acute coronary syndrome 052014

7/22/2019 Acute Coronary Syndrome 052014

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Acute Coronary Syndrome

Sindroma Koroner Akut

Dr M.Diah, SpPD-KKV, FCIC, FINASIM

Departemen KardiologiInstalasi Kateterisasi Jantung

Divisi Kardiologi Departemen Ilmu Penyakit Dalam

FKUNSYAH/RSUZA BANDA ACEH


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MUHMMAD DIAH

SD, SMP, SMA Bireuen

Dokter Umum: FK UNSRI Palembang

Internist : FK UNSRI, Palembang

Konsultan Kardiovaskuler: RCSM-RSMH Kolegium

Intervensi Jantung:

- Angiografi : 2011 (RSCM)

- Fellow Intervention Clinical Cardiologi (FCIC)

Institut Jantung Negara (IJN). Kuala Lumpur

- Sertifikasi Intervensi Cardiologi Tk III (Koleguim)

Pekerjaan:Staf Departemen Kardiologi RSUZA/FK UNSYIAH

Staf Subdivisi Kardiologi Bag Penyakit Dalam RSUZA.FK

UNSYIAH

Ka Instalasi Kateterisasi Jantung RSUZA Banda Aceh

Staf SP2 Kardiologi, Bagian Peny Dalam RSMH/FK UNSRI


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3

DEFINISI

Suatu sindroma klinik yang menandakanadanya iskemia miokard akut, terdiri dari :

Infark miokard akut Q wave (STEMI)

Infark miokard akut non-Q (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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4

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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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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CAD

Atherosclerosis

Risk Factors

( ,BP, DM,

Insulin Resistance, Platelets,

Fibrinogen, etc)

The cardiovascular continuum of events

DYSLIPIDEMIA

Adapted fromDzau et al. Am Heart J. 1991;121:1244-1263

Myocardial

Ischemia

plaque

Ischemia = oxygen supply

and demand imbalance


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CAD

Atherosclerosis

Risk Factors

( ,BP, DM,


Fibrinogen, etc)


DYSLIPIDEMIA


Myocardial

Ischemia

Coronary

Thrombosis


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CAD

Atherosclerosis

Risk Factors

( ,BP, DM,


Fibrinogen, etc)


DYSLIPIDEMIA


Myocardial

Ischemia

Coronary

Thrombosis

ACS


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Stable anginaPlaque ruptureCoronary thrombosisUA/NSTEMISTEMI


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PenyempitanPembuluh darah


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Clinical Spectrum of Acute Coronary Syndrome

Acute Coronary Syndrome

Non-ST Segment

Elevation

ST SegmentElevation

Unstable

Angina Pectoris

Non-Q-wave Q-wave

Acute Myocardial Infarction

STEMI

NSTEMI


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Unstable

AnginaSTEMINSTEMI

Non occlusive

thrombus

Non specificECG

Normal

cardiac

enzymes

Occluding thrombus

sufficient to cause

tissue damage & mild

myocardial necrosis

ST depression +/-

T wave inversion on

ECG

Elevated cardiac

enzymes

Complete thrombus

occlusion

ST elevations on

ECG or new LBBB

Elevated cardiac

enzymes

More severe

symptoms


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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 angina1/3 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 infarctsOccasionally 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, Levine sign (fistsign: costricting, pressing pain typical of angina pectoris)

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 RATEVariable 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 riseHalf of pts with inferior MI parasympathetic stimulation

: hypotension, bradycardia or both (Bezold Jarischreflex)

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, feverresolves by 4thor 5thday

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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ST-segment elevation


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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 sangat menyokong 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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KRITERIA DIAGNOSTIK (WHO) :

1. Klinis : keluhan terbanyak adalah nyeri dada

2. Perubahan gambaran EKG :

Dengan elevasi segmen ST : STEMI

Tanpa elevasi segmen ST : UAP, NSTEMI

3. Peningkatan kadar enzim jantung :

1. Kadar CK, CK-MB

2. Kadar Troponin I/ Troponin T


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Kasus 1

Laki-laki, usia 50 tahun Nyeri dada semakin memberat sejak 7 jam

sebelum masuk rumah sakit

Riwayat nyeri sebelumnya (-) FR : merokok, HT dan DM tidak diketahui

Riw Keluarga : PJK (+)

PF : CM, TD=140/90 mmHg

Cor dan Pulmo : dalam batas normalAbdomen : dalam batas normal

Ekstremitas : edema -/-


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Kasus 1


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Interpretasi EKG ?

