CHAPTER I

PRELIMINARY

A. Background

According to WHO, hypertension is an increase in systolic pressure

greater than or equal to 160 mmHg and or equal or greater than 95 mmHg
diastolic pressure. (Nasrin, 2003). In industrialized countries, hypertension is
one of the main health problems. In Indonesia, hypertension is also a health
problem that needs to be considered by doctors who work in primary health
services because of the high pre-valence rate and the long-term consequences
it causes.

Based on the cause, hypertension is divided into 2 groups, namely

primary hypertension with no known cause or idiopathic and secondary
hypertension, namely hypertension caused by other diseases. Primary
hypertension includes approximately 90% of all hypertensive patients and the
other 10% are caused by secondary hypertension. Only 50% of the secondary
hypertension groups can be identified, and from this group only a few percent
can be corrected. Therefore, efforts to treat primary hypertension get more
priority. Many studies have been carried out on primary hypertension both
regarding pathogenesis and its treatment.

B. Problem Formulation

1. What is the definition of hypertension in general?

2. Why can hypertension occur? What caused it ?

3. What are the types of hypertension?

4. What are the signs and symptoms of hypertension?

5. How to treat and prevent hypertension?

1
C. Purpose

The purpose of this paper is:

1. To help people know what hypertension is.

2. To find out the cause of hypertension.

3. To find out the types of hypertension.

4. Helps know the signs and symptoms of hypertension.

5. Helps know the treatment and prevention of hypertension.

D. Benefits

To give understanding to the community about hypertension, what are

the signs of symptoms, causes of hypertension and how to treat and prevent
it.

2
 CHAPTER II

THEORY REVIEW

A. Definition of Hypertension

Hypertension is defined as persistent blood pressure where the systolic

pressure is above 140 mmHg and diastolic pressure is above 90 mmHg.
(Smeltzer, 2001).

According to WHO, hypertension is an increase in systolic pressure

greater than or equal to 160 mmHg and or equal or greater than 95 mmHg
diastolic pressure. (Nasrin, 2003). Hypertension is defined by the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure JNC as a pressure higher than 140/90 mmHg and
classified according to its severity, has a range of high normal blood pressure
to malignant hypertension.

So it can be concluded that hypertension is a constant blood pressure

where the systolic pressure is above 140 mmHg and the diastolic pressure is
above 90 mmHg and is classified according to its severity, has a range of
normal blood pressure. Clinically the degree of hypertension according to
Rahardjo (2000) can be grouped according to the recommendations of "The
Sixth Report of the Join National Committee, Prevention, Detection and
Treatment of High Blood Pressure" (JNC VI) as follows:

No. Category Systolic(mmHg) Diastolic(mmHg)

1. Optimal <120 <80
2. Normal 120 – 129 80 – 84
3. High Normal 130 – 139 85 – 89
4. Hypertensi

Grade 1 (light) 140 – 159 90 – 99

3
No. Category Systolic(mmHg) Diastolic(mmHg)
Grade 2 (medium) 160 – 179 100 – 109

Grade 3 (weight) 180 – 209 100 – 119

Grade 4 (very heavy) >210 >120

B. Anatomy And Physiology

The cardiovascular system is a transport system that carries respiratory

gas, nutrients, hormones and other substances to and from the body's tissues.
The cardiovascular system is built by:

1. Heart

The heart is an organ consisting of muscles. Cardiac muscle is a

special network because it is seen from the same shape and arrangement as
the latitude muscle, but the way it works is the smooth muscle that is
beyond our will (influenced by the autonomic nervous system).

The shape of the heart resembles the heart of a banana, the upper part
is blunt (the base of the heart) and is called a cord base. At the bottom a bit
pointed called the cord apex.

The location of the heart in the front chest cavity (cavity the anterior
mediastinum), lower left of the mid chest cavity, above the diaphragm, and
the base is behind the left between costal V and VI two fingers below the
papilla of the mamae. In this place there is a heart that is called the cord
heart.

The heart size is about the size of your right hand and weighs
approximately 250 - 300 grams.

a. Heart Layer

4
 The endocardium is a layer of the heart which is located in the
very inner part which consists of endothelial tissue or lender membrane
lining the endothelial cavity or the lining of the lender that lines the
surface of the heart cavity. The myocardium is the core layer of the
heart consisting of the heart muscles, this heart muscle forms a bundle -
the muscle bundle that is

1) Bundle of atria muscle, which is on the left or right and base

2) The cord that forms a porch or cordic auricle.

