Case Report STEMI INFERIOR ONSET 3 hari KILLIP I TIMI RISK 7/14

PEMBICARA
-A L V I N K W A R D I ( 0 9 0 1 0 0 0 4 5 ) -T I A H N U R B A I T I L U B I S ( 0 9 0 1 0 0 0 2 8 )

PEMBIMBING DR. ANDIKA SITEPU SP.JP DR. ALI NAFIAH NASUTION SP.JP

Definition
A Spectrum of clinical syndromes due to sudden, significantly compromised coronary circulation. ACS: Q wave Acute MCI (STEMI) Non-Q wave Acute MCI(NSTEMI) Unstable Angina Pectoris (UAP) These conditions were the further stages of stable angina pectoris.

Pathogenesis
Mostly caused by coronary atherosclerosis Ruptured atherosclerosis plaqueFormation of thrombus which occludes blood vessel. The degree of blood vessel occlusion determines the degree of damage to Myocardium.

Risk Factors
Unmodified Risk factors: 1. Age 2. Sex

3. Race
4. Genetics (Family History)

Modified Risk Factors

Ischemia = oxygen supply and demand imbalance

Myocardial Ischemia

CAD

plaque
Atherosclerosis

Risk Factors ( , BP, DM, DYSLIPIDEMIA Insulin Resistance, Platelets, Fibrinogen, etc)

Coronary Thrombosis Myocardial Ischemia

CAD Atherosclerosis

Risk Factors ( DYSLIPIDEMIA, BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)

ACS
Coronary Thrombosis Myocardial Ischemia

CAD Atherosclerosis

Risk Factors ( DYSLIPIDEMIA, BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)

DIAGNOSIS

HISTORY
PRODROMAL SYMPTOMS History very valuable to establish D/. Prodoma : chest discomfort unstable angina 1/3 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

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 infarcts Occasionally diarrhea, profound weakness, dizziness, palpitation, cold perspiration, sense of impending doom Occasionally : cerebral embolism or systemic arterial embolism

Pain Patterns with Myocardial Ischemia

13

Clinical Classification of Angina Typical angina (definite) substernal chest discomfort with a characteristic quality and duration provoked by exertion or emotional stress 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

PHYSICAL EXAMINATION
GENERAL APPEARANCE Anxious, considerable distress, restless, fist on chest (Levine sign) LV failure & sympathetic stimulation : cold perspiration, pallor, dyspnea, cough with frothy pink or blood-streaked sputum. Shock : cool, clammy skin, facial pallor, cyanosis, confusion or disorientation HEART RATE Variable depending on underlying rhythm and degree or ventr. failure Most commonly, HR 100 110/min; > 95% patients : VPBs within first 4 hours

BLOOD PRESSURE Majority normotensive, but syst. BP may decline and diast. BP may rise Half of pts with inferior MI parasympathetic stimulation : hypotension, bradycardia or both (Bezold Jarisch reflex) 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, fever resolves by 4th or 5th hari Respiration due to anxiety and pain, in LV failure : resp. rate correlates with degree of heart failure

WORKUP
Electrocardiogram
Q-wave Acute Miocard Infarction (STEMI) : Elevated ST segment 1 mm at 2 (extremities leads) Or 2 mm at 2 (Precordial leads which represents the same area or close by)

LBBB (new or presumed new)

17

ECG presentation for NSTEMI(Non-Q wave MCI or UAP) :

ST Segment depression or inverted T wave(1mm) at 2 or more closely positioned lead. ST segment changes from ST depression at the moment of symptom to normal ST segment when symptom is relieved -> UAP

ACS

Heart Biomarker
BIOMARKER TIME OF ELEVATION PEAK NORMALIZED

CK-MB

3 12 hours

24 hours

48 72 days

(cTn)T

3 12 hours

24 hours

5 10 days

(cTn)I

3 12 hours

12 hour s 2 days

5 14 days

ACS
Coronary Thrombosi s Myocardial Ischemia Arrhythmia and Loss of Muscle Remodeling

