopause.
Breasts are situated over ribs 2 through 6 and overlap the pectoral muscle as well as some
portions of the oblique muscles. The lateral margin of the sternum creates an unintentional
margin for the edge of each breast. Each breast also follows the anterior margin of the respective
axilla. Coming within very close proximity to the Axillary vessels, the breasts upward and
laterally toward the axilla, which contributes to the high incidence of breast cancer due to the
axillary process’ lymphatic drainage.
15 to 20 lobes compose the mammary gland, and each lobe is equipped with its own duct to the
outside of the body. Adipose tissue in varying amounts segregates each lobe. While this tissue
controls the size and shape that the breast takes, there is no determination by this tissue when it
comes to the woman’s ability to suckle her young. Lobules are subdivisions of each lobe. These
subdivisions contain mammary alveoli. The milk of a lactating female are produced within the
N407
mammary alveoli. Suspensory ligaments support the breasts which are attached between the
lobules and run deep into the fascia which overlap the pectoral muscles. Breast milk is secreted
into a network of mammary ducts which receive the milk from the clusters of mammary alveoli.
These mammary ducts converge to form lactiferous ducts. Near the nipple, each lactiferous duct
expands into the lumen to allow for outward flow of milk. The lactiferous sinuses store the milk
before the suckling action, or additional pressure, releases it from the body. The milk leaves the
body from the tip of the nipple.
The nipple contains some erectile tissue that protrudes into a cylindrical projection. The circular
area around the nipple that contrasts in color is the areola. Sebaceous areola glands create a
bumpy surface around the areola which resides just under the surface of the areola’s skin. These
glands secrete fluids during lactation as well as when a woman is not lactating, which keep the
nipple supple. The complexion of the areola is based on the complexion of the skin that covers
the rest of the body, varying in pigments and tints. During gestation most areola surfaces darken.
It also becomes larger in most cases. This is thought to be more obvious for a nursing infant to
find.
Branches of the internal thoracic artery are responsible for supplying blood flow to the nipple as
well as the rest of the breast and mammary glands. Between the second, third, and forth
intercoastal spaces these braches of the thoracic artery enter the mammary glands. These spaces
are positioned laterally to the sternum and offer entry to the mammary artery, which only
supplies supportive blood. The return veins run alongside the initial arteries which supply the
blood. During pregnancy and lactation, and sometimes during other periods, a superficial venous
plexus can be seen through the surface of the skin.
N407
The fourth, fifth, and sixth thoracic nerves innervate the breast principally through sensory
somatic neurons. These neurons are derivative of the anterior and lateral branches of the thoracic
nerves. The release of milk is dependant upon the sensory innervations as stimulus is the only
natural release an infant can provide to be nourished.
Menstrual Cycle
Menstruation is the shedding of the lining of the uterus (endometrium) accompanied by bleeding.
It occurs in approximately monthly cycles throughout a woman's reproductive life, except during
pregnancy. Menstruation starts during puberty (at menarche) and stops permanently at
menopause.
By definition, the menstrual cycle begins with the first day of bleeding, which is counted as day
1. The cycle ends just before the next menstrual period. Menstrual cycles normally range from
about 25 to 36 days. Only 10 to 15% of women have cycles that are exactly 28 days. Usually, the
cycles vary the most and the intervals between periods are longest in the years immediately after
menarche and before menopause.
Menstrual bleeding lasts 3 to 7 days, averaging 5 days. Blood loss during a cycle usually ranges
from ½ to 2½ ounces. A sanitary pad or tampon, depending on the type, can hold up to an ounce
of blood. Menstrual blood, unlike blood resulting from an injury, usually does not clot unless the
bleeding is very heavy.
The menstrual cycle is regulated by hormones. Luteinizing hormone and follicle-stimulating
hormone, which are produced by the pituitary gland, promote ovulation and stimulate the ovaries
to produce estrogen and progesterone stimulates the uterus and breasts to prepare for possible
N407
fertilization. The cycle has three phases: follicular (before release of the egg), ovulatory (egg
release), and luteal (after egg release).
HORMONES AND FEMALE CYCLES
The ovarian cycle is
hormonally regulated in two phases.
The follicle secretes estrogen before
the ovulation; the corpus luteum
secretes both estrogen and
progesterone after ovulation.
Hormones from the hypothalamus and
anterior pituitary control the ovarian
cycle. The ovarian cycle covers events
in the ovary; the menstrual cycle
occurs in the uterus.
Menstrual cycles vary from between 15 and 31 days. The first day of the cycle is the
first day of blood flow (day 0) known as menstruation. During menstruation, the uterine lining is
broken down and shed as menstrual flow. FSH and LH are secreted on day 0, beginning both the
menstrual cycle and the ovarian cycle. Both FSH and LH stimulate the maturation of a single
follicle in one of the ovaries and the secretion of estrogen. Rising levels of estrogen in the blood
trigger secretion of LH, which stimulates follicle maturation and ovulation (day 14, or mid
cycle). LH stimulates the remaining follicle cells to form the corpus luteum, which produces both
estrogen and progesterone.
N407
Estrogen and progesterone stimulate the development of the endometrium and
preparation of the uterine lining for implantation of a zygote. If pregnancy does not occur, the
drop in FSH and LH causes the corpus luteum to disintegrate. The drop in hormones also causes
the sloughing off of the inner lining of the uterus by a series of muscle contractions of the uterus.
Fertilization and Pregnancy
If a female and male have sex within several days of the female's ovulation (egg release),
fertilization can occur. When the male ejaculates (which is when semen leaves a man's penis),
between 0.05 and 0.2 fluid ounces (1.5 to 6.0 milliliters) of semen is deposited into the vagina.
Between 75 and 900 million sperm are in this small amount of semen, and they "swim" up from
the vagina through the cervix and uterus to meet the egg in the fallopian tube. It takes only one
sperm to fertilize the egg.
About a week after the sperm fertilizes the egg, the fertilized egg (zygote) has become a multi-
celled blastocyst (pronounced: blas-tuh-sist). A blastocyst is about the size of a pinhead, and it's
a hollow ball of cells with fluid inside. The blastocyst burrows itself into the lining of the uterus,
