Pregnancy Induced Hypertension Case Study 2b376t

HOLY ANGEL UNIVERSITY 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

Pregnancy-Induced Hypertension: A Case Study September 29, 2010

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Pregnancy-Induced Hypertension: A Case Study TABLE OF CONTENTS

INTRODUCTION BRIEF DESCRIPTION OF THE DISEASE

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REASONS FOR CHOOSING THE CASE

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STATISTICS

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STUDENT NURSE-CENTRED OBJECTIVES

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DIAGNOSTIC & LABRATORY PROCEDURES

8

PHYSICAL ASSESSMENT

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ANATOMY & PHYSIOLOGY

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PATHOPHYSIOLOGY SYNTHESIS OF THE DISEASE

44

DEFINITION OF THE DISEASE

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PREDISPOSING & PRECIPITATING FACTORS

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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

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Pregnancy-Induced Hypertension: A Case Study

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“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

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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 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.

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Pregnancy-Induced Hypertension: A Case Study 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.

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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 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%.

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STUDENT NURSE-CENTRED OBJECTIVES

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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.

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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.

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Pregnancy-Induced Hypertension: A Case Study DIAGNOSTIC & LABRATORY PROCEDURES

COMPLETE BLOOD COUNT

Diagnostic Procedure

Indications or Purpose

Possible Results

Normal Values

HGB (g/dL)

To measure the total amount of hemoglobin in the blood.

May be elevated due to hemoconcentration of blood.

120-160 g/dl

HCT (%)

To aid diagnosis of abnormal states of hydration, polycythemia and anemia and aids in calculation of erythrocyte indices.

May be elevated due to hemoconcentration of blood.

36.0 – 47.0

Platelet Count

To evaluate platelet production

Thrombocytoenia or decreased platelet states are often found in PIH

150 – 400

To determine for presence of for further tests such as WBC differential infection and also for determination count

WBC and differential counts may be elevated depending upon the presence of infection for the individual case of the patient.

4.8 – 10.8

To provide a numeric estimate of the client’s immune status.

WBC and differential counts may be elevated depending upon the presence of

55-65%

(x10 9/L)

WBC (x10 9/L)

Differential Count: Segmenters (%)

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Pregnancy-Induced Hypertension: A Case Study infection for the individual case of the patient. Lymphocytes (%)

To check for immune responses


25-35%

Eosinophils (%)

To determine presence of multicellular parasites and certain infections


2-4%

Monocytes (%)

To determine presence of Chronic inflammatory disease, Parasitic infection, Viral infection


2-6%

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Pregnancy-Induced Hypertension: A Case Study 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.

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BLOOD CHEMISTRY Diagnostic Procedure Creatinine

Sodium (Na+)

Potassium (K+)

Bilirubin

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Possible Findings

Normal Values

This test measures the amount of creatinine in the blood. It is used to diagnose impaired renal function and assess glomerular filtration.

Often normal but may be increased in cases of severe preeclampsia.

0.5-1.69 mg/dl

To check for water balance.

Normal in PIH, but may differ due to comorbid existing conditions for the patient

137-145 mmo/l

To measure acid base balance and normal muscle activity.

Normal in PIH, but may differ due to comorbid existing conditions for the patient

3.6-5.0 mmo/l

Tests for the presence of liver disease or dysfunction through evaluation of bilirubin levels in the blood.

Usually below 5 mg/dL

0.2-1.9 mg/dL


Aspartate Aminotransferase (AST)

Alkaline Phosphotase

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The aspartate aminotransferase (AST) test can be used specifically to check for liver or heart problems, or it can be part of standard medical test screening. A test which evaluates 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.

AST is usually below 500 IU

6-34 IU/L

Alkaline phosphotase may increase 2 to 3 fold in PIH

20-140 IU/L

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Pregnancy-Induced Hypertension: A Case Study BLOOD CHEMISTRY NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER 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.


Inform the patient that pain may be felt through prick in the needle

•

Instruct the patient to calm down to avoid uneasiness.


