Ska Barukul

8/11/2019 Ska Barukul

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TATALAKSANA SINDROM

KORONER AKUTDENGAN ELEVASI SEGMEN ST

Saharman Leman, Rony Y Syarif

Sub-bagian Kardiologi Ilmu Penyakit Dalam

Fakultas Kedokteran Universitas Andalas Padang



Acute Coronary Syndrome

What is Acute Coronary Syndrome ?

How can I look at an EKG and tell whatpart of the heart is affected ?

What do Emergency Room need to know ?



Scope of Problem(2004 stats)

CHD single leading cause ofdeath in United States 452,327 deaths in the U.S. in 2004

1,200,000 new & recurrentcoronary attacks per year

38% of those who with

coronary attack die within a yearof having it

Annual cost > $300 billion



Definitions

Acute coronary syndrome is defined asmyocardial ischemia due to myocardialinfarction (NSTEMI or STEMI) or unstable

angina

Unstable angina is defined as angina at rest, newonset exertional angina (<2 months), recent

acceleration of angina (<2 months), or postrevascularization angina



Who is at risk for ACS?

Conditions that may mimic ACS include:

Musculoskeletal chest pain Pericarditis (can have acute ST changes)

Aortic dissection

Central Nervous System Disease (may mimicMI by causing diffuse ST-T wave changes)

Pancreatitis/Cholecystitis



Expanding Risk Factors

Smoking

Hypertension

Diabetes Mellitus

Dyslipidemia

Low HDL < 40

Elevated LDL / TG

Family History — event infirst degree relative >55male/65 female

Age-- > 45 for male/55for female

Chronic Kidney Disease

Lack of regular physicalactivity

Obesity

Lack of Etoh intake

Lack of diet rich in fruit, veggies, fiber



Acute Coronary Syndromes

Similar pathophysiology

Similar presentation andearly management rules

STEMI requires evaluationfor acute reperfusionintervention

Unstable Angina

Non-ST-SegmentElevation MI(NSTEMI)

ST-SegmentElevation MI(STEMI)



Diagnosis of Angina

Typical angina — All three of the following Substernal chest discomfort

Onset with exertion or emotional stress

Relief with rest or nitroglycerin

Atypical angina 2 of the above criteria

Noncardiac chest pain 1 of the above



Diagnosis of Acute MI

STEMI / NSTEMI

At least 2 of the following

Ischemic symptoms

Diagnostic ECGchanges

Serum cardiac marker

elevations



No ST Elevation ST Elevation


Unstable Angina NQMI Qw MI

NSTEMI

Myocardial Infarction

Davies MJHeart 83:361, 2000

Ischemic DiscomfortPresentation

Working Dx

ECG

Biochem.

Marker

Final Dx

Hamm Lancet 358:1533,2001

STEMI



The Three I’s

Ischemia= ST depression or T-wave inversionRepresents lack of oxygen to myocardial tissue



The Three I’s

Injury = ST elevation -- represents prolongedischemia; significant when > 1 mm above the baselineof the segment in two or more leads



The Three I’s

Infarct = Q wave — represented by firstnegative deflection after P wave; must bepathological to indicate MI



Unstable

Angina STEMINSTEMI

Non occlusive

thrombus

Non specific

ECG

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



Acute Management

Initial evaluation &stabilization

Efficient riskstratification

Focused cardiac care



Evaluation

Efficient & direct history Initiate stabilization interventions

Plan for moving rapidly toindicated cardiac care

Directed Therapies

are

Time Sensitive!

Occurs

simultaneously



Chest pain suggestive of ischemia

12 lead ECG Obtain initial

cardiac enzymes

electrolytes, cbclipids, bun/cr,glucose, coags

CXR

Immediate assessment within 10 Minutes

Establishdiagnosis

Read ECG

Identifycomplications

Assess forreperfusion

Initial labsand tests

Emergentcare

History &Physical

IV access Cardiac

monitoring

Oxygen

Aspirin

Nitrates



Focused History

Aid in diagnosis and ruleout other causes

Palliative/Provocativefactors

Quality of discomfort

Radiation

Symptoms associated with discomfort

Cardiac risk factors

Past medical history -especially cardiac

Reperfusion questions

Timing of presentation

ECG c/w STEMI

Contraindication tofibrinolysis

Degree of STEMI risk



Targeted Physical

Recognize factors thatincrease risk

Hypotension

Tachycardia Pulmonary rales, JVD ↑,

pulmonary edema,

New murmurs/heart sounds

Diminished peripheralpulses

Signs of stroke

Examination Vitals

Cardiovascular

system Respiratory system

Abdomen

Neurological status



ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECG

Unstable Angina

ST Depression or dynamic T wave inversions

NSTEMI



Lokasi infark berdasarkan letak

perubahan gambaran EKG

Anterior : V1-V6 Anteroseptal : V1-V4 Anterior ekstensif : V1-V6, I-AVLInferior : II, III, AVFLateral : I, AVL, V5-V6