called the endometrium (pronounced: en-doh-mee-tree-um). The hormone estrogen causes the
endometrium to become thick and rich with blood. Progesterone, another hormone released by
the ovaries, keeps the endometrium thick with blood so that the blastocyst can attach to the
uterus and absorb nutrients from it. This process is called implantation (pronounced: im-plan-
tay-shun).
As cells from the blastocyst take in nourishment, another stage of development, the embryonic
stage, begins. The inner cells form a flattened circular shape called the embryonic disk, which
will develop into a baby. The outer cells become thin membranes that form around the baby. The
N407
cells multiply thousands of times and move to new positions to eventually become the embryo
(pronounced: em-bree-o). After approximately 8 weeks, the embryo is about the size of an adult's
thumb, but almost all of its parts — the brain and nerves, the heart and blood, the stomach and
intestines, and the muscles and skin — have formed.
During the fetal stage, which lasts from 9 weeks after fertilization to birth, development
continues as cells multiply, move, and change. The fetus (pronounced: fee-tus) floats in
amniotic (pronounced: am-nee-ah-tik) fluid inside the amniotic sac. The fetus receives oxygen
and nourishment from the mother's blood via the placenta (pronounced: pluh-sen-tuh), a disk-
like structure that sticks to the inner lining of the uterus and connects to the fetus via the
umbilical (pronounced: um-bih-lih-kul) cord. The amniotic fluid and membrane cushion the
fetus against bumps and jolts to the mother's body.
Pregnancy lasts an average of 280 days — about 9 months. When the baby is ready for birth, its
head presses on the cervix, which begins to relax and widen to get ready for the baby to pass into
and through the vagina. The mucus that has formed a plug in the cervix loosens, and with
amniotic fluid, comes out through the vagina when the mother's water breaks.
When the contractions of labor begin, the walls of the uterus contract as they are stimulated by
the pituitary hormone oxytocin (pronounced: ahk-see-toh-sin). The contractions cause the cervix
to widen and begin to open. After several hours of this widening, the cervix is dilated (opened)
enough for the baby to come through. The baby is pushed out of the uterus, through the cervix,
and along the birth canal. The baby's head usually comes first; the umbilical cord comes out with
the baby and is cut after the baby is delivered.
N407
The last stage of the birth process involves the delivery of the placenta, which is now called the
afterbirth. After it has separated from the inner lining of the uterus, contractions of the uterus
push it out, along with its membranes and fluids.
The renin-angiotensin-aldosterone system
The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood
volume and systemic vascular resistance, which together influence cardiac output and arterial
pressure. As the name implies, there are three important components to this system: 1) renin, 2)
angiotensin, and 3) aldosterone. Renin, which is primarily released by the kidneys, stimulates the
formation of angiotensin in blood and tissues, which in turn stimulates the release of aldosterone
from the adrenal cortex.
Renin is a proteolytic enzyme that is released into the circulation primarily by the kidneys. Its
release is stimulated by:
N407
1. sympathetic nerve activation (acting via β1-adrenoceptors)
2. renal artery hypotension (caused by systemic hypotension or renal artery stenosis)
3. decreased sodium delivery to the distal tubules of the kidney.
Juxtaglomerular (JG) cells associated
with the afferent arteriole entering the
renal glomerulus are the primary site of
renin storage and release in the body. A
reduction in afferent arteriole pressure
causes the release of renin from the JG
cells, whereas increased pressure inhibits
renin release. Beta1-adrenoceptors
located on the JG cells respond to
sympathetic nerve stimulation by releasing renin. Specialized cells (macula densa) of distal
tubules lie adjacent to the JG cells of the afferent arteriole. The macula densa senses the amount
of sodium and chloride ion in the tubular fluid. When NaCl is elevated in the tubular fluid, renin
release is inhibited. In contrast, a reduction in tubular NaCl stimulates renin release by the JG
cells. There is evidence that prostaglandins (PGE2and PGI2) stimulate renin release in response
to reduced NaCl transport across the macula densa. When afferent arteriole pressure is reduced,
glomerular filtration decreases, and this reduces NaCl in the distal tubule. This serves as an
important mechanism contributing to the release of renin when there is afferent arteriole
hypotension.
N407
When renin is released into the blood, it acts upon a circulating substrate, angiotensinogen, that
undergoes proteolytic cleavage to form the decapeptide angiotensin I. Vascular endothelium,
particularly in the lungs, has an enzyme,angiotensin converting enzyme (ACE), that cleaves off
two amino acids to form the octapeptide, angiotensin II (AII), although many other tissues in the
body (heart, brain, vascular) also can form AII.
AII has several very important functions:
• Constricts resistance vessels (via AII [AT1] receptors) thereby increasing systemic
vascular resistance and arterial pressure
• Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to
increase sodium and fluid retention
• Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior
pituitary, which increases fluid retention by the kidneys
• Stimulates thirst centers within the brain
• Facilitates norepinephrine release from sympathetic nerveendings and inhibits
norepinephrine re-uptake by nerve endings, thereby enhancing sympathetic adrenergic function
• Stimulates cardiac hypertrophy and vascular hypertrophy
The renin-angiotensin-aldosterone pathway is regulated not only by the mechanisms that
stimulate renin release, but it is also modulated by natriuretic peptides (ANP and BNP) released
by the heart. These natriuretic peptides acts as an important counter-regulatory system.
N407
Therapeutic manipulation of this pathway is very important in treating hypertension and heart
failure. ACE inhibitors, AII receptor blockers and aldosterone receptor blockers, for example, are
used to decrease arterial pressure, ventricular afterload, blood volume and hence ventricular
preload, as well as inhibit and reverse cardiac and vascular hypertrophy.
N407
BOOK-BASED PATHOPHYSIOLOGY
N407
Endothelial damage Vasospasms
Increased
Increased Fluid
Fluid shifts
shifts from
from Increased
Increased endothelin
endothelin Intravascular
Intravascular Increased
Increased sensitivity
sensitivity to
to
thromboxane intravascular
intravascular to
thromboxane to to to &
& coagulation
coagulation angiotensin II
angiotensin II
prostacydin intracellular
intracellular space
space
prostacydin
decreased
decreased nitric
nitric oxide
oxide
Generalized Uteroplacental Glomerular Cortical Pulmonary

