C.P.

Reyes Hospital
NURSING SERVICE DEPARTMENT

A
Case Presentation
On

HYPERTENSION

Station 3A and 4A Annex

May 2017
 NURSING SERVICE DEPARTMENT
HYPERTENSION

I. OBJECTIVE
The participant will be able to:

Describe diagnostic evaluation and admission criteria for patient

presenting with clinical features of Hypertension
Describe clinical significant and measurable treatment outcomes in
this patient population
Trace the pathophysiology of hypertension and enumerate the
different sign and symptoms of hypertension

II. DEMOGRAPHIC DATA

Name:JRA

Age:30 y/o

Address:Suplang, Tanauan City, Batangas

Birthdate:8/28/1986

Civil Status: Married

Religion: Roman Catholic

Citizenship: Filipino

Sex:Female

Chief Complaint:Headache

Admitting Physician: Dr. Apolonio Javier Jr.

Admitting Diagnosis:t/c Hypertension urgency

III. HISTORY OF PRESENT ILLNESS

Few hours PTA

(+) headache (occipital area)

 (+) weakness
(-) chest pain
(+) consult to emergency room

IV. PAST MEDICAL HISTORY

Prior to her hospitalization , she denies in having any record or medical

history of being admitted due to trauma, accident and disease. She also
denies having allergies to food and drugs.

Family Health History

The patient has family health history of hypertension on her mothers

side.

V. NURSING REVIEW OF SYSTEM

A. CENTRAL NERVOUS SYSTEM

Patient experienced seldom headache, she takes pain reliever and take

a complete bed rest to manage and relieve such disturbance. She also

experiences occasional uncoordinated movements.

B. RESPIRATORY SYSTEM

Patient experienced sore throat but was able to manage by eating

ginger or taking herbal medicine. She claims that it was a proven to be

effective on her because the soreness was relieved. She also claimed that

she had seasonal rhinitis especially when she inhales dust and strong odor

and seldom, she has runny nose when the weather changes especially

during cold days.

C. ENDOCRINE

She claimed that she has not experienced any signs of abnormalities.

Neither has she experienced goiter nor tumor nor some other alterations

related to the system involved.

D. GASTROINTESTINAL SYSTEM
 The patient experienced thirst and hunger like any other normal

person. She also experienced constipation and diarrhea. She experienced

hyperacidity whenever meals are not taken on time. She claimed to have

no allergies in any food and drugs.

E. MUSCULOSKELETAL SYSTEM

She experienced fatigue and muscle pains. She also claimed to have

experienced back pain and joints but relieved by self-massaging, resting

and taking pain reliever. The patient has an aged posture as observed.

F. GENITO-URINARY SYSTEM

She also claimed that her urination is normal as far as she can

remember and urinates frequently depending on the amount of liquid she

has taken in.

VI. PHYSICAL ASSESSMENT

Date Assessed: May 8, 2017

Time Assessed:9:00 AM

Vital signs: Blood Pressure: 140/90, Temperature: 36.7 C,

Pulse rate: 88bpm, Respiratory rate: 20 breaths/min

General appearance: The patient is awake, lying on bed,

conscious and coherent with an IVF of PNSS 1L to run for 16
hours on the right arm.

Anthropometric Data: weight 68kg, height 165cm BMI 24.9

Skin: warm to touch, no active dermatoses, no scars, no edema, no
pallor or jaundice.
Hair/Head: black smooth dry hair, no lice and nits, no abnormal
swelling
Face: symmetrical face, no abnormal facies, no deformities
Eyes: pinkish palpebral conjuctiva, no strabismus, no opacities, no
discharge, (+) ROR on both eyes, no periorbital edema
Ears and mastoids: no deformity, no redness or swelling of ear
canal, tympanic membrane intact
Nose and paranasal sinuses: no deformity, turbinates congested
and not hyperemic
 Mouth and throat: moist lips, pink and moist buccal mucosa, midline
uvula
Chest and Lungs: symmetrical chest expansion
Abdomen: soft, flat, symmetrical abdomen, normoactive bowel
sounds, tympanic, no mass, no tenderness
Extremities: no clubbing, no cyanosis, no swelling, no edema
Neurological Exam: GCS 15, active, Cranial Nerves: I. Turns head to
odor, II. Follows object with eyes, III. Both pupils constrict briskly,
reactive to light, direct and indirect reactions, III, IV, VI. No ptosis,
equal and complete opening of both eyes, V. Able to clench teeth,
VII. Can raise both eyebrows, frown and close eyes, VIII. Turns head
to sounds, IX, X. Uvula is midline, good swallow when drinking milk,
XI. Can turn head side to side, good sternocleidomastoid activity,
XII. Good tongue movements, no lateral deviation of tongue
Motor: Good motor activity was observed during examination
Sensory: Withdrawal when blunt object was stroked on the plantar
and palmar area

IX. Laboratory/ Diagnostic Examination

 Triglycerides are chemical compounds digested by the body to
provide it with the energy for metabolism. Triglycerides are the
most common form of fat in the body. Elevated triglyceride levels
may be a risk factor for atherosclerosis. Highly elevated triglyceride
levels may also cause fatty liver disease and pancreatitis.

High triglyceride levels can also be associated with diabetes, kidney

disease.

Very-low-density lipoproteins (VLDL) are complexes of lipids and

proteins assembled in the liver in response to nutrients and
hormones. When VLDL are secreted, they carry almost all of the
triglyceride in the blood-stream (they are about 85% triglycerides
themselves). Their function is to carry triglycerides from the liver,
possibly to avoid the development of fatty liver, taking them to the
peripheral tissues for storage in adipose tissue or for use in skeletal
muscle.