Posterior : V7-V9 Ventrikel Kanan : V3R-V4R



Normal or non-diagnostic EKG



ST Depression or Dynamic T wave

Inversions



ST-Segment Elevation MI



New LBBB

QRS > 0.12 sec

L Axis deviation

Prominent Q wave V1-V3

Prominent S wave 1, aVL, V5-V6

with T-wave inversion



Cardiac markers

Troponin ( T, I) Very specific and more

sensitive than CK Rises 4-8 hours after

injury May remain elevated for

up to two weeks Can provide prognostic

information

Troponin T may beelevated with renal dz,poly/dermatomyositis

CK-MB isoenzyme

Rises 4-6 hours after injuryand peaks at 24 hours

Remains elevated 36-48

hours Positive if CK/MB > 5%

of total CK and 2 timesnormal

Elevation can be predictive

of mortality False positives with

exercise, trauma, muscle dz,DM, PE



Risk Stratification

UA or NSTEMI- Evaluate for Invasive vs.

conservative treatment

- Directed medical therapy

Based on initial

Evaluation, ECG, and

Cardiac markers

- Assess for reperfusion

- Select & implementreperfusion therapy

- Directed medical therapy

STEMI

Patient? YES NO



Cardiac Care Goals

Decrease amount of myocardial necrosis

Preserve LV function

Prevent major adverse cardiac events

Treat life threatening complications



Tabel . Kelas Rekomendasi

Kelas I Terapi atau prosedur yang telah terbukti secara

klinis atau disepakati secara umum memberikan

manfaat dan efektif

Kelas II

Kelas IIa

Kelas IIb

Bukti klinis yang diperoleh mengenai suatu terapi

atau prosedur masih memiliki kontroversiStudi klinis cenderung lebih banyak menyatakan

suatu terapi atau prosedur memberikan manfaat dan

efektif

Studi klinis menunjukkan suatu terapi atau prosedur

masih diragukan apakah memberikan manfaat danefektif

Kelas III Studi klinis atau kesepakatan umum bahwa suatu

terapi atau prosedur tidak bermanfaat atau tidak

efektif dan bahkan pada beberapa kasus dapat

membahayakan

T l k P R h S ki



1. Bagi orang awam

Mengenali gejala serangan jantung dan segera mengantarkan pasienmencari pertolongan ke rumah sakit atau menelpon rumah sakitterdekat meminta dikirimkan ambulan beserta petugas kesehatanterlatih.

2. Petugas kesehatan/dokter umum di klinik - Mengenali gejala sindrom koroner akut dan pemeriksaan EKG bila ada

- Tirah baring dan pemberian oksigen 2-4 L/menit

- Berikan aspirin 160-325 mg tablet kunyah bila tidak ada riwayat alergi aspirin

- Berikan preparat nitrat sublingual misalnya isosorbid dinitrat 5 mg dapat diulangsetiap 5-15 menit sampai 3 kali

- Bila memungkinkan pasang jalur infus

- Segera kirim ke rumah sakit terdekat dengan fasilitas ICCU ( Intensive Coronary Care

Unit ) yang memadai dengan pemasangan oksigen dan didampingi

dokter/paramedik yang terlatih

Tatalaksana Pra Rumah Sakit



STEMI cardiac care

STEP 1: Assessment Time since onset of symptoms

90 min for PCI / 12 hours for fibrinolysis

Is this high risk STEMI? KILLIP classification

If higher risk may manage with more invasive rx

Determine if fibrinolysis candidate

Meets criteria with no contraindications

Determine if PCI candidate Based on availability and time to balloon rx



Fibrinolysis Indications

ST segment elevation >1mm in twocontiguous leads

New LBBB

Symptoms consistent with ischemia

Symptom onset less than 12 hrs prior topresentation

Absolute contraindications for fibrinolysis



Absolute contraindications for fibrinolysis

therapy in patients with acute STEMI

Any prior ICH Known structural cerebral vascular lesion (e.g., AVM)

Known malignant intracranial neoplasm

(primary or metastatic) Ischemic stroke within 3 months EXCEPT acute

ischemic stroke within 3 hours

Suspected aortic dissection

Active bleeding or bleeding diathesis (excluding menses)

