STEP 1
STEP 2
1. Mengapa pasien merasa nyeri dada sprti diremas remas yg dijalrkan ke rahang kiri
?
2. Mengapa keluhan disertai mual dan muntah?
3. Hubungan px lab yg ada diskenario (nilai normal) dengan keluhan pasien?
4. Mengapa terjadi cardiomegali ?
5. Mengapa didapatkan VS= T 90/60, N 110x/menit , RR 24x/menit ?
6. Mengapa ditemukan ST elevasi pada gambaran EKG?
7. Apa arti gambaran Rogent CTR >50% dan cara mengukurnya?
8. Mengapa dokter memberikan oksigen, infus kristaloid dan ISDN sublingual ?
9. Mengapa didapati pasien dgn KU lemah dan kesadaranya apatis?
10. Fungsi obat-obat yg diberikan dr spesialis ( ISDN, Aspilet, Cloprigogel,simvastatin,
glimepride, metformin)?
DD
Nyeri dada
STEAMI
Angina pectoris
STEP 3
1. Mengapa pasien merasa nyeri dada sprti diremas remas yg dijalrkan ke rahang kiri
?
Referred pain (also reflective pain)[1] is pain perceived at a location other than the site
of the painful stimulus. An example is the case of ischemia brought on by a myocardial
infarction (heart attack), where pain is often felt in the neck, shoulders, and back rather
than in the chest, the site of the injury. The International Association for the Study of
Pain , as of 2001, has not officially defined the term; hence several authors have defined
the term differently. Radiation is different from referred pain. The pain related to a
myocardial infarction could either be referred pain or pain radiating from the chest.
Classically the pain associated with a myocardial infarction is located in the mid or left
side of the chest where the heart is actually located. The pain can radiate to the left
side of the jaw and into the left arm. Referred pain is when the pain is located away
from or adjacent to the organ involved. Referred pain would be when a person has
pain only in their jaw or left arm, but not in the chest. Myocardial infarction can rarely
present as referred pain and this usually occurs in people with[2] diabetes or older
age. Physicians and scientists have known about referred pain since the late 1880s.
Despite an increasing amount of literature on the subject, the mechanism of referred
pain is unknown, although there are several hypotheses
There are several proposed mechanisms for referred pain. Currently there is no
definitive consensus regarding which theory may be correct. The cardiac general visceral
sensory pain fibers follow the sympathetics back to the spinal cord and have their cell
bodies located in thoracic dorsal root ganglia 1-4(5). As a general rule, in the thorax and
abdomen, general visceral afferent (GVA) pain fibers follow sympathetic fibers back to
the same spinal cord segments that gave rise to the preganglionic sympathetic fibers.
The central nervous system (CNS) perceives pain from the heart as coming from the
somatic portion of the body supplied by the thoracic spinal cord segments 1-4(5). Also,
the dermatomes of this region of the body wall and upper limb have their neuronal cell
bodies in the same dorsal root ganglia (T1-5) and synapse in the same second order
neurons in the spinal cord segments (T1-5) as the general visceral sensory fibers from
the heart. The CNS does not clearly discern whether the pain is coming from the body
wall or from the viscera, but it perceives the pain as coming from somewhere on the
body wall, i.e. substernal pain, left arm/hand pain, jaw pain.
Medilexicon International Ltd., 2009. What is pain? What causes pain. Retrieved on
June11, 2010
But you might be way off. Sometimes the brain gets confused, making you think that one
part of the body hurts, when in fact another part of the body, far removed from the pain,
is the real source of trouble. This curious (and clinically important) phenomenon is known
asreferred pain. For example, it's unlikely but possible that your shoulder pain is a sign of
something insidious happening in your liver,gall bladder, stomach, spleen, lungs,
or pericardial sac (the connective tissue bag containing the heart). Strange, isn't it?
