Nstemi Peni

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    NSTEMI

    Non ST ElevationMyocardial Infarction

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    SKA

    Suatu sindroma klinik yang menandakan

    adanya iskemia miokard akut, terdiri dari :

    STEMI

    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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    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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    Penyempitan

    Pembuluh

    darah

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    Clinical Spectrum of Acute Coronary Syndrome

    Acute Coronary Syndrome

    Non-ST Segment

    Elevation

    ST Segment

    Elevation

    Unstable

    Angina Pectoris

    Non-Q-wave Q-wave

    Acute Myocardial

    Infarction

    STEMI

    NSTEMI

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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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    Myocardial infarction:acute, evolving, recent

    Typical rise and gradual fall (troponin) or morerapid rise and fall (CK-MB) of biochemical

    markers of myocardial necrosis with at leastone of the following:

    a) ischemic symptoms;

    b) development of pathologic Q waves on the ECG;

    c) ECG changes indicative of ischemia (ST segmentelevation or depression); or

    d) coronary artery intervention (e.g., coronary angio-plasty).

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    ACC/AHA Guidelines

    NSTEMI is an acute process of myocardial

    ischemia with sufficient severity andduration to result in myocardial necrosis.

    The initial ECG in patients with NSTEMI

    does not show ST-segment elevation.

    NSTEMI is distinguished from UA by the

    detection of cardiac markers indicative of

    myocardial necrosis in NSTEMI and theabsence of abnormal elevation of such

    biomarkers in patients with UA.

    Definition: NSTEMI

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    Definition: unstable angina

    Unstable anginaan acute process of

    myocardial ischemia that is not ofsufficient severity and duration to result in

    myocardial necrosis.

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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 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

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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 infarcts Occasionally 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, fist on chest(Levine sign)

    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 RATE Variable 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 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 day

    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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    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 sangatmenyokong 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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    Recommended Class I:

    Aspirin, Nitrate, B-blockers, morphine, O2 (prn).

    Nondihydropyridine (cardizem/verapamil).

    ACEi for specifics.

    Class 2a:

    ACEi for all.

    Long-acting CCB for recurrent ischemia.

    IABP if all fails.

    Class 2b:

    Extended form of Nondihydropyridine.

    Short acting dihydropyridine in the presence of B-blocker.

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    Oxygen

    For:

    Cyanosis

    Resp distress

    High risk features

    Consume resources Evidence is lacking.

    Nit t

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    Nitrates: Decr MVO2, incr coronariesoxygenation

    Actions

    Dilate venous bed: decr preload and ventricular walltension.

    Smaller dilatation of arterial system: decr afterloadand ventricular wall tension.

    Need B-blocker

    Dilatation of atherosclerotic coronaries

    Decreased platelets adhesiveness.

    For

    ischemia despite nitro X 3 and iv B-blockade

    high-risk patients (non-hypotensive).

    Prethrombolytics: 35% mortality reduction.

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    Morphine

    Potent anxiolytic and analgesic action

    Potentially beneficial

    Venous dilatation

    Decr HR

    Decr sBP (Decr MVO2)

    Activates neutral endopeptidases

    Ann Emerg Med. May 2001;37:445-449.

    Nausea and vomiting in 20%

    Hypotension

    Meperidine if allergic

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    Beta-blockers Decr sBP

    Decr SA node rate, contractility, AV nodeconduction.

    Incr diastole filling time.

    iv form for high-risk pts/on going pain.

    Oral for intermediate/low risks patients.

    No preferred agents except better if B-blockerwithout ISA (metoprolol, atenolol, propramolol,esmolol).

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    B-blockers Contraindications (consensus):

    1st degre AV block >24 msec

    2nd or 3rd degre AV block without pacemaker

    Asthma

    Severe LV dysfunction with CHF

    Caution with:

    COPD

    Bradycardia

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    B-blockers

    13% reduction of progression of UA to

    AMI.

    Extrapolate data from use in AMI, recent

    MI, stable angina, heart failure.

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    Calcium channel blockers

    Inhibit vasculature SM contracture

    Coronary vasodilatation

    Inhibit myocardial muscle contraction

    AV block

    Slow sinus node

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    Calcium channel blockers Dihydropyridines: nifedipine and amlodipine

    peripheral vasodilatation

    Verapamil: DAVIT study (3200 pts)

    Only favorable trend

    Nifedipine: HINT study (500 pts)

    Incr MI by 16%, decr by 20% if with metoprolol

    But metoprolol alone decr by 24%!!!

    Diltiazem showed trends of improved outcome

    CKMB level, reinfarction rate

    Same mortality

    except in LV dysfunction ACS

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    Calcium channel blockers

    Conclusion:

    Good symptom reliever Trend of improved outcome with non-

    dihydropyridine agents

    To use if unable to use B-blockers

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    Antiplatelet agents

    Aspirin ASAP!

    Thienopyridine (clopidogrel or ticlopidine) ifhypersensitivity of major GI intolerance

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    Aspirin

    Cyclooxygenase-1 inhibitor

    Prevents thromboxane A2 formation

    Dosing: 160 mg or 325 mg

    Based on ISIS-2 which definetly established

    its efficacy.

    Can use pr route.

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    Adenosine diphosphate

    inhibitors Clopidogrel acts faster than ticlopidine.

    Ticlodipine: Gi se, neutropenia, TTP

    Clopidogrel: minimal rash and diarrhea

    11 TTP within 14 days (3 millions pts)

    CURE study: NEJM Aug 2001 12000 pts, plavix 300mg po

    9.3 vs 11.4, 16.5 vs 18.8

    ST changes or + markers

    No GP2b3a inh or angio

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    Plavix:Safety if angio or used with

    Gp2b3A inh Lancet August 2001: PCI-CURE study

    2600 pts.

    Plavix 300mg loading

    No increased bleeding problem whether

    plavix +/- GPIIb/IIIa inh were used.

    Better outcome before an after PCI.

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    Other po agents

    Sulfinpyrazone

    Dipyridamole

    Prostacyclin

    Oral GP IIB/IIIA inhibitor:

    4 studies: 1 PCI, 3 NSTEMI 2 increased mortality

    None presently recommended

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    Anticoagulants

    UFH

    LMW heparin

    Hirudin

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    UFH Activates antithrombin III

    Inactives thrombin (f2), f9a and f10a

    Molecular weight: 5 000 to 30 000 D

    Binds to various proteins, cells , endothelium

    Unpredictable.

    Weight adjusted dosage

    Incr need in DM and smoking, lower with age

    Theroux et al. N Engl J Med 1988;319:110511.

    MI rate of 12% down to 0.8% in UA

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    LMW heparin

    Molecular weight of 4200 to 6000 D

    Factor Xa to thrombin inhibition ratio of1.9 to 3.8

    Only 25-50% have >18 saccharides

    both f2 and 10 inhibition

    Rest inhibits only factor Xa

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