Acs-ilham.ppt

ACUTE CORONARY SYNDROME dr. Ilham Uddin SpJP

New Paradigm

Threshold

Decades

Years-Months

healthy

subclinical

Months-Days symptomatic Thrombus

Intima Media

Lumen

Plaque • • • • •

Unstable angina Unstable plaque no narrowing Difficult to diagnose (IVUS, MRI) Frequent MI with sudden death Easy to prevent

Pathophysiology of Atherosclerosis •Foam •Cells

Endothelial Dysfunction

•Fatty •Intermediate •Fibrous •Complicated •Streak •Lesion •Atheroma •Plaque•Lesion/Rupture

•oxidized LDL •homocystein e

•smoking •aging •hyperglycemi a •hypertension

35-45 yrs 45-55 yrs •Endothelial injury•Lipid accumulation •nitric oxide •endothelin-1 •vasodilation

•adhesion molecules (ICAM, VCAM) •monocyte adhesion •macrophage LDL uptake

55-65 yrs

•Inflammation

>65 yrs

•continued macrophage/lipid •MMP's accumulation •CRP (hepatic) •leukocyte accumulation •cytokines (IL-6, TNFa, IFNg )

Pathophysiology Mechanical Obstruction

Thrombosis

Dynamic obstruction

> MVO2 Inflammation/ Infection Mechanical Obstruction

Thrombosis

Dynamic obstruction Inflammation/ Infection Braunwald, Circulation 98:2219,1998

> MVO2

Acute Coronary Syndromes  

Are a continuum initiated by: rupture of an unstable, lipid-rich atheromatous plaque in epicardial artery; activating platelet adhesion, fibrin clot formation and coronary thrombosis

ACUTE CORONARY SYNDROME

ST Elevation

No ST Elevation

NSTEMI

Unstable Angina N Qw Myocardial Infarction

Qw Myocardial Infarction AHA Guidelines, 2000

New terminology for coronary syndromes

Adapted from Aroney C, Boyden AN, Jelinek MV, et al. Management of unstable angina: guidelines 2000. Med J Aust 2000;173(Suppl):S65–S88, with permission.

Pemeriksaan awal pada Sindrom Koroner Akut Masuk RS Diagnosis Kerja ECG Biochemistry Stratifikasi risiko

SAKIT DADA

Anamnesis & pem. fisik

Curiga Sindrom Koroner Akut Elevasi ST menetap Troponin CK/CKMB

Tanpa Elevasi ST menetap

Normal atau Tdk dpt ditentukan ECG Troponin 2 X negative

Troponin

Risiko: :Tinggi Sedang Rendah

Mungkin bukan SKA

Pengobatan Pencegahan sekunder Esc/EHJ 2002

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 sakit perut yg tdk dpt dijelaskan, sendawa, nyeri hulu hati Penjalaran ke leher, rahang, bahu, punggung atau 1 atau ke 2 lengan •Disertai sesak •Disertai mual dan/atau muntah •Disertai berkeringat

Patients with suspected ACS, who have chest pain at rest > 20 minutes, syncope/presyncope, or unstable vital signs ----refer to EMG immediately AFP Guideline 2005

PERKI Guideline 2003 : 10 minutes NHFA &CSANZ Guideline 2006 : 10 minutes European Guideline 2003 : 20 minutes

Suspicious Chest Pains 

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Classic angina - dull, pressure, substernal; arm or neck radiation; SOB, palpitations, sweating, nausea or vomiting Angina Equivalent - no pain but sudden ventricular failure or ventricular dysrhythmias Atypical chest pain - precordial area but with musculoskeletal, positional, or pleuritic features

DIAGNOSIS DIFERENSIAL SAKIT DADA Cardiac    

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ACS : Infarct,angina MVP Aortic Stenosis Hypertrophic cardiomyopathy Pericarditis

Lungs    

Lung Emboli Pnemonia Pneumothorax Pleuritis

Gastrointestinal •Reflux esofagus •Ruptur esofagus •Gall bladder disease •Peptic Ulcer •Pancreatitis