vasoconstric arteriole damage brain edema
tion lesions spasms
Proteinuria
Hypertension -IUGR Headache Dyspnea
Edema of the
-Abruption of
hands face
placenta Hyperreflexia
and
-increased abdomen
uterine Seizure
(dependent)
contractility
Retinal Haemolysis Platelet Hepatic

arteriolar of RBCs aggregation micro
spasms and fibrin emboli;
deposition
Liver damage
-Blurred -Decreased Thrombocytopenia -elevated liver enzymes

vision haemoglobin
-Nausea and vomiting
-Maternal Disseminated
hyperbilirubinemia intravascular -Epigastric pain
coagulation
-Right Upper Quadrant Pain
-Decreased blood glucose
N407
B O O K - B A S E D :
S Y N T H E S I S O F T H E D I S E A S E
Definition of the Disease
Pre-eclampsia is a medical condition where hypertension arises in pregnancy (pregnancy-
induced hypertension) in association with significant amounts of protein in the urine. Because
pre-eclampsia refers to a set of symptoms rather than any causative factor, it is established that
there are many different causes for the syndrome. It also appears likely that there is a substance
or substances from the placenta that may cause endothelial dysfunction in the maternal blood
vessels of susceptible women.
Preeclampsia is a disorder that occurs only during pregnancy and the postpartum period
and affects both the mother and the unborn baby. Affecting at least 5-8% of all pregnancies, it is
a rapidly progressive condition characterized by high blood pressure and the presence of protein
in the urine. Swelling, sudden weight gain, headaches and changes in vision are important
symptoms; however, some women with rapidly advancing disease report few symptoms.
Preeclampsia has been described as a disease of theories, because the cause is unknown.
Some theories include (1) endothelial cell injury, (2) rejection phenomenon (insufficient
production of blocking antibodies), (3) compromised placental perfusion, (4) altered vascular
reactivity, (5) imbalance between prostacyclin and thromboxane, (6) decreased glomerular
filtration rate with retention of salt and water, (7) decreased intravascular volume, (8) increased
central nervous system irritability, (9) disseminated intravascular coagulation, (10) uterine
muscle stretch (ischemia), (11) dietary factors, and (12) genetic factors. The relatively new
theory of endothelial injury explains many of the clinical findings in preeclampsia. The theory
emphasizes that there is more to preeclampsia than hypertension. The vascular endothelium
N407
produces a number of important substances including endothelial-derived relaxing factor or nitric
oxide, endothelin-1, prostacyclin, and tissue plasminogen activator. Thus, endothelial cells
modify the contractile response of the underlying smooth muscle cells, prevent intravascular
coagulation, and maintain the integrity of the intravascular compartment. Several findings
suggest endothelial injury in preeclampsia.
Predisposing / Precipitating Factors
Women with preeclampsia have abnormal blood vessels feeding the placenta, although the
exact cause of this abnormality is not know. There are no tests that can reliably predict who will
get preeclampsia, and there is no way to prevent it. Women with one or more of the following
characteristics have an increased risk of developing preeclampsia:
 First pregnancy (excluding miscarriages)
 High blood pressure, kidney disease, lupus, or diabetes prior to pregnancy
 Gestational diabetes
 Multiple gestation (eg, twins or triplets)
 A family history of preeclampsia in a sister or mother
 A previous history of preeclampsia
 Age under 20 years and possibly age over 35 to 40 years
 Obesity
N407
Conversely, women who do not develop preeclampsia in their first pregnancy are at low risk of
developing it in a subsequent pregnancy.
Other precipating factors may include: pregnancy, long interval pregnancy and urinary tract
infection.
Other predisposing factors may include: genetics, low socioeconomic status, race and heart
disease.
Signs and Symptoms
Signs of severe preeclampsia — Mild preeclampsia can worsen and become severe. This usually
occurs over several days to weeks, but may occur more quickly. Severe preeclampsia may be
characterized by one or more of the following signs or symptoms. However, the signs of both
mild and severe preeclampsia may be subtle, and patients should not hesitate to mention any
concerns about possible signs of preeclampsia to their provider:
 Blood pressure ≥160/110 mmHg. Women with blood pressures in this range have an
increased risk of stroke
 Persistent severe headache
 Visual problems (blurred or double vision, blind spots, flashes of light or squiggly lines,
loss of vision)
 Abnormal kidney tests or decreased urination (urinating less than 500 mL in 24 hours)
 Fluid in the lungs, which may cause new shortness of breath
N407
 Low platelet count; platelets help the blood to clot, which may cause easy bruising or
bleeding
 Liver abnormalities (detected by blood tests); symptoms may include nausea, vomiting,
or pain in the mid- or right upper abdomen (similar to heartburn)
 Destruction of red blood cells (hemolysis, which is detected by blood tests).
Partial or complete separation of the placenta from the uterus (called abruption); symptoms
include vaginal bleeding, uterine pain, and/or decreased fetal activity
N407
MEDICAL MANAGEMENT
I n t r a v e n o u s
Th e r a p y
INTRAVENOUS FLUID THERAPY
Medical Management General Description Indication or Purposes
5% Dextrose in Lactated Hypertonic Solution  To replace fluids and

Ringer’s Solution electrolytes loss
A solution containing sodium  To increase vascular/
(30gtts/min) chloride, potassium chloride, plasma volume necessary
calcium chloride and sodium during bleeding or blood
lactated in distilled water, loss
referred to Lactated Ringer’s  To replenish fluid loss of
solution calories from dextrose the body, maintain
nutritional intake when
patient is unable to tolerate
feedings, also serves as
medium for administration
of medications.
INTRAVENOUS THERAPY
NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER

 Check the doctor’s order regarding to what type of IVF to be used and also its volume
and rate.
 Explain the procedure to the patient.
 Gather all materials needed for the insertion of IVF to save time and not to waste time for
looking for other materials.
 Wash hands before and after the procedure to prevent contamination from insertion site.
N407
 Place patient in a comfortable position to facilitate easy insertion of IV line and to

decrease patient’s fear about the procedure.
 Make sure that we give the proper IV fluid and drop rate accurately because patient may
experience fluid overload or dehydration.
 Check for its patency by observing the backflow of blood upon insertion.
After the Procedure
 Press the site where the needle was inserted and secure it with micropore.
 Check the site of hand where the needle is inserted if bulging is not visible. If so,
reinsertion is to be undertaken.
 Advice patient to avoid scratching the site less movement of the hand where the needle
was inserted to keep it in place.
 Instruct patient and significant others to inform the nurse on duty if bulging of the site is
visible, if there is back flow of blood of if IVF is not infusing well.
 Observe the IV site at least every hour for signs of infiltration or other complications
fluid or electrolyte overload and air embolism.
 IVF regulation should be checked and monitored upon receiving patient.
 Always check the doctor’s order for new orders regarding the IVF supplement of the
patient.
 Always check if the IVF is infusing well and intact.
 Monitor the patient’s skin integrity.
 Provide comfort for the patient.
 Remove and dispose used items.
 Report and record as appropriate.
 Place IV tag
N407
P h a r m a c o l o g i c a l ,
M a n a g e m e n t
Drugs Given Before Delivery
Generic Name Indication or Side effects &

