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NSTEMI
Non ST ElevationMyocardial Infarction
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SKA
Suatu sindroma klinik yang menandakan
adanya iskemia miokard akut, terdiri dari :
STEMI
NSTEMI
Angina pektoris tidak stabil (UAP)
Ketiga kondisi ini sangat berkaitan erat, berbeda
hanya dalam derajat beratnya iskemi dan
luasnya miokard yang mengalami nekrosis.
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PATOGENESIS
Umumnya disebabkan oleh aterosklerosis
koroner
Plak aterosklerosis ruptur terbentuktrombus diatas ateroma yang secara akut
menyumbat lumen koroner
Apabila sumbatan terjadi secara total hampir seluruh dinding ventrikel akan
nekrosis
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Penyempitan
Pembuluh
darah
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Clinical Spectrum of Acute Coronary Syndrome
Acute Coronary Syndrome
Non-ST Segment
Elevation
ST Segment
Elevation
Unstable
Angina Pectoris
Non-Q-wave Q-wave
Acute Myocardial
Infarction
STEMI
NSTEMI
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Uncontrollable
Sex
Hereditary
Race
Age
Controllable
High blood pressure
High blood cholesterol
Smoking
Physical activity
Obesity
Diabetes
Stress and anger
Risk Factors
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Myocardial infarction:acute, evolving, recent
Typical rise and gradual fall (troponin) or morerapid rise and fall (CK-MB) of biochemical
markers of myocardial necrosis with at leastone of the following:
a) ischemic symptoms;
b) development of pathologic Q waves on the ECG;
c) ECG changes indicative of ischemia (ST segmentelevation or depression); or
d) coronary artery intervention (e.g., coronary angio-plasty).
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ACC/AHA Guidelines
NSTEMI is an acute process of myocardial
ischemia with sufficient severity andduration to result in myocardial necrosis.
The initial ECG in patients with NSTEMI
does not show ST-segment elevation.
NSTEMI is distinguished from UA by the
detection of cardiac markers indicative of
myocardial necrosis in NSTEMI and theabsence of abnormal elevation of such
biomarkers in patients with UA.
Definition: NSTEMI
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Definition: unstable angina
Unstable anginaan acute process of
myocardial ischemia that is not ofsufficient severity and duration to result in
myocardial necrosis.
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Diagnosis
Anamnesis
Pemeriksaan Fisik
Pemeriksaan Penunjang :
1. Laboratorium
2. Elektrokardiografi
3. Thoraks Foto
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HISTORY
PRODROMAL SYMPTOMS
History very valuable to establish D/. Prodoma : chest discomfort
unstable angina 1/3 symptoms for 1 4 wks
20% symptoms for < 24 hrs
Malaise, exhaustion
NATURE OF PAIN Most patients
severe prolonged, 30 minutes - hours Constricting, crushing, oppressing, compressing
heavy weight or squeezing in chest
Choking, vise-like, heavy pain or stabbing, knife-like, boring or
burning discomfort
Location : retrosternal, spreading frequently to both sides of the
chest with predilection to the left side
Often pain radiates down ulnar aspect of left arm, producing
tingling sensation in left wrist, hand and fingers
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NATURE OF PAIN
SOME INSTANCES : pain begins in epigastrium, and simulates
abdominal disorder
Sometimes pain radiates to shoulders, upper extremities, neck, jaw
and interscapular region favoring the left side
Elderly : no chest pain but acute left ventricular failure and chest
tightness or marked weakness or syncope
Pain arises from nerve endings in ischemic or injured, but not necrotic,
myocardium
OTHER SYMPTOMS
50% nausea or vomiting in transmural infarcts Occasionally diarrhea, profound weakness, dizziness, palpitation, cold
perspiration, sense of impending doom
Occasionally : cerebral embolism or systemic arterial embolism
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Pain Patterns with MyocardialIschemia
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Anamnesis untuk UAP
3 kategori presentasi klinik UAP:
Angina saat istirahat (resting angina)
Angina awitan baru (new onset angina)
Angina yang bertambah berat (increasingangina)
Riwayat penyakit dahulu :
Riwayat angina on effort, infark atauoperasi pintas
Riwayat penggunaan nitrogliserin
Identifikasi faktor-faktor risiko
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PHYSICAL EXAMINATION
GENERAL APPEARANCE
Anxious, considerable distress, restless, fist on chest(Levine sign)
LV failure & symp. stimulation : cold perspiration, pallor,dyspnea, cough with frothy pink or blood-streakedsputum.