3) The ventricular muscle bundle, which forms the heart chamber, is

removed from

4) The atrioventricular ring reaches the heart apex.

5) Bundal of ventricular muscle is a separation wall between spaces

6) Porch and heart chamber.

b. Heart valves

Inside the heart there are valves that are very important in blood
circulation and human heart movements.

1) Biscuspidal valvula, between the dextra atrium and the ventricles

2) Dextra consists of 3 valves.

3) The biscuspid vein, located between the left atrium and the ventricle

4) Sinistra has 2 valves.

5) Semilunaris vulva arterial pulmonary, located between the

ventricles dextra

6) With the pulmonary artery, where blood flows to the lungs.

5
 7) The semilunar vein of the aorta, located between the ventricular
sisnistra and the aorta

8) Precisely blood flows to the whole body.

c. Blood vessel

1) Arterial blood vessels

Arteries are the type of blood vessels that come out of the heart
that carries blood throughout the left ventricle called the aorta.
Arteries have 3 layers that are strong and thick but elastic and consist
of 3 layers.

a) Intima / internal tunica. Lapisa is at most in relation to blood and

consists of endothelial tissues.

b) Media tunika. The middle layer consists of muscle tissue which

consists of smooth muscle tissue.

c) External tunica / adventesia. The most extreme layer consists of

overtime connective tissue which strengthens the arterial wall.

d. Capillary

The capillary is a very small palpable blood vessel from the thinest
branch of the artery so that it is not visible except from under a
microscope. Forming capillaries in all body tissues. The capillary then
meets one another into a larger blood called a vein.

e. Veins (veins behind)

Veins bring dirty blood back to the heart Some important veins:

6
 1. Superior Vena cava

The vein that enters the right atrium carries dirty blood from
the head area, thorax and upper extremities.

2. Vena cava inferor

Veins that return dirty blood to the heart from all lower body
organs.

3. Vena cava jugularis

Veins that return dirty blood from the brain to the heart.
specifically the atrial delivery system to the ventricles is a 1/10
second slowdown between the pathway of the heart and atrium into
the ventricles. This allows the atrium to contract ahead of the
ventricle, the atrium works as a primary pump for the ventricles
and ventricles and then provides a major source of energy for the
movement of blood through the vascular system.

C. Hypertension Etiology

Based on the etiology, hypertension is divided into primary

hypertension and secondary hypertension.

1. Primary Hypertension

More than 90% of cases of hypertension have unclear causes, and

are called primary hypertension or essential hypertension. Primary
hypertension is a multifactorial genetic disease, which means that the
reduction of abnormal genes in an individual will increase the likelihood
that the person is suffering from hypertension, plus the presence of
environmental factors and lifestyle such as excessive salt consumption and
psychosocial stress. The genes involved in this process have not been
identified, so the determination of the mechanism of the occurrence of

7
 hypertension is more focused on revealing functional disorders that occur
due to hypertension. (Aaronson, Ward, Wiener, Schulman, Gill, 2007).

2. Secondary Hypertension

Less than 10% of cases of hypertension can be identified as the

cause and are called secondary hypertension. The most common causes of
secondary hypertension include: (a) renovascular disease, disrupting fluid
regulation and / or activating the renin-angiotensin-aldosterone system
(RAA), (b) endocrine disorders, usually in the adrenal cortex and
associated with excessive secretion of aldosterone, cortisol, and / or
catecholamines, (c) oral contraception, which results in an increase in
blood pressure through RAA system activation and hyperinsulinemia.
(Aaronson, Ward, Wiener, Schulman, Gill, 2007).

D. Pathophysiology of Hypertension

Blood pressure is a complex trait that is determined by the interaction

of various factors such as genetic and environmental factors that influence
two hemodynamic variables namely cardiac output and total peripheral
resistance (Robbins et al., 2007). Cardiac output is a factor that determines
the value of systolic blood pressure and total peripheral resistance determines
the value of diastolic blood pressure. An increase in blood pressure can occur
due to an increase in cardiac output and / or an increase in total peripheral
resistance (Saseen and Maclaughlin, 2008).