Vascular •Aortic dissection/aneurysma

Others •Musculoskeletal •Herpes zoster

CAD Risk Stratification 

High Risk (≧1 of the following features)    

Prior MI, VT or VF or known CAD Definite clinical angina Dynamic ST changes Marked anterior T-wave changes

CAD Risk Stratification 

Intermediate Risk (no high-risk features plus 1 of the following)    

Definite angina (young age) Probable angina (older age) Possible angina (DM or 3 other risk factors) ST depression  1 mm or T inversion  1 mm

CAD Risk Stratification 

Low Risk (no high- or intermediate-risk features plus 1 of the following)    

Possible angina One risk factor (not DM) T-wave inversion < 1mm Normal ECG

Sasaran utama terapi SKA : • Mengurangi nekrosis miokard pada pasien yg mengalami infark

• Mencegah MACE ( kematian, IMA non fatal, kebutuhan untuk revaskularisasi segera ) • Defibrilasi segera bila terjadi VF

Stratifikasi risiko : EKG 12 lead

3 kelompok triase : • Elevasi segmen ST • Depresi segmen ST • EKG non diagnostik/normal

ER Patient Care Initial assessment (< 10 min)     

Measure vital signs Measure SpO2 Obtain IV access Obtain 12-lead ECG Perform brief, targeted history and PE)

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Obtain initial cardiac marker levels Evaluate initial electrolyte and coagulation studies Request, review portable chest x-ray (<30 min

ER patient care 

Initial general treatment (memory aid: “MONA” greets all patients   

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Morphine, 2-4 mg repeated q 5-10 min Oxygen, 4 L/min; continue if SaO2 < 90% NTG, SL or spray, followed by IV for persistent or recurrent discomfort Aspirin, 160 to 325 mg (chew and swallow)

Triage by ECG 

ST elevation or new LBBB 

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ST depression or dynamic T-wave inversion 

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ST elevation ≧1 mm in 2 or more contiguous leads ST depression > 1 mm Marked symmetrical T-wave inversion in multiple precordial leads Dynamic ST-T changes with pain

Nondiagnostic ECG or normal ECG

ST depresi dan perubahan gelombang T • ST depresi dianggap bermakna bila > 1 mm di bawah garis dasar PT di titik J • Titik J didefinisikan sebagai akhir kompleks QRS dan permulaan segmen ST Bentuk segmen ST : • up-sloping ( tidak spesifik ) • horizontal ( lebih spesifik untuk iskemia ) • down-sloping ( paling terpercaya untuk iskemia )

Perubahan gelombang T pada iskemia kurang begitu spesifik Gelombang T hiperakut kadang2 merupakan satu-satunya perubahan EKG yang terlihat

T Wave

Stable atherosclerotic plaque

Electrocardiography 

ECG necessary to detect ischaemic changes or arrhythmias.

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Initial ECG has a low sensitivity for ACS, and a normal ECG does not rule out ACS.

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However, the ECG is the sole test required to select patients for emergency reperfusion (fibrinolytic therapy or direct PCI).

ECG 

serial ECGs : in patients with NSTEACS w high and intermediate risk features The frequency of ECGs will depend on clinical features (eg, every 10– 15 minutes during ongoing symptoms, immediately if symptoms change while the patient is under observation

Blood tests Measurements should include: • Serum troponin I or T levels ( or CK-MB if troponin is not available). • Full blood count. • Serum creatinine and electrolyte levels, particularly K+ concentration, as hypokalaemia is associated with an increased risk of arrhythmias, especially ventricular fibrillation10 (grade B recommendation). Knowledge of kidney function (expressed as estimated glomerular filtration rate) is strongly encouraged (grade B recommendation) given the association between renal impairment and adverse outcomes (evidence level III).11

Serum creatine kinase (CK) level. • Serum lipid levels (fasting levels of total cholesterol, lowdensitylipoprotein cholesterol, high-density-lipoprotein cholesterol and triglycerides) within 24 hours. • Blood glucose level.