Conditions as diverse as liver abscesses, gallstones, gastric ulcers, splenic rupture,
pneumonia, and pericarditis can all cause shoulder pain. How is that possible?
Neuroscientists still don't know precisely which anatomical connections are responsible for
referred pain, but the prevailing explanation seems to work pretty well. In a nutshell,
referred pain happens when nerve fibers from regions of high sensory input (such as the
skin) and nerve fibers from regions of normally low sensory input (such as the internal
organs) happen to converge on the same levels of the spinal cord. The best known example
is pain experienced during a heart attack. Nerves from damaged heart tissue convey pain
signals to spinal cord levels T1-T4 on the left side, which happen to be the same levels that
receive sensation from the left side of the chest and part of the left arm. The brain isn't
used to receiving such strong signals from the heart, so it interprets them as pain in the
chest and left arm.
So what about that shoulder pain? All of organs listed above bump up against
the diaphragm, the thin, dome-shaped muscle that moves up and down with every breath.
The diaphragm is innervated by twophrenic nerves (left and right), which emerge from
spinal cord levelsC3, C4, and C5 (medical students remember these spinal cord levels using
the mnemonic, "C3, 4, 5 keeps the diaphragm alive"). The phrenic nerves carry
both motor and sensory impulses, so they make the diaphragm move and they convey
sensation from the diaphragm to the central nervous system.
Most of the time there isn't any sensation to convey from the diaphragm, at least at the
conscious level. But if a nearby organ gets sick, it may irritate the diaphragm, and the
sensory fibers of one of the phrenic nerves are flooded with pain signals that travel to the
spinal cord (at C3-C5). It turns out that C3 and C4 don't just keep the diaphragm alive;
neurons at these two spinal cord levels also receive sensation from the shoulders (via
the supraclavicular nerves). So when pain neurons at C3 and C4 sound the alarm, the brain
assumes (quite reasonably) that the shoulder is to blame. Usually that's a good
assumption, but sometimes it's wrong.
Illustration showing sites of
referred pain from abdominal organs. From Moore and Dalley's Clinically Oriented Anatomy.
Please note that I added the "tighty whities" with Photoshop (hey, this is a family friendly
site).
Nyerinyaa kenapaa???
Klo nyeri gt apa cuma jantung??
Rules of referred pain :
RP does not cross the midline. A unilateral lesion can only cause unilateral pain. Example
: a unilateral sacroiliac arthritis or a facet joint lesion give rise to unilateral pain only. A
central disc protrusion, with pressure against the dura mater and /or nerve root could cause
central, unilateral or bilateral pain.
RP is mainly segmental. The pain is referred according to the embryological origin of each
structure. Any structure of C5-origin could cause pain in the C5-dermatome. Example : a
shoulder arthritis or bursitis, supraspinatus or infraspinatus tendinitis all provoke similar
pain in the arm (forearm). Hence, it is important to know the embryological derivation of all
structures and the maps of the dermatomes.
Reference occurs mainly in a distal direction It is abnormal for a local distal lesion to
refer pain mainly in a proximal direction. Example : a shoulder tendinitis may give rise to a
pain felt as far as the base of the thumb (C5-dermatome) ; a tendinous lesion at the wrist
does not cause pain as far as the shoulder. Or : a sacroiliac arthritis (S1-S2) can cause pain as
far as the heel, whereas the pain of a retrocalcanean bursitis would not reach the buttock.
Reference in a proximal direction is only slight.
The lesion does not necessarily lie in the painful area. Palpation of local tenderness, with
no other confirming examination, has poor diagnostic value. It should always be connected
with other data from the clinical examination.
Example : shoulder joint arthritis. The pain is felt in the C5-dermatome and not necessarily
only at the top of the shoulder. (It has to be said that this depends upon the individual
differences in dermatomic distribution.).
Many soft tissues can cause referred pain. There is no difference in pain quality and
ability to refer pain between a muscular, tendinous, ligamentous or other soft tissue pain.