The kidneys have a role in controlling blood pressure through the renin-
angiotensin-aldosterone system. The mechanism for regulating blood pressure
by the kidneys can be seen in Figure 1.

8
 Renin produced by the kidney justaglomerulus cells converts
angiotensinogen to angiotensin-1, then angiotensin-1 is converted to
angiotensin-2 by angiotensin converting enzyme (ACE). Angiotensin-2 can
bind to angiotensin-2 type 1 (AT1) or angiotensin-2 type 2 (AT2) receptors.
AT1 receptor stimulation can increase blood pressure through pressor effects
and blood volume (Saseen and Maclaughlin, 2008).

The effects of pressor angiotensin-2 include vasoconstriction,

stimulation of catecholamine release from the adrenal medulla, and increased
activity of the sympathetic nervous system (Saseen and Maclaughlin, 2008).
In addition, angiotensin-2 stimulates synthetic aldosterone from the adrenal
cortex which causes sodium and water retention.

This sodium and water retention results in an increase in blood volume,

an increase in total peripheral resistance, and finally an increase in blood
pressure (Saseen and Maclaughlin, 2008; Saseen, 2009).

9
 Blood pressure is also regulated by the adrenergic nervous system
which can cause contractions and relaxation of blood vessels. The stimulation
of α-2 receptors in the sympathetic nervous system causes a decrease in the
work of the sympathetic nerve which can reduce blood pressure. Peripheral α-
1 receptor stimulation causes vasoconstriction which can increase blood
pressure. Β-1 receptor stimulation in the heart causes an increase in heart rate
and contractility, whereas β-2 receptor stimulation in the arteries and veins
causes vasodilation (Saseen and Maclaughlin, 2008; Saseen, 2009).

E. Clinical Manifestations

1. Physical examination may show no abnormalities other than high blood

pressure.

2. Retinal changes may occur with hemorrhage, exudates, arteriole

narrowing, and papillary edema.

3. Symptoms usually show vascular damage associated with the organ

system that is caused by the affected blood vessels.

4. Coronary artery disease with angina is a common result.

5. Pathological changes in the kidneys (nocturia and azotemia).

6. Left ventricular hypertrophy occurs; heart failure.

7. Cerebral vascular involvement and transient ischemia (Baughman, Diane

C, 2000).

F. Complications of Hypertension

Hypertension that occurs over a long period of time will be dangerous,

causing complications. These complications can attack various target organs,
namely the brain, eyes, heart, arteries and kidneys. As a result of the

10
occurrence of hypertension complications, the quality of life of patients
becomes low and the worst possibility is the occurrence of death in patients
due to complications of hypertension they have.

Hypertension can cause damage to organs, both directly and indirectly.

Several studies have found that the cause of damage to these organs can be
through direct consequences of increased blood pressure in the organs, or
because of indirect effects, including the presence of autoantibodies against
angiotensin II receptors, oxidative stress, down regulation, and others. Other
studies have also shown that a high-salt diet and sensitivity to salt play a
major role in the emergence of target organ damage, such as damage to blood
vessels due to increased expression of transforming growth factor-β (TGF-β).

Generally, hypertension can cause damage to organs, both directly and

indirectly. Organ damage commonly found in hypertensive patients is:

1. Heart

 left ventricular hypertrophy

 myocardial angina or infarction

 heart failure

2. Brain

 stroke or transient ishemic attack

3. Chronic kidney disease

4. Peripheral artery disease

5. Retinopathy

11
G. Management

1. Non-pharmacological management or live smokers

Reducing salt intake and the effort needed is the first step in the
treatment of hypertension. Limiting salt intake to 60 mmol / day, means
not adding salt when eating. It will be difficult because it will reduce salt
intake tightly and will drastically affect the patient's routine.

At some stage it is found that a low-fat diet can reduce the risk of
cardiovascular disease. By doing activities you can access prisoners.

Lifestyle influences such as smoking, drinking alcohol,

hyperlipidemia, stress. Can be used to improve health levels. Relaxations
such as meditation, yoga or hypnosis can control the autonomous system
as possible.