a. STEMI Anterior dan NSTEMI

Inferior

b. STEMI Anteroseptal dan OMIInferior

c. STEMI Anteroseptald. NSTEMI Inferior


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STEMI Anteroseptal

Terdapat perubahan pada segmen STberupaelevasi yang merupakan terjadinyaacuteinjury di anteroseptal ( leads V1-V4)

Dengan atau tanpa perubahan resiprokalberupa depresi segmen ST pada sandapaninferolateral

Gamb EKG : Acute Injury pada sandapan V1-V3 :

Elevasi segmen ST upsloping Gel T yang tinggi

Perubahan resiprokal pada sandapan II,III-aVF


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Kasus 1


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Interpretasi EKG ?

a. STEMI Anterior dan NSTEMI

Inferior

b. STEMI Anteroseptal dan OMIInferior

c. STEMI Anteroseptald. NSTEMI Inferior


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Kasus 2

Laki-laki, 36 tahun

Nyeri dada hebat sejak40 menit sebelum

datang ke IGD rumah sakit

FR : tidak jelas. Kadar lipid belum diperiksa

PF : CM. TD = 130/90 mmHg

Lain-lain dalam batas normal


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Kasus 2


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Interpretasi EKG ?

a. NSTEMI Anterior dan Inferior

b. STEMI Anterior Ekstensif/Luas

c. STEMI Anterior Ekstensif/Luas dengan

Ventricular ectopic beats

d. STEMI Anteroseptal


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STEMI Anterior Ekstensif/Luas dengan

Ventricular Ectopic beats

Terdapat perubahan berupa elevasi segmenST yang menunjukkan terdapatnya acuteinjury pada hampir seluruh sandapananterior (V1-V6) dan I-aVL

Dengan atau tanpa perubahan resiprokalpada berupa depresi segmen ST padasandapan inferior

Gamb EKG : Gambaran HIPERAKUT : jam-jam pertama infark

Peningkatan tinggi gel R

Elevasi ST upsloping

Gel T yang lebar dan tinggi


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Kasus 2


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Interpretasi EKG ?

a. NSTEMI Anterior dan Inferior

b. STEMI Anterior Ekstensif/Luas

c. STEMI Anterior Ekstensif/Luas dengan

Ventricular ectopic beats

d. STEMI Anteroseptal


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Kasus 3

Wanita, 67 tahun

Nyeri dada semakin memberat sejak3 jam

FR : riw DM (+)


Lab :

GDS = 250 mg/dL Troponin T (-), CK dan CK-MB dalam batas normal


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Kasus 3


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Interpretasi EKG ?

a.OMI Anteroseptal

b.NSTEMI Inferior

c.STEMI Anteroseptal

d.STEMI Lateral


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STEMI Lateral

Terdapat perubahan pada segmen ST berupaelevasidi sandapan lateral (V4-V6) dan I-aVL

Dengan atau tanpa perubahan resiprokal berupadepresisegmen ST pada sandapan inferior

Gamb EKG : Gamb acute injury pada sandapan V4-V6 dan I-aVL :

Elevasi ST upsloping

Gel T yang tinggi

Perubahan resiprokal pada sandapan inferior (leads III

dan aVF) Kemungkinan terdapat infark lama di daerah

anteroseptal :poor R wave progression


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Kasus 3


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Interpretasi EKG ?

a.OMI Anteroseptal

b.NSTEMI Inferior

c.STEMI Anteroseptal

d.STEMI Lateral


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Kasus 4

Laki-laki, usia 60 tahun

Nyeri dada beberapa jam sebelum masuk RS

(onset tidak jelas)

FR : DM (+)


Cor dan Pulmo dalam batas normal

Lain-lain tidak ditemukan kelainan

Lab : Troponin T (+)


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Kasus 4


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Interpretasi EKG

a. STEMI Inferior

b. STEMI Inferior dan Infark Ventrikel

Kananc. NSTEMI Inferior dan Infark Ventrikel

Kanan

d. Infark Ventrikel Kanan


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STEMI Inferior

dengan Infark Ventrikel Kanan

Perubahan pada segmen ST di daerah inferior(leads II, III dan aVF) berupa elevasi,menunjukkan terjadinya acute injury .

Infark inferior sering berhubungan dan Infark padaVentrikel Kanan. Ditandai dengan elevasisegmenST > 1 mm pada sandapan V4R .