Recommendations on Cardiac Biomaker

Cardiac Troponin •On arrival -------- Troponin indicates myonecrosis --high feature in NSTEACS -------- 1/3 pts high Troponin but normal CK & CKMB will develop adverse outcome •Not repeated if positif --- not useful for identifying ealy reinfarction •If initial negative --- repeat > 8 hours after last episode of chest pain or other symptoms •Serial troponin ----in pts NSTEACS suspected to be at high risk.Rise indicates more aggressive thx.

Recommendations on Cardiac Biomarkers

CK-MB Level •Measured in All pts with an ACS if Troponin assay unavailable ( if Trop unavailable, CK-MB is more spesific than CK for myocardial injury. CK-MB may be used to confirm a re-infarction)

Total CK Level •Serial measurements for 48 hrs in MCI •Remeasurement if reinfarction suspected

Chest x-ray 

A chest x-ray is useful for assessing cardiac size, evidence of heart failure and other abnormalities (grade D recommendation), but should not delay reperfusion treatment where indicated.

Kriteria infark miokard akut

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Kriteria infark miokard akut adalah terdapat 2 dari 3 kriteria dibawah ini : Nyeri khas infark Perubahan serial EKG Peningkatan diikuti dengan penurunan serum cardiac marker.

Penanganan Khusus Terapi reperfusi, dengan sasaran: • Fibrinolitik : door-to-needle < 30 menit • Primary PTCA: door-to-dilatation < 90 menit

Terapi Conjunctive ( kombinasi dengan obat fibrinolitik ) • Aspirin • Heparin ( khususnya dengan TPA )

Terapi Tambahan •  blocker oral , bila memungkinkan • Nitrogliserin iv ( iskemik menetap, kontrol hipertensif dan udem paru ) • ACE Inhibitor ( IMA anterior, LVEF < 40%, gagal jantung tanpa hipotensi - TD sistolik > 100 mmHg )

Terapi Fibrinolitik Tissue Plasminogen Activator ( tPA ) Diberikan pada AMI yang luas, datang dini dan kemungkinan komplikasi pendarahan kecil Diberikan dengan dosis bertahap • 15 mg bolus iv • 0.75 mg/kg - jangan > 50 mg, 30 menit • 0.50 mg/kg - jangan > 35 mg, 60 menit Streptokinase Diberikan pada pasien IMA yang kemungkinan komplikasi perdarahan otak tinggi, datang lambat dan infarknya tak luas • 1.5 juta unit dalam 1 jam

Terapi Fibrinolitik Reteplase (rPA) 10 U + 10 U iv bolus selang 30’ Tenecteplase (TNK-tPA) Single iv bolus • 30 mg = < 60 kg • 35 mg = 60-70 kg • 40 mg = 70-80 kg • 45 mg = 80-90 kg • 50 mg = > 90 kg

Heparin IV ( U F H )

AHA, 2004

Direkomendasikan untuk : • Pasien yang strategi reperfusinya menggunakan PTCA / CABG • Pasien yang diberi TPA, Reteplase atau Tenecteplase • Pasien yang diberi Streptokinase, Anistreplase atau Urokinase dengan risiko tromboemboli ( IMA anterior / luas, AF, riwayat emboli atau diketahui Trombus LV ) • Trombosit harus diperiksa setiap hari

Perhatian : Kontraindikasi seperti pada terapi fibrinolitik LMWH ( Enoxaparin ) 30 mg bolus iv, diikuti 1 mg / kg / sc tiap 12 jam

