INTRODUCTION

HYPERTENSION

Hypertension is one of the most common worldwide diseases

afflicting humans. Because of the associated morbidity and mortality and
the cost to society, hypertension is an important public health challenge.
Over the past several decades, extensive research, widespread patient
education, and a concerted effort on the part of health care professionals
have led to decreased mortality and morbidity rates from the multiple
organ damage arising from years of untreated hypertension.

Defining abnormally high blood pressure is extremely difficult and

arbitrary. Furthermore, the relationship between systemic arterial
pressure and morbidity appears to be quantitative rather than
qualitative. A level for high blood pressure must be agreed upon in
clinical practice for screening patients with hypertension and for
instituting diagnostic evaluation and initiating therapy. Because the risk
to an individual patient may correlate with the severity of hypertension,
a classification system is essential for making decisions about
aggressiveness of treatment or therapeutic interventions.

Based on recommendations of the Seventh Report of the Joint

National Committee of Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure (JNC VII), the classification of blood pressure
(expressed in mm Hg) for adults aged 18 years or older is as follows:

 Normal - Systolic lower than 120, diastolic lower than 80

 Prehypertension - Systolic 120-139, diastolic 80-99
 Stage 1 - Systolic 140-159, diastolic 90-99
 Stage 2 - Systolic equal to or more than 160, diastolic equal to or
more than 100

Non-modifiable risk factors for hypertension includes family history,

age in which primary hypertension typically appears between ages of 30-
50 years, gender in which overall incidence is higher in men than in
women until about the age 55 years and ethnicity where blacks are at
high risks.

On the other hand, modifiable factors includes diabetes, stress,

obesity, excessive sodium consumption and substance abuse such as
cigarette smoking, heavy alcohol consumption and some illicit drugs are
risks for having hypertension.
 This is based on the average of 2 or more readings taken at each of 2
or more visits after initial screening. Normal blood pressure with respect
to cardiovascular risk is less than 120/80 mm Hg. However, unusually
low readings should be evaluated for clinical significance.

Prehypertension, a new category designated in the JNC VII report,

emphasizes that patients with prehypertension are at risk for progression
to hypertension and that lifestyle modifications are important preventive
strategies. Hypertension may be either essential or secondary. Essential
hypertension is diagnosed in the absence of an identifiable secondary
cause. Approximately 95% of American adults have essential
hypertension, while secondary hypertension accounts for fewer than 5%
of the cases.

Blacks have a higher prevalence and incidence of hypertension than

whites. The prevalence of hypertension was increased by 50% in African
Americans. In Mexican Americans, the prevalence and incidence of
hypertension is similar to or lower than in whites. The National Health
and Nutrition Examination Survey (NHANES) III reported an age-adjusted
prevalence of hypertension at 20.6% in Mexican Americans and 23.3% in
non-Hispanic whites.

A progressive rise in blood pressure with increasing age is observed.

The third NHANES survey reported that the prevalence of hypertension
grows significantly with increasing age in all sex and race groups.
National health surveys in various countries have shown a high
prevalence of poor control of hypertension. These studies have reported
that prevalence of hypertension is 22% in Canada, of which 16% is
controlled; 26.3% in Egypt, of which 8% is controlled; and 13.6% in
China, of which 3% is controlled. Hypertension is a worldwide epidemic;
in many countries, 50% of the population older than 60 years has
hypertension. Overall, approximately 20% of the world's adults are
estimated to have hypertension. The 20% prevalence is for hypertension
defined as blood pressure in excess of 140/90 mm Hg. The prevalence
dramatically increases in patients older than 60 years.

HYPOKALEMIA

Potassium, the most abundant intracellular cation, is essential for

the life of the organism. Potassium is obtained through the diet, and
common potassium-rich foods include meats, beans, fruits, and potatoes.
Gastrointestinal absorption is complete, resulting in daily excess intake
of approximately 1 mEq/kg/d (60-100 mEq). Ninety percent of this excess
is excreted through the kidneys, and 10% is excreted through the gut.
Potassium homeostasis is maintained predominantly through the
regulation of renal excretion.
 Potassium is predominantly an intracellular cation; therefore,
serum potassium levels can be a very poor indicator of total body stores.
Because potassium moves easily across cell membranes, serum
potassium levels reflect movement of potassium between intracellular
and extracellular fluid compartments, as well as total body potassium
homeostasis.

