Asuhan keperawatan pada

Penyakit Arteri Koronaria

Emil Huriani

Heart Anatomy

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Figure
2 18.1

Dinding Jantung

Epikardium Lapisan terluar perikardium

Miokardium Lapisan otot jantung yang
membentuk lapisan tebal pada jantung
Endokardium lapisan endotelium di bagian
dalam miokardium

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External Heart: Anterior View

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Figure
4 18.4b

Jantung bagian luar: Pembuluh darah yang

membawa darah ke dan dari dinding jantung
(Anterior)

Arteri koronaria kiri dan kanan, marginal,

circumflex, dan arteri interventricular anterior
Vena vena besar, anterior dan kecil

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External Heart: Posterior View

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Figure 18.4d

Jantung bagian luar: Pembuluh darah yang

membawa darah ke dan dari dinding jantung
(Posterior)
Arteri arteri koronaria kanan dan arteri
interventricular posterior
Vena vena besar, vena posterior ventrikel kiri,
sinus coroner dan vena tengah

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Sirkulasi Koroner

Sirkulasi coroner adalah suplay darah fungsional ke

otot jantung
Jalur kolateral memastikan aliran darah ke jantung
walaupun pembuluh darah besar tersumbat

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Coronary Circulation: Arterial Supply

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Figure 18.7a

Coronary Circulation: Venous Supply

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10

Figure 18.7b

Penyakit arteri koronaria

Etiologi: Aterosklerosis
Istilah atherosclerosis, berasal dari bahasa Yunani atheros (artinya
gruel or paste) and sclerosis (artinya pengerasan),
menunjukkan adanya pembentukan lesi fibro-fatty di lapisan
intima pada arteri ukuran besar dan menengah seperti aorta dan
percabangannya, arteri koronaria, dan pembuluh darah besar yang
membawa darah ke otak.

Penumpukan Kolesterol dan Lemak fokal yang umumnya

terjadi pada tunika intima arteri
Pengerasan dinding arteri

Atherosklerosis

Teori Aterosklerosis
Cedera endothelium Endothelial injury caused by
hyperlipidemia, hypertension or other irritant agents
Defense factors released into the endothelial lining and causes
migration of smooth muscle cells into the intima
The presence of smooth muscle cells initiate the synthesis of
collagen, proteins and proteoglycans
The accumulation of intracellular and extracellular lipids and
platelets
Formation of such lesions, such as thrombus

Tahapan Atherosklerosis
Fatty Streak
Intermediate lesion
Atheroma
Complicated lesion
rupture
Fibrosis plaque

Atherosklerosis Tahap 1
Endothelial
disfunction caused
by LDL cholesterol,
infection and free
radicals
Migration of
monosite, T
lymphosites and
macrophages

Atherosklerosis Tahap 2

Prolipheration of
smooth muscle
cell and platelet
aggregation

Atherosklerosis Tahap 3

Necrosis of core
lesion

Atherosklerosis Tahap 4

Fibrous cap
thinning and
rupture due to the
influx and
activation of
macrophages

Atherosklerosis Tahap 5
The release of
proteolytic
enzymes
followed by
hemorrhage,
thrombus
formation and
arterial occlusion

Risk Factors (1)

Unmodifiable
Age: > 65 years
Gender: men> women
Family history
Heredity: congenital arterial wall defect

Faktor Resiko (2)

Modifiable
Serum lipid increase
Cholesterol > 200 mg/dl (5,2 mmol/L)
Triglyceride > 200 mg/dl (1,7 mmol/L)
LDL > 160 mg/dl
HDL < 35 mg/dl

Hypertension. BP > 140/90 mmHg

Diabetes mellitus
Diabetes elevates blood lipid levels and otherwise increases the risk of
atherosclerosis.

Smoking: nicotine & carbonmonoksida

Physical Inactivity < 30 min, 3 x per week
Obesity > 30 % above standard

Risk factors (3)

There are a number of other less well-established risk factors for
atherosclerosis, including:
High serum homocysteine levels
Homocysteine is derived from the metabolism of dietary
methionine
Homocysteine inhibits elements of the anticoagulant cascade and is
associated with endothelial damage.
Elevated serum C-reactive protein
It may increase the likelihood of thrombus formation;
Inflammation marker;
Infectious agents
The presence of some organisms (Chlamydia pneumoniae,
herpesvirus hominis, cytomegalovirus) in atheromatous lesions has
been demonstrated by immunocytochemistry, but no cause-andeffect relationship has been established.
The organisms may play a role in atherosclerotic development by
initiating and enhancing the inflammatory response.

Clinical Manifestations
The clinical manifestations of atherosclerosis depend on the vessels involved
and the extent of vessel obstruction.
Atherosclerotic lesions produce their effects through:
narrowing of the vessel and production of ischemia;
sudden vessel obstruction caused by plaque hemorrhage or rupture;
thrombosis and formation of emboli resulting from damage to the vessel
endothelium;
In larger vessels such as the aorta, the important complications are those of
thrombus formation and weakening of the vessel wall.
In medium-size arteries such as the coronary and cerebral arteries, ischemia
and infarction caused by vessel occlusion are more common.
Although atherosclerosis can affect any organ or tissue, the arteries supplying
the heart, brain, kidneys, lower extremities, and small intestine are most
frequently involved.