The pain can be felt anywhere in the dermatome, not necessarily in the entire
dermatome. We should not be mislead by the fact that RP can be confined to one part of
the dermatome only.
Example : osteoarthrosis at the hip joint (L3) : the pain can be felt at the groin and down the
front of the thigh, or just at the knee, or just in the upper buttock, or at the front of the leg
as far as the medial malleolus. Hence, a patient who complains about an anterior knee pain,
may have a hip lesion instead of a knee lesion.
Discrepancies exist between dermatomes and myotomes. A muscular structure does not
necessarily lie underneath its dermatome ; it needs to be pointed out that this fact does not
necessarily has important clinical value.
Example : supraspinatus tendinitis (C5) : the C5-dermatome ends at the base of the thumb,
but there are no C5-muscles beyond the elbow.
The thumb and index finger lie in the C6-dermatome but the muscles in the hand are of C8-
and T1-origin. The proximal end of the C5-dermatome is at the mid-deltoid area. The supra-
and infra-spinatus muscles are C5-structures.
http://www.om-cyriax.com/577-glossary/Referred-pain.htm
The term "cardiomegaly" most commonly refers to an enlarged heart seen on chest
X-ray before other tests are performed to diagnose the specific condition causing
your cardiomegaly. You may develop an enlarged heart temporarily because of a
stress on your body, such as pregnancy, or because of a medical condition, such as
the weakening of the heart muscle, coronary artery disease, heart valve problems
or abnormal heart rhythms.
Cardiomegaly, or an enlarged heart, is actually a symptom and not a disease. Typically found
when an X-ray is performed, it may be indicative of a number of different conditions such as
valve damage or high blood pressure. While not always preventable, once detected, the
cause of cardiomegaly is usually treatable.
Diseased Heart Valves
The job of the four valves of your heart is to ensure the blood flows in the proper direction
at all times. Various conditions and infections, such as rheumatic fever or birth defects, can
damage these valves, causing the heart to enlarge and pump that much harder to work
the way it was intended.
Sedentary Lifestyle
The Better Health Channel states that a sedentary lifestyle, or one lacking exercise, is a
major risk factor for developing an enlarged heart. This is because lack of exercise can
contribute to both coronary heart disease and high blood pressure, both of which are
conditions that cause the heart to enlarge.
Lack of exercise may also lead to obesity, another risk factor of cardiomegaly. When you are
obese, your body contains excess body fat which not only places undue stress on your
heart, but may also cause your blood pressure to rise. Both of these situations, especially
when combined, force the heart to work harder, thus resulting in an enlarged heart.
High Blood Pressure
The American Heart Association states that people can suffer for years from high blood
pressure before realizing it is a problem for them. Known as the silent killer, this condition
has few or no symptoms. When left untreated for a prolonged period of time, it damages
the heart by forcing it to pump harder, leading to its enlargement.
To prevent this from occurring, have your blood pressure checked regularly by your
physician, or purchase a home monitoring kit and check your pressure yourself on a regular
basis. Anything under 120/80 is considered healthy according to the National Heart Lung
and Blood Institute.
Birth Defects
In certain cases, people are born with congenital heart defects, such as a hole in the heart.
Defects like this force the heart to work harder, affecting the way the blood flows through
the heart. The harder the heart has to pump, the greater the risk of developing an enlarged
heart.
Weak Muscles
Conditions such as a heart attack, cardiomyopathy and congestive heart failure cause the
muscles of the heart to become stiff and thick, which, over time, results in a weakening of
your heart muscles according to the American Heart Association. Just as with the
previously mentioned conditions, these not only weaken the muscles of the heart, but force
it to work harder; this results in cardiomegaly.
References
Better Health Channel: Heart Disease-Enlarged Heart
American Heart Association: Diagnose and Monitor High Blood Pressure
Mayo Clinic: Enlarged Heart Causes
Conditions associated with an enlarged heart include:
High blood pressure. Having high blood pressure can make it so that your heart has to
pump harder to deliver blood to the rest of your body, enlarging and thickening the muscle.