High levels of VLDL cholesterol have been associated with the

development of plaque deposits on artery walls, which narrow the
passage and restrict blood flow.
 Sodium is an essential electrolyte that helps maintain the balance of
water in and around your cells. Sodium is important for proper
muscle and nerve function. It also helps to maintain
stable blood pressure levels. Low blood sodium occurs when water
and sodium are out of balance.
Potassium is both an electrolyte and a mineral. It helps keep the water
(the amount of fluid inside and outside the body's cells) and
electrolyte balance of the body. Potassium is also important in how
nerves and muscles work.
 Leukocyte- esterase is an enzyme present in most white blood cells
(WBCs). A few white blood cells are normally present in urine and
usually give a negative chemical test result. When the number of
WBCs in urine increases significantly, this screening test will become
positive.
When this test is positive and/or the WBC count in urine is high, it may
indicate that there is inflammation in the urinary tract or kidneys. The
most common cause for WBCs in urine (leukocyturia) is a
bacterial urinary tract infection (UTI), such as a bladder or kidney
infection.
Blood - This test is used to detect hemoglobin in the urine
(hemoglobinuria). Hemoglobin is an oxygen-transporting protein found
inside red blood cells (RBCs). Its presence in the urine indicates blood
in the urine (known as hematuria).
Red Blood Cells (RBCs) - Normally, a few RBCs are present in urine
sediment (0-5 RBCs per high power field, HPF). A positive chemical test
for hemoglobin and an increase in the number of RBCs seen under the
microscope indicates that there is blood in the urine. However, this
test cannot be used to identify where the blood is coming from.
White Blood Cells (WBCs) - The number of WBCs in urine sediment is
normally low (0-5 WBCs per high power field, HPF).An increased
number of WBCs seen in the urine under a microscope and/or positive
test for leukocyte esterase may indicate
an infection or inflammation somewhere in the urinary tract.
Bacteria - Bacteria from the surrounding skin can enter the urinary
tract at the urethra and move up to the bladder, causing a urinary
tract infection (UTI). If the infection is not treated, it can eventually
move to the kidneys and cause kidney infection (pyelonephritis).
 VII. Medication
Name of Indication Contraindicati Adverse Nursing
Drugs on effect Consideration

Brand name: Used because -Heart failure -febrile

-Assess the patient
Plain NSS it has little to response,
-Pulmonary frequently.
no effect on
Other name: the tissues edema -infection at
0.9%Sodium and make the the site of -Look for signs and
Chloride - Renal injection, symptoms of
person feel Impairment
Solution hydrated dehydration or
-venous fluid overload. Two
Form: IV preventing - -Sodium thrombosis or
hypovolemic retention or more signs or
phlebitis symptoms indicate
Dosage: 1000 shock extending
ml to run for 16 or hypotensio a fluid imbalance.
from the site
hours n of injection,
-Document the
CLASSICFICATI - patient's weight
ON: Isotonic extravasation daily and keep an
Intravenous , accurate record of
 Solution -and intake and output
hypervolemia imbalance.
.
-Assess lung
sounds frequently
for crackles, which
could indicate fluid
overload. Also
assess skin turgor
and jugular vein
distension.

-Assess the I.V. site

frequently.

-Encourage oral
fluids, if
appropriate

Name of Indication Contraindicati Adverse Nursing

Drugs on effect Consideration

Generic name: Indicated in Pain, -Assess patients

Hypersensitivity
Ceftriaxone patients induration, previous sensitivity
with to phlebitis,
Brand name: reaction to penicillin or
neurologic rash, other cephalosphorins.
Ceftriax cephalosporins
complicatio diarrhea,
ns, carditis and related thrombocyt -Assess patient for
Classification:
3rd generation and antibiotics; osis, signs and symptoms
cephalosporin arthritis. It is leucopenia, of infection before and
also pregnancy glossitis, during the treatment.
Dosage: 2gms effective in (category B). respiratory
tiv once a day Gram super -Obtain c&s before
(8pm) after negative infections beginning drug
negative skin infections, therapy to identify if
test meningitis, correct treatment has
gonorrhea. been initiated.
It is also for -Repost signs such as
 bone joint petechiae, epistaxis or
infectious, other forms of
lower bleeding.
respiratory
-Monitor hematologic,
tract
renal, electrolytes and
infections,
hepatic function.
middle ear
infection,
PID, -Check for fever if
septicemia diarrhea occurs:
and UTI
Report both promptly.
The incidence of
antibiotic-produced
pseudomembranous
colitis is higher than
with most
cephalosporins.

-Inspect injection sites

for induration and
inflammation. Rotate
sites. Note IV injection
sites for signs of
phlebitis (redness,
swelling, pain).

Name of Indication Contraindicati Adverse Nursing

Drugs on effect Consideration

Contraindicated Monitor BP
Dizziness
Generic name: This with carefully
medication is
Clonidine hypersensitivity Orthostatic whendiscontinuing
used alone or
hypotension
Brand name: with other to clonidine or clonidine; hyperte
medications
Catapres any adhesive Somnolence ( nsion usually
to treat high
layer dose- returns within 48
Classification: blood
dependent)
pressure (hyp components of hr.
Alpha-agonist ertension)
the transdermal Xerostomia (d
hypotensive ag ry mouth)
ent
system. Take this drug
Headache
Dosage: Use cautiously exactly as
(dose-
75 mcg/tab, with severe dependent) prescribed. Do not
STAT dose
coronary miss doses. Do
Fatigue
insufficiency, not discontinue
recent Hypotension the drug unless so
MI, cerebrovasc instructed.
ular disease; chr
onic renal
Attempt lifestyle
failure;
changes that will
pregnancy,
reduce your blood
lactation.
pressure: Stop
smoking and
using alcohol; lose
weight; restrict
intake of sodium
(salt); exercise
regularly.

Report urinary
retention, changes
in vision,
blanching of
fingers, rash.

Name of Indication Contraindicati Adverse Nursing

Drugs on effect Consideration
 Hypersensitivity
Allergic
Generic name: Acute and to any reactions Assess patient for
chronic including
Etoricoxib component of signs and
treatment of rash, itching
the signs and this product. A and hives symptoms of
symptoms of
Brandname: history of infection before
osteoarthritis severe skin
and asthma, reactions, and during the
Arcoxia
rheumatoid urticarial or which may treatment.
arthritis occur without
other allergic warning
Dosage: Monitor
reactions after
management taste hematologic,
90mg/tab, 1 taking aspirin or
of ankylosing alteration
tab once a day renal, electrolytes
spondylitis other NSAIDs.
(8am)
wheezing and hepatic
function.
relief of congestive insomnia
chronic
musculoskelet heart failure. Take this drug
anxiety
al pain exactly as

hypertension drowsiness prescribed. Do not

relief of acute whose blood miss doses. Do
pain mouth ulcers
pressure is not discontinue
diarrhea the drug unless so
persistently
above 140/90 instructed.

mmHg and has

Report urinary
not been
retention, changes
adequately
in vision,
controlled.
blanching of
fingers, rash.
 Name of Indication Contraindicati Adverse Nursing
Drugs on effect Consideration

Generic name: In patients who Back pain;