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23

Coronary heart disease

The term coronary heart disease (CHD) describes heart disease caused by
impaired coronary blood flow.
In most cases, it is caused by atherosclerosis.
Diseases of the coronary arteries can cause:
Angina
Myocardial infarction or heart attack
Cardiac dysrhythmias
Conduction defects
Heart failure
Sudden death

Angina Pectoris

Definition
Generally described as retrosternal
heavy or gripping sensation with
radiation to left arm or neck, provoked
by exertion and eased with rest or
nitrates

Angina can be:

Stable
Unstable caused by
unstable plaque, occurs at
rest, unpredictable, pain can
increase for no obvious
reason
Prinzmetals occurs
without provocation, usually
at rest, as a result of
coronary artery spasm

Stable angina pectoris

Provoked by physical exertion,
especially in cold weather, after
meals and commonly aggravated
by anger or excitement
The pain fades quickly with rest
In some patients pain occurs
predictably at a certain level of
exertion

WOC CAD
Hiperlipidemia

Stress
Kepribadian tipe A

Merokok

Nikotin

Karbon monoksida

Pelepasan
Katekolamin

Berikatan kuat
dgn Hb

Akumulasi & deposit lipid

pada dinding arteri

Fatty streak

Pembentukan
plaque

Atherosklerosis
MK: Intoleransi
aktivitas
Penurunan curah
jantung

Penyempitan &
pengerasan lumen PD

Suplai O2 sistemik
menurun
MK: Risti ggn
perfusi jaringan

MK: Pean CO

Suplai O2 miokard
menurun

Pembebasan
enzim lisosomal

Ketidakseimbangan
suplai dan kebutuhan

Penurunan
curah jantung

Angina
Pektoris

Injuri sel

Disritmia
Perubahan
potensial aksi
Penurunan
kontraktilitas

MK: Kcemasn

Glikolisis
anaerob
Produksi
asam laktat

Asidosis
metabolik

Iskemia sel
Infark
Miokard

Nekrosis sel

MK: Ggn rasa

nyaman

MK: Perub
pola nafas

Signs and symptoms

Chest pain
Nausea & vomitting
Stimulation of Sympathetic nervous system
Fever
Cardiovascular manifestation

Myocardial infarction
Acute myocardial infarction (AMI), also known as a heart attack, is
characterized by the ischemic death of myocardial tissue associated with
atherosclerotic disease of the coronary arteries.
Diagnosis:
1. Pain
The pain typically is severe and crushing, often described as being
constricting, suffocating. It usually is substernal, radiating to the
left arm, neck, or jaw, although it may be experienced in other areas
of the chest.
Gastrointestinal complaints are common. There may be a sensation
of epigastric distress; nausea and vomiting may occur.
2. ECG
Elevation of the ST segment usually indicates acute myocardial
injury.
When the ST segment is elevated without associated Q waves, it is
called a nonQ-wave infarction. A nonQ-wave infarction usually
represents a small infarct that may evolve into a larger infarct.
3. Enzymes

Enzymes
Myoglobin is an oxygen-carrying protein, similar to hemoglobin, that is
normally present in cardiac and skeletal muscle. It is a small molecule that
is released quickly from infarcted myocardial tissue and becomes elevated
within 1 hour after myocardial cell death, with peak levels reached within 4
to 8 hours. It rapidly eliminates through urine (low molecular weight).
Because myoglobin is present in both cardiac and skeletal muscle, it is not
cardiac specific.

Creatine kinase (CK), formerly called creatinine phosphokinase, is an

intracellular enzyme found in muscle cells. Muscles, including cardiac
muscle, use ATP as their energy source. Creatine, which serves as a storage
form of energy in muscle, uses CK to convert ADP to ATP. CK exceeds
normal range within 4 to 8 hours of myocardial injury and declines to
normal within 2 to 3 days. There are three isoenzymes of CK, with the MB
isoenzyme (CK-MB) being highly specific for injury to myocardial tissue.

Enzymes

The troponin complex consists of three subunits (i.e., troponin C, troponin I,

and troponin T) that regulate calcium-mediated contractile process in striated
muscle. These subunits are released during myocardial infarction. Cardiac
muscle forms of both troponin T and troponin I are used in diagnosis of
myocardial infarction. Troponin I (and troponin T; not shown) rises more
slowly than myoglobin and may be useful for diagnosis of infarction, even up
to 3 to 4 days after the event. It is thought that cardiac troponin assays are
more capable of detecting episodes of myocardial infarction in which cell
damage is below that detected by CK-MB level.

