A.

Concept Of Diseases
1. Anatomy And Physiology Of

1.1. The Brain

Brainbrain is divided into three major parts: cerebrum, brain stem, and
cerebellum. All are in one part of the bone structure called the skull, which
also protects the brain from injury. Four bones that relate to form skull bones:
frontal, parietal, temporal and occipital bones At the base of the skull are three
parts of the fossa. The anterior fossa section contains the cerebral frontal lobes
of the hemisphere; the middle part of the fossa contains the parietal, temporal
and occipital lobes and the posterior fossa section contains the brain stem and
medulla. Another opinion suggests, the brain is a very important body tool
because it is a computer center of all body organs, part of the central nerve
located in the skull cavity (cranium) is wrapped in a strong brain membrane.
● Cerebrum The cerebrum
consists of two hemispheres and four lobes. Grafty substancia is
found on the outer wall of the cerebrum and white matter covering the
inner cerebral wall. In principle, the composition of gray matter formed
from nerve cell bodies meets the cerebral cortex, nucleus and basal
ganglia. The substance of alba consists of nerve cells that connect parts of
the brain with other parts. Most cerebral hemispheres (telensefalon)
contain central nervous system tissue (CNS). This area controls the
highest motor function
 The Cerebrum
stemstem is located in the anterior fossa. The parts of the brain
stem consist of the midbrain, pons and medulla oblongata. The midbrain
(midbrain or mesensefalon connects the pons and cerebellum to the
cerebral hemisphere. This section contains sensory and motor pathways
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 and is the center of the auditory and visual reflexes. The pons are located
in front of the cerebellum between the midbrain and medulla and are
bridges between the two parts of the cerebellum, and also between
medulla and cerebellum Pons contain sensory and motor pathways.The
medula
oblongata transmits motor fibers from the brain to the spinal cord
and sensory fibers from the spinal cord to the brain and these fibers cross
in this area.The pons contain the most important centers in controlling the
heart, breathing and blood pressure and as the origin of the fifth to eighth
● The cerebellum
cerebellum of the cerebellum lies in the posterior fossa and is
separated from the cerebral hemisphere, folds of the dura mater, tentorium
of the cerebellum.The cerebellum has two actions which are stimulating
and inhibiting and broad responsibilities towards coordination and smooth
movements, plus me control the correct movement, balance, position and
integrate inputsensory".
1.2. Cerebral Circulation
circulation receives approximately 20% of the heart or 750 ml per minute.
This circulation is needed, because the brain does not store food, while having
high metabolic needs. This brain blood flow is unique, because it is against the
direction of gravity. Where arterial blood flows from the bottom and the veins
flow from above. Lack of additional collateral blood flow can cause
irreversible tissue damage; this is different from other body organs that
quickly tolerate when blood flow decreases due to adequate collateral flow.
● Arteries
blood supplied to the brain comes from two internal carotid
arteries and two vertebral arteries and extends to the branching system.
The internal carotid is formed from the branching of two carotides and
gives the anterior brain blood circulation. The vertebral arteries are
branches of the subclavian artery, flowing backwards and rising on one
side of the vertebrae vertically and entering the skull through the foramen
magnum. Then interconnected into the basilar artery in the brain stem.
Vertebrobasilary arteries supply blood to the posterior brain most. The
basilar artery divides into two branches in the posterior cerebral artery.
● Willisi Circles