Used to treat
high blood are
Losartan hypersensitive diarrhea; Monitor BP at drug
pressure
trough (prior to a
Brand name: (hypertension to any dizziness; scheduled dose).
). It is also component of symptoms of
Losartol used to lower upper
this product. Monitor drug
Classification: the risk of respiratory
effectiveness
stroke in tract infection
For
angiotensin II certain people (eg, cough,
receptor with heart coadministratio Inadequate
runny or
antagonists disease. n with aliskiren response may be
stuffy nose,
in patients improved by
sneezing,
Dosage: Losartan is splitting the daily
with diabetes. sore throat);
used to slow dose into twice-
50mg/tab, 1 tiredness.
long-term daily dose.
tab once a day kidney
(8am) damage in Lab tests: Monitor
people with CBC, electrolytes,
type 2 liver & kidney
diabetes who function with long-
also have term therapy.
high blood
pressure.
 Name of Indication Contraindicati Adverse Nursing
Drugs on effect Consideration

Hyperkalemia.
Generic name: Hypokalemia, Hyperkalemia Monitor I&O ratio
Chronic renal
including that , GI and pattern in
Potassium disease. Acute discomfort patients receiving
caused by
chloride and irritation, the parenteral
diuretics. dehydration.
Digitalis diarrhea, rash drug. If oliguria
Heat cramps. (rare). occurs, stop
intoxication
Brand name: without AV Severe tissue Tablets: infusion promptly
block. Esophageal and notify
K-lyte destruction. physician.
and GI
Adrenal ulceration,
bleeding, Monitor for and
insufficiency. report signs of GI
Dosage: obstruction,
perforation. ulceration
600mg/tab, (esophageal or
1tab TID x 6 Familial periodic
epigastric pain or
doses (8am, paralysis. hematemesis).
1pm, 8pm)
Acidosis
Be alert for
(potassium potassium
chloride intoxication
(hyperkalemia,
products). may result from
Alkalosis any therapeutic
dosage, and the
(potassium patient may be
bicarbonate asymptomatic.
products).
Tablets:
Esophageal
compression
due to enlarged
left atrium.

Decreased GI
motility.
 Name of Indication Contraindicati Adverse Nursing
Drugs on effect Consideration

Generic name: Assess patient for

Helps reduce mild stomach
Fenofibrate cholesterol Patients with pain; signs and
and severe renal
symptoms of
triglycerides impairment,
Brand name: (fatty acids) infection before
in the blood. Patients with back pain; and during the
Fenoflex High levels of active liver
these types of disease, treatment.
fat in the including those
Classification: blood are with primary headache; or Monitor
associated biliary hematologic,
antilipemics with an cirrhosis and
and fibric acid increased risk unexplained renal, electrolytes
of persistent liver and hepatic
runny or
atherosclerosi function
stuffy nose function.
Dosage: s (clogged test abnormaliti
arteries). es
160mg/tab, 1 Take this drug
tab ODHS
Patients with severe pain in exactly as
(9pm)
preexisting gallb your upper prescribed. Do not
Fenofibrate is ladder disease stomach
used to treat spreading to miss doses. Do
high Patients with your back, not discontinue
cholesterol known hypersen nausea and
and high sitivity to vomiting, fast the drug unless so
triglyceride fenofibrate or heart rate instructed.
levels. fenofibric acid
Report urinary
retention, changes
in vision,
blanching of
fingers, rash.
XI. ANATOMY AND PHYSIOLOGY

Anatomy and Physiology

When most people hear the term cardiovascular system, they immediately
think of the heart. We have all felt our own heart "pound" from time to
time, and we tend to get a bit nervous when this happens. The crucial
importance of the heart has been recognized for a long time. However, the
cardiovascular system is much more than just the heart, and from a
scientific and medical standpoint, it is important to understand why this
system is so vital to life.

Most simply stated, the major function of the cardiovascular system is

transportation. Using blood as the transport vehicle, the system carries
oxygen, nutrients, cell wastes, hormones, and many other substances vital
for body homeostasis to and from the cells. The force to move the blood
around the body is provided by the beating heart. The cardiovascular
system can be compared to a muscular pump equipped with one-way
valves and a system of large and small plumbing tubes within which the
blood travels.

HEART

The heart is a muscular organ found in all vertebrates that is responsible

for pumping blood throughout the blood vessels by repeated, rhythmic
contractions.
The heart is enclosed in a double-walled sac called the pericardium. The
superficial part of this sac is called the fibrous pericardium. This sac
protects the heart, anchors its surrounding structures, and prevents
overfilling of the heart with blood. It is located anterior to the vertebral
column and posterior to the sternum. The size of the heart is about the
size of a fist and has a mass of between 250 grams and 350 grams. The
heart is composed of three layers, all of which are rich with blood vessels.
The superficial layer, called the visceral layer, the middle layer, called the
myocardium, and the third layer which is called the endocardium. The
heart has four chambers, two superior atria and two inferior ventricles.
The atria are the receiving chambers and the ventricles are the
discharging chambers. The pathway of blood through the heart consists of
a pulmonary circuit and a systemic circuit. Blood flows through the heart
in one direction, from the atrias to the ventricles, and out of the great
arteries, or the aorta for example. This is done by four valves which are
the tricuspid atrioventicular valve, the mitral atrioventicular valve, the
aortic semilunar valve, and the pulmonary semilunar valve.
Systemic circulation is the portion of the cardiovascular system which
carries oxygenated blood away from the heart, to the body, and returns
deoxygenated blood back to the heart. The term is contrasted with
pulmonary circulation.

Pulmonary circulation

is the portion of the cardiovascular system which carries oxygen-depleted

blood away from the heart, to the lungs, and returns oxygenated blood
back to the heart. The term is contrasted with systemic circulation. A
separate system known as the bronchial circulation supplies blood to the
tissue of the larger airways of the lung.
Arteries

are blood vessels that carry blood away from the heart. All arteries, with
the exception of the pulmonary and umbilical arteries, carry oxygenated
blood.

Pulmonary arteries

The pulmonary arteries carry deoxygenated blood that has just returned
from the body to the heart towards the lungs, where carbon dioxide is
exchanged for oxygen.

Systemic arteries

Systemic arteries can be subdivided into two types muscular and elastic
according to the relative compositions of elastic and muscle tissue in
their tunica media as well as their size and the makeup of the internal and
external elastic lamina. The larger arteries (>10mm diameter) are
generally elastic and the smaller ones (0.1-10mm) tend to be muscular.
Systemic arteries deliver blood to the arterioles, and then to the
capillaries, where nutrients and gasses are exchanged.