CAD Atherosclerosi s Risk Factors ( , BP, DM, DYSLIPIDEMIA Insulin Resistance, Platelets, Fibrinogen, etc)

Ventricular Dilatation Congestive Heart Failure End-stage Heart Disease

ACS
ACS ALGORITHM

Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Time from onset of symptoms 12 hours - Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) - ACE-I/ARB within 24 h of symptom onset) - Statin - High risk: early invasive strategy - Continue ASA, heparin, ACE-I, statin ST-depression or dynamic T-wave inversion strongly suspicious for injury Normal or nondiagnostic changes in ST-segment or Twaves Develops high or intermediate risk criteria or troponin-positive Monitored bed in ED Develops high or intermediate risk criteria or troponin-positive

Start adjunctive treatment 12 hrs Admit to monitored bed Assess risk status

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

Chest discomfort suggestive of ischemia

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

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)

study
Portable chest x-ray ( 30 minutes)

Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Time from onset of symptoms 12 hours - Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) - ACE-I/ARB within 24 h of symptom onset) - Statin - High risk: early invasive strategy - Continue ASA, heparin, ACE-I, statin ST-depression or dynamic T-wave inversion strongly suspicious for injury Normal or nondiagnostic changes in ST-segment or Twaves Develops high or intermediate risk criteria or troponin-positive Monitored bed in ED Develops high or intermediate risk criteria or troponin-positive

Start adjunctive treatment 12 hrs Admit to monitored bed Assess risk status

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

Adjunctive Therapy
Heparin (UFH/LMWH)

Glycoprotein IIb/IIIa receptor inhibitors

-Adrenoreceptor blockers
Clopidogrel

From: 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2013;61(4):e78-e140. doi:10.1016/j.jacc.2012.11.019

Figure Legend:
Reperfusion therapy for patients with STEMI. The bold arrows and boxes are the preferred strategies. Performance of PCI is dictated by an anatomically appropriate culprit stenosis. *Patients with cardiogenic shock or severe heart failure initially seen at a nonPCIcapable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from MI onset (Class I, LOE: B). Angiography and revascularization should not be performed within the first 2 to 3 hou rs after administration of fibrinolytic therapy. CABG indicates coronary artery bypass graft; DIDO, door-indoor-out; FMC, first medical contact; LOE, Level of Evidence; MI, myocardial PCI, percutaneous coronary intervention; and STEMI, ST-elevation Date of download: Copyrightinfarction; The American College of Cardiology. myocardial infarction. 6/3/2013 All rights reserved.

RISK STRATIFICATION
HIGH-RISK PATIENT
Repetitive or prolonged (> 10 minutes) pain Elevated level of 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 Haemodynamic compromise Sustained ventricular tachycardia Syncope LV systolic dysfunction (ejection fraction <40%); Prior PCI or CABG within 6 months or prior Diabetes Chronic kidney disease (estimated GFR< 60 mL/min)
Guideline ACS 2006 National Heart Foundation Australia

Outpatient Care
Medication to relieve symptoms and prevent Aspirin Beta-blocker ACE inhibitor

Modification of Risk Factors

Stop Smoking Body Weight Physical Activity (based on patients performance, preferably determined by cardiac stress test [treadmill]) Diet (Low fat, with LDL target below 100mg/dL) Control BP Control of blood glucose level for patients with DM

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.

KILLIP CLASSIFICATION
Stage I- No heart failure. No clinical signs of cardiac

decompensation; Stage II- Heart failure. Diagnostic criteria include rales, S3 gallop and pulmonary hypertension. Pulmonary congestion with wet rales in the lower half of the lung fields; Stage III- Severe heart failure. Frank pulmonary oedema with rales troughout the lung fields; Stage IV- Cardiogenic shock. Signs include hypotension (SBP <= 90 mmHg), and evidence of peripheral vasoconstriction such as oliguria, cyanosis, and diapohoresis.