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 At the base of the brain around the pituitary gland, a circle of
arteries forms between a series of internal and vertebral carotid arteries.
This circle is called theWillisi circuswhich is formed from the branches of
the internal carotid artery, anterior and middle cerebral arteries, and the
anterior and posterior connecting arteries. Blood flow from the Willisi
circulation directly affects the anterior and posterior circulation of the
cerebral, the arteries in the circular Willis provide an alternative route in
the bloodstream if one of the major arterial roles is blocked.
Arterial anastomosis along the circular Willis is an area that often
has aneurysms, may be congenital. Aneurysms can occur when blood
pressure increases, which causes the artery wall to balloon out like a
balloon. Aneurysms that are close to the cerebral structure can cause
cerebral structural suppression, such as an emphasis on optical properties
that cause visual disturbances. If the artery is blocked due to vascular
spasm, embolism, or due to thrombus, can cause blockage of blood flow
to the distal neurons and this results in rapid neuronal cells necrosis. This
situation results in stroke (cerebrovascular injury or infarction). The effect
of blood vessel obstruction depends on the blood vessels and on the
affected brain area.
● Venous
flow for the brain does not accompany arterial circulation as in
other organ structures. Veins in the brain reach the brain area and join into
large veins. Subarachnoid crossing and wide emptying of the dural sinus,
affecting the vascular spread in the strong dura mater. The tissue in the
sinuses takes the vein out of the brain and emptyes the internal jugular
vein into the central circulation system. Cerebral veins are unique,
because these veins are not like other veins. Cerebral veins do not have
valves to prevent blood flow.
2. Definition Of Diseases
According to WHO, stroke is a clinical manifestation of cerebral dysfunction, both
focal and global, which progresses rapidly, lasts more than 24 hours or ends with
death, without finding a cause other thandisorders vascular.
According to Chang (2010), brain attack is a contemporary term for stroke or
cerebrovascular injury which refers to a sudden disruption of cerebral blood supply
as a result of partial or total vascular occlusion, or due to rupture of the cerebral
blood vessels.
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 According to Williams (2008), stroke is a sudden disorder in the cerebral
circulation in one or more blood vessels that supply the brain. Stroke interrupts or
reduces oxygen supply and generally causes serious damage or necrosis in brain
tissue.
Strokes are classified into two, namely hemorrhagic strokes (primary hemorrhagic
strokes) and non-hemorrhagic strokes (ischemic strokes).
According to Padila (2012), non-hemorrhagic stroke is a brain injury associated
with obstruction of cerebral blood flow resulting from thrombus formation in the
cerebrum artery or embolis that flows to the brain and other places in the body.
According to Arif Muttaqin (2008), non-hemorrhagic stroke is a process of
ischemia due to embolism and cerebral thrombosis usually occurs after a long rest,
just wakes up or in the morning and there is no bleeding. But there is ischemia which
causes hypoxia and secondary edema can occur.
3. Etiology
Non himorragic stroke is divided into 3, namely:
● Thrombotic stroke: thrombus formation process that makes blood
clots
● Embolic strokes: closed arteries by blood clots
● Systemic hypoperfusion: reduced blood flow throughout the body
because there is a disturbance in heart rate
The causative factor of stroke

● factors that cannot be changed (non reversible)

o Gender: men are more often found to have a stroke
o Age: the higher the age, the higher the risk of stroke The
o offspring Changeable
● factors
o Hypertension
o Heart disease
o High cholesterol
o Obesity
o Diabetes mellitus
o Polysetemia
o Emotional stress
● Life habits
o Smoking