The Aorta

The aorta is the root systemic artery. It receives blood directly from the left
ventricle of the heart via the aortic valve. As the aorta branches, and
these arteries branch in turn, they become successively smaller in
diameter, down to the arteriole. The arterioles supply capillaries which in
turn empty into venules. The very first branches off of the aorta are the
coronary arteries, which supply blood to the heart muscle itself. These are
followed by the branches off the aortic arch, namely the brachiocephalic
artery, the left common carotid and the left subclavian arteries.

Aorta the largest artery in the body, originating from the left ventricle of
the heart and extends down to the abdomen, where it branches off into
two smaller arteries (the common iliacs). The aorta brings oxygenated
blood to all parts of the body in the systemic circulation.

The aorta is usually divided into five segments/sections:

Ascending aortathe section between the heart and the arch of

aorta
Arch of aortathe peak part that looks somewhat like an inverted
"U"
Descending aortathe section from the arch of aorta to the point
where it divides into the common iliac arteries
o Thoracic aortathe half of the descending aorta above the
 diaphragm
o Abdominal aortathe half of the descending aorta below the
diaphragm

Arterioles

Arterioles, the smallest of the true arteries, help regulate blood pressure
by the variable contraction of the smooth muscle of their walls, and deliver
blood to the capillaries.
Veins are blood vessels that carry blood towards the heart. Most veins
carry deoxygenated blood from the tissues back to the lungs; exceptions
are the pulmonary and umbilical veins, both of which carry oxygenated
blood. Veins differ from arteries in structure and function; for example,
arteries are more muscular than veins and they carry blood away from the
heart.
Veins are classified in a number of ways, including superficial vs. deep,
pulmonary vs. systemic, and large vs. small.

Superficial veins

Superficial veins are those whose course is close to the surface of the
body, and have no corresponding arteries.

Deep veins

Deep veins are deeper in the body and have corresponding arteries.

Pulmonary veins

The pulmonary veins are a set of veins that deliver oxygenated blood from
the lungs to the heart.

Systemic veins

Systemic veins drain the tissues of the body and deliver deoxygenated
blood to the heart.
Atrium sometimes called auricle, refers to a chamber or space. It may be
the atrium of the lateral ventricle in the brain or the blood collection
chamber of a heart. It has a thin-walled structure that allows blood to
return to the heart. There is at least one atrium in animals with a closed
circulatory system.

Right atrium is one of four chambers (two atria and two ventricles) in the
human heart. It receives deoxygenated blood from the superior and
inferior vena cava and the coronary sinus, and pumps it into the right
ventricle through the tricuspid valve. Attached to the right atrium is the
right auricular appendix.

Left atrium is one of the four chambers in the human heart. It receives
oxygenated blood from the pulmonary veins, and pumps it into the left
ventricle, via the atrioventricular valve.
Ventricle is a chamber which collects blood from an atrium (another heart
chamber that is smaller than a ventricle) and pumps it out of the heart.
Right ventricle is one of four chambers (two atria and two ventricles) in
the human heart. It receives deoxygenated blood from the right atrium via
the tricuspid valve, and pumps it into the pulmonary artery via the
pulmonary valve and pulmonary trunk.

Left ventricle is one of four chambers (two atria and two ventricles) in the
human heart. It receives oxygenated blood from the left atrium via the
mitral valve, and pumps it into the aorta via the aortic valve.

XII. PATHOPHYSIOLOGY
Narrative Pathophysiology
Cardiac output and peripheral vascular resistance (PVR)

Cardiac output and PVR are two important factors that maintain normal
blood pressures and it has been suggested that increased cardiac output
resulting from sympathetic dysfunction is the trigger for the development
of HTN and increases in PVR is essentially the physiologic response to
accommodate change in pressure and maintain homeostasis.

Sympathetic nervous system

Over the last decade the role of SNS in the development and maintenance
of blood pressure has been studied exhaustively and it has been identified
that sympathetic stimulation of the heart, peripheral vasculature, and
kidneys, resulting in increased cardiac output, increased vascular
resistance, plus fluid retention is important in the development and
maintenance of this disease. As evidenced in the Coronary Artery Risk
Development in Young Adults (CARDIA) study, sympathetic overdrive is
often accompanied by low parasympathetic tone, which further
exacerbates the condition. Additionally, several studies have
demonstrated evidence of sympathetic over activity by documenting
increases in norepinephrine spill over in patients with HTN confirming that
sympathetic over activity is a core component in the pathophysiology of
this disease. The renal sympathetic nervous system is a major player in
the development and maintenance of HTN affecting blood pressure via two
pathways, namely, the efferent and afferent pathways. The efferent
pathway carries signals from the SNS to the kidney and increases renin
release thereby activating the RAAS system and increasing sodium and
water retention, all resulting in increased circulating volumes and
therefore increased blood pressures. In addition to the aforementioned
processes the efferent pathway also decreases renal blood flow and to
increase perfusion the kidney triggers the afferent pathway that carries
impulses to the SNS exacerbating sympathetic over activity and thereby
maintaining the high blood pressures.

Renin-angiotensin-aldosterone system (RAAS)

The RAAS system plays a major role in orchestrating the maintenance of

normal blood pressures and is activated by dual mechanisms, stimulation
of the SNS and glomerular under perfusion. These stimuli trigger the
release of renin from the juxtaglomerular apparatus which converts
angiotensinogen to inactive angiotensin I, the latter is further cleaved by
endothelium bound angiotensin converting enzyme (ACE) into angiotensin
II, the active component of this cascade and a potent vasoconstrictor.
Although this conversion of angiotensin I to angiotensin II was initially
believed to occur primarily in the lungs, it has since been established that
the process occurs practically in all tissues. In response to decreased salt
intake RAAS also triggers the release of aldosterone from the adrenal
glands that increases salt reabsorption coupled with water retention
resulting in further increase of blood pressure. Under these circumstances
one would expect that patients with HTN would invariably have high
circulating levels of renin and angiotensin II, however, studies have
demonstrated that plasma renin activity is increased in 15 percent
patients, normal in 60 percent patients, and reduced in approximately 25
percent patients. This can be reconciled by growing evidence for the
presence of local renin systems regulating regional blood flow that might
play an essential part in the pathophysiology of HTN.