Heart valve disease. Four valves within your heart keep blood flowing in the right direction.
If the valves are damaged by such conditions as rheumatic fever, a heart defect, infections
(infectious endocarditis), connective tissue disorders, certain medications or radiation
treatments for cancer, your heart may enlarge.
Heart attack. Damage done during a heart attack may cause an enlarged heart.
A heart condition you're born with (congenital heart defect).Many types of congenital
heart defects may lead to an enlarged heart, as defects can affect blood flow through the
heart, forcing it to pump harder.
Abnormal heartbeat (arrhythmia). If you have an arrhythmia, your heart may not pump
blood as effectively as it would if your heart rhythm were normal. The extra work your
heart has to do to pump blood to your body may cause it to enlarge.
High blood pressure in the artery connecting your heart and lungs (pulmonary
hypertension). If you have pulmonary hypertension, your heart may need to pump harder
to move blood between your lungs and your heart. As a result, the right side of your heart
may enlarge.
Low red blood cell count (anemia). Anemia is a condition in which there aren't enough
healthy red blood cells to carry adequate oxygen to your tissues. Left untreated, chronic
anemia can lead to a rapid or irregular heartbeat. Your heart must pump more blood to
make up for the lack of oxygen in the blood when you're anemic. Rarely, your heart can
enlarge if you have anemia for a long time and you don't seek treatment.
Rare diseases that can affect your heart, such as amyloidosis.Amyloidosis is a condition in
which abnormal proteins circulate in the blood and may be deposited in the heart,
interfering with your heart's function. If amyloid builds up in your heart, it can cause it to
enlarge.
You may have a greater risk of developing an enlarged heart if you have any of the following
risk factors:
High blood pressure. Having a blood pressure measurement higher than 140/90 millimeters
of mercury puts you at an increased risk of developing an enlarged heart.
Blocked arteries in your heart (coronary artery disease). If you have coronary artery
disease, fatty plaques in the arteries of your heart make it so blood can't easily flow
through the vessels of your heart. Sometimes this leads to a heart attack, where a section
of heart muscle dies. If this happens, your heart has to pump harder to get an adequate
amount of blood to the rest of your body, causing it to enlarge.
Congenital heart disease. If you're born with a condition that affects the structure of your
heart, you may be at risk for developing an enlarged heart, especially if your condition isn't
treated.
Valvular heart disease. The heart has four valves the aortic, mitral, pulmonary and
tricuspid valves that open and close to direct blood flow through your heart. Valves may
be damaged by a variety of conditions leading to narrowing (stenosis), leaking (regurgitation
or insufficiency) or improper closing (prolapse). Any of these conditions may cause the heart
to enlarge.
Heart attack. Having a heart attack increases your risk of developing an enlarged heart.
http://www.mayoclinic.com/health/enlargedheart/DS01129/DSECTION=risk-factors
http://www.mayoclinic.com/health/enlarged-heart/DS01129/DSECTION=causes
1. Definisi
Suatu sindrom dimana memiliki spektrum mulai dari unstabil angina sampai infark
miokard akut yang muncul ketika suplay oksigen tidak sesuai dg yang dibutuhkan. Memiliki
patofisiologi sama yaitu oklusi arteri koronaria meliputi unstabil angina, STEMI,NONSTEMI
USU
Sindroma koroner akut adalah suatu peralihan (spektrum) manifestasi dari penyakit
jantung iskemik meliputi angina tak stabil hingga infark miokard akut(IMA) dengan
gelombang Q atau pun tanda gelombang Q
HARRISON
Sekumpulan keluhan dan tanda klinis yang sesuai dengan iskemia miokardium akut.
SKA merupakan suatu spektrum dari perjalanan penderita penyakit jantung koroner
(aterosklerosis koroner).