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 o Alkohon drinkers Illegal
o drugs unhealthy. (Kusuma H, 2015)
4. Pathway / Phatofisiology
Pathway (attached)
Cerebral infarction is a reduction in blood supply to certain areas of the brain.
The extent of the infarct depends on factors such as the location and size of the
vessels and the presence of collateral circulation to the area supplied by blocked
vessels. The blood supply to the brain can change (slower or faster) in local disorders
(thrombus, embolism, bleeding, and vascular spasm) or due to general disorders
(hypoxia due to pant and heart disorders). Atherosclerosis is often a factor in the
infarction of the brain. Thrombus can originate from atherosclerotic plaques, or blood
can freeze in stenotic areas, where blood flow is slowed or turbulence occurs
(Muttaqin, 2008).
Thrombus can rupture from the walls of blood vessels carried as emboli in the
bloodstream. Thrombus suggests ischemia of brain tissue supplied by the blood
vessels concerned and edema and congestion around the area. This edema area
causes greater dysfunction than the infarct area itself. Edema can be reduced in a few
hours or sometimes after a few days. With reduced edema the client begins to show
improvement. Because thrombosis is usually not fatal "if there is no massive
bleeding. Occlusion of the cerebral blood vessels by the embolus causes edema and
necrosis followed by thrombosis. If septic infection develops on the vessel wall,
abscesses or encephalitis will occur, or if the remaining infection is in a blocked
blood vessel. causes dilation of blood vessel aneurysms. This will cause cerebral
bleeding, if the aneurysm breaks or ruptures (Muttaqin, 2008).
Bleeding in the brain is caused by arteriosclerotic rupture and vascular
hypertension. Extensive intracerebral hemorrhage will more often lead to death than
overall cerebrovascular disease; because extensive bleeding occurs destruction of the
brain mass, increased intracranial pressure and the heavier ones can cause brain
herniation in the cerebral falk or through the foramen magnum (Muttaqin, 2008).
Death can be caused by compression of the brain stem, hernisfer of the brain, and
secondary brain stem bleeding or extension of bleeding to the brain stem. Blood
permeation to the ventricles of the brain occurs in one third of cases of cerebral
hemorrhage in the caudate nucleus, thalamus, and puncher (Muttaqin, 2008). If
cerebral circulation is inhibited, cerebral anoxia can develop: Changes caused by
cerebral anoxia can be reversible for 4-6 minutes. Irreversible changes if anoxia is
more than 10 minutes. Cerebral anoxia can occur due to various disorders such as
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 cardiac arrest (Muttaqin, 2008). In addition to damage to the brain parenchyma, due
to the relatively large volume of hemorrhage, there will be an increase in intracranial
pressure and a decrease in brain perfusion pressure and brain drainage disorders. The
vasoactive elements of the blood that come out and the ischemic cascade are due to
decreased perfusion pressure, causing the nerves in the affected area and the
surrounding area to be depressed again (Muttaqin, 2008). The amount of blood
coming out determines the prognosis. If the blood volume is more than 60 cc, the risk
of death is 93% in internal bleeding and 71% in lobar bleeding. Whereas if there is
cerebellar hemorrhage with a volume between 30-60 cc it is estimated that the
probability of death is 75%, but the blood volume of 5 cc and contained in the pons
have fatal consequences (Misbach, 1999 in Muttaqin, 2008).
5. Clinical Manifestations
● Suddenly half-weakness or paralysis
● Suddenly sensitized
● Speech or pelo
● Impaired speech and language
● Vision impairment
● Mouth stroking or asymmetry when grin
● Memory impairment Severe
● headache
● Vertigo
● Decreased consciousness
● Urinary disturbance
● Disruption of brain function ( Kusuma H, 2015)
6. Supporting Investigation / Diagnostic
6.1. Stroke Thrombosis
● blood examination: complete blood, LED, GDA, cholesterol.
● Electrocardiography: to see the presence of an infectious myocardium,
arrhythmias, atrial fibrialis which can be a predictive factor in stroke.
● CT scan or MRI: to distinguish whether a stroke is caused by an
infarction or bleeding, and to get rid of lesions due to tumors or
abscesses that can have symptoms such as stroke
● Cerebral angigraphy: intracranial angiography is used to identify the
presence of extracranial carotid lesions that can be operated on.
● Ultrasonography: to detect the presence of stenosis or occlusion in the
internal carotid artery
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 ● Echocardiography: to see whether there is a heart abnormality that can
cause an embolic stroke. (Munir, Badrun. 2015)
6.2. Embolic stroke
● Radiological examination: head CT scan, MRI, and MRA.
● 12-lead ECG examination: to detect postpartum with suspected AF and
acute myocardial infarction.
● Framingham score examination and CHADS score were used for
stroke risk in AF patients
● Examination of thoracic photographs
● Blood glucose examination, electrolytes, BUN, creatinine, blood
platelet level, international normalized ration and prothrombin time,
activated thromboplastin time. C reactive protein or erythrocyte
sedimentation rate and blood culture.
● Echocardiography examination. (Munir, Badrun. 2015)
7. The management
7.1. Hyperacute stadium
action is carried out in an emergency care facility and is an act of
resuscitation of cerebro-cardio-pulmonary aimed at preventing brain tissue
damage. At this stage the patient is given oxygen 2 L / min and crystalloid /
colloid fluid; avoid administering dextrose or saline fluids in H2O. brain CT
scan, electrocardiography, chest X-ray, complete blood counts with platelet
count, prothrombin time / INR, APTT, blood glycose, blood chemistry, if
hypoxia, blood gas analysis is performed. Another action in the emergency
care facility is the provision of mental support to the patient and giving an
explanation to his family to remain calm.
a. Acute stage
Non himorragic stroke is general therapy: place the patient at position 30o,
head and chest in one area; change sleep position every 2 hours; mobilization
begins gradually if hemodynamics are stable. Next, free the airway, give
oxygen 1-2 liters / minute until you get the results of blood gas analysis. If
necessary, intubation. Fever is treated with compresses and antipyretics, then
the cause is sought; if the bladder is full, empty (preferably with an
intermittent catheter). Giving nutrition with isotonic liquid, crystalloid or
colloidal 1500-2000 ml and electrolytes as needed, avoid liquids containing
glucose or isotonic saline.

