dr. berlian i. idris, spjp(k), fiha, mph, dscidicabangtangerang.org/upload/20190209112507-stemi pit...

dr. Berlian I. Idris, SpJP(K), FIHA, MPH, DSc

• Dokter Umum: FKUI 1995-2002

• Master of Public Health (MPH) - Doctor of Science

(DSc): Belanda 2003-2006

• Spesialis Jantung dan Pembuluh Darah (SpJP):

FKUI - Pusat Jantung Nasional Harapan Kita 2007-

2011

• Pendidikan Konsultan (K) Intervensi Kardiologi:

Vietnam & Thailand 2012 – 2013

• Dokter di RSUD Kota Tangerang

Berlian I. Idris

RSUD Kota Tangerang

Fibrinolytic for STEMI patients:

How we could save lives

Disclaimer

• This is a sponsored lecture by Dexa

Medica (Fibrion, streptokinase)

Acute coronary syndrome

A spectrum of clinical syndromes due to

sudden, significantly compromised coronary

circulation ranging from unstable angina to

NSTEMI and STEMI.

Further stages of stable angina pectoris

Topol EJ, ed. Textbook of cardiovascular medicine 2007.

DEFINITION

Atherogenesis and Atherothrombosis: A Progressive Process

NormalFatty

StreakFibrousPlaque

Athero-scleroticPlaque

PlaqueRupture/Fissure &

Thrombosis

Myocardial

Infarction

Ischemic

Stroke

Critical Leg

Ischemia

Clinically Silent

Cardiovascular Death

Increasing Age

Angina

Transient Ischemic Attack

Claudication/PAD

3

Normal

vessel

Minimal

CAD

Severe

CAD

Moderate

CAD

Progression

Pathophysiology

Autopsy

Stable plaque

Davies MJ. Heart 2000;83;361-366.

Thrombosis caused by erosion

Thrombosis caused by disruption

Thrombosis caused

by disruption

Presentation: angina

(Clinical, Initial ECG)

ST-Seg Elevation

Myocardial Infarction

Non-STSeg Elevation

Acute Coronary Syndr

ST-Seg Elevation

MCI

Non-ST-seg-

Elevation MCI

Unstable

Angina

Workingdiagnosis

Time

Evolution ofECG &

Biomarkers

Finaldiagnosis

National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006

Biomarker (-)Biomarker (+)

Transmural injury: ST ↑

Ischemia: ST ↓, tall T, inverted T

ECG pattern in ACS

10

ECG evolution

Important: check ECG serially; at least 2 times, 4-6 hours apart

11

Early repol

• Monitor and support ABCs

• Check vital signs, incl oxygen saturation

• Establish IV access

• Administer– Oxygen 2-4L/min

– Aspirin 160-325 mg chewed

– Clopidogrel loading dose 300 mg, or ticagleror 180 mg

– Statin loading dose

– Nitrate (ISDN) sublingual

– Morphine if pain not relieved with NTG

Initial management

Anticoagulation & reperfusion

• Heparin administration (LMWH enoxaparine, fondaparinux or UFH)

• Reperfusion in STEMI

– Fibrinolysis or primary percutaneous coronary intervention (PCI)

– Assess onset & contraindication

Indication • Typical symptom: angina

• ST elevation in 2 or more related leads/ new or presumably newLBBB baru

• Chest pain onset < 12 hours, most effective <2h after onset.1

Preparation• Contraindication check list

• Informed consent

• Resuscitation personnel and equipments

Fibrinolytic drugs• Streptokinase

• Tissue Plasminogen Activator

• Tenecteplase (TNK-tPA)

Fibrinolytic therapy

1Boersma E, et al. Lancet 1996;348(9030):771–775

Mortality reduction in ISIS-2

0

100

200

300

400

500

600

0 7 14 21 28 35

Placebo 13.2%

ASA 10.7%

SK 10.4%

SK + ASA 8.0%

Time (days)

Cumulative

Mortality (No of patients)

Results of ISIS-2

Streptokinas

e

Event

SK

n=13,607

tPA

13,569

APSAC

13,599

Thrombo-

lysis +

heparin

20,400

Thrombo-

lysis alone

20,375

Death (%)

10.6

(%)

10.3

(%)

10.5

(%)

10.3

(%)