Buku Panduan Kursus Bantuan Hidup Jantung Lanjut ACLS Indonesia, IDI.
2. Etiologi
a. Trombosis Koroner
Pada penelitian angiografi dan studi post-mortem yang dilakukan pada pasien SKA
segera setelah timbulnya keluhan menunjukan lebih dari 85% terdapat adanya oklusi
trombus pada arteri penyebab (culprit artery). Trombus yang terbentuk merupakan
campuran trombus putih (white trombus) dan trombus merah (red trombus).
Buku Panduan Kursus Bantuan Hidup Jantung Lanjut ACLS Indonesia, IDI.
3. Patofisiologi
a. Plak yang tidak stabil
Penyebab utama terjadinya SKA adaah rupturnya plak yang kaya lipid dengan
cangkang yang tipis. Umumnya plak yang mengalami ruptur secara hemodinamik
tidak signifikan lesinya. Adanya komponen sel inflamasi yang berada di bawah
subendotel merupakan titik lemah dan merupakan perdisposisi terjadinya ruptur
plak. Kecepatan aliran darah, turbulensi, dan anatomi pembuluh darah juga
memberikan kontribusi .terhadap hal tersebut.
b. Ruptur plak
Setelah ruptur plak, sel-sel platelet akan menutupi atau menempel pada plak
yang ruptur merangsang dan mengaktifkan agregasi platelet. Fibrinogen akan
menyelimuti platelet merangsang pembentukan trombin.
c. Angina tidak stabil
Sumbatan trombus yang parsialakan menimbulkan gejala iskemik yang lebih
lama dan dapat terjadi saat istirahat. Pada fase ini trombus kaya akan platelet
sehingga terapi aspirin, clopidrogel, dan GP Iib/IIIa inhibitor paling efektif. Pemberian
trombolisis pada fase ini tidak efektif dan malah sebaliknya dapat mengakselerasi
oklusi dengan melepaskan bekuan yang berikatan dengan trombin yang dapat
mempromosi terjadinya koagulasi. Oklusi trombus yang bersifat intermitten dapat
menyebabkan nekrosis mikard sehingga menimbulkan NSTEMI.
d. Mikroemboli
Mikroemboli dapat berasal dari trombus distal dan bersarang di dalam
mikrovaskular koroner yang menyebabkan troponin jantung meningkat (penanda
adanya nekrosis di jantung) Kondisi ini merupakan risiko tinggi terjadinya infark
miokard.
e. Oklusif trombus
Jika trombus menyumbat total pembuluh darah koroner dalam jangka waktu
yang lama, maka akan menyebabkan STEMI. Bekuan ini kaya akan trombin, oleh
karena itu pemberian fibrinolisis yang cepat dan tepat atau langsung dilakukan PCI
dapat membatasi perluasan infark miokard.
Buku Panduan Kursus Bantuan Hidup Jantung Lanjut ACLS Indonesia, IDI.
4. Manifestasi Klinis
a. Rasa tekanan yang tidak nyaman, rasas penuh, diremas atau rasa nyeri di tengah dada
dalam beberapa menit
b. Nyeri yang menjalar ke bahu, leher, satu atau kedua lengan atau rahang bawah, ke
punggung
c. Nyeri dada yang disertai rasa sempoyongan, mau jatuh, berkeringat atau mual
d. Sesak nafas yang tidak dapat dijelaskan, yang dapat terjadi dengan atau tanpa nyeri
dada
Sumber: Buku Panduan Kursus Bantuan Hidup Jantung Lanjut ACLS Indonesia, IDI.