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 Providing perorah nutrition only if the function of swallowing is good,
blood sugar levels> 150 mg% must be corrected to 150 mg% with continuous
intravenous insulin drip for the first 2-3 days. Hypoglycemia (blood sugar
level <60 mg% or <80 mg% with symptoms) is resolved immediately with
40% dextrose iv until it returns to normal and must be looked for again.
Headache or nausea and vomiting are treated with medication according
to symptoms. Blood pressure does not need to be lowered immediately, except
if systolic pressure is> 220 mmhg, and diastolic> 120 mmhg, mean arterial
bold preasure (MAP)> 130 mmhg (at 2 measurements with an interval of 30
minutes), or acquired acute myocardial infarction, heart failure congestive and
kidney failure.
Blood pressure reduction is a maximum of 20%, and drugs are
recommended: sodium nitroprusid, alpha-beta receptor blockers, ACE
blockers and calcium antagonists. If there is hypotension or systolic pressure
<90 mmhg and distolic <70 mmhg, given NaCl 0.9% 250 ml for 1 hour,
followed by 500 ml for 4 hours, and 500 ml for 8 hours or until hypotension
can be overcome. If it has not been corrected, the systolic blood pressure is
still <90mmhg, can be given dopamine 2-20 ug / kg / minute until systolic
blood pressure> 110mmhg. If seizures, given diazepam 5-20 mg iv slowly for
3 minutes, a maximum of 100 mg / day; followed by oral anticonvulsants
(penitoin, carbamazepine). If seizures occur after 2 weeks, long-term oral
anticonvulsants are given. If increased intracranial pressure is obtained,
intravenous mannitol bolus is 0.25-1 g / kg body weight / 30 minutes, and if a
rebound phenomenon is suspected or the general condition worsens, continued
0.25 g / kg / 30 minutes every 6 hours for 3-5 days . Osmolality stabilizers
(<320 mmol); alternatively, hypertonic solutions (3% NaCl) or furosemide can
be given.
Special therapy: is intended for reperfusion with administration of
antiplatelet agents such as aspirin and anti-coagulants, or those recommended
with rt-PA thrombolytics (recombinant tissue, plasminogen activator). Can
also be given a neuroprotection agent, namely sitikolin or pirasetam (if
obtained aphasia). (Kusuma H, 2015)
8. Complication
● cerebral edema and an increase in intracranial pressure that can cause
herniation or compression of the brain stem
● Seizures
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 ● Hemorrhagic transformation
● Infection: pneumonia, UTI
● Thrombosis
● life activity disorders (Munir. B, 2015)
● Veins DailySwallowing disorders b.d decreased function of nerfus vagus
or loss of reflux vomiting
● Nutritional imbalance
● Acute pain
● Damage to skin integrity
● Risk of ineffectiveness of brain tissue perfusion. (Kusuma H, 2015)
B. The Basic Concept Of Nursing Care
1. Assessment
According to Muttaqin, (2008) the history of stroke includes client identity, main
complaint, current disease history, past medical history, family history, and
psychosocial assessment.
a. Client Identity
Includes name, age (mostly in old age), gender, education, address, occupation,
religion, ethnicity, MRS date and time, register number, and medical diagnosis.
b. The main complaint
Often the client's reason for asking pertolongau health is the weakness of the
limbs of the body, talking pelo, unable to communicate, and decreasing the level
of consciousness.
c. Current disease history
Attacks of hemorrhagic strokes often occur very suddenly, when the client is
carrying out activities. Usually headache occurs, nausea, vomiting and even
seizures until unconscious, in addition to symptoms of paralysis of the body or
other disorders of brain function.
There is a decrease or change in the level of consciousness caused by
changes in the intracranial. Complaints about behavior change are also common.
In accordance with the development of the disease, lethargy, unresponsiveness
and conia can occur.
d. Past medical
history A history of hypertension, a history of previous stroke, diabetes mellitus,
heart disease, anemia, history of head trauma, prolonged oral contraception, use
of anti-coagulant medications, aspirin, vasodilators, addictive drugs, and
obesity. Assessment of the use of drugs that are often used by clients, such as
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 the use of antihypertensive drugs, antilipidemia, beta blockers, and others. There
is a history of smoking, alcohol use and use of oral contraceptives. This history
assessment can support the assessment of the current disease history and is a
basic data for further study and to provide further action.

