CHAPTER I

PRELIMINARY

1. BACKGROUND
Hypertension is a risk of premature morbidity and mortality, which
increases with increasing systolic and diastolic pressure. Emergency
hypertension occurs when elevated blood pressure should be decreased within 1
hour. This increased life-threatening acute blood pressure requires immediate
treatment in intensive care because it can cause serious damage to other organs
in the body.
Emergency hypertension occurs in patients with uncontrolled hypertension
or those who suddenly discontinue treatment. The presence of left ventricular
failure or brain dysfunction indicates a need for the need to lower blood pressure
immediately. This requires nurse care in handling the treatment.
Given the increase in blood pressure that can be life-threatening, the
authors are interested in preparing nursing care with this hypertension.

2. OBJECTIVE
A. General Purpose
To gain an understanding of the implementation of Nursing Care on
Hypertension.

B. Special Purpose
1) Can carry out assessment on clients with hypertension.
2) Can arrange nursing planning on clients with hypertension.
3) Can perform nursing actions on clients with hypertension.
4) Can carry out evaluation of nursing actions on clients with hypertension.
5) Can document the results of Care of Nursing properly and correctly.

3. WRITING METHOD
The techniques used to arrange it is by observation, interview, literature
study and collect some sources that can support in the elaboration of this paper.
 CHAPTER II
THEORY REVIEW

A. UNDERSTANDING
Hypertension can be defined as persistent blood pressure where the
diastolic pressure above 140 mmHg and diastolic pressure above 90 mmHg. In
the elderly population hypertension is defined as 160 mmHg systolic pressure
and diastolic pressure of 90 mmHg. Hypertension is a major cause of heart
failure, stroke, and kidney failure.

B. CLASSIFICATION
Blood pressure classification in adults aged 18 and above.

Category Systolic, mmHg Diastolic, mmHg

Normal <130 <85

Normal high 130-139 85-89

Hypertension

Stage 1 (light) 140-159 90-99

Stage 2 (medium) 160-169 100-109

160-209 110-119
Stage 3 (heavy)

Stage 4 (very heavy) ≥ 210 ≥ 120

C. PATHOPHYSIOLOGY
The mechanisms that control the contraction and relaxation of blood
vessels lie at the center of the vasomotor, the medulla in the brain. From this
vasomotor center begins the sympathetic nerve pathway, which continues
downward into the spinal cord out of the spinal column of the colullus to the
sympathetic ganglia in the thorax and abdomen. Vasomotor center stimulation is
delivered in the form of impulses that move downward through the sympathetic
nervous system to the sympathetic ganglia. At this point, the preganglion neuron
releases acetylcholine, which will stimulate the post-ganglion nerve fibers into the
blood vessels, which with the release of norepinephrine results in constriction of
blood vessels. Various fears and anxiety can affect the vascular response to
vasoconstrong stimulants. Individuals with hypertension are very sensitive to
norepinephrine, although it is not clear why this is possible.
At the same time that the sympathetic nervous system stimulates the blood
vessels in response to emotional stimulation, the adrenal glands are also aroused,
resulting in additional vasoconstraction activity. The adrenal medulla secretes
epinephrine, which causes vasoconstriction. The adrenal cortex secretes cortisol
and other steroids, which can strengthen the vasoconstrictor response of the blood
vessels. Vasoconstriction leading to decreased blood flow to the kidneys, resulting
in renin release. Renin stimulates the formation of angiotensin I which is then
converted into angiotensin II, a powerful vasoconstrictor, which in turn stimulates
aldosterone secretion by the adrenal cortex. This hormone causes an increase in
intravascular volume. All these factors tend to trigger the state of hypertension.
Gerontological Considerations. Structural and functional changes in the peripheral
vascular system are responsible for changes in blood pressure that occur in old age.
These changes include arterosclerosis, loss of elasticity of connective tissue, and a
decrease in relaxation of smooth muscle of blood vessels, which in turn decreases
the ability of distention and tensile strength of blood vessels. Consequently, the
large aorta and arteries decrease their ability to accommodate the volume of blood
pumped by the heart (stroke volume), resulting in decreased cardiac output and
increased peripheral resistance.