Endothelial dysfunction

Whether endothelial dysfunction is a cause or an effect of hypertension is

debatable, nonetheless there is substantial evidence linking endothelial
dysfunction with hypertension. In fact, there is evidence of a positive
association between the degree of endothelial dysfunction and the
severity of hypertension. The major underlying mechanism for endothelial
dysfunction seen in HTN is the decrease in the availability of nitric oxide
(NO), a consequence of increased oxidative stress in these patients. To
this, extent although effective antihypertensive therapy restores impaired
nitric oxide production, endothelium dependent vasorelaxation continues
to be altered suggesting an irreversible course once HTN is established.
This evidence as well as studies demonstrating that inhibition of
endothelium-derived nitric oxide synthase (eNOS) results in hypertension
in humans, insinuates endothelial dysfunction as a potential aetiological
factor in the initiation of HTN. On the other hand the Multiethnic Study of
Atherosclerosis (MESA) showed that impaired flow-mediated dilation (FMD)
was not a significant independent predictor of the future development of
hypertension and Juonala et al demonstrated an association of higher
blood pressures in adolescence with endothelial dysfunction in adulthood.
In addition to NO other vasorelaxing factors such as arachidonic acid
metabolites, reactive oxygen species (ROS), vasoactive peptides and
microparticles of endothelial origin play important roles in maintenance of
vascular tone. Emerging data suggests that these factors contribute to
excessive vascular oxidative stress and vascular inflammation resulting in
endothelial dysfunction. In the recent years endothelial progenitor cells
(EPCs) that develop to form mature endothelial cells has been implicated
in the maintenance of arterial stiffness and as such are now considered as
determinants of endothelial function. Thus endothelial dysfunction is
multifactorial and a myriad of alterations in the vascular milieu lead to
structural and functional changes within the arteries and therapies
targeting key pathways involved in the process have shown to decrease
vascular remodeling, improve vascular function and therefore attenuate
overall cardiovascular risk.

Whilst due to its relevance endothelial function was initially measured in

the coronary arteries invasively using acetylcholine or other
pharmacologic flow manipulation, current methodologies include venous
plethysmography, digital pulse tonometery, laser Doppler flowmetry and
the most common high-resolution ultrasound. These methods have not
only made early identification of endothelial dysfunction possible and but
has also broadened the horizon of FMD in determining efficacy of
treatment and assessing prognosis in patients with HTN and
other cardiovascular diseases.

Vasoactive substances

Endothelin, a potent vasoconstrictor is one of the major substances

involved in maintaining vascular tone. Identified by Hickey et al in 1985, it
is secreted by endothelial cells and exerts its affects in a paracrine or
autocrine manner on vascular smooth muscle cells and counteracts the
relaxing activity of NO. Studies have demonstrated that both in animals
and humans infusion of endothelin-1 (ET-1) results in increased blood
pressures and blocking the system using antagonists reverts the
phenomenon. However, plasma levels of ET-1 are normal in patients with
essential hypertension suggesting that activity of this system might not
play a role in all types of HTN but rather in specific disease states such as
salt-sensitive HTN and renal HTN. Large clinical trials aimed at determining
both the importance of endothelin in the development and maintenance of
HTN and, ascertaining necessity of treatments targeted towards
maintenance of this system are warranted.

Bradykinin a vasodilatory peptide with autocrine and paracrine function

has long had an indirect association with HTN since apart from its direct
vasodilatory affects, bradykinin stimulates release of other vasoactive
substances like prostaglandins. This peptide from the kinin-kallikrein
system is shown to reduce blood pressures by vasodilation as well as
enhanced natriuresis and diuresis both achieved via increased renal blood
flow mediated by NO and prostaglandin release. Although vastly
overlooked due to side effects of coughing and angioedema the
hypotensive effects of ACE inhibitors is due to increased bradykinin levels
owing to its reduced degradation therefore therapies targeted directly at
bradykinin system are likely in the not so distant future.

Atrial natriuretic peptide (ANP) belongs to a family of structurally and

functionally related peptide hormones with cardio-renal functions. ANP
mediates its functions via membrane-bound guanylatecyclase linked
receptor (NPR-A), which further activates intracellular cGMP mediated
processes. Released from the atria in response to atrial distention
stemming from hemodynamic overload, ANP causes natriuresis and
diuresis resulting in modest reductions in blood pressures with
concomitant decreases in plasma renin and aldosterone. Thus, the
natriuretic peptide system by decreasing peripheral vascular resistance
balances the activity of the SNS and the RAAS system in maintaining blood
pressures.

The pathogenesis of primary hypertension, also known as essential

hypertension, is a highly complex and multifactorial interaction
between the environment and genetics. Combined, these increase
vascular tone (increased peripheral resistance), and blood volume,
thus resulting in sustained increases in blood pressure. Multiple
pathophysiologic mechanisms mediate these effects and include the
RAAS (Renin-Angiotensin-Aldosterone System), SNS (Sympathetic
Nervous System), natriuretic peptides and mutations in the gene
Adducin. Inflammation, endothelial dysfunction, obesity-related
hormones, and insulin resistance also contribute to both increased
peripheral resistance and increased blood volume.

Insulin Resistance:
Damage and dysfunction of endothelial cells results in decreased
production of vasodilators (nitric oxide), resulting in hypertension.
Insulin can increase blood pressure by activating the SNS, increasing
 renal sodium reabsorption, hypertrophy of resistance vessels, and/or
alteration of transmembrane ion transport. Conversely,
hypertension can cause altered delivery of insulin and glucose to
the skeletal muscle cells, leading to insulin resistance.

Natriuretic hormones (Adducin):

Modulate (lowers) renal sodium excretion, increasing vascular
resistance, leading to hypertension.

Overactive SNS:
Increased production of catecholamines (epinephrine and
norepinephrine) results in SNS overactivity. This results in an
increased heart rate, increased peripheral vascular resistance due to
systemic vasoconstriction, and hypertension. Additionally, an
overactive SNS effects insulin resistance, vascular remodeling, has
procoagulant effects, which can lead to neospasm and narrowing of
the blood vessels.

Pressure-Natriuresis Relationship Shift:

Commonly known as Shift in Pressure-natriuresis relationship.
Caused by increased vascular volume related to a decrease in renal
excretion of salt in the urine, leading to hypertension.

Inflammation:
Commonly known as Shift in Pressure-natriuresis relationship.
Caused by increased vascular volume related to a decrease in renal
excretion of salt in the urine, leading to hypertension.

Overactive RAAS:
Contributes to salt and water retention, leading to increased
vascular resistance and hypertension.

Mutation of the gene Adducin:

Adducin is an essential component of the sodium-potassium pump,
and mutations cause an increased tubular renal retention of sodium,
increasing vascular volume, causing hypertension.