Apply brief pressure to prevent bleeding

•

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

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URINALYSIS Diagnostic Procedure Urinalysis


Possible Findings

For general health screening to detect renal and metabolic disease; diagnosis of disease or disorders of the kidney or urinary tract; monitoring patient’s with diabetes.

Urinalysis reveals Proteinuria (positive albumin levels) and occasional hyaline casts.

Normal Values Color: Straw yellow to amber. Transparency: transparent Sugar: negative Albumin: negative

Specific Gravity: 1.015 – 1.025 Pus cells: 510/HPF RBC: o-2 HPF Epithelial cells: Moderate

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Pregnancy-Induced Hypertension: A Case Study URINALYSIS NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER PROCEDURE


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


The specimen should be delivered to the lab within 1 hour.

•

Obtain result and secure it to the chart

Refer result to the physician

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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

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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 local edema. Subarachnoid or intraventricular hemorrhages may be seen in the most severe cases. N-407


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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 istration 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

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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 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

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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. 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.

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Refractoriness to angiotensin II can be restored in patients with preeclampsia by the istration 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. 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

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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 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

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plasma renin activity, plasma renin concentration, and angiotensin II levels. Plasma aldosterone levels rise even higher than can be ed 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 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. N-407


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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 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.

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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-Larginine. 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. 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.

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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. 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.

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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 ively 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 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,

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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

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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.

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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.

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The fimbriae nearly surround the surface of the ovary. As a result, as soon as the oocyte is ovulated, it comes into 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 s 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 ed by the broad ligament and the round ligament. In addition to these ligaments that the uterus, much is provided inferiorly to the uterus by skeletal muscles of the pelvic floor. If ligaments that 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.

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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 es 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

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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 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

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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

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mammary alveoli. Suspensory ligaments 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 ive 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.

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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

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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 progesterone

both

estrogen after

and

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.

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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 multicelled 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-plantay-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

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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 disklike 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 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.

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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:

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Pregnancy-Induced Hypertension: A Case Study 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.

42

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.

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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.

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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.

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Pregnancy-Induced Hypertension: A Case Study BOOK-BASED PATHOPHYSIOLOGY

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Endothelial damage

Generaliz ed vasoconst riction

Vasospasms

Fluid shifts from intravascular to intracellular space

Increased thromboxane to prostacydin

Uteroplacen tal arteriole lesions

-Abruption of placenta -increased uterine contractili ty

Retinal arteriolar spasms

-Blurred vision

Increased endothelin &

Intravascular coagulation

Increased sensitivity to angiotensin II

Cortical brain spasms

Pulmonar y edema

Headach e

Dyspnea

decreased nitric oxide

Glomerul ar damage

Proteinur ia

-IUGR

Hypertensi on

Edema of the hands face and abdomen

Hyperrefl exia

(depende nt)

Haemolys is of RBCs

-Decreased haemoglobin -Maternal hyperbilirubin emia

Seizure

Platelet aggregati on and fibrin depositio n Thrombocytop enia

Hepatic micro emboli; Liver -elevated liver damage enzymes -Nausea and vomiting -Epigastric pain

Disseminated intravascular coagulation

-Right Upper Quadrant Pain -Decreased blood glucose

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B

O O K - B A S E D :

S

Y N T H E S I S

O F

T H E

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D I S E A S E

Definition of the Disease Pre-eclampsia is a medical condition where hypertension arises in pregnancy (pregnancyinduced 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

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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

Conversely, women who do not develop preeclampsia in their first pregnancy are at low risk of developing it in a subsequent pregnancy.

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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

•

Low platelet count; platelets help the blood to clot, which may cause easy bruising or bleeding

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Pregnancy-Induced Hypertension: A Case Study •

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

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51

MEDICAL MANAGEMENT

I

n t r a v e n o u s

T

h e r a p y

INTRAVENOUS FLUID THERAPY Medical Management 5% Dextrose in Lactated Ringer’s Solution (30gtts/min)

General Description Hypertonic Solution

Indication or Purposes •

A solution containing sodium • chloride, potassium chloride, calcium chloride and sodium lactated in distilled water, • referred to Lactated Ringer’s solution calories from dextrose

To replace fluids and electrolytes loss To increase vascular/ plasma volume necessary during bleeding or blood loss To replenish fluid loss of the body, maintain nutritional intake when patient is unable to tolerate feedings, also serves as medium for istration of medications.

