Post on 11-Mar-2016
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Anatomi Koroner dan EKG 12 sandapan
Sandapan V1 dan V2 menghadap septal area ventrikel kiri
Sandapan V3 dan V4 menghadap dinding anterior ventrikel kiri
Sandapan V5 dan V6 ( ditambah I dan avL ) menghadap dinding lateral ventrikel kiri
Sandapan II, III dan avF menghadap dinding inferior ventrikel kiri
Lokalisasi Dinding Ventrikel PadaEKG (Ventrikel Kiri)
Anteroseptal : V1-V4 Anterior ekstensif : V1-V6, I dan aVL Anterolateral : V4-V6, I dan aVL Anterior terbatas : V3-V5 Inferior : II, III dan aVF Lateral tinggi : I dan aVL Posterior murni : bayangan cermin V1, V2,
V3 pada garis horisontal
ISCHEMIA : ST depresi atau T inverted
INFARCT : ST Elevasi
NECROSIS (OLD INFARCT) : gel. Q patologis atau QS
Iskemia Depresi ST Inversi T Inversi U
ST depresi dan perubahan gelombang T
ST depresi dianggap bermakna bila > 1 mm di bawah garis dasar PT di titik J Titik J didefinisikan sebagai akhir kompleks QRS dan permulaan segmen ST
Bentuk segmen ST :
up-sloping ( tidak spesifik ) horizontal ( lebih spesifik untuk iskemia ) down-sloping ( paling terpercaya untuk iskemia )
Perubahan gelombang T padaiskemia kurang begitu spesifik
Gelombang T hiperakutkadang2 merupakan satu-satunyaperubahan EKG yang terlihat
Nonpathologic (nonischemic) and pathologic (ischemic) ST-segment and T-wave changes. A, Characteristic nonischemic ST-segment change called J-depression; note
that the ST slope is upward. B and C, Examples of pathologic ST-segment changes; note that the
downward slope of the ST segment (B) or the horizontal segment is sustained (C).
(From Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. Philadelphia, Mosby, 2006.)
Iskemia Inversi T
Gelombang T yang negatif(vektor T berlawanan arahdengan vektor QRS)
Tanda ini tidak terlalu spesifikYang lebih spesifik gelombang
T ini simetris dan berujung lancip
Inversi T pada iskemia miokarda. Inversi T : kurang spesifik untuk iskemiab. Inversi T berujung lancip & simetris (ujung anak
panah) : spesifik untuk iskemia
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ST Depresi
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T Inverted
Infark miokard
Progression of an Acute Myocardial Infarction
An acute MI is a continuum that extends from the normal state to a full infarction:
IschemiaLack of oxygen to the cardiac tissue, represented by ST segment depression, T wave inversion, or both
InjuryAn arterial occlusion with ischemia, represented by ST segment elevation
InfarctionDeath of tissue, represented by a pathological Q wave
Normal
Ischemia
Injury
Infarction
Figure. ST, QRS, and T vectors in myocardial infarction.
a. ST injury vector. b. b. QRS vector in necrosis. c. c. T ischemia vector
Hubungan antara lokasiinfark dan oklusi arterikoroner (panah), dan lead elektrocardiogram. a. Anteroseptal infark.b. Anterior infark
Extensive (anterolateralinfarction)
c. Infark lateral isolatedction
a b
c
d
e f
d. Infark Inferior
e. Infark Posterior
f. Right ventricular infarction (combined to inferior infarction)
Ishemia Injury - InfarctAccurate ECG interpretation in a patient with chest pain is critical. Basically, there can be three types of problems - ischemia is a relative lack of blood supply (not yet an infarct), injury is acute damage occurring right now, and finally, infarct is an area of dead myocardium. It is important to realize that certain leads represent certain areas of the left ventricle; by noting which leads are involved, you can localize the process. The prognosis often varies depending on which area of the left ventricle is involved (i.e. anterior wall myocardial infarct generally has a worse prognosis than an inferior wall infarct).
V1-V2 anteroseptal wallV3-V4 anterior wallV5-V6 anterolateral wallII, III, aVF inferior wallI, aVL lateral wall
V1-V2 posterior wall (reciprocal)
depresion
elevation
NON-TRANSMURAL = SUB ENDOCARDIAL = non Q-WAVE M.I.
TRANSMURAL = MYOCARDIAL = Q-WAVE M.I.
Figure. a. Acute infarction: correlation between
the electrocardiogram (ECG) and the stage of myocardial ischemia. Monophasic ST deformation /transmural lesion = lesion / injury.
b. Subacute infarction. Correlation between the ECG and the stage of myocardial ischemia (ST elevation = lesion, plus pathologic Q wave = necrosis, plus negative T wave = ischemia).
c. Evolution of subacute infarction to chronic infarction
Figure V3 lead: Evolution of QRS and ST/T morphologies in STEMI due to occlusion of LAD.(a) Few minutes; (b) 1 hour; (c) 1 day; (d) 1 week.
Figure 9.3. The evolution of an inferior wall myocardial infarction, as seen in lead III of a 55-year-old white male. Note that the admission tracing shows only ST elevation. A Q wave is beginning to form by 1 hour, and ST elevation is on the way down. By 24 hours, Q wave formation is complete,and the T wave is fully inverted. By 1 year, a pathologic Q wave is the only remaining evidence of infarction.
Mid LAD occlusion after the first septalperforator (arrow) ECG : large anterior MI
Proximal large RCA occlusion
ST elevation in leads II, III, aVF, V5, and V6with precordial ST depression
Small inferior distal RCA occlusion
ECG changes in leads II, III, and aVF
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ST Elevasi
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Fase Evolusi Lengkap
Elevasi ST spesifik : konveks keatas
T negatif dan simetris Q patologis
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Qs Patologis
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Early Repolarisasi
LATIHAN
Unstable angina
Subendocardial ischemia. Anterolateral ST-segment depression
Acute anteroseptal myocardial infarction. Hyperacute T-wave changes are noted
Acute anterolateral myocardial infarction
Lateral myocardial infarction
Inferior myocardial infarction
Inferior myocardial infarction. Inferior Q waves with T-wave inversions
Acute inferoposterior myocardial infarction
Right bundle branch block
RBBB + Anterior Infarction
Left bundle branch block
Thank you