Shock : cool, clammy skin, facial pallor, cyanosis,confusion or disorientation
HEART RATE Variable depending on underlying rhythm and degree or
ventr. failure
Most commonly, HR 100 110/min; > 95% patients :
VPBs within first 4 hours
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BLOOD PRESSURE
Majority normotensive, but syst. BP may decline and
diast. BP may rise Half of pts with inferior MI parasympathetic
stimulation : hypotension, bradycardia or both (Bezold Jarisch reflex)
half of pts with anterior MI, sympathetic excess :hypertension, tachycardia or both
TEMPERATURE AND RESPIRATION
Most pts with extensive MI fever within 24-48 hrs,fever resolves by 4th or 5th day
Respiration due to anxiety and pain, in LV failure : resp.rate correlates with degree of heart failure
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JUGULAR VENOUS PULSE
JVP usually normal
RV infarction : marked jug. venous distension
CAROTID PULSE
Small pulse reduced stroke volume
Pulse alternans : severe LV dysfunction
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CHEST
LV failure and/or LV compliance : moist rales
Severe failure : diffuse wheezing, cough + hemopthysis
1967 : Killip & Kimball : prognostic classification
Class I : patients free of rales or S3
II : rales < 50% lung fields +/- S3
III : rales > 50% lung fields, frequently
pulm. edema IV : cardiogenic shock
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Pemeriksaan Penunjang
Pemeriksaan EKG
Gambaran EKG infark miokard akut Q-wave (STEMI):
Elevasi segmen ST 1 mm pada 2 sadapanextremitas
Atau 2 mm pada 2 sadapan prekordial yangberurutan
Atau gambaran LBBB baru atau diduga baru
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Gambaran EKG infark miokard akut non-Q-wave
(NSTEMI) atau angina pektoris tidak stabil
(UAP) :
Depresi segment ST atau gelombang T
terbalik pada 2 sadapan berurutan
Inversi gelombang T minimal 1 mm pada 2
sadapan atau lebih yang berurutan.
Perubahan segment ST saat keluhan dan
kembali normal saat keluhan hilang sangatmenyokong UAP
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ST-segment depression
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T-wave inversion
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Current-of-injury patterns with acuteischemia
ELEKTROKARDIOGRAM
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Pemeriksaan Penanda Jantung/Enzim jantung
(Cardiac Markers):
Yang lazim adalah CKMB, dapat pula troponin T
(TnT) atau troponin I (TnI)
Peningkatan marka jantung akan terlihat pada
infark miokard akut Q-wave (STEMI) dan non-Q-wave
(NSTEMI)
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Plot of the appearance of cardiac markers inblood versus time after onset of symptoms
A myoglobin C CK-MB
B troponin D troponin in UA
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1. Diseksi aorta
2. Perikarditis
3. Nyeri angina atipikal pada kardiomiopati
hipertrofi
4. Penyakit esofageal, GI atas atau traktus biliaris
5. Penyakit paru-paru : pneumotoraks, emboli,
pleuritis
6. Sindroma hiperventilasi7. Gangguan dinding dada : muskuloskeletal,
neurogen
8. Psikogen
Diagnosis Banding
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Recommended Class I:
Aspirin, Nitrate, B-blockers, morphine, O2 (prn).
Nondihydropyridine (cardizem/verapamil).
ACEi for specifics.
Class 2a:
ACEi for all.
Long-acting CCB for recurrent ischemia.
IABP if all fails.
Class 2b:
Extended form of Nondihydropyridine.
Short acting dihydropyridine in the presence of B-blocker.
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Oxygen
For:
Cyanosis
Resp distress
High risk features
Consume resources Evidence is lacking.
Nit t
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Nitrates: Decr MVO2, incr coronariesoxygenation
Actions
Dilate venous bed: decr preload and ventricular walltension.