Gamb EKG : Incomplete RBBB Infark miokard inferior akut

Infark ventrikel kanan akut Perubahan resiprokal pada berupa depresi ST pada

sandapan anterior Junctional Premature Beat (JPB) Ventricular Premature Beat pada sandapan V4-V6


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Kasus 4

JPB

VES


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Interpretasi EKG

a. STEMI Inferior

b. STEMI Inferior dan Infark Ventrikel

Kananc. NSTEMI Inferior dan Infark Ventrikel

Kanan

d. Infark Ventrikel Kanan


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Interpretasi EKG :

Curiga iskemi/infark inferior, harus dilakukanpemeriksaan ventrikel kanandan posterior

Gejala klinis tidak khas pada pasien DM dan usialanjut

Komplikasi infark inferiordan infark ventrikelkanan :

infark inferior : blok pada AV node

infark ventrikel kanan : gangguan

hemodinamik

EVOLUSI EKG PADA STEMI


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EVOLUSI EKG PADA STEMI


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EVOLUSI EKG

ELECTROCARDIOGRAPHIC HIGHLIGHTS


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Anatomic

Region

Coronary Artery Descriptive

Leads

Anterior wallAnteroseptal

Anteroseptal Lateral

Septal wall

Inferior wall

Inferior and RV

Inferoposterior

Posterior wall

Lateral wall

Anterolateral

Inferolateral

posterolateral

LADLAD

Proximal LAD

LAD

RCA; LCX

Proximal RCA

RCA; LCX

RCA; LCX

LAD

LAD; LCX

LAD; LCX

LAD; LCX

V3 and V4V1 to V4

V1-V6, I and aVL

V1 and V2

II, III and aVF

II, III, aVF, V1, V2

and V3R-V6R

II, III, aVF, V1,

V2 and V7-V9

V1, V2 and V7-V9

V5, V6, I and aVL

V3-V6, I and aVL

II, III, aVF, I, aVL,

V5 and V6

V1, V2, V7 to V9,

V5, V6, I and aVL

ELECTROCARDIOGRAPHIC HIGHLIGHTS


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Kasus 5

Laki-laki, usia 42 tahun

Nyeri dada yang memberat sejak 2 hari

sebelum datang ke IGD

RPD : infark miokard akut 1 tahun yang lalu,

belum dilakukan intervensi selain obat-obatan

FR : merokok


Lain-lain dalam batas normal

Kasus 5


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Interpretasi EKG ?

a. Angina Pektoris Stabil

b. Angina Pektoris tidak Stabil (UAP)

c. Angina pasca infark

d. NSTEMI Anteroseptal


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Deep and symmetr ical T waveinvers ion pada sandapan anterior

(V1-V5, I-aVL)

Inversi gelombang T seringkalimerupakan perubahan yang non-

spesifik kecuali inversi yang

bentuknya dalam dan simetris

Kasus 5


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Interpretasi EKG ?

a. Angina Pektoris Stabil

b. Angina Pektoris tidak Stabil (UAP)

c. Angina pasca infark

d. NSTEMI Anteroseptal


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Manajemen



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ACS

Coronary

Thrombosis

Myocardial

Ischemia

CAD

Atherosclerosis

Risk Factors

( ,BP, DM,Insulin Resistance, Platelets,

Fibrinogen, etc)Adapted from

Dzau et al. Am Heart J. 1991;121:1244-1263

DYSLIPIDEMIA

Arrhythmia and

Loss of Muscle

Remodeling

Ventricular

Dilatation

Congestive

Heart Failure

End-stage Heart

Disease

DELAY TO THERAPY


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DELAY TO THERAPY

1. From onset of symptoms to patient recognition

2. Out-hospital transport

3. In-hospital evaluation

ISCHEMIC CHEST PAIN ALGORYTHM


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ISCHEMIC CHEST PAIN ALGORYTHM

Chest pain suggestive of ischemia


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ISCHEMIC CHEST PAIN

TYPICAL ANGINA EQUIVALENT ANGINA

1. CHEST DISCOMFORT

2. LOCATION

3. RADIATION

4. UNLIKELINESS

1. NO CHEST DISCOMFORT

2. LOCATION

3. INDIGESTION

4. UNEXPLAINED WEAKNESS

5. DIAPORESIS

6. SHORTNESS OF BREATH


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Chest discomfort suggestive of ischemia

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

Immediate ED assessment and immediate ED general treatment

Acute coronary syndrome algorithm



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Immediate ED assessment ( 10 min)Vital sign