INTRAVENOUS THERAPY NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER Before the Procedure •

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.


Place patient in a comfortable position to facilitate easy insertion of IV line and to decrease patient’s fear about the procedure.

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Pregnancy-Induced Hypertension: A Case Study •

52

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.


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

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P

h a r m a c o l o g i c a l

,

M

53

a n a g e m e n t

Drugs Given Before Delivery Generic Name (Brand Name)

Magnesium Sulfate Injection (Magnesium Sulfate/ Epsom Salt)

General Action

Mineral/ Anticonvulsant Magnesium is the second most plentiful cation of the intracellular fluids. It is essential for the activity of many enzyme systems and plays an important role with regard to neurochemical transmission and muscular excitability. Deficits are accompanied by a variety of structural and functional disturbances.

Hydralazine

Anti-hypertensive

(Apresoline)

Hydralazine apparently lowers blood pressure by exerting a peripheral vasodilating effect through a direct relaxation of vascular smooth muscle. Hydralazine, by altering cellular calcium metabolism, interferes with the calcium movements within the vascular

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Dose and Route

For Eclampsia: Initially 1 to 2 g in 25% or 50% solution is given intramuscularly. Subsequently, 1 g is given every 30 minutes until relief is obtained. The blood pressure should be monitored after each injection.

Indication or Purposes the most common medicine used for preventing eclampsia (seizures) during pregnancy

Side effects & Adverse Reactions Flushing, sweating, sharply lowered blood pressure, hypothermia, stupor and ultimately, respiratory depression.

Contraindications

Magnesium sulfate should be given very cautiously in the presence of serious impairment of renal function since it is excreted almost entirely by the kidneys. This product contains aluminum that may be toxic. Aluminum may reach toxic levels with prolonged parenteral istration if kidney function is impaired. Magnesium sulfate should not be istered parenterally in patients with heart block or myocardial damage.

Start with 10 mg four times daily for the first 2-4 days, increase to 25 mg four times daily for the balance of the first week. For the second and subsequent weeks, increase dosage to 50 mg four times daily. For maintenance, adjust dosage to the lowest effective levels.

an intravenous medicine for quickly lowering severely high blood pressure during pregnancy

(Common)\ Headache, anorexia, nausea, vomiting, diarrhea, palpitations, tachycardia, angina pectoris.

MAO inhibitors should be used with caution in patients receiving hydralazine. Used with caution in patients with suspected coronary artery disease. Apresoline should be used with caution in patients with advanced renal damage


54

smooth muscle that are responsible for initiating or maintaining the contractile state

Methyldopa

Anti-hypertensive

(Aldomet)

ALDOMET is an aromatic-aminoacid decarboxylase inhibitor in animals and in man. Although the mechanism of action has yet to be conclusively demonstrated, the antihypertensive effect of methyldopa probably is due to its metabolism to alphamethylnorepinephr ine, which then lowers arterial pressure by stimulation of central inhibitory alpha-adrenergic receptors, false neurotransmission, and/or reduction of plasma renin activity. Methyldopa has been shown to cause a net reduction in the tissue concentration of serotonin, dopamine, norepinephrine, and epinephrine.