PATHOPHYSIOLOGY OF PRIMARY HYPERTENSION

The hemodynamic hallmark of hypertension is persistently increased SVR.

Water and sodium retention: A high-sodium intake may activate a number of

pressor mechanisms and cause water retention.
Altered renin-angiotensin mechanism: High plasma renin activity (PRA) results
in the increased conversion of angiotensinogen to angiotensin I causing
arteriolar constriction, vascular hypertrophy, and aldosterone secretion.

Stress and increased SNS activity: Arterial pressure is influenced by factors

such as anger, fear, and pain. Physiologic responses to stress, which are
normally protective, may persist to a pathologic degree, resulting in
prolonged increase in SNS activity. Increased SNS stimulation produces
increased vasoconstriction, increased HR, and increased renin release.

Insulin resistance and hyperinsulinemia: Abnormalities of glucose, insulin, and

lipoprotein metabolism are common in primary hypertension. Additional
pressor effects of insulin include vascular hypertrophy and increased renal
sodium reabsorption.

Endothelial cell dysfunction: Some hypertensive people have a reduced

vasodilator response to nitric oxide. Nitric oxide, an endothelium-derived
relaxing factor (EDRF), helps maintain low arterial tone at rest, inhibits growth
of the smooth muscle layer, and inhibits platelet aggregation. Endothelin
produces pronounced and prolonged vasoconstriction.

Clinical Presentation

(Treatment and Procedures)

Signs and Symptoms:

Undiagnosed high blood pressure can lead to many physical problems

including damage to major organs over a period of time. The symptoms of
hypertension, if ignored, can lead to deterioration in kidney / liver function
and cardiac problems. Hypertension can also damage vision, cause strokes
and more.
 Here are some of the common hypertension symptoms to be aware of.

Recurrent / persistent headaches

Vision problems including blurring of vision
Giddiness
Convulsions
Tremors in the hands or other body parts
Walking difficulties (formally called ataxia)

Clinical Manifestations of Hypertension

Often called the silent killer because it

is frequently asymptomatic until it
becomes severe and target organ disease occurs.

Target organ diseases occur in the heart (hypertensive heart disease), brain
(cerebrovascular disease), peripheral vasculature (peripheral vascular
disease), kidney (nephrosclerosis), and eyes (retinal damage).

Hypertension is a major risk factor for coronary artery disease (CAD).

Sustained high BP increases the cardiac workload and produces left
ventricular hypertrophy (LVH). Progressive LVH, especially in association with
CAD, is associated with the development of heart failure.

Hypertension speeds up the process of atherosclerosis in the peripheral blood

vessels, leading to the development of peripheral vascular disease, aortic
aneurysm, and aortic dissection.

Intermittent claudication (ischemic muscle pain precipitated by activity and

relieved with rest) is a classic symptom of peripheral vascular disease
involving the arteries.
Hypertension is one of the leading causes of end-stage renal disease. The
earliest manifestation of renal dysfunction is usually nocturia.

The retina provides important information about the severity and duration of
hypertension. Damage to retinal vessels provides an indication of concurrent
vessel damage in the heart, brain, and kidney. Manifestations of severe retinal
damage include blurring of vision, retinal hemorrhage, and loss of vision.

Classification of Hypertension: WHO/ISH

Category Systolic Diastolic

Optimal < 120 <80

Normal <130 <85
High Normal 130-139 85-89

Grade 1 (mild hypertension) 140-159 90-99

Subgroup: borderline 140-149 90-94

Grade 2 (moderate hypertension) 160-179 100-109

Grade 3 (severe Hypertension) 180 110

Isolated Systolic Hypertension (ISH) 140 <90

Subgroup (borderline) 140-149 <90

World Health Organization ISH International Society of Hypertension

Category Systolic Diastolic

Optimal < 120 <80

Pre-hypertensive 120-139 80-89

Hypertensive 140 90

Stage 1 140-159 90-99

Stage 2 160 100

 National Institutes of Health Classification

Diagnostic Studies

Basic laboratory studies are performed to (1) identify or rule out causes of secondary
hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular
risk, or (4) establish baseline levels before initiating therapy.

Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to
screen for renal involvement and to provide baseline information about kidney
function.

Measurement of serum electrolytes, especially potassium levels, is done to detect

hyperaldosteronism, a cause of secondary hypertension.

Blood glucose levels assist in the diagnosis of diabetes mellitus.

Lipid profile provides information about additional risk factors that predispose to
atherosclerosis and cardiovascular disease.

ECG and echocardiography provide information about the cardiac status.

Treatment and Procedures

Nursing and Collaborative Management

Treatment goals are to lower BP to less than 140 mm Hg systolic and less than 90 mm
Hg diastolic for most persons with hypertension (less than 130 mm Hg systolic and
less than 80 mm Hg diastolic for those with diabetes mellitus and chronic kidney
disease).

Lifestyle modifications are indicated for all patients with prehypertension and
hypertension and include the following:

Weight reduction. A weight loss of 10 kg (22 lb) may decrease SBP by approximately
5 to 20 mm Hg.

Dietary Approaches to Stop Hypertension (DASH) eating plan. Involves eating several
servings of fish each week, eating plenty of fruits and vegetables, increasing fiber
intake, and drinking a lot of water. The DASH diet significantly lowers BP.

Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g of
sodium per day.

This involves avoiding foods known to be high in sodium (e.g., canned soups) and not
adding salt in the preparation of foods or at meals.

Restriction of alcohol

Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a day most
days of the week. Moderately intense activity such as brisk walking, jogging, and
swimming can lower BP, promote relaxation, and decrease or control body weight.
It is strongly recommended that tobacco use be avoided.

Stress can raise BP on a short-term basis and has been implicated in the development
of hypertension. Relaxation therapy, guided imagery, and biofeedback may be useful
in helping patients manage stress, thus decreasing BP.

Drug Therapy

Drug therapy is not recommended for those persons with prehypertension unless it is
required by another condition, such as diabetes mellitus or chronic kidney disease.

The overall goals for the patient with hypertension include (1) achievement and
maintenance of the goal BP; (2) acceptance and implementation of the therapeutic
plan; (3) minimal or no unpleasant side effects of therapy; and (4) ability to manage
and cope with illness.

Drugs currently available for treating hypertension work by (1) decreasing the volume
of circulating blood, and/or (2) reducing SVR.