Muscle contains the bulk of body potassium, and the notion that
muscle could play a prominent role in the regulation of serum potassium
concentration through alterations in sodium pump activity has been
promoted for a number of years. Insulin stimulated by potassium
ingestion increases the activity of the sodium pump in muscle cells,
resulting in an increased uptake of potassium. Studies in a model of
potassium deprivation demonstrate that acutely, skeletal muscle
develops resistance to insulin-stimulated potassium uptake even in the
absence of changes in muscle cell sodium pump expression. However,
long term potassium deprivation results in a decrease in muscle cell
sodium-pump expression, resulting in decreased muscle uptake of
potassium.

Thus, there appears to be a well-developed system for sensing

potassium by the pancreas and adrenal glands, resulting in rapid
adjustments in immediate potassium disposal and for long-term
potassium homeostasis. High potassium states stimulate cellular uptake
via insulin-mediated stimulation of sodium-pump activity in muscle and
stimulate potassium secretion by the kidney via aldosterone-mediated
enhancement of distal renal expression of secretory potassium channels
(ROMK). Low potassium states result in insulin resistance, impairing
potassium uptake into muscle cells, and cause decreased aldosterone
release, lessening renal potassium excretion.

In the general population, data are difficult to estimate; however,

probably fewer than 1% of people on no medications have a serum
potassium level of lower than 3.5 mEq/L. Potassium intake varies
according to age, sex, ethnic background, and socioeconomic status.
Whether these differences in intake produce different degrees of
hypokalemia or different sensitivities to hypokalemic insults is not
known. Up to 21% of hospitalized patients have serum potassium levels
lower than 3.5 mEq/L, with 5% of patients achieving potassium levels
lower than 3 mEq/L. Of elderly patients, 5% demonstrate potassium
levels lower than 3 mEq/L.

Hypokalemia generally is associated with higher morbidity and

mortality, especially due to cardiac arrhythmias or sudden cardiac death.
However, an independent contribution of hypokalemia to increased
morbidity/mortality has not been conclusively established.
 Patients who develop hypokalemia often have multiple medical
problems, making the separation and quantitation of the contribution by
hypokalemia, per se, difficult. Some suggestion is observed of increased
frequency of diuretic-induced hypokalemia in African Americans. The
higher frequency of hypokalemia in this group may be due to the lower
intake of potassium among African American men (approximately 25
mEq/d) than in their white counterparts (70-100 mEq/d).

Some suggestion also is observed of increased frequency of

diuretic-induced hypokalemia in women. With age, frequency increases,
due to increased use of diuretics and poor diet, which often is low in
potassium.

HYPONATREMIA

Serum sodium concentration and serum osmolarity normally are

maintained under precise control by homeostatic mechanisms involving
stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal
handling of filtered sodium. Clinically significant hyponatremia is
relatively uncommon and is nonspecific in its presentation; therefore, the
physician must consider the diagnosis in patients presenting with vague
constitutional symptoms or with altered level of consciousness.
Irreparable harm can befall the patient when abnormal serum sodium
levels are corrected too quickly or too slowly. The physician must have a
thorough understanding of the pathophysiology of hyponatremia to
initiate safe and effective corrective therapy. The patient's fluid status
must be accurately assessed upon presentation, as it guides the
approach to correction.

Though clearly not indicative of the overall prevalence

internationally, hyponatremia has been observed in as high as 42.6% of
patients in a large acute care hospital in Singapore and in 30% of
patients hospitalized in an acute care setting in Rotterdam.

Pathophysiologic differences between patients with acute and

chronic hyponatremia engender important differences in their morbidity
and mortality.

Patients with acute hyponatremia (developing over 48 h or less)

are subject to more severe degrees of cerebral edema for a given serum
sodium level. The primary cause of morbidity and death is brainstem
herniation and mechanical compression of vital midbrain structures.
Rapid identification and correction of serum sodium level is necessary in
patients with severe acute hyponatremia to avert brainstem herniation
and death.

Patients with chronic hyponatremia (developing over more than 48

h) experience milder degrees of cerebral edema for a given serum
sodium level. Brainstem herniation has not been observed in patients
with chronic hyponatremia. The principal causes of morbidity and death
are status epilepticus (when chronic hyponatremia reaches levels of 110
mEq/L or less) and cerebral pontine myelinolysis (an unusual
demyelination syndrome that occurs in association with chronic
hyponatremia).

The distinction between acute hyponatremia and chronic

hyponatremia has critical implications in terms of morbidity and
mortality and in terms of proper corrective therapy. Overall incidence of
hyponatremia is approximately equal in males and females, though
postoperative hyponatremia appears to be more common in menstruant
females. Hyponatremia is most common in the extremes of age; these
groups are less able to experience and express thirst and less able to
regulate fluid intake autonomously.

