ESC Guidelines for the management of Acute Coronary

Syndrome in patients without persistent ST Elevation.2011

Unstable
NSTEMI STEMI
Angina
Non-occlusive
thrombus Complete thrombus
Non occlusive sufficient to cause occlusion
thrombus tissue damage & mild
myocardial necrosis ST elevations on
Non specific ECG or new LBBB
ECG ST depression +/-
T wave inversion on Elevated cardiac
Normal cardiac ECG enzymes
enzymes
Elevated cardiac More severe
enzymes symptoms
EKG Normal
ST elevation on the ECG
ST elevation on the ECG
 ACS PATHOPHYSIOLOGY

Distruption of coronary artery

plaque -> platelet
activation/aggregation
/activation of coagulation
cascade -> endothelial
vasoconstriction ->intraluminal
thrombus/embolisation ->
obstruction -> ACS
Severity of coronary vessel
obstruction & extent of
myocardium involved
determines characteristics of
clinical presentation
Unstable Plaque
Plaque (lipid rich core,
fibrious cap)
Monocytes,
in ACS macrophages,
inflammation
Plaque rupture
deposition of platelet
aggregates, thrombosis

Partial Partial Complete

occlusion occlusion occlusion

thrombolysis thrombosis Collaterals

Lysis and repair Unstable angina Q wave MI

No symptoms Non Q wave MI Non Q-wave MI
Rapid progression of Angina,ECG changes, Angina,ECG changes,
atherosclerosis Troponin release Troponin release
Vulnerable plaque
a large lipid core
a low density of smooth
muscle cells
a high concentration of
inflammatory cells
a thin fibrous cap covering
the lipid core
acute thrombosis induced
by a plaque rupture
Vulnerable plaque
Vulnerable patient
Multiple sites of plaque rupture with or without
intracoronary thrombosis
Elevated levels of various systemic markers of inflammation,
thrombosis and coagulation system activation
Hypercholesterolaemia
Tobacco smoking
Classification of MI
Type 1 spontaneous MI related to ischemia due to a primary
coronary event such as plaque erosion and/or rupture,
fissuring, or dissection
Type 2 MI secondary to ischemia due to either increased oxygen
demand or decreased supply, e.g. coronary artery spasm,
coronary embolism, anemia, arrhythmias, hypertension, or
hypotension
Type 3 sudden unexpected cardiac death, including cardiac arrest
but death occurring before blood samples could be
obtained
Type 4 associated with PCI:
Type 4a MI associated with the procedure of PCI
Type 4b MI associated with stent thrombosis

Type 5 MI associated with CABG

Myocardial infarction
1. Atherosclerotic aetiology (type 1)
2. Non-atherosclerotic aetiology: (type 2-5)
arteritis
trauma
dissection
congenital anomalies
cocaine abuse
complications of cardiac catheterization, CABG
Diagnosis of acute MI
2 from 3 criteraia must be fulfilled :
Clinical symtoms
Chest pain
ECG changes
ST elevation or depression
negative T wave
Elevated cardiac biomarkers
Troponin I or T
CK-MB
myoglobin
Diagnosis of ACS
Clinical presentation
History of patient
Physical examination
Electrocardiogram
Biochemical markers - troponin
Non-invasive imaging - Echo
Imaging of coronary arteries - coronary angiography
 KELUHAN UTAMA SINDROM KORONER AKUT
Sakit dada atau nyeri hulu hati yang berat, asalnya
non-traumatik, dengan ciri-ciri tipikal iskemia miokard
atau infark:
Dada bgn tengah/substernal rasa tertekan atau sakit
seperti diremas
Rasa sesak, berat/tertimpa beban , mencengkeram,
terbakar, sakit perut yg tdk dpt dijelaskan, sendawa,
nyeri hulu hati
Penjalaran ke leher, rahang, bahu, punggung atau 1
atau ke2 lengan
Disertai sesak
Disertai mual dan/atau muntah
Disertai berkeringat

Start EKG
Clinical presentation
STE/NSTE-ACS:
Intense prolonged (20 min) pain at rest - retrosternal pressure or
heaviness (angina) radiating up to the neck, shoulder and jaw and
down to the ulnar aspekt of the left arm
May be accompanied by other symptoms such as
diaphoresis, nausea, abdominal pain, dyspnoea,
Unstable angina:
New onset severe angina (class III of CCS)
Recent destabilization of previously stable angina with
at least CCS III angina characteristics (crescendo
angina)
Post-MI angina.
 Clinical presentation
1) Typical chest pain