Myocardial infarction

Effects of AMI
The principal biochemical consequence of AMI is the conversion from aerobic
to anaerobic metabolism with inadequate production of energy to sustain
normal myocardial function.
The ischemic area ceases to function within a matter of minutes, and
irreversible myocardial cell damage occurs after 20 to 40 minutes of severe
ischemia.
The term reperfusion refers to re-establishment of blood flow through use of
thrombolytic therapy or revascularization procedures.
Early reperfusion (within 15 to 20 minutes) after onset of ischemia can
prevent necrosis.
Reperfusion after a longer interval can salvage some of the myocardial
cells that would have died because of longer periods of ischemia.

ECG
ST segment elevations
typically due to complete occlusion of a coronary
artery.

NSTEMIs
typically a sudden narrowing of a coronary artery
with preserved (but diminished) flow to the distal
myocardium.
Anticoagulation and antiplatelet agents
prevent the narrowed artery from occluding.

Klasifikasi KILLIP
Used in individuals with an acute myocardial infarction
to risk stratify
Individuals with a low Killip class are less likely to die within
the first 30

KILLIP I Sesak + tanda gagal jantung (-) Mortality rate = 6%

KILLIP II Sesak + Rhonkhi (+/+) Mortality rate = 17%
KILLIP III Sesak + Rhonkhi luas (Edema Pulmonal) Mortality
rate = 38%.

KILLIP IV Syok Kardiogenik. Mortality rate = 81%

Management
EARLY MANAGEMENT
The patients history and 12-lead ECG are the primary methods
used to determine initially the diagnosis of MI.
The ECG is examined for the presence of ST segment
elevations of 1 mV or greater in contiguous leads.
1. Administer aspirin, 160 to 325 mg chewed.
2. After recording the initial 12-lead ECG, place the patient on
a cardiac monitor and obtain serial ECGs.
3. Give oxygen by nasal cannula.

 4. Administer sublingual nitroglycerin (unless the

systolic blood pressure is less than 90 mm Hg or the
heart rate is less than 50 or greater than 100
beats/minute).
5. Provide adequate analgesia with morphine sulfate.
Provide adequate analgesia with morphine sulfate.

Thrombolytic Therapy

Thrombolytic drugs lyse coronary thrombi by converting

plasminogen to plasmin.
Thrombolytic therapy provides maximal benefit if given
within the first 3 hours after the onset of symptoms.
Significant benefit still occurs if therapy is given up to 12
hours after onset of symptoms.

Complications
Arrhythmias
Congestive Heart Failure
Cardiogenik Shock
Papillary muscle dysfunction
Ventricular aneurism
Pericarditis
Pulmonary Emboli

Treatment (continued)
1) Stenting
a stent is introduced into a blood vessel on a balloon
catheter and advanced into the blocked area of the artery
the balloon is then inflated and causes the stent to expand
until it fits the inner wall of the vessel, conforming to
contours as needed
the balloon is then deflated and drawn back
The stent stays in place permanently, holding the vessel
open and improving the flow of blood.

Treatment
(continued)

2) Angioplasty
a balloon catheter is passed through the guiding catheter to the
area near the narrowing. A guide wire inside the balloon catheter is
then advanced through the artery until the tip is beyond the
narrowing.
the angioplasty catheter is moved over the guide wire until the
balloon is within the narrowed segment.
balloon is inflated, compressing the plaque against the artery wall
once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.

Treatment (continued)
3) Bypass surgery
healthy blood vessel is removed from leg, arm or chest
blood vessel is used to create new blood flow path in your heart
the bypass graft enables blood to reach your heart by flowing
around (bypassing)
the blocked portion
of the diseased
artery. The increased
blood flow reduces
angina and the risk
of heart attack.

Get regular medical checkups.

Control your blood pressure.
Check your cholesterol.
Dont smoke.
Exercise regularly.
Maintain a healthy weight.
Eat a heart-healthy diet.
Manage stress.

Myocardial infarction
Nursing process
Assessment

A careful history
Description of symptoms ( chest pain, palpitation,
dyspnea, syncope or sweating). Each symptoms
must be evaluated with regard to time, duration,
precipitating & relieving factors. In addition
complete physical assessment for:
*level of consciousness

Nursing process (cont)

*Heart sounds

*Peripheral pulses

*Lung sound

Nursing Diagnoses
Acute Pain related to oxygen supply and demand
imbalance
Risk for ineffectively of cardiac tissue perfusion
Anxiety related to chest pain, fear of death, threatening
environment
Decreased Cardiac Output related to impaired
contractility
Activity Intolerance related to insufficient oxygenation
to perform activities of daily living, deconditioning
effects of bed rest
Risk for Injury (bleeding) related to dissolution of
protective clots

Nursing process (cont)

Patient's goals
Report that pain is decreased
Breath effectively
Experience less anxiety level
Have improved tissue perfusion
Adhere to the self care program

Nursing process (cont)

Nursing intervention
Relief or control of chest pain
Alleviate respiratory difficulties
Reduce the anxiety level
Maintain adequate tissue perfusion
Help the patient to adhere to the self care program

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52