ECG PLD Ischemia and Infarction (Daniel)

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Department of Cardiology and Vascular Medicine Faculty of Medicine University of Indonesia National Cardiovascular Center Harapan Kita ECG CHANGES IN ISCHEMIA, INJURY AND INFARCTION Daniel Tobing, MD, FIHA

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Transcript of ECG PLD Ischemia and Infarction (Daniel)

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Department of Cardiology and Vascular MedicineFaculty of Medicine University of Indonesia

National Cardiovascular Center Harapan Kita

ECG CHANGES IN ISCHEMIA, INJURY AND

INFARCTIONDaniel Tobing, MD, FIHA

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The Electrocardiogram ( ECG )

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No ST ElevationNo ST Elevation ST ElevationST Elevation

Acute Coronary SyndromeAcute Coronary Syndrome

Unstable AnginaUnstable Angina NQMINQMI Qw MIQw MI

NSTEMINSTEMI

Myocardial InfarctionMyocardial Infarction

Davies MJ Davies MJ Heart 83:361, 2000Heart 83:361, 2000

Ischemic DiscomfortIschemic DiscomfortPresentationPresentation

Working DxWorking Dx

ECGECG

Biochem. Biochem. MarkerMarker

Final DxFinal DxHamm Lancet 358:1533,2001Hamm Lancet 358:1533,2001

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Visualization of the generation ofthe Left Ventricular portion ofthe ECG complex in Lead II

1. Septum depolarizes from the inside out and resulting depolarization wave moves away from the electrode recording Lead II

2. The rest of the ventricle depolarizes counter-clockwise from the inside out and creates the (large arrow) which is essentially, the algebraic sum of all of the small depolarization vectors. This vector is, in a normal heart, almost always moving directly toward Lead II, generating a mostly positive QRS complex

main cardiac vector

Lead II electrode60 downwardrotation angle from the horizontal 0

o

o

60o

Note: compared tothe left ventricle, the right ventricle is muchsmaller and contributeslittle to the overall mainvector of depolarization

(DEPOLARIZATION)

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3. Repolarization can be thought of as beginning where depolarization left off

and proceeding clockwise from the lateral wall back to the septum..

4. The repolarization process proceeds at a much slower rate than depolarization so the wave inscribed (T-wave) is wide and rounded. The repolarization vector is moving away from the Lead II electrode so the inscribed T-wave is always positive

the Left Ventricular portion ofthe ECG complex in Lead II(REPOLARIZATION)

Visualization of the generation of

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ISCHEMIA

• Imbalance between metabolic needs of the myocardium (demand) and the flow of oxygenated blood to it (supply)

• Affects the generation and impulse conduction delays in depolarization and repolarization

ST and T changes (on ECG)• Significant ST depression, if

– ST segment depression >0.05 mVolt at a point 0.04 second to the right of J point.

– In two or more leads facing the same anatomic area

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INJURY

• Prolonged ischemia more than few minutes will cause injury

• Injured cells are still alive but will infarct (die) if ischemia is not corrected

• Do not depolarize completely, electrically more positive than the uninjured areas

viewed on ECG as ST segment elevation

Significant if: elevated > 1 mm in two or more contiguous leads

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INFARCTION

• Occurs when blood flow to the heart muscle stops or suddenly decreased

• Infarcted (dead) cells are without function and can not respond to electrical stimuli

• Q wave on ECG

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ST depresi dan perubahan gelombang T

• ST depresi dianggap bermakna bila > 0.05 mVolt• 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 pada iskemia kurang begitu spesifik Gelombang T hiperakut kadang2 merupakan satu-satunyaperubahan EKG yang terlihat

ECG CHANGES OF ISCHEMIA

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“J point”

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SPESIFISITAS DEPRESI SEGMEN ST PADA ISKEMIA

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VARIASI SEGMEN ST

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Unstable angina DD/ Acute NSTEMI

Tn AS, 65 th, nyeri dada khas infark

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ECG CHANGES OF INJURY (ACUTE MYOCARDIAL INFARCTION)

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CONCEPT OF RECIPROCITY

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ECG CHANGES OF OLD INFARCTION

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Recent Inferior MCI with T-wave inversions

Tn DS, 56 th, riwayat nyeri dada khas infark 2 minggu yang lalu

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LOCATING

THE MYOCARDIAL INFARCTION

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• 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

Anatomi Koroner dan EKG 12 sandapan

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LOCATING THE MYOCARDIAL INFARCTION

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Mid LAD occlusion after the first septal perforator (arrow)

ECG : large anterior MI

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Proximal large RCA occlusion

ST elevation in leads II, III, aVF, V5, and V6

with precordial ST depression

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Small inferior distal RCA occlusion

ECG changes in leads II, III, and aVF

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Subendocardial ischemia. Anterolateral ST-segment depression

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Acute anteroseptal myocardial infarction. Hyperacute T-wave changes are noted

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Acute anterolateral myocardial infarction

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Lateral myocardial infarction

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Inferior myocardial infarction. Inferior Q waves with T-wave inversions

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Acute inferoposterior myocardial infarction

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RBBB + Anterior Infarction

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Left bundle branch block

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Pseudo Infarct PaternW P W

negative delta wave II,III,aVF

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Early repolarization

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Left ventricular aneurysm

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