5. Algoritma SKA
- Pasang jalur IV, dapatkan / kaji EKG 12 sadapan Pertahankan saturasi > 90%
- Dapatkan px sinar X dada yg portable (<30mnt) - Morfin IV (nyeri tdk brkrng dgn
nitroglicerin
ST elevasi atau baru curiga LBBB ST Depresi atau inversi Perubahan normal/ non
baru; sangat mungkin terjadi luka gelombang T dinamis, sangat diagnostik pada segmen ST atau
ST- Elevasi MI (STEMI) mungkin terdapat iskemi ; gelombang T UA intermediate /
Angina tidak stabil, risiko risiko remdah
tinggi NSTEMI
Pertimbangkan admisi ke
Kirim ke tempat tidur Kirim ke tempat tidur unit nyeri dada ED atau
yang termonitor, Nilai >12jam yang termonitor, Nilai ke tempat tidur
status risiko status risiko termonitor di ED.
Monitor:
-penanda jantung
<12 jam (termasuk troponin),
monitor EKG,
Pasien risiko tinggi :
Strategi reperfusi : pertimbangkan tes stress
7. Komplikasi
1. aritmia
2. syok kardiogenik
a. akut defek septum ventrikel
b. regurgitasi mitral akut
3. edema paru akut
4. dinding ventrikel bebas pecah
www.aic.cuhk.edu.hk/web8/coronary%20sy.htm
8. Prognosis
Mortalitas sekitar 8% dari pasien yang bertahan hidup untuk mencapai
rumah sakit
www.aic.cuhk.edu.hk/web8/coronary%20sy.htm
10. Klasifikasi
12. Patogenesis
Infark Miokard :
o Ruptur plak yang terjadi di tepi lesi pada MI saat istirahat, atau di
daerah penipisan topi pada MI karena olah raga, menghasilkan
pembentukan thrombus dengan cepat dan oklusi pembulih darah
secara komplit
o Bukti-bukti menunjukkan bahwa peristiwa aterotrombosis
memiliki komponen inflamasi yang turut menyebabkan terjadinya
agregasi trombosit seperti yang ditunjukkan dengan tingginya
kadar protein C-reaktif pada pasien yang menderita iskemia
koroner akut.
o Iskemia berkepanjangan mengakibatkan kerusakan permanen sel-
sel miokard dengan kehilangan kontraktilitas dan pelepasan enzim
seluler
o Bila thrombus pecah sebelum terjadi nekrosis jaringan distal
secara komplet, infark hanya akan mengenai miokardium yang
berada tepat dibawah endokardium, dan tidak akan berhubungan
dengan sadapan gelombang-Q klasik pada EKG (MI subendokardial
atau MI non-gelombang Q). sangat penting mengenali bentuk
sindrom koroner akut ini karena pembentukan bekuan darah
berulang pada plak aterosklerotik yang pecah sangat mungkin
terjadi.
o Bila thrombus lebih permanen menghambat pembuluh darah,
maka infark akan melebar di sepanjang miokardium mulai dari
endokardium sampai epikardium mengakibatkan disfungsi jantung
berat dan gelombang-Q yang khas pada EKG(MI transmural atau
MI gelombang Q).
o Kerusakan iskemik mengakibatkan nekrosis dengan infiltrasi sel
sel inflamasi dan fibroblas yang mendasari jaringan parut (fibrosis)
dan mengakibatkan penurunan kontraktilitas dan komplians
secara permanen.
o stunning miokardium dapat terjadi di daerah sekitar jaringan
infark, suatu proses yang menyebabkan miosit kehilangan fungsi
konduktif dan kontraktilitas yang normal dalamwaktu lama
bahkan setelah perfusi dikembalikan. Dimediasi oleh peroksidasi
lipid yang diinduksi radikal bebas, defek enzim (pompa Na/K), dan
perubahan homeostasis kalsium.