Diuretics promote sodium and water excretion, reduce plasma volume, decrease
sodium in the arteriolar walls, and reduce the vascular response to catecholamines.

Adrenergic-inhibiting agents act by diminishing the SNS effects that increase BP.
Adrenergic inhibitors include drugs that act centrally on the vasomotor center and
peripherally to inhibit norepinephrine release or to block the adrenergic receptors on
blood vessels.

Direct vasodilators decrease the BP by relaxing vascular smooth muscle and reducing
SVR.

Calcium channel blockers increase sodium excretion and cause arteriolar vasodilation
by preventing the movement of extracellular calcium into cells.

Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of

angiotensin I to angiotensin II and reduce angiotensin II (A-II)mediated
vasoconstriction and sodium and water retention.

A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in
the walls of the blood vessels.

Thiazide-type diuretics are used as initial therapy for most patients with hypertension,
either alone or in combination with one of the other classes.

When BP is more than 20/10 mm Hg above SBP and DBP goals, a second drug should
be considered. Most patients who are hypertensive will require two or more
antihypertensive medications to achieve their BP goals.

Side effects and adverse effects of antihypertensive drugs may be so severe or

undesirable that the patient does not comply with therapy.

Hyperuricemia, hyperglycemia, and hypokalemia are common side effects with both
thiazide and loop diuretics.

ACE inhibitors lead to high levels of bradykinin, which can cause coughing. An
individual who develops a cough with the use of ACE inhibitors may be switched to an
ARB.
Hyperkalemia can be a serious side effect of the potassium-sparing diuretics and ACE
inhibitors.

Sexual dysfunction may occur with some of the diuretics. Orthostatic hypotension and
sexual dysfunction are two undesirable effects of adrenergic-inhibiting agents.

Tachycardia and orthostatic hypotension are potential adverse effects of both

vasodilators and angiotensin inhibitors.

Patient and family teaching related to drug therapy is needed to identify and
minimize side effects and to cope with therapeutic effects. Side effects may be an
initial response to a drug and may decrease with continued use of the drug.

Hypertensive crisis

Hypertensive crisis is a severe and abrupt elevation in BP, arbitrarily defined as a DBP
more than 140 mm Hg.

Hypertensive crisis occurs most often in patients with a history of hypertension who
have failed to comply with their prescribed medications or who have been
undermedicated.

Hypertensive crisis related to cocaine or crack use is becoming a more frequent

problem. Other drugs such as amphetamines, phencyclidine (PCP), and lysergic acid
diethylamide (LSD) may also precipitate hypertensive crisis that may be complicated
by drug-induced seizures, stroke, MI, or encephalopathy.

Hypertensive emergency develops over hours to days and is defined as BP that is

severely elevated (more than 180/120 mm Hg) with evidence of acute target organ
damage.

Hypertensive emergencies can precipitate encephalopathy, intracranial or

subarachnoid hemorrhage, acute left ventricular failure with pulmonary edema, MI,
renal failure, dissecting aortic aneurysm, and retinopathy.

Hypertensive emergencies require hospitalization, intravenous (IV) administration of

antihypertensive drugs, and intensive care monitoring.

Nursing Management

The primary nursing responsibilities for long-term management of hypertension are to

assist the patient in reducing BP and complying with the treatment plan. Nursing
actions include patient and family teaching, detection and reporting of adverse
treatment effects, compliance assessment and enhancement, and evaluation of
therapeutic effectiveness.

Patient and family teaching includes the following: (1) nutritional therapy, (2) drug
therapy, (3) physical activity, (4) home monitoring of BP (if appropriate), and (5)
tobacco cessation (if applicable).
FDAR

DATE/TIME FOCUS DATA/ACTION/RESPONSE

05/07/17 Risk for decreased cardiac
11:00 AM output related to increased
vascular vasoconstriction
D: Subjective Data: I do not
really feel well, right now.
My blood pressure is always
high and I feel light headed
when I
suddenly move. as claimed
by patient.

Objective Data:-Pale in color-

Skin cool and moist to
touch-Jugular vein can be
easily seen and bounding
upon palpation-Verbalized
light headedness on sudden
change of position-Easy
fatigability and occasional
dyspnic occurrences upon
exertion-Blood pressure
ranging from140/90 to
150/100 mmHg, BP as of
6:00 A.M. 04/17/12 is150/90
11:30 AM mmHg-Pulse rate of 110
beats per

A: Monitor blood pressure

periodically. Measure both
arms three times; 3-5 mins
apart while patient is at rest
for initial evaluation.
12:00 PM
Note presence
of,quality of central
and peripheral
pulses.
Auscultate heart
tones and breath
sounds

Observe skin color,

moisture,
temperature and
capillary refill time.
Note independent or
general edema
Provide a calm
environment;
minimizing noise;
 limiting visitors and
length of stay.
Maintain activity
restrictions (bed rest)
and assist patient
with self- care
activities.
Provide comfort
measures,
i.e.elevation of head
Encourage relaxation
techniques like
guided imagery and
distractions

Monitor response to
medications to
control blood
pressure

Administer
medications like
diuretics, alpha and
beta antagonists,
1:00 PM calcium channel
blockers, and
vasodilators.
Instruct and
implement to patient
dietary restrictions in
sodium, fat and
cholesterol
The patient will
participate in
activities that reduce
cardiac workload by

R:The patient will maintain

blood pressure within
acceptable range by

The patient will demonstrate

stable cardiac rhythm and
rate within patients
normal range by
Juan Dela Cruz, RN
 DATE/TIME FOCUS DATA/ACTION/RESPONSE
05/07/17 Difficulty in breathing D: Nahihirapan akong
11:00 AM huminga. As verbalized
by the patient. Rapid
breathing. Dyspneic. Vital
signs: T: 36.8C, P: 89bpm,
RR: 30cpm, BP: 130/80
mmHg
11:30 AM
A: Assisted patient into
moderate high back rest
position
Auscultated lung
fields, noting areas
of decreased or
absent airflow and
12:00 PM adventitious breath
sounds
Monitored rate,
rhythm, depth and
effort of
respirations
Encouraged deep
breathing exercises
Assisted patient in
coughing exercises
Increased fluid
1:00 PM intake as
appropriate

R: Patient was able to

demonstrate deep
breathing exercises every
1-2 hours during the day.
RR: 19 cpm

Juan Dela Cruz, RN

 DATE/TIME FOCUS DATA/ACTION/RESPONSE
05/07/17 Risk for Deficient Fluid D: Hindi siya
11:00 AM Volume nakakainom ng sapat na
dami ng tubig. As
verbalized by the
patients relative.
Decreased oral intake.
Vital signs: T: 36.8C, P:
88bpm, RR: 24cpm, BP:
1:30 PM 130/80 mmHg

A: Assessed vital signs

changes: increasing
temperature, tachycardia.
Assessed skin
turgor, moisture of
mucous
membranes
Checked IVF rate
Advised to eat
waterier content
foods
Monitored intake
and output (I&O),
noting color,
2:00 PM character of urine.
Calculate fluid
balance. Be aware
of insensible
losses.