10.6

Stroke:

any

1.04* 1.39 1.26 1.28 1.18

Stroke:

haemorrhagic

0.24*

0.66

0.55

0.56***

0.40

Bleeds:

any

4.5*

5.2

5.4

6.3***

3.9

Bleeds:

major

0.9

0.8

1.0

1.0***

0.8

Reinfarction 3.47 2.93** 3.55 3.16 3.47

Allergic

reactions

0.3

0.1**

0.5

0.3

0.3

Hypotension 6.7 4.4** 7.0 6.0 5.9

* significantly lower than tPA and APSAC

** significantly lower than SK and APSAC

*** significantly higher than thrombolysis alone

ISIS-3 results in relation to treatment regimen

Mortality and major clinical eventsin the ISIS-3 trial

Procedure

Attached defibrillator EKG

IV line :

IV Cath no. 22 left arm for fibrinolytic

IV Cath no. 20 right arm,for other durgs and NS infusion

Streptokinase 1.5 mill Unit in NS100 cc for 30-60 minutes

Alteplase : 15 mg IV bolus then 0.75 mg/Kg for 30 mnt, and

0.5 mg/Kg for next 60 mnt

Monitor vital signs, symptom, EKG every 5 menit.

Anticipate complications ( P A H A )

Evaluate result 60-90 minutes after fibrinolytic.

• Significant symptomatic relieve

• ECG: decrease in ST elevation >50%

Success criteria

Perdarahan (bleeding)

Minor : observe, slow infusion rate.

Major : stop, transfusion if necessary

Alergy

Stop fibrinolytic, antihistamin / cortikosteroid iv

Hipotension

Withhold fibrinolytic

Tredelenburg position

Loading 100-250 cc Nacl 0,9%

Start again, slow the rate

Arrhythmia

Benign: observe

Malignant: treat accordingly

Complications

8. Terapi 1. Fase akut di UGD

a. Bed rest total

b. Oksigen 2-4 ilter/menit

c. Pemasangan IVFD

d. Obat-obatan :

- Aspilet 160 mg kunyah

- Clopidogrel (untuk usia <75th dan tidak rutin mengkonsumsi clopidogrel) berikan 300 mg

jika pasien mendapatkan terapi fibrinolitik atau

- Clopidogrel 600 mg atau Ticagrelor 80 mg jika pasien mendapatkan primary PCI

- Atorvastatin 40 mg

- Nitrat sublingual 5mg, dapat diulang sampai 3(tiga) kali jika masih ada keluhan, dan

dilanjutkan dengan nitrat iv bila keluhan persisten

- Morfin 2-4 mg iv jika masih nyeri dada

e. Monitoring jantung

f. Jika onset <12 jam:

- Fibrinolitik (di IGD) atau

- Primary PCI (di cathlab) bila fasilitas dan SDM di cathlab siap melakukan dalam 2 jam

2017 ESC Guidelines for the management of acute myocardial infarction in patients

presenting with ST-segment elevation. European Heart Journal (2018) 39, 119–177

Fibrinolytic with Streptokinase in JKN

Special top-up CMG Streptokinase

Total budget STEMI with streptokinase

=

Budget InaCBG

(acute myocardial infarction)

+

Budget Top Up streptokinase

Thank you

HEPARINISASI PADA UAP/NSTEMI

UFH ( Unfractionated Heparin )

• Initial I.V BOLUS 60 UI/Kg max 4000 UI

• Infus : 12 UI/kg BB/jam max 1000 UI/jam

• Monitor APTT : 3, 6, 12, 24 jam setelah mulai

terapi

• Target APTT 50-70 msec (1,5 -2 x kontrol )

LMWH ( Low Molecular Weight Heparin ):

Enoxaparine 2 x 0,6 mg

Nadroparine 0,1 ml/10 kg, SC 2 x 0,6 mg

Factor Xa inhibitor:

Fondaparinux 1 x 2,5 mg

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low

Algorithm in Acute Coronary Syndrome

Modified from ESC 2007

- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

±revascularization

Medical therapy,

coronary angiography

Perform

ed in 10 min

{on serial

ECG}

Troponin,

CKMB (+)

Initial tx

Clinical classification of chest pain

Typical angina (definite)