General Action Dose and Route Contraindications
(Brand Name) Purposes Adverse Reactions
Magnesium Mineral/ For Eclampsia: the most Flushing, Magnesium sulfate

Anticonvulsant Initially 1 to 2 g common sweating, sharply should be given
Sulfate Injection in 25% or 50% medicine used lowered blood very cautiously in
Magnesium is the solution is given for preventing pressure, the presence of
(Magnesium second most intramuscularly. eclampsia hypothermia, serious impairment
Sulfate/ Epsom plentiful cation of Subsequently, 1 (seizures) stupor and of renal function
the intracellular g is given every during ultimately, since it is excreted
Salt) fluids. It is 30 minutes until pregnancy respiratory almost entirely by
essential for the relief is depression. the kidneys. This
activity of many obtained. The product contains
enzyme systems blood pressure aluminum that
and plays an should be may be toxic.
important role with monitored after Aluminum may
regard to each injection. reach toxic levels
neurochemical with prolonged
transmission and parenteral
muscular administration if
excitability. kidney function is
Deficits are impaired.
accompanied by a
variety of Magnesium sulfate
structural and should not be
functional administered
disturbances. parenterally in
patients with heart
block or
myocardial
damage.
Hydralazine Anti-hypertensive Start with 10 mg an intravenous (Common)\ MAO inhibitors

four times daily medicine for Headache, should be used
Hydralazine for the first 2-4 quickly anorexia, nausea, with caution in
(Apresoline) apparently lowers days, increase to lowering vomiting, diarrhea, patients receiving
blood pressure by 25 mg four severely high palpitations, hydralazine. Used
exerting a times daily for blood pressure tachycardia, angina with caution in
peripheral the balance of during pectoris. patients with
vasodilating effect the first week. pregnancy suspected coronary
through a direct For the second artery disease.
relaxation of and subsequent Apresoline should
vascular smooth weeks, increase be used with
muscle. dosage to 50 mg caution in patients
Hydralazine, by four times daily. with advanced
altering cellular For renal damage
calcium maintenance,
metabolism, adjust dosage to
interferes with the the lowest
calcium effective levels.
movements within
N407
the vascular
smooth muscle that
are responsible for
initiating or
maintaining the
contractile state
Methyldopa Anti-hypertensive starting dosage an oral edation, usually With active hepatic
of ALDOMET medicine for transient, may disease, such as
ALDOMET is an is 250 mg two or controlling high occur during the acute hepatitis and
(Aldomet) aromatic-amino- three times a blood pressure initial period of active cirrhosis.
acid decarboxylase day in the first during therapy or With liver
inhibitor in 48 hours. When pregnancy whenever the dose disorders
animals and in ALDOMET is is increased. previously
man. Although the given with Headache, associated with
mechanism of antihypertensive asthenia, or methyldopa
action has yet to be s other than weakness may be therapy. With
conclusively thiazides, the noted as early and hypersensitivity to
demonstrated, the initial dosage of transient any component of
antihypertensive ALDOMET symptoms. these products.
effect of should be
methyldopa limited to 500 On therapy with
probably is due to mg daily in monoamine
its metabolism to divided doses; oxidase (MAO)
alpha- when inhibitors.
methylnorepinephr ALDOMET is
ine, which then added to a
lowers arterial thiazide, the
pressure by dosage of
stimulation of thiazide need
central inhibitory not be changed.
alpha-adrenergic daily dosage of
receptors, false ALDOMET is
neurotransmission, 500 mg to 2 g in
and/or reduction of two to four
plasma renin doses. Although
activity. occasional
Methyldopa has patients have
been shown to responded to
cause a net higher doses, the
reduction in the maximum
tissue recommended
concentration of daily dosage is 3
serotonin, g
dopamine,
norepinephrine,
and epinephrine.
Labetalol Anti-hypertensive DOSAGE an intravenous Body as a Whole: The drug is

MUST BE medicine for Fever. contraindicated in
Labetalol HCl INDIVIDUALI quickly bronchial asthma,
(Trandate) combines both ZED. The lowering Cardiovascular: overt cardiac
selective, recommended severely high Hypotension, and failure, greater-
competitive, initial dosage is blood pressure rarely, syncope, than-first-degree
alpha1-adrenergic 100 mg twice in the hospital, bradycardia, heart heart block,
blocking and daily whether and also an oral block. cardiogenic shock,
nonselective, used alone or medicine for severe bradycardia,
competitive, beta- added to a controlling high Central and other conditions
adrenergic diuretic blood pressure Peripheral Nervous associated with
blocking activity in regimen. After 2 during Systems: severe and
a single substance. or 3 days, using Paresthesia, most prolonged
N407
In man, the ratios standing blood pregnancy frequently hypotension, and

of alpha- to beta- pressure as an described as scalp in patients with a
blockade have indicator, dosage tingling. In most history of
been estimated to may be titrated cases, it was mild hypersensitivity to
be approximately in increments of and transient and any component of
1:3 and 1:7 100 mg b.i.d. usually occurred at the product
following oral and every 2 or 3 the beginning of
intravenous (IV) days. The usual treatment.
administration, maintenance
respectively. dosage of Collagen
Beta2-agonist labetalol HCl is Disorders:
activity has been between 200 and Systemic lupus
demonstrated in 400 mg twice erythematosus,
animals with daily. positive
minimal beta1- antinuclear factor.
agonist (ISA)
activity detected. Eyes: Dry eyes.
In animals, at
doses greater than Immunological
those required for System:
alpha- or beta- Antimitochondrial
adrenergic antibodies.
blockade, a
membrane Liver and Biliary
stabilizing effect System: Hepatic
has been necrosis, hepatitis,
demonstrated. cholestatic
jaundice, elevated
liver function tests.
Musculoskeletal
System: Muscle
cramps, toxic
myopathy.
Respiratory
System:
Bronchospasm.
Skin and
Appendages:
Rashes of various
types, such as
generalized
maculopapular,
lichenoid,
urticarial, bullous
lichen planus,
psoriaform, and
facial erythema;
Peyronie's disease;
reversible alopecia.
Urinary System:
Difficulty in
micturition,
including acute
urinary bladder
retention.
Hypersensitivity:
Rare reports of
N407
hypersensitivity
(e.g., rash,
urticaria, pruritus,
angioedema,
dyspnea) and
anaphylactoid
reactions.
Nifedipine Anti-hypertensive Dosage should an oral Body as a Concomitant