2. Pharmacological management or treatment of hypertension

The decision to start giving antihypertensive drugs based on factors

such as blood elevation, target organ damage and clinical manifestations of
cardiovascular disease or other risk factors. or 95 mmHg and systolic
above 130 to 139 mmHg it is necessary to start drug therapy. (Smeltzer,
2001) Types of hypertension drugs are as follows:

a. Diuretics

The way this drug works is by increasing the volume of urine and
removing sodium (salt) through the urine. The diuretic drug commonly
given is thiazide. Side effects of the occurrence of "gout" and sugar
levels in DM slightly increase.

b. Beta Bloker

Works by inhibiting the work of stress hormones, namely

adrenaline against the heart and blood vessels. Side effects of feeling

12
 tired and lethargic, weak legs and cold hands. Which include
asebutolol, alprenolol, propanolol, timolol, pindolol, etc.

c. Calcium antagonists

Calcium antagonists work by reducing the amount of calcium that

enters muscle cells in the blood vessel and heart walls and reduces
muscle tension. This reduced muscle tension causes blood pressure to
drop. Side effects are headache, red face and ankle swelling. This class
of drugs such as nifedipine, diltiazim, verapamil, amlodipine, felodipine
and nicardipine.

d. Angiotensin converting enzyme inhibitors (ACE inhibitors). ACE

inhibitors inhibit the substances produced by the kidneys, which are
responsible for narrowing the small arteries. Side effects: a drastic drop
in blood pressure, tingling and coughing disturbances. for example
losartan, valsartan and irbesartan.

e. Vasodilator

Work by dilating the arteries directly. Side effects of vasodilator

slightly increase heart rate and cause swelling of the ankles. Included in
this group are doksazosin, prazosin, hydralazine, minoxidil, diazoside
and sodium nitroprusid.

f. Sympathetic inhibitors

Inhibition of sympathetic activity can occur in the vasomotor center

of the brain as in methyldopa and clonidine or at peripheral nerve
endings such as reserpine and guanetidine.

13
H. Supporting Examination

Investigations for clients with hypertension are as follows:

1. Hematocrit

In patients with hypertension hematocrit levels in the blood increases

with increasing levels of sodium in the blood. Hematocrit examination is
also needed to follow the development of hypertension treatment.

2. Serum potassium

Increased serum calcium levels can increase hypertension

3. Serum creatinine

The results obtained from the examination of creatinine is increased

creatinine levels in the blood, which has an impact on kidney function.

4. Urinalisa

Blood, protein, glucose indicate kidney dysfunction and / or diabetes.

5. Electrocardiogram

Left ventricular enlargement and cardiomyegaly can be detected by

this examination. It can also describe whether hypertension has been
ongoing for a long time.

14
I. DIAGNOSIS AND NURSING INTERVENTIONS

1. Assessment

The study was conducted on May 9, 2012 on B11 multazam ward,

PKU Muhammadiyah Surakarta Hospital. Data obtained from patients,
families, and medical records.

a. Patient's self identity

Mr. H, Age 60 years, male sex. Address betongan, 01/07, mangu,

ngemplak, boyolali, marital status is married, Islam, Javanese tribe,
elementary education, work as a farmer, No. RM 068309, Medical
diagnosis of hypertension.

b. Main complaint The patient complains of headache. Current medical

history before being taken to the hospital, the patient complained that his
head was dizzy, the client said the pain was throbbing and stiff neck, the
pain came at any time, the client seemed to hold his head, before the
client had been treated by a shaman but there was no change, the client
also said pain the joints and vision are blurred, the client wonders about
the disease, and at this time the disease that is felt by the client is
hypertension. Then by Mr. H immediately brought to PKU
Muhammadiyah Surakarta Hospital to get further treatment. Previous
medical history 3 months ago Mr. H ever felt dizziness, joint pain and
itching.

15
 2. Nursing diagnoses

a. Data Analisys

No. Data Etiology Problem

1. DS: Large arteries Pain relief disorder

- Client says headache

lose flexibility and
- The client said a
become stiff
throbbing headache

- The client say sick

comes at times blood vessels cannot
expand
- The client of his
vision blurred

DO: vascular
vasocontriction
- Clients often seem to
hold the term.