Oxygen saturation

Obtain IV access

Obtain ECG 12 lead

Brief history and physical exam

Check contraindication for fibrinolytic

Initial serum cardiac markers

Initial electrolyte and coagulation

study

Portable chest x-ray ( 30 minutes)

Immediate ED general treatment

O2 at 4 L/min (maintain O2 sat 90%)

Aspirin 160-325 mg

Nitroglycerin SL, spray, or IV

Morphine IV 2-4 mg repeated every

5-10 minutes (if pain not relieved

with nitroglycerine)

Memory: MONAgreets all patients




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Review initial 12 lead ECG






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ST elevation or new or

presumably new LBBB

strongly suspicious for

injury







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ST-depression or

dynamic T-wave

inversion strongly

suspicious for injury


presumably new LBBB


injury







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ST-depression or

dynamic T-wave

inversion stronglysuspicious for injury

(UA/NSTEMI)


presumably new LBBB

strongly suspicious forinjury (STEMI)




Normal or non-

diagnostic changes

in ST-segment or T-waves (intermediate/

low-risk UA)




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Start adjunctive treatment

Normal or non-

diagnostic changes

in ST-segment or T-waves (intermediate/

low-risk UA)

ST-depression or

dynamic T-wave

inversion stronglysuspicious for injury

(UA/NSTEMI)


presumably new LBBB

strongly suspicious forinjury (STEMI)





ADJUNCTIVE TREATMENT


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1. Beta-adrenergic receptor blocker

2. Clopidogrel

3. Heparin (UFH or LMWH)

ADJUNCTIVE TREATMENT

(Do not delay reperfusion)



Ch t di f t ti f i h i


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Normal or non-

diagnostic changes in

ST-segment or T-

waves

ST-depression or dynamic

T-wave inversion strongly



presumably new LBBB


injury




Time from onset of

symptoms

- Reperfusion strategy: PCI (90

min) or fibrinolysis (30 min)

- ACE-I/ARB

- Statin

12 hours



Chest discomfort s ggesti e of ischemia


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Time from onset of

symptoms

- Reperfusion strategy: PCI (90 min) or

fibrinolysis (30 min)

- ACE-I/ARB within 24 hours of onset

- Statin

12 hours


Normal or non-


ST-segment or T-

waves





presumably new LBBB


injury






Adj ncti e t eatment


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Heparin (UFH/LMWH)

Glycoprotein IIb/IIIa receptor inhibitors

-Adrenoreceptor blockers Clopidogrel

Adjunctive treatment




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Time from onset of

symptoms



- ACE-I/ARB within 24 h of

symptom onset)

- Statin

12 hours


Normal or non-


ST-segment or T-

waves





presumably new LBBB


injury





12 hrs Admit to monitored bed

Assess risk status

-High risk: early invasive

strategy

-Continue ASA, heparin,

ACE-I, statin

VERY HIGH-RISK PATIENT


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VERY HIGH RISK PATIENT

1. Refractory chest pain

2. Recurrent/persistent ST deviation

3. Ventricular tachycardia

4. Hemodynamic instability

5. Sign of pump failure

6. Shock within 48 hours




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Time from onset of

symptoms



- ACE-I/ARB within 24 h of

symptom onset)

- Statin

12 hours

12 hrs


Normal or non-


ST-segment or T-

waves





presumably new LBBB


injury




Admit to monitored bed

Assess risk status

-High risk: early invasivestrategy

-Continue ASA, heparin,

ACE-I, statin

Develops high or

intermediate risk criteria

or troponin-positive

Monitored bed in ED

Develops high or

intermediate risk criteria

or troponin-positive

No evidence of ischemia and MI: discharge with follow-up


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Pengobatan Pasca Perawatan


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Obat-obat untuk mengontrol keluhan iskemiaharus dilanjutkan

Aspirin Beta-blocker

ACE inhibitor

Berhenti merokok

Pertahankan BB optimal

Aktivitas fisik sesuai dengan hasil treadmill

Diet

Rendah lemak jenuh dengan kolesterol, bila perludengan target LDL < 100 mg/dL

Pengendalian hipertensi

Pengendalian ketat gula darah pada penderita DM

Modifikasi Faktor Risiko


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Get regular medical checkups.

Control your blood pressure.Check your cholesterol.

Dont smoke.

Exercise regularly.

Maintain a healthy weight.

Eat a heart-healthy diet.Manage stress.


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Thank you for your attention

acute coronary syndrome 052014

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