Objectives of the study

1. Gain knowledge about the pathophysiology of Hypertension and

electrolyte imbalances, what are the risk factors and how it is
treated.
2. Gain insights about its manifestations and etiology.
3. Be familiar with its possible complications
4. Be well versed with its management
5. Apply our learning to our nursing practice in the present and in the
future as well

Reasons for choosing the disease

1. To have a full understanding of this disease since it is very common

in the community
2. To determine the distinctions of this disease from other diseases
similar to it in terms of manifestations.
3. To evaluate if we became an effective health care providers to the
patient who suffered from this illness.
4. To established a comprehensive knowledge of this disease.
 5. We find it very interesting

NURSING PROCESS

Biographical Data

The name of the patient is Mr. Precious Brando, a 47 year-old,

male, born at Bagac, Bataan. He is Roman Catholic and a natural born
Filipino citizen, currently residing at Bagac, Bataan, with his wife and his
four children.

The patient works as a tricycle driver in their town. He works the

whole day and perspires a lot. According to his wife, Mr. Precious Brando
is a heavy drinker and a chronic smoker for almost 25 years. He
consumes almost 21 bottles of gin and 2 packs of cigarette sticks/day.
According to his wife, before the patient was diagnosed to have
Hypertension in 1990, he stops from eating high-salty foods. The wife
also stated that the patient is not fond of consuming fruits.
Pertinent Family History:

A. Genogram:
F + M

+ +


Legend:
 MALE

FEMALE

F FATHER

M MOTHER

 MR. DIABET

+ POSITIVE FOR HYPERTENSION

B. Narrative: As reflected in the genogram, the patient’s father

and his oldest sister also suffered from hypertension which
indicates that the said disease runs in their family. No other
disease was seen similar to the patient except from hypertension.

History of Past Illness

According to the patient’s wife, the patient has no known serious

illness, only occasional cough and colds.

History of Present Illness

The patient was diagnosed as having hypertension in the year

1990. He was able to control his high blood pressure by taking the
prescribed anti-hypertensive drug for 8 months which he could not
remember the name. However, the patient wasn’t able to comply with
his medication regimen and didn’t have follow up consultation because
of financial problem.
 Few days prior to patient’s admission, the patient experienced
headache, nausea and vomiting from unknown reasons, increase in his
blood pressure, muscle weakness and drowsiness. He was rushed in a
local hospital in Bagac and experienced seizures during his stay. They
were advised for transfer to another hospital for further management.

On September 01, 2009 at 3:05 pm, the patient was admitted to

the emergency department of Isaac and Catalina Medical Center (ICMC)
with chief complaints of increased in blood pressure and decrease
sensorium. The attending physician asked the patient’s relative
regarding the symptoms experienced by the patient and ordered a series
of diagnostic exams which include SGPT, H. pylori test, HCT, BUN, serum
creatinine, serum Na, serum K, Complete blood count, FBS, Chest X-ray,
cranial CT-scan, and RBS
 Normal Findings Abnormal Findings

PHYSICAL ASSESSMENT
Hair And Scalp
Vital Signs:
BP:160/100
Face and Skull
T: 35.9
Evenly distributed thick, silky, resilient hair. No
infection or infestation.
Rounded, smooth skull contour, absence of
nodules or masses, symmetric or slightly
P: 87 asymmetric facial features, symmetric facial
R: 15 movements
Skin From light to deep brown
Uniform in color
No edema lesions noted, no pigmentation
Brings back to previous state after pinching
Normal temperature @ 37C
Eyes Symmetrically aligned with equal movements Slightly yellowish sclera
Ears Symmetrical in shape and aligned in the outer
canthus of the eye
No tenderness, recoils after it is foiled
No discharge
Nose No discharge, no lesion and tenderness, no
obstruction
Lips No blister/cracks, moist
Tooth and gums Pink gums, not swollen Dark gums
Smooth and white shiny enamel Yellowish teeth
Tongue Centered, no lesions, smooth movement
Neck Equal in size, head centered with muscles
( trapezius and sternocleidomastoid) equal in
size
No unusual mass noted upon palpation
No enlargement of lymph nodes
Trachea is in midline position
No distention of veins, No enlargement of thyroid
gland
Thorax and Lungs Spine is vertically aligned, no tenderness, pain,
or unsual mass upon palpation
Tactile fremitus present
Clear breath sounds
Heart Has a regular rate and rhythm
Abdomen Unblemished skin
Uniform in color, no swelling or lump noted
Tympanic sound heard upon auscultation
Symmetric contour
Symmetric movements caused by respirations
No tenderness
Extremities No edema, deformities, tenderness noted Dirty fingernails
Have symmetrical lower and upper extremities
Clean fingernails and toenails
NEUROVITAL SIGNS MONITORING
Glasgow coma Scale:

Guidelines: 09/01/09 09/02/09

Eye opening 4 4
Motor response 6 6
Verbal response 4 5
Total DIAGNOSTIC EXAMS14 15

Laboratory Date Indications/ Normal values Results Interpretation

procedures ordered purposes
Results in
BLOOD CHEMISTRY DO: To determine any BUN:
09/01/09 abnormalities in 2.9-9.3 mmol/L 5.03 This is a normal
@ 3pm the chemical Creatinine: mmol/L finding
composition, 4-150 umol/L
structure, and S odium: 114.92 This is a normal
 properties of the 135-145 mmol/L umol/L finding
blood Potassium:
3.5-5.3 mmol/L 101.2 This indicates
mmol/L hyponatremia
This indicates
1.75 hypokalemia
mmol/L
HGT DO: HGT in mg/dl:
09/01/09 60-130 mg/dL 165
@ 3pm HGT in
mmol/dl: 9.07
3.3-7.2 mmol/dL
SGPT DO: 0.38 IU/L 23.2 IU/L
09/01/09

ASSURE TEST DO: To determine Negative Negative This is a normal

(Helicobacter pylori 09/01/09 presence H. pylori finding
Test) in the blood
HGT DO: HGT in mg/dl:
09/01/09 60-130 mg/dL 127 mg/dL This is a normal
@ 7:15 HGT in finding
pm mmol/dl: 7.0
3.3-7.2 mmol/dL This is a normal
mmol/dL finding
Hematology DO: To determine any WBC:
09/01/09 abnormalities in 5-10 x 10 g/l 8.7x10 g/l This is a normal
blood composition Hct: finding
such as WBS, 0.40 0.53
RBC, etc. Hgb:
120-170 175
Bleeding time:
1-5 mins n/a
Clotting time:
3-7 mins n/a
Reticulocyte:
0.5-1.5% n/a

Differential
Count
Segmenters: 0.84
0.50-0.70
Lymphocytes: 0.12
0.20-0.40
Bands/stabs: n/a
0-0.05
Eosinophils: 0.0-0.12
0.01-0.05
Monocytes: 0.04
0.01-0.08 This is a normal
Basophils: 0-0.12 finding
0-0.01
Platelet Count: 248x10g/l
150-450 x 10 g/l
Erythrocyte This is a normal
finding
BLOOD CHEMISTRY 09/02/09 To determine any FBS in mg/dl:
abnormalities in 70-105 129
the chemical FBS in mmol/L:
composition, 3.9-5.8 7.1
structure, and Cholesterol:
properties of the 3.1-7.3 3.4 mmol This is a normal
blood Triglycerides: finding
0.45-1.81 0.45 mmol
HDL This is a normal
0.78-195 0.78 mmol finding
LDL:
1.72-4.63 2.54 mmol This is a normal
Na: finding
135-145 n/a
K: This is a normal
3.5-5.5 n/a finding
Calcium:
2.1-2.8 1.75 mmol
Magnesium:
1.58-2.55 2.38 mmol

This indicates
hypocalcemia
ANATOMY AND PHYSIOLOGY

 Myocardi
um-
middle
layer
 Endocardi
um- inner
layer

Heart
Chambers
CARDIOVASCULAR  Atria- upper
SYSTEM – responsible receiving
for the transport of O2 chambers
and CO2, nutrients and  Ventricles- lower
waste products. pumping
chambers
I. Anatomy of the
Heart Heart Valves
AV Valves- between
Location: atria and ventricles
 Apex- left at 5th  Bicuspid- left AV
intercostals space valve
 Base-towards the  Tricuspid- right
nd
shoulder at 2 rib AV valve
Semilunar Valves
Coverings and walls  Pulmonic- at the
Pericardium- a pulmonary trunk
double layer sac  Aortic- at the
that encloses the aorta
heart Cardiac Circulation
 Coronary
Three layers
arteries-
 Epicardium- supplies blood to
outer layer the heart
II. Physiology of the
Heart

Conduction System of
the Heart

Two types of
controlling system
1. Autonomic
Nervous System
 Symphatetic
stimulation-
increases heart
rate
 Parasymphateti
c stimulation–
decreases heart
rate
2. Nodal System
 SA Node – atrial
contraction
 AV Node
 AV Bundle
 Bundle Branches
 Purkinje Fibers