be adjusted medicine for Whole/Systemic: administration with
The mechanism by according to controlling high chest pain, leg pain strong P450
(Adalat) which nifedipine each patient's blood pressure inducers, such as
reduces arterial needs. It is during Central Nervous rifampin, are
blood pressure recommended pregnancy System: contraindicated
involves peripheral that Adalat CC paresthesia, since the efficacy
arterial be administered vertigo of nifedipine
vasodilatation and, orally once daily tablets could be
consequently, a on an empty Dermatologic: rash significantly
reduction in stomach. Adalat reduced.
peripheral vascular CC is an Gastrointestinal:
resistance. The extended release constipation Nifedipine must
increased dosage form and not be used in
peripheral vascular tablets should be Musculoskeletal: cases of
resistance, an swallowed leg cramps cardiogenic shock.
underlying cause whole, not bitten
of hypertension, or divided. In Respiratory:
results from an general, titration epistaxis, rhinitis
increase in active should proceed Known
tension in the over a 7-14 day Urogenital: hypersensitivity to
vascular smooth period starting impotence, urinary nifedipine.
muscle. Studies with 30 mg once frequency
have demonstrated daily. Upward
that the increase in titration should
active tension be based on
reflects an increase therapeutic
in cytosolic free efficacy and
calcium. safety. The usual
maintenance
dose is 30 mg to
60 mg once
daily. Titration
to doses above
90 mg daily is
not
recommended.
Betamethasone Glucocorticoid/ Injectable To Accelarate Allergic Reactions: contraindicated in

Corticosteroid Suspension may the Anaphylactoid patients who are
vary from 0.25 development of reaction, hypersensitive to
(Diprolene/ Naturally to 9.0 mg per surfactant in anaphylaxis, any components of
Celestone) occurring day depending infants in angioedema. this product.
glucocorticoids on the specific mothers with
(hydrocortisone disease entity PIH Cardiovascular:
and cortisone), being treated. Bradycardia,
which also have cardiac arrest, Intramuscular
salt-retaining cardiac corticosteroid
properties, are arrhythmias, preparations are
used as cardiac contraindicated for
replacement enlargement, idiopathic
therapy in circulatory thrombocytopenic
adrenocortical collapse,
N407
deficiency states. congestive heart purpura.

Their synthetic failure, fat
analogs are embolism,
primarily used for hypertension,
their anti- hypertrophic
inflammatory cardiomyopathy in
effects in disorders premature infants,
of many organ myocardial rupture
systems. A following recent
derivative of myocardial
prednisolone, infarction,
betamethasone has pulmonary edema,
a 16β-methyl syncope,
group that tachycardia,
enhances the anti- thromboembolism,
inflammatory thrombophlebitis,
action of the vasculitis.
molecule and
reduces the Dermatologic:
sodium- and water- Acne, allergic
retaining dermatitis,
properties of the cutaneous and
fluorine atom subcutaneous
bound at carbon 9. atrophy, dry scaly
skin, ecchymoses
and petechiae,
edema, erythema,
hyperpigmentation
,
hypopigmentation,
impaired wound
healing, increased
sweating, rash,
sterile abscess,
striae, suppressed
reactions to skin
tests, thin fragile
skin, thinning
scalp hair,
urticaria.
Endocrine:
Decreased
carbohydrate and
glucose tolerance,
development of
cushingoid state,
glucosuria,
hirsutism,
hypertrichosis,
increased
requirements for
insulin or oral
hypoglycemic
adrenocortical and
pituitary
unresponsiveness
(particularly in
times of stress, as
in trauma, surgery,
or illness),
N407
suppression of
growth in pediatric
patients.
Fluid and
Electrolyte
Disturbances:
Congestive heart
failure in
susceptible
patients, fluid
retention,
hypokalemic
alkalosis,
potassium loss,
sodium retention.
Gastrointestinal:
Abdominal
distention,
bowel/bladder
dysfunction (after
intrathecal
administration),
elevation in serum
liver enzyme levels
(usually reversible
upon
discontinuation),
hepatomegaly,
increased appetite,
nausea,
pancreatitis, peptic
ulcer with possible
perforation and
hemorrhage,
perforation of the
small and large
intestine
(particularly in
patients with
inflammatory
bowel disease),
ulcerative
esophagitis.
Metabolic:
Negative nitrogen
balance due to
protein catabolism.
Musculoskeletal:
Aseptic necrosis of
femoral and
humeral heads,
calcinosis
(following intra-
articular or
intralesional use),
Charcot-like
arthropathy, loss of
N407
muscle mass,
muscle weakness,
osteoporosis,
pathologic fracture
of long bones,
postinjection flare
(following intra-
articular use),
steroid myopathy,
tendon rupture,
vertebral
compression
fractures.
Neurologic/Psychi
atric:
Convulsions,
depression,
emotional
instability,
euphoria,
headache,
increased
intracranial
pressure with
papilledema
(pseudotumor
cerebri) usually
following
discontinuation of
treatment,
insomnia, mood
swings, neuritis,
neuropathy,
paresthesia,
personality
changes, psychic
disorders, vertigo.
Arachnoiditis,
meningitis,
paraparesis/paraple
gia, and sensory
disturbances have
occurred after
intrathecal
administration
Ophthalmic:
Exophthalmos,
glaucoma,
increased
intraocular
pressure, posterior
subcapsular
cataracts, rare
instances of
blindness
associated with
periocular
injections.
N407
Other:
Abnormal fat
deposits, decreased
resistance to
infection, hiccups,
increased or
decreased motility
and number of
spermatozoa,
malaise, moon
face, weight gain.
Dexamethasone Glucocorticoid/ 0.75 to 9 mg a To Accelarate Anaphylactoid Contraindicated in