PROGNOSIS

STATUS PASIEN
No : 00.55.87.56 Tanggal : 16 Mei 2013 Nama pasien: Saiman

Umur

: 73th/ 10 bln/4 hr Seks : LK Pekerjaan: Wiraswasta Alamat : Jl. Aek Raso Kec. Torgamba Agama: Islam Tlp: Hp: -

 Keluhan utama: Nyeri dada Anamnesis: Hal ini dialami os 3 hari yang lalu (Senin, 13/5,

sekitar pukul 9 pagi) saat os jalan pagi. Nyeri dada dirasakan os seperti terhimpit benda berat. Penjalaran (+) ke bahu dan punggung. Durasi > 30 menit, disertai mual (+), keringat dingin (+), muntah (-). Nyeri dada yang seperti ini merupakan pertama kali dirasakan os. Sesak nafas (-), DOE (+), PND (-), OP (-), kaki bengkak (-). Riwayat nyeri dada sebenarnya telah dirasakan os 1 tahun ini, bersifat hilang timbul. Nyeri dada terutama dirasakan os bila beraktifitas berat, durasi 5-10 menit, menghilang dengan beristirahat. Oleh karena keluhan nyeri dada tersebut, os lalu dibawa keluarga ke RSUD Rantau Prapat dan dirawat oleh SpPD selama 3 hari.

 Menurut pengakuan os, saat di IGD RSUD Rantau

Prapat, os telah diberikan obat 4 tablet yang dimakan sekaligus dan 2 tablet kunyah, serta dapat obat suntikan di perut sebanyak 2 kali. Kemudian os dirujuk ke RSHAM untuk penanganan selanjutnya. Riwayat hipertensi dan DM disangkal os. Os adalah pasien baru RSHAM, saat di IGD keluhan nyeri dada sudah berkurang. Riwayat merokok (+) 2 bungkus perhari selama >50 tahun.

 Faktor Resiko PJK: Laki laki, usia >45 tahun,

merokok Riwayat Penyakit Terdahulu: Riwayat obat: Clopidrogel, Fasorbid, Fluxum, tanapres s, Alovastatin, Ranitidin, Aspilet.

STATUS PRESENS
Status presens: KU: Nyeri dada.

Kesadaran: CM

TD: 90/70

mmHg Pols:94 x/i, irreguler RR: 24 x/i Suhu: 36,5C Sianosis : (-) Ortopnu: (+) Dispnu: (-) Ikterus: (-) Edema (-) pucat (-) BB: 50 kg TB: 158 cm IMT : BB/(TB)2 = 50/(1.58)2 = 20.08 (normoweight)

PEMERIKSAAN FISIK
Pemeriksaan Fisik: Kepala : sklera ikterik (-/-) konjungtiva palpebra inferior

anemis (-/-) Leher: TVJ : R+3 cmH2O Dinding toraks: Inspeksi : simetris fusiformis Palpasi : stem fremitus kanan = kiri, kesan normal Perkusi : sonor pada kedua lapangan paru Batas jantung : Atas : ICS III sinistra Kanan : Linea parasternalis dextra Kiri : 1 cm lateral LMCS

 Auskultasi Jantung: S1 (N) S2 (N) S3 (-) S4 (-) irregular, HR 94x/i irreguler

Murmur : (-) , Tipe : (-). Paru : suara pernafasan vesikuler suara tambahan : ronki (+) wheezing (-/-) Abdomen: Palpasi Hepar/Lien : tidak teraba Bising Usus (+) Asites (-) Ekstremitas: akral hangat edema (-)

SINUS RHYTM, QRS RATE 96X/MNT, QRS AXIS (N), GEL. P (N), PR INTERVAL 0,16, QRS DURATION 0,08, Q PATOLOGIS DI II, III, AVF, ST DEPRESI DI I, AVL, V2-V6. LVH (-), VES (-), AES (-), (ECG POST: Q PATH DENGAN ST ELEVASI V8 V9/EKG KANAN: ST ELEVASI V3R-V4R.) KESAN EKG: SR + STEMI INFEROPOSTERIOR + RV INFARK

 Interpretasi Foto Thorax: CTR 55%, segmen aorta dilatasi, segmen Po normal,

pinggang jantung (+), kongesti(-). Infiltrat(-). Kesan: Cardiomegali + aorta dilatasi