• Substernal chest discomfort with a characteristic quality and duration that is

• provoked by exertion or emotional stress and

• relieved by rest or nitroglycerin

Atypical angina (probable)

• meets 2 of the above characteristics

Noncardiac chest pain

• meets <=1 of the typical angina characteristics

Diamond GA. J Am Coll Cardiol 1983;1:574

Assessing chest pain

• Character

• Time of onset, duration, frequency

• Changes in tempo

• Exacerbating and alleviating factors

• Pain during situation associated with increased myocardial O2 demand (e.g. exertion, stress)

Character of anginal pain

• Localized usually at precordium

• Radiate to arm, neck, shoulder, back or epicardium

• Feels like being pressed by heavy object, orconstricting or crushing.

• Concomitant systemic symptoms: dyspnea, dizziness, nausea, diaphoresis

• Not related to movement/body position, cough, other obvious cause e.g. herpes, trauma

Character of anginal pain

• Some feels epigastrial pain, similar to gastritis• Only 54% report typical angina• 34% “burning”, or “indigestion”• 32% chest pain • 20% stabbing, sharp pain• 42% undescribable• Can be atypical in the elderly, diabetic• Patient without CAD: sharp localized pain,

pleuritic, positional, increased with tactile pressure almost always not ischemia.

Classification of Angina

• Typical vs atypical angina vs non cardiac• Angina equivalent• Stable Angina• Unstable angina

– Angina in myocardial infarct

Stable Angina Pectoris

• Provoked by exertion or emotional stress; increasing demand triggers ischemia

• Relieved by rest or nitroglycerin

Pedoman tatalaksana SKA tanpa ST elevasi, PERKI 2008

Severity in Stable Angina

• I : angina occurring with strenous but not ordinary physical activity

• II : Slight limitation of ordinary physical activity

• III : Marked limitation of ordinary physical activity

• IV : Inability to carry on any physical activity without discomfort, symptoms may be present at rest.

Unstable angina

1. Angina at rest

2. Angina first onset

3. Progressive anginaSignificant worsening of stable angina, increasingintensity/frequency, longer duration, triggeredeasier, harder to alleviate

4. Angina after infarctAngina after infarct recovery

Pedoman tatalaksana SKA tanpa ST elevasi, PERKI 2004

Differential Diagnosis

of Chest Pain

Cardiac• ACS : Infarct,angina

• MVP

• Aortic Stenosis

• Hypertrophic cardio-

myopathy

• 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

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

±revascularization

Medical therapy,


Perform

ed in 10 min

{on serial

ECG}

Troponin,

CKMB (+)

Initial tx

Dalam 10 menit !!

Membuat dan menganalisa

E K G

Case

• Tn mahmudin 50th..os merasa lemas pada sisi

kiri tubuh sejak 1 hari yg lalu secara

mendadak..mulut mencong (-), bicara pelo (-),

minum tersedak (-), nyeri dada (-)..riwayat

merokok sejak remaja 1-2 bungkus sehari,

berhenti sejak 10 thn yll..riwayat HT (+), tidak

terkontrol, DM (-), riwayat serangan jantung 10

thn yll..KU baik, kes CM, GCS 15, TD 150/90, N

90, RR 20, suhu 37, 9..motorik 5/5, 5/5. CKMB

16, serial ecg N

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

±revascularization

Medical therapy,


Perform

ed in 10 min

{on serial

ECG}

Troponin,

CKMB (±)

Initial tx

• Recommendation: CK, CKMB & Troponin upon admission and serial in 4-6 hours if initially normal

• LDH, SGOT/SGPT and other enzymes not recommended

• Increase of plasma CK plasma & CK-MB happens early, but less specific

• Increase of TnI & TnT are more specific in diagnosingmarker MI; level corresponds with prognosis.