Corticosteroid day depending the reaction, systemic fungal
on the disease development of anaphylaxis, infections and
Glucocorticoids, being treated. surfactant in angioedema. patients with
naturally occurring infants in Bradycardia, known
and synthetic, are mothers with cardiac arrest, hypersensitivity to
adrenocortical PIH cardiac the product and its
steroids that are arrhythmias, consituents.
readily absorbed cardiac
from the enlargement,
gastrointestinal circulatory
tract. collapse,
Glucocorticoids congestive heart
cause varied failure, fat
metabolic effects. embolism,
In addition, they hypertension,
modify the body's hyper-trophic
immune responses cardiomyopathy
to diverse stimuli. in premature
Naturally infants, myocardial
occurring rupture following
glucocorticoids recent myocardial
(hydrocorti-sone infarction. Acne,
and cortisone), allergic dermatitis,
which also have dry scaly skin,
sodium-retaining ecchymoses and
properties, are petechiae,
used as erythema,
replacement impaired wound
therapy in healing, increased
adrenocortical sweating, rash,
deficiency states. striae, suppression
Their synthetic of reactions to skin
analogs including tests, thin fragile
dexamethasone are skin, thinning
primarily used for scalp hair,
their anti- urticaria.
inflammatory
effects in disorders
of many organ
systems.
N407
Nursing Responsibilities for All Drugs
Before the administration of drug:
 Verify Doctor’s order

 Remember the 10R’s of Drug administration
During the administration of drug:
 Verify patient’s identification

 Inform the patient with regards to drug administration
 Clean the IV port prior to administration of the drug
After the administration of drug:
 Monitor patient for adverse effects

 Inform patient that easy bruising may occur
 Caution patient not to stop taking drug abruptly without first consulting prescriber
N407
D i e t &
A c t i v i t y
M a n a g e m e n t
LOW SALT, LOW FAT DIET
Indication or Examples of
Type of Diet General Description
Purposes Restricted foods
Low Salt, Low Fat Reduced sodium and To prevent risk for -Fried foods
diet. cholesterol content of other complications -Salty Sauces (Fish
food which may arise from sauce and soy sauce)
hypertension. -Snack foods
-Processed foods
LOW SALT, LOW FAT DIET
NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER
 Check the doctor’s order.

 Check the right client.
 Be sure that the diet is properly instructed.
 Monitor if the client complies with the given diet.

 Be sure patient is taking or eating food he can tolerate
After the Procedure
 Assess for patient’s condition; how he responds to the diet
N407
Chronic Obstructive Pulmonary Disease: A Case Study 62
NURSING CARE PLAN
DECREASED CARDIAC OUTPUT
Nursing Scientific
Cues Objectives Nursing Interventions Rationale
Diagnosis Explanation
S=  Decreased A hypertensive Short Term: 1. Assess other Enhances ideas to

cardiac output pregnant woman precipitating factors. prioritize things.
r/t altered heart is caused by After 2-3
rate AEB sudden weight hours oh
O= pt. May nursing
increased blood gain. This would 2. Involve client in Enhances sense of control
manifest: interventions
pressure bring formulation of plan of care and aids in cooperation
complications in the pt. will be
>pallor at level of ability. and maintenance of
the body because able to
demonstrate independence.
>non-pitting/ there is an
pitting edema inadequate blood stable cardiac Bounding carotid, jugular,
rhythm and 3. Note presence, quality of radial, femoral pulses may
pumped by the
>hypertension rate within central and peripheral
heart to meet the be observed or palpated.
patient’s pulses. Pulses in the legs or feet
>body metabolic
demands of the normal range. may be diminished,
malaise
body, there is an reflecting effects of
>variations in alteration of her vasoconstriction and
blood V/S especially on Long Term: venous congestion.
pressure the blood pressure
After 2-3 days
>anxiety and and heart rate. As 4. Monitor blood pressure
the pt. will be Comparison of pressures
restlessness a result, a of the patient. Measure in
able to provides a more complete
decreased volume both arms/thighs three
blood pumped by participate in times, 3-5 min., then picture of vascular

either ventricle of activities that sitting, then standing for involvement or scope of
the heart each reduce blood initial evaluation. Use the problem.
minute. pressure or correct cuff size and
cardiac accurate technique.
workload.
5. Observe skin color, Presence of pallor, cool,

moisture, temperature and moist skin and delayed
capillary refill time. capillary refill time may be
due to peripheral
vasoconstriction.
6. Note independent or May indicate heart failure,

general edema. renal or vascular
impairment.
To promote venous return

7.Position the client with to the heart
legs elevated
8. Encourage leg exercise To improve blood flow

such as flexion and and reduce venous
extension of the feet, stagnation
active and relaxation of the
calf muscles
9. Place the client in a To decrease preload and

highfowler’s position reduce pulmonary
N407
congestion
10. Instruct the client the

importance of maintaining
regular physical ability To promote circulation
and vascular health
11. Provide calm, restful

surroundings, minimize
environmental activity or Can reduce stressful
noise. stimuli produce calming
effect thereby reduces
blood pressure.
12. Maintain activity

restrictions; provide
comfort measures, e.g. Help reduce sympathetic
back and neck massage, stimulation promotes
elevation of head. relaxation.
13. Instruct pt. in

relaxation technique and Reduces physical stress
guided imagery. and tension that affect
blood pressure and causes
hypertension.
Response to drug therapy