- The client looks blood pressure

weak Pain scale 5

- TD: 160/90 mmHg

increased cerebral
- N: 87x / minutes vasculer pressure

- RR: 20x / minutes

- BB: 45 kg

2. DS : Hypertension Lack of knowledge

- Client say doesn’t

know about
Lack of information
hypertension

16
No. Data Etiology Problem
- Client does not know about disease
the cause of
hypertension

- The client said eating

the same food as his
family

DO :

- The client asks about

the disease

- TD : 160/90 mmHg

- Pulse : 87x/ minutes

- RR : 20x/ minutes

- T : 36,70C

- Weight : 45 kg

3. DS : Lifestyle Risk of excess volume

of fluid
- The client said the
was not happy to
Hypertention
eat without salt

DO :
renal vasocontriction
- TD : 160/90
mmHg

- Pulse : 87x/ menit decrease in blood flow

17
No. Data Etiology Problem
- RR : 20x/ menit

- T : 36,70C increase in aldosterone

- weight : 45 kg

Retention Na

Edema

b. Formulation of The Problem

Based onthe analysis of the data that the author obtained, the
priority of the problem that can be enforced;

1) pain relief is associated with an increase in cerebral vascular pressure.

2) Lack of knowledge is related to lack of information about disease and

therapy.

3) The risk of excess fluid volume is related to edema.

3. Intervention

No. Diagnosa Aim Intervention Rational

1. 1 After nursing action 1. Review the 1. General
for 2 X 60 minutes general condition shows
can control the pain condition of the client’s
or headache lost or the patient. condition as a
reduced by the result whole and to
criteria : know vital

18
 - The client does signs
not reveal any
2. To find out the
pain or headache.
pain level of the
2. Review the
- Client looks client
client’s pain
comfortable.
level.
- Vital signs are
within normal
limits. 3. To find out the
pain that is felt
3. Review the
location of
pain intensity
and scale.

4. Analgesic can

4. Collaboration reduce pain

administering
analgesic
drugs as
indicated
2. 2 After nursing action 2 1. Explain about 1. Provide a basis
X 60 minutes the the normal for
patient is expected to blood understanding
know information pressure, high of increased
about hypertension blood pressure blood pressure
with outcome criteria: limit and
2. So that clients
effect
The client expresses know and help
knowledge of with continued
hypertension treatment
2. Explain the
nature of the 3. So client can

19
 disease and control stress
the purpose of
the treatment
and procedure

3. Explain the
importance of
a quite
environment
3. 3 After nursing action 2 1. Review the 1. Decreased renal
X 60 minutes the client’s diet or flow resulting
patient is expected diet against in antidiuritic
that there will be no inadekuat increases
excess volume of protein intake leading to water
fluid with outcome and sodium
criteria: retention
2. Send the
No edema 2. An increase in
client to
sodium levels
Normal BB decrease the
in the blood can
salt input
Normal breath and cause edema
heart sounds
3. Skin edema,
3. Take can be easily
measures to injured and dry
protect the skin is more
body from prone to
injury and damage and
edema injurry

CHAPTER III

20
 COVER

A. Conclusion

Hypertension is a constant blood pressure where the systolic pressure is

above 140 mmHg and the diastolic pressure is above 90 mmHg and is
classified according to its severity, has a range of normal blood pressure. Based
on the etiology, hypertension is divided into primary hypertension and
secondary hypertension.
Hypertension that occurs over a long period of time will be dangerous,
causing complications. These complications can attack various target organs,
namely the brain, eyes, heart, arteries and kidneys.

B. Suggestions

People should be aware of their health such as diet and regular exercise.
Because this hypertensive disease can attack all ages and for treatment is
carried out for a lifetime.

Index

21
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Cardiovaskuler System At A Glance.UK: Blackwell Science
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Robbins S.P, dan Judge,2008. Perilaku Organisasi, Jakarta: Salemba Empat

Hal)256(

Robbins S.P, dan Judge,2002. Perilaku Organisasi, Jakarta: Salemba Empat Hal
284

Robbins S.P, at al, 2006. Perilaku organisasi ed 12, Jakarta : Salemba Empat Hal
283

Rahardjo, 2000. Penyakit Gagal Ginjal Kronik, Buku Ajar Ilmu Penyakit Dalam
Jilid II Edisi III. Jakarta :BPFKUI

Saseen, J.J., & Maclaughlin, E.J., Cardiovaskuler Disorder: Editor : Dipiro JT

Talbert., R.L.Yee, G.C., Matzke, G.R Wells, B.G., Posey, L.M,
Pharmachotherapy A Phatophyisilogical Approach, Seventh Edtion,
New York : Mcgraw-Hill Medical Publishing Division

22