Labetalol

Anti-hypertensive

(Trandate)

Labetalol HCl combines both selective, competitive, alpha1-adrenergic blocking and nonselective, competitive, betaadrenergic blocking activity in a single substance. In man, the ratios of alpha- to beta-

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starting dosage of ALDOMET is 250 mg two or three times a day in the first 48 hours. When ALDOMET is given with antihypertensive s other than thiazides, the initial dosage of ALDOMET should be limited to 500 mg daily in divided doses; when ALDOMET is added to a thiazide, the dosage of thiazide need not be changed. daily dosage of ALDOMET is 500 mg to 2 g in two to four doses. Although occasional patients have responded to higher doses, the maximum recommended daily dosage is 3 g

an oral medicine for controlling high blood pressure during pregnancy

DOSAGE MUST BE INDIVIDUALI ZED. The recommended initial dosage is 100 mg twice daily whether used alone or added to a diuretic regimen. After 2 or 3 days, using standing blood

an intravenous medicine for quickly lowering severely high blood pressure in the hospital, and also an oral medicine for controlling high blood pressure during pregnancy

edation, usually transient, may occur during the initial period of therapy or whenever the dose is increased. Headache, asthenia, or weakness may be noted as early and transient symptoms.

With active hepatic disease, such as acute hepatitis and active cirrhosis. With liver disorders previously associated with methyldopa therapy. With hypersensitivity to any component of these products. On therapy with monoamine oxidase (MAO) inhibitors.

Body as a Whole: Fever. Cardiovascular: Hypotension, and rarely, syncope, bradycardia, heart block. Central and Peripheral Nervous Systems: Paresthesia, most frequently described as scalp

The drug is contraindicated in bronchial asthma, overt cardiac failure, greaterthan-first-degree heart block, cardiogenic shock, severe bradycardia, other conditions associated with severe and prolonged hypotension, and

Pregnancy-Induced Hypertension: A Case Study blockade have been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) istration, respectively. Beta2-agonist activity has been demonstrated in animals with minimal beta1agonist (ISA) activity detected. In animals, at doses greater than those required for alpha- or betaadrenergic blockade, a membrane stabilizing effect has been demonstrated.

pressure as an indicator, dosage may be titrated in increments of 100 mg b.i.d. every 2 or 3 days. The usual maintenance dosage of labetalol HCl is between 200 and 400 mg twice daily.

tingling. In most cases, it was mild and transient and usually occurred at the beginning of treatment. Collagen Disorders: Systemic lupus erythematosus, positive antinuclear factor. Eyes: Dry eyes. Immunological System: Antimitochondrial antibodies. Liver and Biliary System: Hepatic necrosis, hepatitis, 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 hypersensitivity (e.g., rash,

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in patients with a history of hypersensitivity to any component of the product


56

urticaria, pruritus, angioedema, dyspnea) and anaphylactoid reactions.

Nifedipine

Anti-hypertensive

(Adalat)

The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilatation and, consequently, a reduction in peripheral vascular resistance. The increased peripheral vascular resistance, an underlying cause of hypertension, results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.

Betamethasone (Diprolene/ Celestone)

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Glucocorticoid/ Corticosteroid Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states.

Dosage should be adjusted according to each patient's needs. It is recommended that Adalat CC be istered orally once daily on an empty stomach. Adalat CC is an extended release dosage form and tablets should be swallowed whole, not bitten or divided. In general, titration should proceed over a 7-14 day period starting with 30 mg once daily. Upward titration should be based on therapeutic efficacy and safety. The usual maintenance dose is 30 mg to 60 mg once daily. Titration to doses above 90 mg daily is not recommended.

an oral medicine for controlling high blood pressure during pregnancy

Injectable Suspension may vary from 0.25 to 9.0 mg per day depending on the specific disease entity being treated.

To Accelarate the development of surfactant in infants in mothers with PIH

Body as a Whole/Systemic: chest pain, leg pain Central Nervous System: paresthesia, vertigo Dermatologic: rash Gastrointestinal: constipation Musculoskeletal: leg cramps

Concomitant istration with strong P450 inducers, such as rifampin, are contraindicated since the efficacy of nifedipine tablets could be significantly reduced. Nifedipine must not be used in cases of cardiogenic shock.

Respiratory: epistaxis, rhinitis Urogenital: impotence, urinary frequency

Allergic Reactions: Anaphylactoid reaction, anaphylaxis, angioedema. Cardiovascular: Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive heart

Known hypersensitivity to nifedipine.

contraindicated in patients who are hypersensitive to any components of this product.

