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ACUTE CORONARY

SYNDROME
Pembimbing
C

Kepaintraan Klinik Ilmu


Dr. Tommy Sibuea Sp. PD Penyakit Dalam Periode
Dr. Sorta Sibuea Sp.PD
06 Mei – 20 July 2019
Disusuh Oleh: Fakultas Kedokteran
Anggi Thalita Adelia Simatupang Universitas Kristen Indonesia
1965050034 Jakarta
CLASSIFICATION
• Acute coronary syndrome is a term used to describe a range of conditions associated
with sudden, reduced blood flow to the heart.

• Acute Coronary Syndrome


• Unstable Angina Pectoris
• Non- ST Segment Elevation
• ST- Segment Elevation
Non- ST Segment Elevation (Subendocardial
Myocardial Infarct) and Unstable Angina
• NSTE-ACS caused by imbalance between oxygen supply and oxygen demand
resulting from a partially occluding thrombus forming on a disrupted atherothrombotic
coronary plaque.
• Increased cardiac enzymes (NSTE-ACS)
• Clinical presentation:
• Chest discomfort is severe and has at least one of three features
• It occurs at rest lasting/min exertion >10 minutes but <30 minutes
• It is of relatively recent onset (onset 1 month)
• It occurs with a crescendo pattern
• Chest pain is typically located in the substernal region or epigastrium and radiates to the left
arm, shoulder and or neck.
TREATMENT
Anti Ischemic
ST-Segment Elevation Myocardial Infarction
(Transmural Myocardial Infarct)
• STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic
occlusion of a coronary artery previously affected by atherosclerosis.
• Clinical presentation
• Pain most common  deep and visceral. Described as heavy, squeezing, crushing, stabbing, burning
• Occurs at rest, is usually more sever, last longer
• Physical findings
• Anxious, restless, altering position, stretching
• Pallor, coolness of extremities
• Chest pain >30 min and diaphoresis
• STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury.
 injury if facilitated by factors such as cigarette smoking, hypertension, and lipid
accumulation.  surface of an atherosclerotic plaque becomes disrupted and conditions
favor thrombogenesis.  thrombus forms at the site of plaque  occluded.
• Coronary plaques prone to disruption are those with a rich lipid core and thin fibrous cap
Diagnosis
• Electrocardiogram

• Cardiac Enzymes
• CK-MB
• Troponin T, I
• Cardiac imaging
• If patient cannot exercise adequately
• Magnetic Resonance (CMR)
• Echocardiography (ECHO)
• Position emission tomography (PET)
Emergency Department
• Goals for the management: control of cardiac discomfort, rapid identification of
patients who are candidates for urgent reperfusion therapy, triage of lower-risk patients
to the appropriate location in the hospital.
• Aspirin is essential in the management of patients with suspected STEMI and is effective
across the entire spectrum of acute coronary syndromes.
• Sublingual nitro-glycerine can be given safely to most patients with STEMI. Up to three
doses of 0.4 mg should be administered at about 5-min intervals. Nitro-glycerine may
be capable of both decreasing myocardial oxygen demand and increasing
myocardial oxygen supply.
• The primary tool for screening patients and making triage decisions is the initial 12-lead
ECG. When ST-segment elevation of at least 2 mm in two contiguous precordial leads
and 1 mm in two adjacent limb leads is present, a patient should be considered a
candidate for reperfusion therapy.
Hospital Phase Management
• Coronary care unit
• Continuous monitoring of cardiac rhythm, hemodynamic monitoring
• Patients should be admitted to a coronary care unit  duration of stay is dictated by the
ongoing need for intensive care
• Activity
• Patients should be kept at bed rest for the first 6-12 hours
• Absence of complication: upright position by dangling their feet over the side of the bed and
sitting in a chair within the first 24 h.
• Psychologically beneficial and usually results in a reduction in the pulmonary capillary wedge
pressure.
Pharmacotherapy
• Antithrombotic agents
• primary goal :to maintain patency of the infarct-related artery, in conjunction with reperfusion
strategies.
• secondary goal: to reduce the patient’s tendency to thrombosis
• Beta – adrenoreceptor blocker
• Acute intravenous beta blockade improves the myocardial O2 supply-demand relationship,
decreases pain, reduces infarct size, and decreases the incidence of serious ventricular
arrhythmias.
• Inhibition of Renin - Angiotensin – Aldosterone system
• The mechanism involves a reduction in ventricular remodelling after infarction with a
subsequent reduction in the risk of CHF.

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