+ECG Changes in Myocardial InfarctionClerk Karen G. Amoloza

+Myocardial Infarction

Death or necrosis of myocardial cells Diagnosis at the end of the spectrum of myocardial

ischemia or acute coronary syndromes Ischemia Injury Infarction

Occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis

+ECG on diagnosis of MI

cornerstone in diagnosis of acute and chronic IHD

Factors: Nature of the process: reversibility (ischemia vs

infarction) Duration: acute vs chronic Extent: transmural vs subendocardial Localization: anterior vs inferoposterior Presence of other underlying abnormalities: chamber

enlargement/hypertrophy, conduction defects

+Ischemia

Decrease in the perfusion of a certain area of the myocardium

Temporary, reversible reduction of blood supply

Earliest manifestation of reduced coronary blood flow

+Ischemia: ECG changesT wave Normal T waves

ventricular repolarization Same direction as and smaller

than QRS complex Upright, asymmetrical

T wave changes Deeply inverted, symmetrical

+Ischemia: ECG changes

Pseudonormalization of the T wave Reversal to a normal upright T wave Acute ischemia in patients with pre-existing

T wave inversion from a past event

+Injury

Acute, prolonged, reduction in blood supply to the myocardium

Reversible

+Injury: ECG changes

ST segment elevation Subepicardial injury (outer ventricular wall) Minutes to hours of an acute event “Coved” or convex upward displacement of the ST segment

from the baseline Factors:

Atherosclerosis with sudden clot formation

Coronary Artery Spasm (Prinzmetal’s Angina)

+Injury: ECG changes

ST segment depression

Subendocardial injury (inner ventricular wall) Small penetrating branches of the superficial

epicardial coronary arteries Poor perfusion First area of the myocardium to sustain injury

+Injury: ECG changes

ST segment depression

Clinical indicator of coronary artery disease during stress test

Assessment of Severity Morphology (magnitude ands slope) during

exercise Duration of ST segment depression after

exercise

+

+Infarction: ECG Changes

Q wavesIndicate a loss of viable myocardium May develop 1 to 2 hours after the

onset of symptoms but can take anywhere from 12 to 24 hours to develop

+Infarction: ECG Changes

Q waves Insignificant Q waves

Small Q waves <25% of the height of the adjacent R wave Normal: Leads I, aVL, V5, V6 Result from the normal process of septal

depolarization

Significant Q waves Deeper than 25% of the height of the adjacent R

wave >0.04s in duration

+Infarction: ECG Changes

+Infarction: ECG Changes

R wave progression

+Localizing Ischemia, Injury and Infarction

Leads Leads Site of occulusion

Anterior V1 – V4 LAD

Septal V1 – V2 LADLateral I, aVL, V5,

V6Circumflex, RCA

High Lateral

I, aVL Circumflex, RCA

Inferior II, III, aVF RCA, circumflexPosterior V1 – V2 RCA

+Anterior InfarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary artery

+Inferior InfarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

+Lateral InfarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

+Evolution of ECG Changes in AMI

Development of acute ECG changes with gradual reversion of the ST segments and T waves to normal over time.

The Hyper-acute Phase

Less than 12 hours

“ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996)

The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal

Usually occurs within a few hours of infarction May vary in severity from 1mm to ‘tombstone’

elevation

+The Fully Evolved Phase

24 - 48 hours from the onset of a myocardial infarction

ST segment elevation is less (coming back to baseline).

T waves are inverting. Pathological Q waves are developing (>2mm)

+The Chronic Stabilised Phase

Isoelectric ST segments T waves upright. Pathological Q waves. May take months or weeks.

+Reciprocal Changes

II, III, aVFI, aVL, V leads

• Are seen as ST depression in the opposite leads from where the ST elevation is seen

• Leads II, III and aVF are opposite to Leads I, aVL, and all of the V leads

• Therefore, if there is ST elevation in leads II, III and aVF any ST depression (if present) would be seen in leads I, aVL and any of the V leads

+Reciprocal Changes ST segment depression seen in the opposite leads from ST segment elevation Highly sensitive as an indicator of acute MI Frequently seen in larger infarctions

ST elevation Reciprocal ST depression

+Thrombolytic Therapy

Indications ST segment elevation in two or more leads

associated with acute chest pain Time between onset of chest pain to

initiation of therapy less than 24 hours (optimal time to initiate therapy is less than 6 hours, and the earlier the better).

+Thrombolytic Therapy

Absolute Contraindications History of cerebrovascular hemorrhage at

any time History of non cerebrovascular hemorrhage,

stroke or other CV event within 1 year Marked hypertension (SBP > 180 or DBP >

110) at any time during acute presentation Suspicion of aortic dissection Active internal bleeding including menses

+Thrombolytic Therapy

Relative Contraindications Current use of any anti-coagulant (INR ≥ 2) Recent (< 2 weeks) invasive or surgical procedure or

prolonged (> 10 min) CPR Pregnancy Hemorrhagic ophthalmic condition (ie. Hemorrhagic

DM nephropathy) Active PUD History of severe hypertension that is adequately

controlled Streptokinase with preceding 5 days to 2 years

(allergic reaction)