(Valentina L. Brashes Aplikasi klinis patofisiologi,Pemeriksaan dan Manajemen.EGC)
Patogenesis
SKA merupakan salah satu bentuk manifestasi klinis dari penyakit jantung koroner (PJK),
salah satu akibat dari proses aterotrombosis selain strok iskemik serta peripheral arterial
disease (PAD). Aterotrombosis merupakan suatu penyakit kronik dengan proses yang sangat
kompleks dan multifaktor serta saling terkait.4
Perjalanan proses aterosklerosis (inisiasi, progresi, dan komplikasi pada plak aterosklerotik),
secara bertahap berjalan dari sejak usia muda bahkan dikatakan juga sejak usia anak-anak
sudah terbentuk bercak-bercak garis lemak (fatty streaks) pada permukaan lapis dalam
pembuluh darah, dan lambat-laun pada usia tua dapat berkembang menjadi bercak
sklerosis (plak atau kerak pada pembuluh darah) sehingga terjadinya penyempitan dan atau
penyumbatan pembuluh darah. Kalau plak tadi pecah, robek atau terjadi perdarahan
subendotel, mulailah proses trombogenik, yang menyumbat sebagian atau keseluruhan
suatu pembuluh koroner. Pada saat inilah muncul berbagai presentasi klinik seperti angina
atau infark miokard. Proses aterosklerosis ini dapat stabil, tetapi dapat juga tidak stabil atau
progresif. Konsekuensi yang dapat menyebabkan kematian adalah proses aterosklerosis
yang bersifat tidak stabil atau progresif yang dikenal juga dengan SKA.4,6
Sedangkan trombosis merupakan proses pembentukan atau adanya darah beku yang
terdapat di dalam pembuluh darah atau kavitas jantung.4 Ada dua macam trombosis, yaitu
trombosis arterial (trombus putih) yang ditemukan pada arteri, dimana pada trombus
tersebut ditemukan lebih banyak platelet, dan trombosis vena (trombus merah) yang
ditemukan pada pembuluh darah vena dan mengandung lebih banyak sel darah merah dan
lebih sedikit platelet.6 Komponen-komponen yang berperan dalam proses trombosis adalah
dinding pembuluh darah, aliran darah dan darah sendiri yang mencakup platelet, sistem
koagulasi, sistem fibrinolitik, dan antikoagulan alamiah.7
Patogenesis terkini SKA menjelaskan bahwa SKA disebabkan oleh obstruksi dan oklusi
trombotik pembuluh darah koroner, yang disebabkan oleh plak aterosklerosis yang rentan
mengalami erosi, fisur, atau ruptur. Penyebab utama SKA yang dipicu oleh erosi, fisur, atau
rupturnya plak aterosklerotik adalah karena terdapatnya kondisi plak aterosklerotik yang
tidak stabil dengan karakteristik inti lipid besar, fibrous cups tipis, dan bahu plak penuh
dengan aktivitas sel-sel inflamasi seperti limfosit T dan lain sebagainya. Tebalnya plak yang
dapat dilihat dengan persentase penyempitan pembuluh koroner pada pemeriksaan
angiografi koroner tidak berarti apa-apa selama plak tersebut dalam keadaan stabil. Dengan
kata lain, risiko terjadinya ruptur pada plak aterosklerosis bukan ditentukan oleh besarnya
plak (derajat penyempitan) tetapi oleh kerentanan plak.