Intramuscular corticosteroid preparations are contraindicated for idiopathic thrombocytopenic purpura.

Pregnancy-Induced Hypertension: A Case Study Their synthetic analogs are primarily used for their antiinflammatory effects in disorders of many organ systems. A derivative of prednisolone, betamethasone has a 16β-methyl group that enhances the antiinflammatory action of the molecule and reduces the sodium- and waterretaining properties of the fluorine atom bound at carbon 9.

failure, fat embolism, hypertension, hypertrophic cardiomyopathy in premature infants, myocardial rupture following recent myocardial infarction, pulmonary edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis. Dermatologic: Acne, allergic dermatitis, cutaneous and subcutaneous 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), suppression of growth in pediatric

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Pregnancy-Induced Hypertension: A Case Study 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 istration), 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 intraarticular or intralesional use), Charcot-like arthropathy, loss of muscle mass, muscle weakness, osteoporosis,

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Pregnancy-Induced Hypertension: A Case Study pathologic fracture of long bones, postinjection flare (following intraarticular 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 istration Ophthalmic: Exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts, rare instances of blindness associated with periocular injections. Other: Abnormal fat deposits, decreased resistance to

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infection, hiccups, increased or decreased motility and number of spermatozoa, malaise, moon face, weight gain.

Dexamethasone

Glucocorticoid/ Corticosteroid Glucocorticoids, naturally occurring and synthetic, are adrenocortical steroids that are readily absorbed from the gastrointestinal tract. Glucocorticoids cause varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli. Naturally occurring glucocorticoids (hydrocorti-sone and cortisone), which also have sodium-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs including dexamethasone are primarily used for their antiinflammatory effects in disorders of many organ systems.

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0.75 to 9 mg a day depending on the disease being treated.

To Accelarate the development of surfactant in infants in mothers with PIH

Anaphylactoid reaction, anaphylaxis, angioedema. Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive heart failure, fat embolism, hypertension, hyper-trophic cardiomyopathy in premature infants, myocardial rupture following recent myocardial infarction. Acne, allergic dermatitis, dry scaly skin, ecchymoses and petechiae, erythema, impaired wound healing, increased sweating, rash, striae, suppression of reactions to skin tests, thin fragile skin, thinning scalp hair, urticaria.

Contraindicated in systemic fungal infections and patients with known hypersensitivity to the product and its consituents.

Pregnancy-Induced Hypertension: A Case Study Nursing Responsibilities for All Drugs Before the istration of drug: •

Doctor’s order

•

the 10R’s of Drug istration

During the istration of drug: •

patient’s identification

•

Inform the patient with regards to drug istration

•

Clean the IV port prior to istration of the drug

After the istration 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

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D

i e t &

A

c t i v i t y

M

62

a n a g e m e n t

LOW SALT, LOW FAT DIET

Type of Diet Low Salt, Low Fat diet.

Indication or Purposes

General Description Reduced sodium and cholesterol content of food

To prevent risk for other complications which may arise from hypertension.

LOW SALT, LOW FAT DIET NURSING RESPONSIBILITIES BEFORE, DURING, AND AFTER Before the Procedure •

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

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Examples of Restricted foods -Fried foods -Salty Sauces (Fish sauce and soy sauce) -Snack foods -Processed foods

Chronic Obstructive Pulmonary Disease: A Case Study

NURSING CARE PLAN DECREASED CARDIAC OUTPUT

Cues

S= ∅

O= pt. May manifest: >pallor >nonpitting/ pitting edema >hypertensi on >body malaise >variations in blood pressure

Nursing Diagnosis

Scientific Explanation

Decreased cardiac output r/t altered heart rate AEB increased blood pressure

A hypertensive pregnant woman is caused by sudden weight gain. This would bring complications in the body because there is an inadequate blood pumped by the heart to meet the metabolic demands of the body, there is an alteration of her V/S especially on the blood

Objectives

Short Term: After 2-3 hours oh nursing intervention s the pt. will be able to demonstrat e stable cardiac rhythm and rate within patient’s normal range.