e. History of family disease

Usually there is a family history of hypertension, diabetes mellitus, or a history
of stroke from previous generations.

f. Psychososiospiritual
assessment Psychological assessment of stroke clients includes several
dimensions that allow the nurse to obtain a clear perception of the emotional,
cognitive, and behavioral status of the client. Assessment of coping mechanisms
used by clients is also important to assess the client's emotional response to the
illness and changes in the role of the client in the family and society and their
response or influence in their daily lives, both in the family and in society.
g. Physical Examination
After taking the history that leads to client complaints, a physical
examination is very useful to support the data from the history review. Physical
examination should be carried out per system (B1-B6) with a focus on physical
examination on B3 (Brain) examination which is directed and linked to
complaints from clients.

1) B1 (Breathing)
On inspection, the client coughs, increases sputum production,
shortness of breath, use of aids muscle, and increased respiratory frequency.
Auscultation of additional breath sounds such as ronkhi in clients with
increased secretion production and decreased coughing ability that is often
found in stroke clients with decreased levels of coma awareness.
For clients with a level of awareness of compos mends, there is no
abnormality in the assessment of respiratory inspections. Thoracic palpation
is obtained right and left balanced tactile premitus. Auscultation does not
get additional breath sounds.

2) B2 (Blood)
Assessment of the cardiovascular system is obtained shock
(hypovolemic shock) which often occurs in stroke clients. Blood pressure

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 usually increases and massive hypertension can occur (blood pressure> 200
mmHg).

3) B3 (Brain)
Stroke causes a variety of neurological deficits, depending on the
location of the lesion (which blood vessel is blocked), the size of the area
with inadequate perfusion, and collateral (secondary or accessory) blood
flow. Damaged brain lesions cannot improve completely. B3 (Brain)
assessment is a focus and more complete examination than other systems.

4) B4 (Bladder)
After a stroke the client may experience transient urinary
incontinence due to confusion, inability to communicate needs, and an
inability to control the bladder due to damage to motor and postural control.
Sometimes the control of external urine sphincter is lost or reduced. During
this period, intermittent catheterization with sterile techniques was carried
out. Continued urinary incontinence shows extensive neurological damage.

5) B5 (Bowel)
There is a complaint of difficulty in swallowing, decreased appetite,
nausea and vomiting in the acute phase. Nausea to vomiting is caused by an
increase in the production of gastric acid, which results in nutritional
fulfillment problems. Defecation patterns usually occur constipation due to
decreased intestinal peristalsis. Alvial incontinence continues to show
extensive neurological damage.

6) B6 (Bone)
Stroke is a disease of UMN and results in loss of voluntary control
of motor movements. Because the motor neurons over cross, voluntary
motor control disturbances on one side of the body can show damage to the
upper motor neurons on the opposite side of the brain. The most common
motor dysfunction is hemiplegia (paralysis on one side) due to lesions on
the opposite side of the brain. Hemiparesis or weakness of one side of the
body, is another sign. On the skin, if the client lacks 02 the skin will look
pale and if there is a lack of fluids the skin turgor will be bad. In addition, it
is also necessary to examine the signs of decubitus especially in areas that
are prominent because stroke clients experience physical mobility
problems.
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 Difficulties for activity due to weakness, sensory loss or paralysis /
hemiplegia, as well as fatigue easily cause problems in the pattern of
activity and rest.