2) Nauzea
3) Sweating
Clinical presentation
Atypical presentations are not uncommon
epigastric pain
recent-onset indigestion
stabbing chest pain
chest pain with some pleuritic features
increasing dyspnoea

- often can be observed in younger (25-40y.), older (75y.),

in women, in pts. with diabetes, chronic renal failure, or
dementia.
Clinical presentation
The presence of tachycardia, hypotension,
or heart failure needs rapid diagnosis and management,
often indicating a poor prognosis of this patient with ACS

It is important to identify the clinical circumstances such

as anaemia, infection, inflammation, fever, and metabolic
or endocrine (in particular thyroid) disorders (may
exacerbate or precipitate ACS)
Physical examination
Frequently normal
Signs of heart failure or haemodynamic instability
Dif. dg.:
- nonischaemic cardiac disorders: pulmonary
embolism, aortic dissection, pericarditis,
valvular heart disease)
- extra-cardiac causes: pulmonary
diseases - pneumothorax, pneumonia,
pleural effusion)
Physical examination
Heart failure
Tachycardia, tachypnoe
Pulmonary rales (pulmonary congestion)
RV failure - jugular congestion, hepatomegaly
Hypotension 100/60 mmhg
cardiac shock (tachycardia)
vagal nerve activity (bradycardia - inferior IM)
Bradycardia
AV block
Inferior IM - non-serious, frequent
Anterior IM - serious, rare
Electrocardiogram
The resting 12-lead ECG is the first-line diagnostic tool in
the assessment of patients with suspected ACS.
STE-ACS ST-elevation
NSTE-ACSST-segment shifts and T-wave changes
A completely normal ECG does not exclude the possibility of
ACS.
Location of MI
Location of MI
ST elevation only:
Anteroseptal -V1-V3
Anterolateral - V1-V6
Inferior wall - II, III, aVF
Lateral wall - I, aVL, V4-V6
Right ventricular - RV4, RV5
Posterior- R/S ratio >1 in V1 and T
wave inversion
Location of MI
Location of MI
Location of MI
Biochemical markers
Markers of myocardial injury:
cardiac troponins (I and T)
creatinine kinase (CK)
CK isoenzyme MB (CK-MB)
Myoglobin

repeated blood sampling and measurements are required 6

12 h after admission and after any further episodes of severe
chest pain
Imaging of the coronary anatomy
The imaging of the coronary anatomy is the most
importat diagnostics method in evaluation of acute
coronary syndrome

The gold standard of patients with ACS is conventional

invasive coronary angiography
Early Invasive

Conservative
Tindakan Umum &
Langkah Awal
Tirah Baring (Kelas 1C)

Oksigen utk pasien dg Saturasi<95% atau distres nafas(I-C)

2
Suplemen Oksigen diberikan utk semua SKA dlm 6 jam pertama tanpa mempertimbangkan Saturasi
(IIa-C)

4 Aspirin tanpa salut 160-320 mg pd semua ps yg toleran thdp Aspirin (I-C)

5 Clopidogrel dosis awal 300 mg, dilanjutkan 75 mg/hari(I-C)

5 Suplemen Oksigen diberikan utk semua SKA dlm 6 jam pertama tanpa mempertimbangkan Saturasi (IIa-C)

Anti Iskemik: NTG spray/tab (I-C), Morfin sulfat 1-5 mg IV dpt diulang setiap 10-30 menit (IIa-
5B)

37
 Psn Nyeri Dada SINDROM KORONER AKUT
Rwyat nyeri dada Aspirin 300 mg dikunyah dan Nitrat s.l.
khas
EKG 12 sandapan*
Penatalaksanaan Petanda biokimia
SKA
EKG Non diagnostik Perubahan ST/T Elevasi seg
Petanda biokimia (-) Petanda biokimia (+)
ST
Nyeri dada (-) Nyeri dada menetap

EKG tdk Observasi

berubah EKG serial
Evaluasi utk
Petanda(-) Ulang petanda
6-12 jam stlh reperfusi
Nyeri dada(-)
onset nyeri dada*
Rawat Terapi
Pulang Nitrat
Perubahan seg ST ASA
Risiko rendah Risiko tinggi Petanda (+) APTS/NSTEMI Clopidogrel
Periksa di Periksa Nyeri dada UFH/LMWH
Rawat jalan segera (+/- Antagonis
menetap
Receptor GPIIb/IIIa
Malaysian Clinical Practice Guideline on UA/NSTEMI 2002