Long Term:

Nursing Interventions

Rationale

1. Assess other precipitating factors.

Enhances ideas to prioritize things.

2. Involve client in formulation of plan of care at level of ability.

Enhances sense of control and aids in cooperation and maintenance of independence.

3. Note presence, quality of central and peripheral pulses.

Bounding carotid, jugular, radial, femoral pulses may be observed or palpated. Pulses in the legs or feet may be diminished, reflecting effects of vasoconstriction and venous congestion.

4. Monitor blood pressure of the patient. Measure in both

63

Pregnancy-Induced Hypertension: A Case Study >anxiety and restlessness

pressure and heart rate. As a result, a decreased volume blood pumped by either ventricle of the heart each minute.

After 2-3 days the pt. will be able to participate in activities that reduce blood pressure or cardiac workload.

arms/thighs three times, 3-5 min., then sitting, then standing for initial evaluation. Use correct cuff size and accurate technique.

5. Observe skin color, moisture, temperature and capillary refill time.

6. Note independent or general edema.

Presence of pallor, cool, moist skin and delayed capillary refill time may be due to peripheral vasoconstriction.

7.Position the client with legs elevated

May indicate heart failure, renal or vascular impairment.

8. Encourage leg exercise such as flexion and extension of the feet, active and relaxation of the calf muscles

9. Place the client in a

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Comparison of pressures provides a more complete picture of vascular involvement or scope of the problem.

To promote venous return to the heart

To improve blood flow and reduce venous stagnation

64

Pregnancy-Induced Hypertension: A Case Study highfowler’s position

10. Instruct the client the importance of maintaining regular physical ability

11. Provide calm, restful surroundings, minimize environmental activity or noise.

12. Maintain activity restrictions; provide comfort measures, e.g. back and neck massage, elevation of head.

To decrease preload and reduce pulmonary congestion

To promote circulation and vascular health

Can reduce stressful stimuli produce calming effect thereby reduces blood pressure.

Help reduce sympathetic stimulation promotes relaxation.

13. Instruct pt. in relaxation technique and guided imagery. Reduces physical stress and tension that affect blood pressure

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14. Monitor response to medications to control high blood pressure.

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and causes hypertension.

Response to drug therapy is dependent on both individuals well as the 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.

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INEFFECTIVE UTEROPLACENTAL TISSUE PERFUSION

Cues S=∅

O=patient may manifest the following: >edema >maternal blood pressure of 160/100 mmHg >increased or decreased fetal heart tone >positive homan’s sign

Nursing Diagnosis


Ineffective uteroplacenta l tissue perfusion related to vasospasm of spiral arteries secondary to preeclampsia

Preeclampsia is characterized by an increased in blood pressure resulting from vasospasm of arteries (for this case, we are pertaining to the spiral artery) that causes vasoconstriction . This then leads to decrease in oxygen supply to the placenta which is otherwise known as ineffective uroplacental perfusion.

Objectives

Short Term: After 2 hours of nursing intervention s, the patient will be able to verbalize understandi ng of condition, therapy regimen and side effects of medications .

Long

Nursing Interventions

Rationale

1. Assist the patient in identifying lifestyle adjustment (e.g., avoiding prolonged sitting, sitting with crossed legs, or standing; developing exercise plan for cardiovascular fitness during pregnancy; avoiding wearing constrictive clothing; maintaining a balance diet with adequate hydration) that may be needed because of changes in physiologic function during pregnancy.

Decreases factors that could lead to decreased perfusion of oxygen to uterus, placenta, and fetus

2. Check and monitor vital signs hourly.

Permits monitoring of cardiovascular response to illness state and provides early warning of perfusion problems.

67

Pregnancy-Induced Hypertension: A Case Study Term: After 2-3 days of nursing intervention , the patient will be able to demonstrat e increased perfusion as individually appropriate (e.g. vital signs, especially blood pressure, within client’s normal range and absence of edema)

3. Monitor fetal heart rate and well being.

4. Institute O2, with an initial volume of at least 2L/min.

5. Monitor intake and output every hour.

6. Instruct the patient to assume the left side lying position when lying down.

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Provides early warning of perfusion problems, and promotes early intervention.

