1. ECG Changes in Myocardial Infarction
Clerk Karen G. Amoloza

2. 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
Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells.
It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes.
Myocardial 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.
Ischemia at this critical threshold level for an extended time period results in irreversible myocardial cell damage or death.1-3

3. 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
The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. The findings depend on several key factors: the nature of the process [reversible (i.e., ischemia) versus irreversible (i.e., infarction)], the duration (acute versus chronic), extent (transmural versus subendocardial), and localization (anterior versus inferoposterior), as well as the presence of other underlying abnormalities (ventricular hypertrophy, conduction defects).

4. 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

5. Ischemia: ECG changes T wave Normal T waves ventricular repolarization
Same direction as and smaller than QRS complex
Upright, asymmetrical
T wave changes
Deeply inverted, symmetrical

6. 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

7. Injury Acute, prolonged, reduction in blood supply to the myocardium
Reversible

8. 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)

9. 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

10. 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

12. Infarction: ECG Changes
Q waves
Indicate 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

13. 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

14. Infarction: ECG Changes

15. Infarction: ECG Changes
R wave progression

16. Localizing Ischemia, Injury and Infarction
Leads
Site of occulusion
Anterior
V1 – V4
LAD
Septal
V1 – V2
Lateral
I, aVL, V5, V6
Circumflex, RCA
High Lateral
I, aVL
Inferior
II, III, aVF
RCA, circumflex
Posterior
RCA

17. Anterior Infarction Anterior infarction I II III aVR aVL aVF V1 V2 V3
Location of infarction and its relation to the ECG: anterior infarction
As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V1–6) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations.
Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V2–6, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V1–6 , I, and aVL.
Left
coronary
artery

18. Inferior Infarction Inferior infarction I II III aVR aVL aVF V1 V2 V3
Location of infarction and its relation to the ECG: inferior infarction
ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node.
Right
coronary
artery

19. Lateral Infarction Lateral infarction I II III aVR aVL aVF V1 V2 V3
Location of infarction and its relation to the ECG: lateral infarction
Occlusion of the left circumflex artery may cause lateral infarctions.
Lateral infarctions are diagnosed by ST elevation in leads I and aVL.
Left
circumflex
coronary
artery

20. 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.

21. 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

23. The Fully Evolved Phase
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)

24. The Chronic Stabilised Phase
Isoelectric ST segments
T waves upright.
Pathological Q waves.
May take months or weeks.

25. Reciprocal Changes II, III, aVF I, 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
II, III, aVF
I, aVL, V leads

26. Reciprocal Changes ST elevation Reciprocal ST depression
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

27. 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).

28. 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

29. 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)