Significant closed-head or facial trauma within 3 months

Relati e contraindications for fibrinol sis



Relative contraindications for fibrinolysis

therapy in patients with acute STEMI

History of chronic, severe, poorly controlled hypertension Severe uncontrolled hypertension on presentation ( SBP greater than 180 mm Hg

or DBP greater than 110 mmHg) History of prior ischemic stroke greater than 3 months , dementia, or known

intracranial pathology not covered in contraindications Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less

than 3 weeks) Recent (within 2-4 weeks) internal bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior

allergic reaction to these agents Pregnancy

Active peptic ulcer Current use of anticoagulants: the higher the INR, the higher the risk of

bleeding



STEMI cardiac care

STEP 2: Determine preferred reperfusion strategy

Fibrinolysis preferred if: <3 hours from onset

PCI not available/delayed

door to balloon > 90min

door to balloon minusdoor to needle > 1hr

Door to needle goal <30min

No contraindications

PCI preferred if: PCI available

Door to balloon < 90min

Door to balloon minusdoor to needle < 1hr

Fibrinolysiscontraindications

Late Presentation > 3 hr High risk STEMI

Killup 3 or higher

STEMI dx in doubt

Medical Therapy



Medical Therapy

MONA + BAH

Morphine (class I, level C)

Analgesia

Reduce pain/anxiety — decrease sympathetic tone, systemic

vascular resistance and oxygen demand Careful with hypotension, hypovolemia, respiratory

depression

Oxygen (2-4 liters/minute) (class I, level C) Up to 70% of ACS patient demonstrate hypoxemia

May limit ischemic myocardial damage by increasingoxygen delivery/reduce ST elevation



Nitroglycerin (class I, level B)

Analgesia — titrate infusion to keep patient pain free Dilates coronary vessels — increase blood flow

Reduces systemic vascular resistance and preload

Careful with recent ED meds, hypotension, bradycardia,tachycardia, RV infarction

Aspirin (160-325mg chewed & swallowed) (class I, level A)

Irreversible inhibition of platelet aggregation

Stabilize plaque and arrest thrombus

Reduce mortality in patients with STEMI

Careful with active PUD, hypersensitivity, bleedingdisorders



Beta-Blockers (class I, level A)

14% reduction in mortality risk at 7 days at 23% long term

mortality reduction in STEMI Approximate 13% reduction in risk of progression to MI

in patients with threatening or evolving MI symptoms

Be aware of contraindications (CHF, Heart block,Hypotension)

Reassess for therapy as contraindications resolve

ACE-Inhibitors / ARB (class I, level A)

Start in patients with anterior MI, pulmonary congestion,

LVEF < 40% in absence of contraindication/hypotension Start in first 24 hours

ARB as substitute for patients unable to use ACE-I



Heparin (class I, level C to class IIa, level C) LMWH or UFH (max 4000u bolus, 1000u/hr)

Indirect inhibitor of thrombin

less supporting evidence of benefit in era of reperfusion

Adjunct to surgical revascularization and thrombolytic /PCI reperfusion

24-48 hours of treatment

Coordinate with PCI team (UFH preferred)

Used in combo with aspirin and/or other platelet inhibitors

Changing from one to the other not recommended



Additional medication therapy

Clopidogrel (class I, level B)

Irreversible inhibition of platelet aggregation

Used in support of cath / PCI intervention or ifunable to take aspirin

3 to 12 month duration depending on scenario

Glycoprotein IIb/IIIa inhibitors(class IIa, level B)

Inhibition of platelet aggregation at final common

pathway In support of PCI intervention as early as possible

prior to PCI



Additional medication therapy

Aldosterone blockers (class I, level A)

Post-STEMI patients

no significant renal failure (cr < 2.5 men or 2.0 for women)

No hyperkalemis > 5.0 LVEF < 40%

Symptomatic CHF or DM



Rekomendasi pengobatan SKA

Rekomendasi terapi antitrombotik tampa terapireperfusi

Rekomendasi terapi antirombotik pada pemberianterapi fibrinolitik

Rekomendasi antitrombotik pada terapi angioplastikoroner perkutan (PCI) primer

Dosis ACE-Inhibitor pada tatalaksana SKA

Dosis ARB pada SKA Rekomendasi terapi untuk mengatasi nyeri, sesak dan

anxietas



STEMI care CCU

Monitor for complications: recurrent ischemia, cardiogenic shock, ICH, arrhythmias

Review guidelines for specific management ofcomplications & other specific clinical scenarios PCI after fibrinolysis, emergent CABG, etc…

Decision making for risk stratification at hospitaldischarge and/or need for CABG