ST-Elevation ASA Beta Blocker

<12h Eligible for thrombolytic therapy

Thrombolytic therapy contraindicated

Thrombolytic therapy From loaded t-PA or SK

Primary PTCA or CABG

>12h Not a Candidate for reperfusion therapi

Persistent Symptoms

No

Other medical therapy: ACE inhibitor ? Nitrates

Yes

Consider Reperfusion Therapy

1999 Updated ACC/AHA AMI Guidelines (Web Version:March 22, 2002)

Benefit of Thrombolytics Time Lives saved/1000 < 1h 65 1-2 h 37 2-3 h 29 3-6 h 26 6-12 18 12-24 9

Thrombolytics and Stroke 

Risk factors: > 65 years  BW < 70 Kg  BP > 180/110  on anticoagulants 

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Strokes no risks = 0.25%  3 risks = 2.5% 

Fibrinolytic Use in Myocardial Infarction ( AHA 2004 ) Absolute Contraindications

Cautions/Relative Contraindications

• Previous hemorrhagic

• Severe uncontrolled HT on presentation

stroke at any time

(BP >180/110 mm Hg)

• Ischemic strokes 3 mo ( except 3 hrs )

• History of prior CV accident or known intracerebral pathology not covered in CI

• Known intracranial malignant neoplasm

• Current use of anticoagulants (INR ≥2-3); known bleeding diathesis

• Active internal bleeding / bleeding diasthesis ( not include menses )

• Recent trauma ( 2-4 wks ), head trauma

• Suspected aortic dissection • Head / facial trauma within 3 mo

• Noncompressible vascular punctures • Recent ( 2-4 wks ) internal bleeding • For streptokinase : prior exposure ( within 5d-2y ) or prior allergic rx • Pregnancy • Active peptic ulcer • History of chronic HT

Absolute contraindications • Haemorrhagic stroke or stroke of unknown origin at any time • Ischaemic stroke in preceding 6 months • Central nervous system damage or neoplasms • Recent major trauma/surgery/head injury ( within 3 weeks ) • Gastro-intestinal bleeding within the last month • Known bleeding disorder • Aortic dissection

Relative contraindications • Transient ischaemic attack in 6 months • Oral anticoagulant therapy • Pregnancy or within 1 week post partum • Non-compressible punctures • Traumatic resuscitation • Refractory hypertension ( SBP >180 mm Hg ) • Advanced liver disease • Infective endocarditis • Active peptic ulcer

High risk for progression to MI or death • recurrent ischaemia / dynamic ST-segment changes ( in particular STsegment depression, or transient ST-segment elevation ) • early post-infarction unstable angina • elevated troponin levels • haemodynamic instability within observation period • major arrhythmias ( repetitive VT, VF ) • DM • with an ECG pattern which precludes assessment of ST-segment changes ESC, 2002

High Risk Unstable Angina Pectoris ( TIMI Risk Score ) • • • • • • •

Usia > 65 tahun Angina > 2x dalam 24 jam 3 faktor resiko CAD Aspirin dalam 7 hari terakhir CAD ( stenosis > 50%, CABG, PTCA, MI ) ST changes Troponin +

Risk Factors for CAD • Family history of premature CAD • Hypertension • Hypercholesterol • DM • Smoker

Anatomi Koroner dan EKG 12 sandapan • Sandapan V1 dan V2 menghadap septal area ventrikel kiri

• Sandapan V3 dan V4 menghadap dinding anterior ventrikel kiri • Sandapan V5 dan V6 ( ditambah I dan avL ) menghadap dinding lateral ventrikel kiri

• Sandapan II, III dan avF menghadap dinding inferior ventrikel kiri

ECG demonstrates large anterior infarction

A: Proximal large RCA occlusion

B: ST elevation in leads II, III, aVF

A : Small inferior distal RCA occlusion

B : ECG changes in leads II, III, and aVF

Unstable angina

Acute anterolateral myocardial infarction

Lateral myocardial infarction. ST segment elevation in leads I and aVL

Acute inferior myocardial infarction

Acute inferoposterior myocardial infarction. ST segment elevation in II, III and aVF with ST depression in leads V1 and V2

Subendocardial ischemia. Anterolateral ST-segment depression

RBBB + Anterior Infarction