Erosi, fisur, atau ruptur plak aterosklerosis (yang sudah ada dalam dinding arteri koroner)
mengeluarkan zat vasoaktif (kolagen, inti lipid, makrofag dan faktor jaringan) ke dalam
aliran darah, merangsang agregasi dan adhesi trombosit serta pembentukan fibrin,
membentuk trombus atau proses trombosis. Trombus yang terbentuk dapat menyebabkan
oklusi koroner total atau subtotal. Oklusi koroner berat yang terjadi akibat erosi atau ruptur
pada plak aterosklerosis yang relatif kecil akan menyebabkan angina pektoris tidak stabil
dan tidak sampai menimbulkan kematian jaringan. Trombus biasanya transien atau labil dan
menyebabkan oklusi sementara yang berlangsung antara 1020 menit. Bila oklusi
menyebabkan kematian jaringan tetapi dapat diatasi oleh kolateral atau lisis trombus yang
cepat (spontan atau oleh tindakan trombolisis) maka akan timbul NSTEMI (tidak merusak
seluruh lapisan miokard).4
Trombus yang terjadi dapat lebih persisten dan berlangsung sampai lebih dari 1 jam. Bila
oklusi menetap dan tidak dikompensasi oleh kolateral maka keseluruhan lapisan miokard
mengalami nekrosis (Q-wave infarction), atau dikenal juga dengan STEMI. Trombus yang
terbentuk bersifat stabil dan persisten yang menyebabkan perfusi miokard terhenti secara
tiba-tiba yang berlangsung lebih dari 1 jam dan menyebabkan nekrosis miokard transmural. 4
Trombosis pada pembuluh koroner terutama disebabkan oleh pecahnya plak aterosklerotik
yang rentan akibat fibrous caps yang tadinya bersifat protektif menjadi tipis, retak dan
pecah. Fibrous caps bukan merupakan lapisan yang statik, tetapi selalu mengalami
remodeling akibat aktivitas-aktivitas metabolik, disfungsi endotel, peran sel-sel inflamasi,
gangguan matriks ekstraselular akibat aktivitas matrix metalloproteinases (MMPs) yang
menghambat pembentukan kolagen dan aktivitas sitokin inflamasi.4
Vasokonstriksi pembuluh darah koroner juga ikut berperan pada patogenesis SKA.
Vasokonstriksi terjadi sebagai respon terhadap disfungsi endotel ringan dekat lesi atau
sebagai respon terhadap disrupsi plak dari lesi itu sendiri. Endotel berfungsi mengatur tonus
vaskular dengan mengeluarkan faktor relaksasi yaitu nitrit oksida (NO) yang dikenal sebagai
Endothelium Derived Relaxing Factor (EDRF), prostasiklin, serta faktor kontraksi seperti
endotelin-1, tromboksan A2, prostaglandin H2. Pada disfungsi endotel, faktor kontraksi
lebih dominan dari pada faktor relaksasi. Pada plak yang mengalami disrupsi terjadi platelet
dependent vasoconstriction yang diperantarai oleh serotonin dan tromboksan A2, serta
thrombin dependent vasoconstriction yang diduga akibat interaksi langsung antara zat
tersebut dengan sel otot polos pembuluh darah.4,6
Referensi:
. Anderson, J, Adams, C, Antman, E, et al. ACC/AHA 2007 guidelines for the
management of patients with unstable angina/non-ST-elevation myocardial
infarction: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines 50:e1. Diunduh
dari: www.acc.org/qualityandscience/clinical/statements.htm (accessed
September 18, 2007).
. Gibler, WB. Evaluation of chest pain in the emergency department. Ann Intern Med
1995; 123:315;.
. Tatum, JL, Jesse, RL, Kontos, MC, et al. Comprehensive strategy for the evaluation and
triage of the chest pain patient. Ann Emerg Med 1997; 29:116. Ornato, JP.
. Chest pain emergency centers: improving acute myocardial infarction care. Clin
Cardiol 1999; 22:IV3.
. Departemen Kesehatan RI. Pharmaceutical Care untuk Pasien Penyakit Jantung
Koroner. Jakarta: Depkes RI; 2006.
Kalim H, et al. Pedoman Praktis Tatalaksana Sindrom Koroner Akut. Jakarta: Departemen
Kardiologi dan Kedokteran Vaskular FKUI; 2008.p.3-7.
Penatalaksanaan
Angina pectoris
Definis
Etiologi
Patofisiologi
Diagnosis
penatalaksanaan
Syok kardiogenik
Definis
Etiologi
Patofisiologi
Diagnosis
penatalaksanaan
EKG
Fisiologi Kontraksi otot polos jantung
PEMBENTUKAN ATEROSKLEROSIS
STEP 4
STEP 5
STEP 6
STEP 7