Acute Coronary Syndrome

Presentasi berjudul: "Acute Coronary Syndrome"— Transcript presentasi:

1 Acute Coronary Syndrome
Sindroma Koroner Akut Toni Mustahsani Aprami, dr., SpPD, SpJP Department of Cardiology and Vascular Medicine Division of Cardiovascular, Department of Internal Medicine Padjadjaran University School of Medicine/Hasan Sadikin Hospital , Bandung

2 DEFINISI Suatu sindroma klinik yang menandakan
adanya 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.

3 PATOGENESIS Umumnya disebabkan oleh aterosklerosis koroner
Plak aterosklerosis ruptur  terbentuk trombus diatas ateroma yang secara akut menyumbat lumen koroner Apabila sumbatan terjadi secara total  hampir seluruh dinding ventrikel akan nekrosis

4 Risk Factors Uncontrollable Controllable High blood pressure Sex
High blood cholesterol Smoking Physical activity Obesity Diabetes Stress and anger Sex Hereditary Race Age

5 The cardiovascular continuum of events
Ischemia = oxygen supply and demand imbalance Myocardial Ischemia CAD plaque Atherosclerosis Risk Factors ( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc) DYSLIPIDEMIA Adapted from Dzau et al. Am Heart J. 1991;121:

6 The cardiovascular continuum of events
Coronary Thrombosis Myocardial Ischemia CAD Atherosclerosis Risk Factors ( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc) DYSLIPIDEMIA Adapted from Dzau et al. Am Heart J. 1991;121:

7 The cardiovascular continuum of events
ACS Coronary Thrombosis Myocardial Ischemia CAD Atherosclerosis Risk Factors ( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc) DYSLIPIDEMIA Adapted from Dzau et al. Am Heart J. 1991;121:

8 STEMI UA/NSTEMI Coronary thrombosis Plaque rupture Stable angina

9 Penyempitan Pembuluh darah

10 Clinical Spectrum of Acute Coronary Syndrome
ST Segment Elevation Non-ST Segment Elevation STEMI NSTEMI Unstable Angina Pectoris Non-Q-wave Q-wave Acute Myocardial Infarction

11 NSTEMI Angina STEMI Complete thrombus Occluding thrombus Non occlusive
Unstable Angina STEMI 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

12 Diagnosis Anamnesis Pemeriksaan Fisik Pemeriksaan Penunjang :
1. Laboratorium 2. Elektrokardiografi 3. Thoraks Foto

13 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

14 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

15 Pain Patterns with Myocardial Ischemia

16 Anamnesis untuk UAP 3 kategori presentasi klinik UAP:
Angina saat istirahat (resting angina) Angina awitan baru (new onset angina) Angina yang bertambah berat (increasing angina) Riwayat penyakit dahulu : Riwayat angina on effort, infark atau operasi pintas Riwayat penggunaan nitrogliserin Identifikasi faktor-faktor risiko

17 PHYSICAL EXAMINATION GENERAL APPEARANCE
Anxious, considerable distress, restless, fist on chest (Levine sign) LV failure & symp. 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 : VPB’s within first 4 hours

18 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 hrs, fever resolves by 4th or 5th day Respiration  due to anxiety and pain, in LV failure : resp. rate correlates with degree of heart failure

19 JUGULAR VENOUS PULSE JVP usually normal RV infarction : marked jug. venous distension CAROTID PULSE Small pulse  reduced stroke volume Pulse alternans : severe LV dysfunction

20 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

21 Pemeriksaan Penunjang Pemeriksaan EKG
Gambaran EKG infark miokard akut Q-wave (STEMI) : Elevasi segmen ST  1 mm pada  2 sadapan extremitas Atau  2 mm pada  2 sadapan prekordial yang berurutan Atau gambaran LBBB baru atau diduga baru

22 ST-segment elevation

23

24

25 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

26 ST-segment depression

27 T-wave inversion

28 Current-of-injury patterns with acute ischemia
ELEKTROKARDIOGRAM Current-of-injury patterns with acute ischemia

29 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)

30 Plot of the appearance of cardiac markers in blood versus time after onset of symptoms
A myoglobin C CK-MB B troponin D troponin in UA

31 Diagnosis Banding Diseksi aorta Perikarditis
Nyeri angina atipikal pada kardiomiopati hipertrofi Penyakit esofageal, GI atas atau traktus biliaris Penyakit paru-paru : pneumotoraks, emboli, pleuritis Sindroma hiperventilasi Gangguan dinding dada : muskuloskeletal, neurogen Psikogen

32 Manajemen

33 The cardiovascular continuum of events
ACS Coronary Thrombosis Arrhythmia and Loss of Muscle Myocardial Ischemia Remodeling Ventricular Dilatation CAD Atherosclerosis Congestive Heart Failure Risk Factors ( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc) End-stage Heart Disease DYSLIPIDEMIA Adapted from Dzau et al. Am Heart J. 1991;121:

34 DELAY TO THERAPY 1. From onset of symptoms to patient recognition
2. Out-hospital transport Public education campaigns increase public awareness and knowledge of symptoms of heart attack but have only transient effects (Blohm M, Herlitz J, Schroder U et al. Reaction to a media campaign focusing on delay in acute myocardial infarction. Heart Lung 1991;20:661-6). Half of the patients who die of AMI do so before reaching the hospital. VF or pulseless VT is the precipitating rhythm in most of the cases (Cohen MC, Rohtla EM, Lavery CE, Muller JE, Mittleman MA. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997;79: and Colquhoun MC, Julien DG. Sudden Death in the community: the arrhythmias causing cardiac arrest and result of immediate resuscitation. Resuscitation 1992;24:177A) and in most cases developed during the first 4 hours after the onset of symptoms (Campbell RW, Murray A, Julian DG. Ventricular arrhythmias in first 12 hours of acute myocardial infarction: natural history study. Br Heart J 1981;46: and Chiriboga D, Yarzebski J, Goldberg RJ, Gore JM, Alpert JS. Temporal trends (1975 through 1990) in the incidence and case-fatality rate of primary ventricular fibrillation complicating acute myocardial infarction: a community perspective. Circulation 1994;89: ). The activation of the emergency medical services (EMS) system and prompt respond to out-hospital cardiac arrest by the community and emergency medical team is therefore necessary to be developed. ACC/AHA guidelines recommend that the patient or family members activate the EMS system rather than call their physician or driving to the hospital if chest discomfort is unimproved if chest discomfort is unimproved or worsening 5 minutes after taking 1 nitroglycerin tablet or using nitroglycerin spray (Antman EM, Anbe DT, Amstrong PW et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary: a report of the American College of Cardiology/American Heart Association ask Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction. Circulation 2004;110: ). Physician should also tell the patient to take aspirin. 3. In-hospital evaluation

35 ISCHEMIC CHEST PAIN ALGORYTHM
Chest pain suggestive of ischemia

36 ISCHEMIC CHEST PAIN TYPICAL ANGINA EQUIVALENT ANGINA
CHEST DISCOMFORT LOCATION RADIATION UNLIKELINESS NO CHEST DISCOMFORT INDIGESTION UNEXPLAINED WEAKNESS DIAPORESIS SHORTNESS OF BREATH Early recognition of symptoms of STEMI by the patient or someone with the patient is the first step that must occur before evaluation and life-saving treatment can be obtained. Although many lay persons are generally aware that chest pain is a presenting symptom of STEMI, they are unaware of the common associated symptoms, such as arm pain, lower jaw pain, shortness of breath, and diaphoresis (Goff DC, Sellers DE, McGovern PG, et al. Knowledge of heart attack symptoms in a population survey in the United States: the REACT Trial. Rapid Early Action for Coronary Treatment. Arch Intern Med 1998;158: ). The average patient with STEMI does not seek medical care for approximately 2 hours after symptom onset, and this pattern appears unchanged over the last decade ( [1] Goldberg RJ, Yarzebski J, Lessard D, Gore JM. A two-decades (1975 to 1995) long experience in the incidence, in-hospital and long-term case-fatality rates of acute myocardial infarction: a community-wide perspective. J Am Coll Cardiol 1999;33:1533-9, [2] Goff DC, Sellers DE, McGovern PG, et al. Knowledge of heart attack symptoms in a population survey in the United States: the REACT Trial. Rapid Early Action for Coronary Treatment. Arch Intern Med 1998;158: [3] Welsh RC, Ornato J, Armstrong PW. Prehospital management of acute ST-elevation myocardial infarction: a time for reappraisal in North America. Am Heart J 2003;145:1-8.). Average and median delays for patients with STEMI were 4.7 and 2.3 hours, respectively, from the 14-country Global Registry of Acute Coronary Events (GRACE) project. Half of the patients who die of AMI do so before reaching the hospital. VF or pulseless VT is the precipitating rhythm in most of the cases (Cohen MC, Rohtla EM, Lavery CE, Muller JE, Mittleman MA. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997;79: and Colquhoun MC, Julien DG. Sudden Death in the community: the arrhythmias causing cardiac arrest and result of immediate resuscitation. Resuscitation 1992;24:177A) and in most cases developed during the first 4 hours after the onset of symptoms (Campbell RW, Murray A, Julian DG. Ventricular arrhythmias in first 12 hours of acute myocardial infarction: natural history study. Br Heart J 1981;46: and Chiriboga D, Yarzebski J, Goldberg RJ, Gore JM, Alpert JS. Temporal trends (1975 through 1990) in the incidence and case-fatality rate of primary ventricular fibrillation complicating acute myocardial infarction: a community perspective. Circulation 1994;89: ).