14. Monitor response to is dependent on both
N407
medications to control high individuals well as the

blood pressure. synergistic effects of the
drugs. Because side
effects, drug interactions
and patient’s motivation
for taking
antihypertensive
medication, it is important
to use the smallest
number and lowest
dosage of medications.
N407
INEFFECTIVE UTEROPLACENTAL TISSUE PERFUSION
Nursing Scientific
S= Ineffective Preeclampsia is

uteroplacental characterized by
tissue perfusion an increased in Short Term: 1. Assist the patient in Decreases factors that
related to blood pressure identifying lifestyle could lead to decreased
O=patient After 2 hours adjustment (e.g., avoiding perfusion of oxygen to
may manifest vasospasm of resulting from of nursing
spiral arteries vasospasm of prolonged sitting, sitting uterus, placenta, and
the following: interventions, with crossed legs, or fetus
secondary to arteries (for this the patient
>edema preeclampsia case, we are standing; developing
will be able to exercise plan for
pertaining to the verbalize
>maternal cardiovascular fitness
spiral artery) that understanding
blood during pregnancy; avoiding
causes of condition,
pressure of wearing constrictive
vasoconstriction. therapy
160/100 clothing; maintaining a
This then leads to regimen and
mmHg balance diet with adequate
decrease in side effects of
oxygen supply to hydration) that may be
>increased or medications.
the placenta which needed because of changes
decreased
is otherwise in physiologic function
fetal heart
known as during pregnancy.
tone Long Term:
ineffective
>positive uroplacental Permits monitoring of
After 2-3 days
homan’s sign perfusion. 2. Check and monitor vital cardiovascular response to
of nursing
signs hourly. illness state and provides
intervention,
early warning of perfusion
the patient
problems.
will be able to
demonstrate
increased
perfusion as 3. Monitor fetal heart rate Provides early warning of
individually and well being. perfusion problems, and
appropriate promotes early
(e.g. vital intervention.
signs,
especially
4. Institute O2, with an It enhances uteroplacental
blood
initial volume of at least perfusion thereby
pressure,
2L/min. decreasing fetal heart
within client’s
normal range workload.
and absence
of edema)
5. Monitor intake and To check for renal

output every hour. perfusion and to
determine fluid loss and
need for replacement or
fluid excess which further
increases BP
6. Instruct the patient to

To promote placental
assume the left side lying
perfusion and prevent the
position when lying down.
compression of vena cava.
N407
7. Provide quiet, non-

stimulating environment for It reduces anxiety and
the patient. promotes rest. Both
measures will assist in
maintaining peripheral
circulation by avoiding
vasoconstriction.
8. Provide the patient and

family factual information It reduces anxiety and
and support as needed. provides teaching
opportunity.
9. Provide low-sodium diet

(not more than 6g daily or It assists in controlling
less than 2.5 g daily). blood pressure. Restriction
Restrict intake of protein. of protein helps limit BUN.
10. Refer to other health Provides support and

care professionals as fosters cost-effective
necessary collaboration through use
of readily available
resources
N407
ACTIVITY INTOLERANCE
Nursing Scientific
S= Activity When there is a After 2-3 days 1. Assess for other Fatigue is a side effect of
intolerance r/t high blood the pt. will be precipitators or causes of some medications. Pain
imbalance pressure, there is able to treatment and pain. and stressful regimens
O= oxygen supply an inadequate achieve also extract energy and
and demand blood flow. measurable produce fatigue.
Pt. may AEB abnormal Inadequate blood increase in
manifest heart rate or flow decreases the activity
blood pressure nutrients and intolerance, 2. Involve client in Enhances sense of
-pallor formulation of plan of care
response oxygen in the evidenced by control and aids in
>non-pitting tissues in the body reduced at level of ability cooperation and
edema as well as in fatigue and maintenance of
metabolic weakness and independence.
>hypertension demands. By then, by V/S within
a person will not acceptable
>body 3. Assess the patient’s
be able to meet limits during
malaise response to activity, The stated parameters are
her desired activity.
nothing pulse rate more helpful in assessing
>variations in activities because
than 20 beats/min. faster physical responses to the
blood of depleted energy
than resting rate ; marked stress of activity and if
pressure that the body
increase in blood pressure present are indicators of
needs to sustain
>anxiety and during or after activity; over exertion.
normal metabolic
restlessness rate. dyspnea or chest pain;
excessive fatigue and
weakness; diaphoresis;
dizziness or syncope.
N407
4. Determine current Comprehensive functional

cap[abilities and barriers to assessment includes
participation in self care. independent performance
of basic ADLs, social
activities, sensory abilities,
cognition and ability to
ambulate.
5. Evaluate accelerating
activity intolerance. May denote increasing
cardiac decompensation
rather than over activity.
6. Provide assistance with Meets client’s personal

self-care activity as care needs without undue
indicated, intersperse myocardial stress or
activity period with rest excessive oxygen
period. demand.
7. Instruct client energy- Energy saving techniques