R: Demonstrated fluid
balance evidenced by
 moist mucous
membranes, good skin
turgor, ans stable vital
signs.

Juan Dela Cruz, RN

DATE/TIME FOCUS DATA/ACTION/RESPONSE

05/08/17 Risk for Imbalanced D: Wala akong gana
8:00 AM Nutrition Less Than Body kumain ngayon. As
Requirements verbalized by the patient.
Abdominal distention/gas
associated with
swallowing air during
dyspneic episodes
9:00 AM
A: Assessed vital signs
changes
Monitored intake
and output
Schedule
respiratory
treatments at least
1 hour before
meals
Maintain adequate
nutrition, asked the
dietary department
 to provide a high-
calorie, high
protein diet
consisting of soft,
easy-to-eat foods.
Auscultate for
bowel sounds.
Observe for
abdominal
10:00 AM distention
Provide small,
frequent meals,
including dry foods
(toast, crackers)
and/or foods that
are appealing to
patient

R: Patient was able to

demonstrate increased
appetite. Maintain/regain
desired body weight.

Juan Dela Cruz, RN

DATE/TIME FOCUS DATA/ACTION/RESPONSE

05/08/17 Pain D:Reports continuous
8:00 AM
pain in the abdomen. (+)
Increased ureteral
contractions, (+) facial
grimace, (+) guarding
 behavior

Vital signs: T: 36.8C, P:

11:30 AM 89bpm, RR: 25cpm, BP:
130/80 mmHg, Pain scale
of 8/10
12:00 PM A: Encourage deep
breathing exercises and
relaxation techniques
12:15 PM Kept patient
comfortable and safe
such as back rub
BP monitoring q30
mins until stable
Provided quiet and
calm environment
Informed attending
1:00 PM physician re: patients
updated status
Reposition as
indicated such as
semi-fowlers and
lateral sims

R:Patient reports pain was

lessen. Pain scale of 5/10

Juan Dela Cruz, RN

DISCHARGE PLAN
Discharge Diagnosis: Hypertensive Urgency
Medications:
Advised to comply with all of the home medications.
Advised not to miss any doses.
Home medications instructed to patient.
Learn to take your own blood pressure. Keep a record of your results.
Take your blood pressure medicine exactly as directed. Don't skip
doses. Missing doses can cause your blood pressure to get out of
control.

Teachings:
 Encouraged to have a good sleeping time and adequate nutrition.

Reminded to always assess patients needs

Lifestyle changes

Maintain a healthy weight. Get help to lose any extra pounds.

Cut back on salt.
o Limit canned, dried, packaged, and fast foods.
o Don't add salt to your food at the table.
o Season foods with herbs instead of salt when you cook.
o Request no added salt when you go to a restaurant.
Begin an exercise program. Ask your doctor how to get started.
Simple activities like walking or gardening can help.
Limit drinks that contain caffeine (coffee, black or green tea, cola)
to 2 per day.
Control your stress. Learn stress-management techniques.
Limit alcohol to no more than 1 drink a day for women and 2 drinks
a day for men.

Hygiene:

Wash your hands

Washing your hands with a good antibacterial soap is essential for

removing harmful bacteria and germs that cause colds, flu, diarrhea and
other infections. Be sure to dry your hands properly and wash your hand
towels regularly.

Observation:

When to seek medical care

Call your doctor immediately or seek emergency care if you have any of
the following:

Chest pain or shortness of breath

Moderate to severe headache
Weakness in the muscles of your face, arms, or legs
Trouble speaking
 Extreme drowsiness
Confusion
Fainting or dizziness
Pulsating or rushing sound in your ears
Unexplained nosebleed
Weakness, tingling, or numbness of your face, arms, or legs
Change in vision
Blood pressure measured at home that is greater than 180/110

Diet:

a. Prescribed Diet: low salt, low fat

b. Restrictions:

Cut back on salt.

o Limit canned, dried, packaged, and fast foods.
o Don't add salt to your food at the table.
Limit drinks that contain caffeine (coffee, black or green tea, cola)
to 2 per day.

Follow-up care

Make a follow-up appointment as directed by attending physician.

BIBLIOGRAPHY

Smeltzer, Bare, Hinkle, and Cheever; Brunner and Suddarths TEXTBOOK

OF MEDICAL-SURGICAL NURSING; 11th ed. 2008
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Marieb, E. et al: ESSENTIALS OF ANATOMY AND PHYSIOLOGY, 6th edition,
Addison-Wesley Publishing Company Inc., America; 2005
Deluane and Landner et al: FUNDAMENTALS OF NURSING: Standards and
Practice, 3rd edition, Delmar learning, a division of Thomson Learning;
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Health Science Asia, 2004
Doenges, M. et al: NURSING CARE PLAN, 6th edition, F.A Davis Company,
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Gulanink and Myers et al NURSING CARE PLANS: Diagnosis and
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Singapore 239519, 2007
Doenges, Moorhouse, Murr, et al: NURSES POCKET GUIDE: Diagnoses,
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Philadelphia, Pennsylvania, 2008
Smith T. et al: THE HUMAN BODY: An Illustrated Guide to its Structure,
Function and Disorders, Dorling Kindersley Limited, London. 2000
Mosby E. et al: Pocket Dictionary of Medicine, Nursing and Health
Professions, 5th ed, 3 Killiney Road #08-01 Winsland House I Singapore
239519, 2006
Lippincott, William and Wilkins, et al: NURSING DRUG HANDBOOK, 23rd
edition, Wolters Kluwer Company, Philadelphia; 2005
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Delmar learning, a division of Thomson Learning, 2008
mims.com
ACKNOWLEGEMENT

We would like to express our deepest appreciation to all those who

provided us the possibility to complete this report. A special thanks goes
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We w o u l d l i ke t o t h a n k G o d a s fi n a l l y w e w e r e a b l e t o fi nish
our assignment that have been given to us. This task had been
done with all afford by group members even though a little bit problem
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