Smaller dilatation of arterial system: decr afterloadand ventricular wall tension.
Need B-blocker
Dilatation of atherosclerotic coronaries
Decreased platelets adhesiveness.
For
ischemia despite nitro X 3 and iv B-blockade
high-risk patients (non-hypotensive).
Prethrombolytics: 35% mortality reduction.
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Morphine
Potent anxiolytic and analgesic action
Potentially beneficial
Venous dilatation
Decr HR
Decr sBP (Decr MVO2)
Activates neutral endopeptidases
Ann Emerg Med. May 2001;37:445-449.
Nausea and vomiting in 20%
Hypotension
Meperidine if allergic
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Beta-blockers Decr sBP
Decr SA node rate, contractility, AV nodeconduction.
Incr diastole filling time.
iv form for high-risk pts/on going pain.
Oral for intermediate/low risks patients.
No preferred agents except better if B-blockerwithout ISA (metoprolol, atenolol, propramolol,esmolol).
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B-blockers Contraindications (consensus):
1st degre AV block >24 msec
2nd or 3rd degre AV block without pacemaker
Asthma
Severe LV dysfunction with CHF
Caution with:
COPD
Bradycardia
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B-blockers
13% reduction of progression of UA to
AMI.
Extrapolate data from use in AMI, recent
MI, stable angina, heart failure.
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Calcium channel blockers
Inhibit vasculature SM contracture
Coronary vasodilatation
Inhibit myocardial muscle contraction
AV block
Slow sinus node
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Calcium channel blockers Dihydropyridines: nifedipine and amlodipine
peripheral vasodilatation
Verapamil: DAVIT study (3200 pts)
Only favorable trend
Nifedipine: HINT study (500 pts)
Incr MI by 16%, decr by 20% if with metoprolol
But metoprolol alone decr by 24%!!!
Diltiazem showed trends of improved outcome
CKMB level, reinfarction rate
Same mortality
except in LV dysfunction ACS
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Calcium channel blockers
Conclusion:
Good symptom reliever Trend of improved outcome with non-
dihydropyridine agents
To use if unable to use B-blockers
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Antiplatelet agents
Aspirin ASAP!
Thienopyridine (clopidogrel or ticlopidine) ifhypersensitivity of major GI intolerance
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Aspirin
Cyclooxygenase-1 inhibitor
Prevents thromboxane A2 formation
Dosing: 160 mg or 325 mg
Based on ISIS-2 which definetly established
its efficacy.
Can use pr route.
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Adenosine diphosphate
inhibitors Clopidogrel acts faster than ticlopidine.
Ticlodipine: Gi se, neutropenia, TTP
Clopidogrel: minimal rash and diarrhea
11 TTP within 14 days (3 millions pts)
CURE study: NEJM Aug 2001 12000 pts, plavix 300mg po
9.3 vs 11.4, 16.5 vs 18.8
ST changes or + markers
No GP2b3a inh or angio
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Plavix:Safety if angio or used with
Gp2b3A inh Lancet August 2001: PCI-CURE study
2600 pts.
Plavix 300mg loading
No increased bleeding problem whether
plavix +/- GPIIb/IIIa inh were used.
Better outcome before an after PCI.
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Other po agents
Sulfinpyrazone
Dipyridamole
Prostacyclin
Oral GP IIB/IIIA inhibitor:
4 studies: 1 PCI, 3 NSTEMI 2 increased mortality
None presently recommended
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Anticoagulants
UFH
LMW heparin
Hirudin
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UFH Activates antithrombin III
Inactives thrombin (f2), f9a and f10a
Molecular weight: 5 000 to 30 000 D
Binds to various proteins, cells , endothelium
Unpredictable.
Weight adjusted dosage
Incr need in DM and smoking, lower with age
Theroux et al. N Engl J Med 1988;319:110511.
MI rate of 12% down to 0.8% in UA
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LMW heparin
Molecular weight of 4200 to 6000 D
Factor Xa to thrombin inhibition ratio of1.9 to 3.8
Only 25-50% have >18 saccharides
both f2 and 10 inhibition
Rest inhibits only factor Xa
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