conserving techniques. reduced the energy
expenditures, thereby
assisting in equalization of
oxygen supply and
demand.
N407
Gradual activity
intolerance progression
8. Encourage progressive prevents a sudden
activity when tolerated. increase in cardiac
workload.
N407
DISCHARGE PLANNING
M- Instructed the patient to take the following home medication as ordered by the physician.
E- Instructed patient to avoid strenuous activities and practice deep breathing exercise.
Instructed patient that she may resume regular exercise as tolerated.
T- n/a
H- Emphasized the importance of breast feeding.
Instructed patient to have proper hygiene.
Instructed patient to continue oral medication as prescribed by the physician.
O- Advice patient to have follow up check up after 1 week.
D- LSLF
LEARNING DERRIVED
A case study is a requirement which all nursing students must complete in order to gain
the appropriate knowledge, skills, and attitude in the field of nursing. It allows the students to
delve into the synthesis and meaning of the disease, the signs and symptoms, as well as the
corresponding nursing care management for the case. A book-based case study is no different,
and in actuality, students are given the opportunity to learn beyond what clients may feel and into
the different dimensions of the disease. In short, the case is not limited to merely the treatments
of the patient to his or her signs and symptoms.
In the four days it took to complete this case study, it can be said that the students have
really learned alot about the “toxemia of pregnancy” or pregnancy induced hypertension. It eas
also beneficial on the part of the group because the case served as a review on previous lessons
discussed in NCM 101. In completing this case, however, the group encountered many
difficulties and one such difficulty was the creation of the pathophysiology.
Many books and researches have different theories on the development of PIH and the
etiology of the disease. Some theories explain the phenomenon as a result of a “toxin” whilst
others go into an explanation of the possibility of a “uterine stretch” from the growing fetus,
which in turn causes ischemia and vasoconstriction. In an effort to include these well-respected
theories of different doctors, the student nurses briefly explained each in order to bring to light a
possible explanation to the occurance of the disease process.
Although it remains true that his case study was difficult to accomplish due to a lack of
supporting evidence to elaborate the occurance of this disease, still, many learnings regarding the
case have been derived. Despite the sleepless nights sacrificed to complete the case study, the
efforts in the end have paid off.Even though the case had been done in such a busy and turbulent
time (CON days), still the manuscript serves as proof that with the belief and faith in God and
the unity of team work, all things are possible. PRAISE BE TO GOD!
N407
REFERENCES
Black, J.M., Hawks, J. H. (2009). Medicalsurgical nursing: clinical management for
positive outcomes. Vol.2. New York. Saunders.
Blanchard, R., Loeb, S. (2004) Blanchard & Loeb publishers nurse’s drug handbook.
Michigan. Blanchard & Loeb.
Fischbach, F.T., Dunning, M.B. (2008). A manual of laboratory and diagnostic tests.
Springhouse, PA. Lippincott, Williams, & Wilkins.
Gutierrez, K. J., Peterson, P.G. (2007). Saunders sursing survival guide pathophysiology.
2nd Edition. New Orleans Louisiana. Saunders & Elsevier.
Hole, J.W. (1993). Human anatomy and physiology. 6th edition. Dubuque, IA. Wm C.
Brown Publishers, inc
Huether, S.E., McCance, K.L. (2000). Understanding pathophysiology.2nd edition.
Singapore: Elsevier Science.
Karch, A. M. (2000). Lippincott’s nursing drug guide 2000. University of Michigan.
Lippincott, Williams, & Wilkins.
Keogh, J. (2009). Nursing laboratory and diagnostic tests demystified. Boston. McGraw
Hill Professional.
McCann, J. A., Holmes, H. N., Robinson, J.M., et al. (2003). Professional guide to
pathophysiology. Springhouse, PA. Lippincott, Williams, & Wilkins.
Nicoll, D., McPhee, S.J., Pignone, M., Chuanyi, M.L. (2007). Pocket guide to diagnostic
tests: Lange clinical science series. Springhouse, PA. McGrawHill.
N407
Porth, Carol M., (2005). Pathophysiology: Concepts of altered health states. 7th Edition.
Boston: Lippincott, Williams, & Wilkins.
Stockley, R. A. (2007). Chronic obstructive pulmonary disease. Chicago, IL. Wiley
Blackwell.
Spratto, G.R., Woods, A.L. (2004). PDR nurse’s drug handbook. Springfield, IL.
Cengage Learning, inc.
Wallach, J.B. (2007). Interpretation of diagnostic tests: Doody’s all reviewed collection.
Springhouse, PA. Lippincott, Williams, & Wilkins.
Weber, J., Kelley, J. (2007). Health assessment in nursing. 2nd edition. Boston.
Lippincott, Williams & Wilkins.
Lam, M., (2010) Estrogen Dominance: The silent epidemic. The Authority on Natural
Healing. http://www.drlam.com/articles/Estrogen_Dominance.asp. Accessed on
September 14, 2010
N407

Pregnancy Induced Hypertension Case Study

Caricato da

Informazioni sul documento

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

Pregnancy Induced Hypertension Case Study

Caricato da

Copyright:

Formati disponibili

H O LY A N G E L U N I V E R S I T Y

In Partial Fulfilment of Requirements for RLE 104

“ PREGNANCY INDUCED HYPERTENSION”

Teacher’s Full Name MAN, RN

September 29, 2010

BRIEF DESCRIPTION OF THE DISEASE 3

REASONS FOR CHOOSING THE CASE 5

STUDENT NURSE-CENTRED OBJECTIVES 7

DIAGNOSTIC & LABRATORY PROCEDURES 8

ANATOMY & PHYSIOLOGY 29

SYNTHESIS OF THE DISEASE 44

DEFINITION OF THE DISEASE 46

PREDISPOSING & PRECIPITATING FACTORS 47

SIGNS AND SYMPTOMS WITH RATIONALE 48

NURSING CARE PLAN 62

“W e learn more by looking for the answer to a question

and not finding it than we do from learning the answer itself .”

disease process, it symptoms, and corresponding treatments.

Pregnancy-induced hypertension is one of the conditions which student-nurses encounter

Pregnancy induced hypertension (PIH) is a condition in which vasospasms occurs

pregnancy induced hypertension, no such toxin has ever identified.

mothers during subsequent pregnancies.

Classification of Hypertensive Diseases in Pregnancy

Chronic Hypertension is defined as blood pressure >140/90 at <20 weeks of gestation.

Pregnancy Induced Hypertension is defined as a sustained blood pressure increase to 140/90 at

Superimposed Pregnancy-Induced Hypertension is defined as coexistence of chronic

Clinical Manifestations of Severe Disease in Patients with PIH

Blood pressure >160-180 mm Hg systolic or >110 mm Hg diastolic

Proteinuria >5 g/24 h or > 1+ on dipstick (normal <300 mg/24 h)

Elevated serum creatinine

Generalized seizures (eclampsia)

Oliguria <500 mL/24 hours

Hepatocellular dysfunction (elevated alanine toxemia preeclampsia, aminotransferase, aspartase

Intrauterine growth restriction or oligohydramnios

Symptoms suggesting significant end-organ involvement: headache, visual disturbances, or

REASONS FOR CHOOSING THE CASE

about 5 percent of nulliparous women develop preeclampsia and 40 to 50 percent of these

women develop severe disease worldwide. In the Philippines, according to Department of

planning can help prevent maternal deaths by 35%.

STUDENT NURSE-CENTRED OBJECTIVES

 Know and understand the disease process and concept of pregnancy-induced

DIAGNOSTIC & LABRATORY PROCEDURES

COMPLETE BLOOD COUNT

Diagnostic Procedure Indications or Purpose Possible Results Normal Values

HCT (%) To aid diagnosis of May be elevated due 36.0 – 47.0

Platelet Count To evaluate platelet Thrombocytocpenia 150 – 400

Differential Count: To provide a numeric WBC and differential 55-65%

infection for the

Lymphocytes (%) To check for immune WBC and differential 25-35%

Eosinophils (%) To determine presence of WBC and differential 2-4%

Monocytes (%) To determine presence of WBC and differential 2-6%

COMPLETE BLOOD COUNT

NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER PROCEDURE

Before the Procedure

 Explain the procedure to the pt. and why it is indicated

 Inform the patient that a blood sample will be taken.

the collection of sample/specimen.

During the Procedure

 Instruct the patient to calm down to avoid uneasiness.

After the Procedure

 Apply brief pressure to prevent bleeding

 Apply warm compress if Hematoma will develop at the venipuncture site.

Diagnostic Procedure Indications or Purpose Possible Findings Normal Values