Biomarkers

2004 ACC/AHA STEMI Guidelines

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

±revascularization

Medical therapy,


Perform

ed in 10 min

{on serial

ECG}

Troponin,

CKMB (±)

Initial tx

High risk

• Repetitive or prolonged (> 10 minutes) ongoing

chest pain;

• Elevated level of at least one cardiac biomarker

(troponin or creatine kinase-MB isoenzyme);

• Persistent or dynamic ST depression 0.5 mm or

new T-wave inversion

• Transient ST-segment elevation ( 0.5 mm) in

more than two contiguous leads;

Guideline ACS 2006 National Heart Foundation Australia

High risk (2)

• Haemodynamic compromise — Syst. BP< 90 mmHg, cool peripheries, diaphoresis, Killip Class > I, and/or new-onset mitral regurgitation;

• Sustained ventricular tachycardia;

• Syncope;

• LV syst dysfunction (ejection fraction < 0.40);

• Prior PCI or CABG within 6 months or prior

• Diabetes;

• Chronic kidney disease (estimated GFR< 60 mL/minute)


Intermediate risk

• Chest pain within 48 hours that occurred at rest, or was repetitive or prolonged (but currently resolved)

• Age >65 years

• Known CAD — prior infarction withEF>0.40, or known 50% coronary stenosis

• No high-risk changes on ECG


Intermediate risk (2)

• Two or more of risk factors: hypertension, family history, active smoking or hyperlipidemia

• Diabetes (with atypical symptoms of ACS);

• Chronic kidney disease (estimated GFR<60 mL/minute) (with atypical symptoms of ACS)

• Prior aspirin use


Low risk

• Acute coronary syndrome without

intermediate-risk or high-risk features.

• This includes

– onset of angina within the last month,

– worsening in severity or frequency of angina,

– lowering of anginal threshold


CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

±reperfusion

Medical therapy,


Perform

ed in 10 min

{on serial

ECG}

Troponin,

CKMB (±)

Initial tx

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

±revascularization

Medical therapy,


Perform

ed in 10 min

{on serial

ECG}

Troponin,

CKMB (±)

A Aspirin and Anticoagulants

B Beta blockers and Blood Pressure

C Cholesterol and Cigarettes

D Diet and Diabetes

E Education and Exercise

F Fun and Faith

Secondary prevention strategy

• Rawat tirah baring

• Puasa 8 jam

• IVFD NaCl 0,9% atau D5W% 1 kolf/24 jam

• Aspirin 160 mg dikunyah,selanjutnya 1 x 80 mg ( besok )

• Clopidogrel 4 tab ( 300 mg ), selanjutnya 1 x 75 mg ( besok )

• ISDN 3 x 5 mg

• Atorvastatin 1 x 40 mg

• Bisoprolol 1 x 2,5 mg

• Diazepam 1 x 5 mg / Clobazam 1 x 10 mg / Alprazolam 1 x 0,5 mg

• Laxadine syrup 1 x CI

• Heparin dg UFH / LMWH selama 5 hari

• Rontgen torak

• EKG tiap hari

• Cek Profil lipid, GDS, Ureum, Kreatinin, elektrolit besok

• ACE inhibitor ( bila ada hipertensi )

CONTOH INSTRUKSI DOKTER

UAP / NSTEMI

Heart failure management –

hemodynamic oriented

Fluid administration Normal BP: vasodilator↓ BP: Inotropic drugs

Diuretic, vasodilator

Lung edema

Volume problem

Administer

• Fluids

• Blood transfusions

• Cause-specific tx

• Consider vasopressors

Rate ProblemPump Problem

Specific algorithm

Clinical signs of hypoperfusion,

congestive HF

BP ?

Syst 70 - 100

Signs of shock (+)

Syst 70-100

Signs of shock (-)

Syst <70

Signs of shock (+)

Norepinefrin Dopamine Dobutamine

Inotropic choice: ACLS algorithm – hypotension / shock

Algorithm in ACLS

A. Normal ECG

B. ‘Tall T’ or Peaked T

waves

C. ‘Injury’, ST elevation

D. Inverted T waves

E. Q-abnormal

“EVOLVING ECG”

FoamCells

FattyStreak

IntermediateLesion Atheroma

FibrousPlaque

ComplicatedLesion/Rupture

Endothelial Dysfunction

Smooth muscleand collagen

From first decade From third decade From fourth decade

Growth mainly by lipid accumulationThrombosis,hematoma

Stary HC et al. Circulation 1995;92:1355-1374.

Atherosclerosis Timeline

New Paradigm

healthy subclinical symptomatic

Threshold

Decades Years-Months Months-Days

Intima

Media

Plaque

Thrombus

Lumen

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

dr. berlian i. idris, spjp(k), fiha, mph, dscidicabangtangerang.org/upload/20190209112507-stemi pit...

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