It enhances uteroplacental perfusion thereby decreasing fetal heart workload.

To check for renal perfusion and to determine fluid loss and need for replacement or fluid excess which further increases BP

To promote placental perfusion and prevent the compression of vena cava.

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7. Provide quiet, nonstimulating environment for the patient.

It reduces anxiety and promotes rest. Both measures will assist in maintaining peripheral circulation by avoiding vasoconstriction.

It reduces anxiety and provides teaching opportunity. 8. Provide the patient and family factual information and as needed.

9. Provide low-sodium diet (not more than 6g daily or less than 2.5 g daily). Restrict intake of protein.

10. Refer to other health care professionals as

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It assists in controlling blood pressure. Restriction of protein helps limit BUN.

Provides and fosters cost-effective collaboration through use of readily available resources

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necessary

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ACTIVITY INTOLERANCE

Cues S=∅

O= Pt. may manifest -pallor >non-pitting edema >hypertensi on >body malaise >variations in blood pressure >anxiety and restlessness

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Nursing Diagnosis


Activity intolerance r/t imbalance oxygen supply and demand AEB abnormal heart rate or blood pressure response

When there is a high blood pressure, there is an inadequate blood flow. Inadequate blood flow decreases the nutrients and oxygen in the tissues in the body as well as in metabolic demands. By then, a person will not be able to meet her desired activities because of depleted energy that the body needs to sustain normal metabolic rate.

Objectives After 2-3 days the pt. will be able to achieve measurable increase in activity intolerance, evidenced by reduced fatigue and weakness and by V/S within acceptable limits during activity.

Nursing Interventions 1. Assess for other precipitators or causes of treatment and pain.

2. Involve client in formulation of plan of care at level of ability

3. Assess the patient’s response to activity, nothing pulse rate more than 20 beats/min. faster than resting rate ; marked increase in blood pressure during or after activity; dyspnea or chest pain; excessive fatigue and weakness; diaphoresis; dizziness or syncope.

Rationale Fatigue is a side effect of some medications. Pain and stressful regimens also extract energy and produce fatigue.

Enhances sense of control and aids in cooperation and maintenance of independence.

The stated parameters are helpful in assessing physical responses to the stress of activity and if present are indicators of over exertion.

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4. Determine current cap[abilities and barriers to participation in self care.

5. Evaluate accelerating activity intolerance.

6. Provide assistance with self-care activity as indicated, intersperse activity period with rest period.

7. Instruct client energy-conserving techniques.

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Comprehensive functional assessment includes independent performance of basic ADLs, social activities, sensory abilities, cognition and ability to ambulate.

May denote increasing cardiac decompensation rather than over activity.

Meets client’s personal care needs without undue myocardial stress or excessive oxygen demand.

Energy saving techniques reduced the energy expenditures, thereby assisting in

72

Pregnancy-Induced Hypertension: A Case Study equalization of oxygen supply and demand.

8. Encourage progressive activity when tolerated.

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Gradual activity intolerance progression prevents a sudden increase in cardiac workload.

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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

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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 ing 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!

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REFERENCES Black, J.M., Hawks, J. H. (2009). Medical-surgical 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. McGrawHill Professional. McCann, J. A., Holmes, H. N., Robinson, J.M., et al. (2003). Professional guide to pathophysiology. Springhouse, PA. Lippincott, Williams, & Wilkins. Nicoll, D., Mhee, S.J., Pignone, M., Chuanyi, M.L. (2007). Pocket guide to diagnostic tests: Lange clinical science series. Springhouse, PA. McGraw-Hill. Porth, Carol M., (2005). Pathophysiology: Concepts of altered health states. 7th Edition. Boston: Lippincott, Williams, & Wilkins.

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Stockley, R. A. (2007). Chronic obstructive pulmonary disease. Chicago, IL. WileyBlackwell. 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

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