HASIL LABORATORIUM
Hematologi Hb 15.60 gr% (Ti) RBC 5.22 x 106 /mm3 WBC 14.22 x 103/mm3 PLT 91 x 103/mm3 Ht 44,40 % (Ti) MCHC 35,10 % RDW 14,40 % Kimia Klinik pH 7,451 pO2 181,2 mmHg (Ti) HCO3 15.6 mmol/L (Tu) CO2 16.3 mmol/L (Tu) BE -6,0 mmol/L (Tu) SO2 99,6%

 Ginjal
Kreatinin: 1.42 mg/dl Ureum: 110 mg/dL Elektrolit Natrium : 121 mEq/L Kalium : 4,2 mEq/L Klorida : 107 mEq/L

Diagnosa Kerja : STEMI inferoposterior Fungsional : STEMI inferoposterior onset 3 hari KILLIP II TIMI Risk Score 7/14 Anatomi : Arteri Koroner Etiologi : Atherosklerosis

Differensial Diagnosa : - STEMI Inferoposterior onset 3 hari KILLIP II TIMI Risk Score 7/14 -NSTEMI -UAP
Pengobatan: Bed Rest O2 4L/i IVFD NaCl 0,9 % 10 gtt/I (mikro) Inj UFH 600 IU/hour Aspilet 1x80 mg Plavix 1x75 mg ISDN 5mg (k/p) Simvastatin 1x40 mg Laxadin 1x1CI

 Rencana Pemeriksaan Lanjutan: KGDN/ 2JPP, HbA1c Faal Hemostasis Lipid profile Echocardiography Angiography coroner Prognosis : Dubia ad bonam

FOLLOW UP PASIEN
FOLLOW UP.docx
FOLLOW UP (16 Mei 2013 30 Mei 2013)

Kesimpulan
Pembentukan thrombus di daerah plak akan mempersempit oklusi,dan gangguan aliran darah menyebabkan ketidakseimbangan yang nyata antara pemasukan oksigen dan kebutuhan oksigen. Bentuk ACS merupakan hasil yang bergantung dari derajat obstruksi koroner dan berhubungan dengan iskemia. Oklusi thrombus parsial menyebabkan sindrom unstable angina (UAP) dan non-ST Elevation Myocardial Infarction (NSTEMI). Jika thrombus menyumbat arteri koroner secara komplit, maka menyebabkan iskemik yang lebih parah dan nekrosis yang lebih banyak, dikenal sebagai ST Elevation Myocardial Infarction (STEMI).

 Pasien datang dengan diagnosa STEMI inferoposterior +

RV infark dengan gejala klinis nyeri dada dirasakan os seperti terhimpit benda berat. Penjalaran (+) ke bahu dan punggung. Durasi > 30 menit, disertai mual (+), keringat dingin (+). Dari interpretasi EKG terlihat kesan SR + STEMI inferoposterior + RV infark. Pasien juga telah mendapat penatalaksaanaan awal dengan ace inhibitor, anti platelet, dan antikoagulan. Pada pasien ini di berikan terapi berupa Bed Rest semi fowler, O2 4L/i, IVFD NaCl 0,9 % 10 gtt/I (mikro), Inj UFH 600 IU/hour , Aspilet 1x80 mg, Plavix 1x75 mg, ISDN 5mg (k/p), Simvastatin 1x40 mg dan Laxadin 1x1ci.

TERIMA KASIH

PDKI 2009 ..\Downloads\Documents\acs-cardiovascular-emergency-jadi.pdf AHA/ACC 2013 ..\Downloads\Documents\Circulation-2013-O-Gara-529-55.pdf ECS 2012 STEMI ..\Downloads\Documents\Guidelines_AMI_STEMI.pdf NSTEMI ..\Downloads\Documents\Guidelines-NSTE-ACS-FT.pdf Ppt ..\Downloads\Documents\Figure.ppt(aha) ..\Downloads\Documents\Slide_Set_AMI_STEMI.ppt(ecs) ..\Downloads\Documents\guidelines_ACS_NSTE_Slides-2011.ppt(ecs)