Risk Stratification to Det

ermine the Likelihood of



Assessment Findings ind icating

HIGH likel ihood of ACS

Findings ind icating

INTERMEDIATEl ikel ihood o f ACS in

absence of high-

l ikel ihood f ind ings

Findings indicating

LOW l ikel ihood of ACS

in absence of high- or

intermediate-l ikel ihood

f ind ings

History Chest or left arm pain or

discomfort as chief

symptom

Reproduction of previous

documented angina

Known history of coronary

artery disease, including

myocardial infarction

Chest or left arm pain or

discomfort as chief

symptom

Age > 50 years

Probable ischemic

symptoms

Recent cocaine use

Physical

examination

New transient mitral

regurgitation,

hypotension, diaphoresis,

pulmonary edema or rales

Extracardiac vascular

disease

Chest discomfort

reproduced by palpation

ECG New or presumably new

transient ST-segment

deviation (> 0.05 mV) or T-

wave inversion (> 0.2 mV)

with symptoms

Fixed Q waves

Abnormal ST segments or

T waves not documented

to be new

T-wave flattening or

inversion of T waves in

leads with dominant R

waves

Normal ECG

Serum cardiac

markers

Elevated cardiac troponin

T or I, or elevated CK-MB

Normal Normal


ACS i k i i



ACS risk criteria

Low Risk ACS

No intermediate or high

risk factors

<10 minutes rest pain

Non-diagnositic ECG

Non-elevated cardiacmarkers

Age < 70 years

Intermediate RiskACS

Moderate to high likelihood

of CAD

>10 minutes rest pain,

now resolved

T-wave inversion > 2mm

Slightly elevated cardiac

markers



High Risk ACS

Elevated cardiac markersNew or presumed new ST depression

Recurrent ischemia despite therapy

Recurrent ischemia with heart failure

High risk findings on non-invasive stress testDepressed systolic left ventricular function

Hemodynamic instability

Sustained Ventricular tachycardia

PCI with 6 monthsPrior Bypass surgery



Low

risk

High

risk

Conservative

therapy

Invasive

therapy

Chest Pain

center

Intermediate

risk



Secondary Prevention

Disease

HTN, DM, HLP

Behavioral smoking, diet, physical activity, weight

Cognitive

Education, cardiac rehab program





disease management

Blood Pressure Goals < 140/90 or <130/80 in DM /CKD

Maximize use of beta-blockers & ACE-I

Lipids LDL < 100 (70) ; TG < 200

Maximize use of statins; consider fibrates/niacin firstline for TG>500; consider omega-3 fatty acids

Diabetes A1c < 7%

Secondary prevention




behavioral intervention

Smoking cessation Cessation-class, meds, counseling

Physical Activity Goal 30 - 60 minutes daily

Risk assessment prior to initiation

Diet DASH diet, fiber, omega-3 fatty acids

<7% total calories from saturated fats

Thinking outside the box



Thinking outside the box…





cognitive

Patient education

In-hospital – discharge – outpatient clinic/rehab

Monitor psychosocial impact Depression/anxiety assessment & treatment

Social support system

Medication Checklist



after ACS

Antiplatelet agent Aspirin* and/or Clopidorgrel

Lipid lowering agent Statin*

Fibrate / Niacin / Omega-3

Antihypertensive agent Beta blocker* ACE-I*/ARB Aldactone (as appropriate)

Pr nti n n



Prevention news…

From 1994 to 2004 the death rate fromcoronary heart disease declined 33%...

But the actual number of deaths declinedonly 18%

Getting better with treatment…

But more patients developing disease – need for primary prevention focus



Summary

ACS includes UA, NSTEMI, and STEMI

Management guideline focus Immediate assessment/intervention (MONA+BAH)

Risk stratification (UA/NSTEMI vs. STEMI)

RAPID reperfusion for STEMI (PCI vs. Thrombolytics)

Conservative vs Invasive therapy for UA/NSTEMI

Aggressive attention to secondary preventioninitiatives for ACS patients

Beta blocker, ASA, ACE-I, Statin

Conclusions; Treatment of




NSTEMI/USA ASA NTG (consider MSO4 if pain not relieved)

Beta Blocker

Heparin/LMWH ACE-I

+/- Statin

+/- Clopidogrel (don’t give if CABG is a possibility)

+/- IIBIIIA inhibitors (based on TIMI risk score)





STEMI ASA NTG (consider MSO4 if pain not relieved)

Beta Blocker

Heparin/LMWH ACE-I

+/-Clopidogrel (based on possibility of CABG)

IIBIIIA

+/- Statin

Activate the Cath Lab!!!

Ska Barukul

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