CARDIOVASCULAR  Interna
SYTEM: THE BLOOD  Media
VESSELS  Externa

Arteries- carries blood Physiology of

away from the the heart Circulation
Veins-brings blood back Arterial Pulse –
to the heart alternating expansion
and recoil of an artery
Tunics
that occurs with each BP of below 100
beat of the ventricles mmHg
Hypertension-
Blood Pressure – 140/90 or higher
pressure the blood
exerts against the inner FLUID AND
walls of the blood ELECTROLYTE
vessels BALANCE
Fluid Compartments-
 Systolic main location of water
Pressure- the within the body
pressure in the
arteries at the Intracellular Fluid
peak of (ICF)- 2/3 of the body
ventricular fluids, contained within
contraction the living cells
 Diastolic
Pressure- the Extracellular Fluid
pressure when (ECF) – 1/3 of the body
the ventricles are fluids;all body fluids
relaxing outside the cells;
includes blood plasma,
Peripheral interstitial, CSF and
Resistance- amount of serous fluids
friction encountered by
a blood as it flows *Very small changes in
through the blood electrolyte balance, the
vessels solute concentration in
various fluid
Factors affecting compartments cause
Blood Pressure water to move from one
compartment to another
 Neural factors
 Renal factors
Sodium- the major
 Temperature
extracellular cation,
 Chemicals important for water
 Diet balance, conduction of
nerve impulse and
Variations in Blood muscle contraction
Pressure
Hypotension- Potassium- the major
low BP; systolic intracellular cation,
necessary for the
conduction of nerve
impulse and muscle
contraction

PATHOPHYSIOLOGY OF HYPERTENSION (client-centered)

Modifiable Non-modifiable
Age (30-50) Smoking
Gender (Male) Heavy alcohol
consumption

Vasoconstrictio
n

Narrowed
lumen

Increased peripheral
Decreased blood flow
resistance

Increased
Decreased O2 supply Decreased blood flow
intravascular
in muscle cells in the brain
pressure

BP of more than Muscle

120/90 weakness

Disorientati Irritabili Dizziness

on ty

SYNTHESIS OF THE DISEASE

 Factors that predisposed the client to
having hypertension includes age in which 30-50
years old are at high risks, being a male is also a
risk according to statistics. Smoking which has a
vasoconstrictive effect secondary to nicotine
content of cigarette played a significant role in
the pathogenesis of Hypertension. Likewise,
excess alcohol consumption may also increase
client’s risks.

Nicotine caused vasoconstriction and

consequently narrowing of the lumen of the
blood vessels. These both increases the
peripheral resistance which increases arterial
blood pressure and decreased blood flow which
deprived O2 to muscle cells causing muscle
weakness and to brain cells which can cause
disorientation and irritability.

PATHOPHYSIOLOGY OF HYPOKALEMIA AND HYPONATREMIA

(client-centered)
Modifiable
Factors
Poor intake
GI losses (vomiting)
Excessive
perspiration
Chronic alcoholism

Decreased Decreased
potassium in Sodium in
extracellular extracellular
fluid fluid

Decreased Osmotic shift of

depolarization water

Decreased
Intracellular
action potential
edema

Increased brain
Slowed smooth Decreased cell volume
Muscle
muscle neuronal
weakness
contraction excitability
Increased ICP

Nausea and Irritability

vomiting Dizziness
Disorientation Headache

Seizures
SYNTHESIS OF THE DISEASE

Factors that predisposed the client to

having electrolyte imbalances include poor
intake, GI losses (vomiting), excessive
perspiration and chronic alcoholism. These
factors caused decreased Sodium in extracellular
spaces leading to osmotic shift of water. Osmosis
can in turn result to increased intracellular
edema. The most sensitive cells are the
neurologic cells in the brain. Increased in the
volume of these cells causes increased ICP which
resulted to headache and seizure.

On the other hand, when there is

decreased potassium in extracellular spaces due
to the above factors, there will be a decreased
nerve conduction and muscle contraction. This
will lead to symptoms such as disorientation and
muscle weakness respectively. Slowed smooth
muscle contraction is also the reason for nausea
and vomiting.

SIGNS AND SYMPTOMS WITH ETIOLOGY

Headache – because of increased in intracranial

pressure caused by fluid shift

Seizures – increased ICP that exceeds seizure

threshold
Irritability, dizziness, disorientation –
caused by decrease Oxygen supply in the brain
or decreased nerve conduction

Nausea and vomiting – resulted from

decreased smooth muscle contraction

Muscle weakness – because of decreased

muscle contraction secondary to low levels of
potassium and sodium; caused also by
decreased Oxygen supplies to muscle cells