37 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

38 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 study Portable chest x-ray ( 30 minutes) Immediate ED general treatment O2 at 4 L/min (maintain O2 sat 90%) Aspirin mg Nitroglycerin SL, spray, or IV Morphine IV 2-4 mg repeated every 5-10 minutes (if pain not relieved with nitroglycerine) Memory: “MONA” greets all patients 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

39 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

40 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Review initial 12 lead ECG Immediate ED assessment and immediate ED general treatment ST elevation or new or presumably new LBBB strongly suspicious for injury 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

41 Acute coronary syndrome 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 ST-depression or dynamic T-wave inversion strongly suspicious for injury 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

42 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG Normal or non-diagnostic changes in ST-segment or T-waves (intermediate/ low-risk UA) ST elevation or new or presumably new LBBB strongly suspicious for injury (STEMI) ST-depression or dynamic T-wave inversion strongly suspicious for injury (UA/NSTEMI) 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

43 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG Normal or non-diagnostic changes in ST-segment or T-waves (intermediate/ low-risk UA) ST-depression or dynamic T-wave inversion strongly suspicious for injury (UA/NSTEMI) ST elevation or new or presumably new LBBB strongly suspicious for injury (STEMI) Start adjunctive treatment 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

44 (Do not delay reperfusion)
ADJUNCTIVE TREATMENT (Do not delay reperfusion) Beta-adrenergic receptor blocker Clopidogrel Heparin (UFH or LMWH) 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

45 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG Normal or non-diagnostic changes in ST-segment or T-waves ST-depression or dynamic T-wave inversion strongly suspicious for injury ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Time from onset of symptoms Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) ACE-I/ARB Statin  12 hours 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

46 Acute coronary syndrome algorithm
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG Normal or non-diagnostic changes in ST-segment or T-waves ST-depression or dynamic T-wave inversion strongly suspicious for injury ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Start adjunctive treatment Time from onset of symptoms  12 hours Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) ACE-I/ARB within 24 hours of onset Statin 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

47 Adjunctive treatment Heparin (UFH/LMWH)
Glycoprotein IIb/IIIa receptor inhibitors -Adrenoreceptor blockers Clopidogrel 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

48 Chest discomfort suggestive of ischemia
Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG Normal or non-diagnostic changes in ST-segment or T-waves ST-depression or dynamic T-wave inversion strongly suspicious for injury ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Start adjunctive treatment  12 hrs Admit to monitored bed Assess risk status High risk: early invasive strategy Continue ASA, heparin, ACE-I, statin 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 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

49 VERY HIGH-RISK PATIENT
Refractory chest pain Recurrent/persistent ST deviation Ventricular tachycardia Hemodynamic instability Sign of pump failure Shock within 48 hours 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

50 Chest discomfort suggestive of ischemia
Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG Normal or non-diagnostic changes in ST-segment or T-waves ST-depression or dynamic T-wave inversion strongly suspicious for injury ST elevation or new or presumably new LBBB strongly suspicious for injury Develops high or intermediate risk criteria or troponin-positive Monitored bed in ED Start adjunctive treatment Start adjunctive treatment Time from onset of symptoms  12 hrs Admit to monitored bed Assess risk status  12 hours High risk: early invasive strategy Continue ASA, heparin, ACE-I, statin Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) ACE-I/ARB within 24 h of symptom onset) Statin No evidence of ischemia and MI: discharge with follow-up 2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

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53 Pengobatan Pasca Perawatan
Obat-obat untuk mengontrol keluhan iskemia harus dilanjutkan Aspirin Beta-blocker ACE inhibitor Modifikasi Faktor Risiko Berhenti merokok Pertahankan BB optimal Aktivitas fisik sesuai dengan hasil treadmill Diet Rendah lemak jenuh dengan kolesterol, bila perlu dengan target LDL < 100 mg/dL Pengendalian hipertensi Pengendalian ketat gula darah pada penderita DM

54 Prevention Get regular medical checkups. Control your blood pressure.
Check your cholesterol. Don’t smoke. Exercise regularly. Maintain a healthy weight. Eat a heart-healthy diet. Manage stress. Prevention

55 Thank you for your attention

56 Anamnesis Nyeri dada atau nyeri epigastrium hebat yang mengarah pada iskemia miokard : Seperti dihimpit benda berat Terasa tercekik Rasa ditekan, ditinju, ditikam Rasa terbakar Biasanya dirasakan dibelakang stenum  seluruh dada terutama kiri, dapat ke tengkuk, rahang, bahu, punggung, lengan kiri atau kedua lengan Terutama laki-laki > 35 tahun dan Wanita > 40 tahun Seringkali disertai mual atau muntah, dapat pula rasa tidak enak disertai sesak nafas, lemah, penurunan kesadaran, dan keringat banyak

57 Pemeriksaan Fisik Biasanya penderita tampak cemas, gelisah, pucat, dan keringat dingin Periksa tanda-tanda vital : Denyut nadi cepat, reguler tetapi dapat pula bradi atau tachycardia, irama ireguler Tekanan darah biasanya normal bila belum terjadi komplikasi, dapat pula terjadi hipo atau hipertensi Bunyi jantung dapat terdengar redup S3 dapat terdengar bila kerusakan miokard luas Paru-paru dapat terdengar ronkhi basah dan atau wheezing yang menandakan terjadinya bendungan paru  tergantung ada tidaknya gangguan fungsi ventrikel kiri