7) Awareness Level Assessment The

quality of client awareness is the most basic parameter and the most
important parameter that requires assessment. The level of client security
and environmental response are the most sensitive indicators for nervous
system dysfunction. Some systems are used to rank changes in alertness and
alertness.
In the advanced state the client's stroke awareness level usually
ranges in levels of lethargy, stupor, and semicomatosa. If the client has
experienced a coma, the GCS assessment is very important to assess the
level of client awareness and evaluation material for monitoring care
provision.

8) Assessment of cerebral function

This study includes mental status, intellectual function, language
ability, frontal lobes, and hemispheres.

9) Menta Status
Observe appearance, behavior, value of speech style, facial
expression, and motor motor activity. In advanced stroke clients, the client's
mental status usually changes.

10) Intellectual Functions

There is a decrease in memory and memory, both short and long
term. Decreased numeracy and calculation abilities. In some cases clients
experience brain damage which is the difficulty of getting to know
similarities and differences that are not so obvious.

11) Language Ability

Decreased language ability depends on the area of the lesion that
affects the function of the cerebral. Lesions in the hemisphere area that are
dominant in the posterior part of the superior temporal gyrus (area of
Wernicke) are receptive dysphasia, ie the client cannot understand spoken
language or written language. While the posterior lesion of the inferior
frontal gyrus (Broca's area) has expressive dysphagia,, that isthe client can

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 understand, but cannot respond appropriately and his speech is not smooth.
Dysarthria (difficulty speaking), is indicated by elusive speech caused by
muscle paralysis responsible for producing speech. Apraksia (inability to
take action previously learned), as seen when the client takes a comb and
tries to comb his hair.

h. Study of Cranial Nerves

According to Muttaqin, (2008) This examination includes examination of
cranial nerves I-X11.

1) Nerve I: Usually in the client stroke there is no abnormality in the olfactory

function.
2) Nerves II. Visual perception dysfunction due to primary sensory pathway
disorders between the eye and visual cortex. Disruption of visual-spatial
relationships (obtaining a relationship of two or more objects in the spatial
area) is often seen in Mien with left hemiplegia. Clients may not be able to
wear clothes without help because of the inability to match clothes to body
parts.
3) Nerves III, IV and VI. If due to stroke results in paralysis, on
4) one side the ocular muscles are found to decrease the ability of the
unilateral conjugate movement on the affected side.
5) V. Nerves. In some conditions stroke causes trigenimus nerve paralysis,
decreased coordination ability of chewing movements, lower jaw
irregularities to the ipsilateral side, and one-sided paralysis of the internal
and external pterygoid muscles.
6) Nerve VII. Perception of taste is within normal limits, face is asymmetrical,
and facial muscles are attracted to the healthy side.
7) Nerves VIII. No conductive and deafness perception was found.
8) Nerves IX and X. Ability to swallow is not good and difficulty opening the
mouth.
9) Nerve XI. There is no atrophy of the sternocleidomastoid and trapezius
muscles.
10) Nerve XII. Symmetrical tongue, there is deviation on one side and
fasciculation, and normal taste senses.
i. Assessment of Motor System
Stroke is upper motor nerve disease (UMN) and results in loss of
voluntary control of motor movements. Because UMN crosses, interference
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 with voluntary motor control on one side of the body can show damage to UMN
on the opposite side of the brain.

1) General Inspection. Hemiplegia (paralysis on one side) is due to lesions on

the opposite side of the brain. Hemiparesis or weakness of one side of the
body is another sign.
2) Fasciculation. Obtained in the muscles of the extremities.
3) Muscle Tonus. Increased.
2. Nursing Diagnoses Nursing
1. Perfusion of the cerebral tissue is not effective r.o O2 brain decreases
2. Nutritional imbalance: less than the body's needs r.o inability to absorb nutrients
Nutritional
3. mobility is a decrease r.o muscle strength.
4. Risk of damage to skin integrity r.o risk factors: dampness
5. Verbal communication disorders r.o neuromuscular damage, central damage to
speech

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