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ECG findings myocardial infarction ST elevation Q waves

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Here is a comprehensive guide to ECG findings in Myocardial Infarction (MI), drawing from Harrison's Principles of Internal Medicine (2025), Guyton & Hall, and clinical ECG image libraries.

ECG Findings in Myocardial Infarction

Overview

The ECG is central to the diagnosis of acute and chronic ischemic heart disease. Ischemia exerts complex time-dependent effects on myocardial electrical properties, producing characteristic changes in the ST segment, T waves, and QRS complex.

1. Pathophysiology: Current of Injury

Severe acute ischemia lowers the resting membrane potential and shortens the action potential duration, creating a voltage gradient between normal and ischemic zones. This generates "currents of injury" seen as ST-segment deviation:

Transmural (epicardial) ischemia → ST vector directed outward → ST elevation in overlying leads
Subendocardial ischemia → ST vector directed inward → ST depression in overlying leads (with ST elevation in aVR)

2. Temporal Evolution of ECG Changes

This is the classic progression of STEMI:

ECG evolution from normal through acute MI to chronic — showing hyperacute T wave, ST elevation, Q wave development, T wave inversion over time (Guyton & Hall)

Phase	Timing	ECG Change
Hyperacute	Minutes	Tall, broad, peaked T waves ("hyperacute T waves")
Acute	Hours	ST elevation (convex/tombstone morphology)
Evolving	Hours–days	T-wave inversion; Q waves begin to appear
Chronic/Old	Weeks–years	Pathological Q waves persist; ST normalizes

3. The Three Key Signs

A. ST-Segment Elevation (STEMI)

≥1 mm in ≥2 contiguous limb leads
≥2 mm in ≥2 contiguous precordial leads (V1–V6)
Convex ("tombstone") morphology in severe cases

B. Pathological Q Waves

Width ≥40 ms (1 small square) or depth ≥25% of the R wave
Represent electrically silent necrotic myocardium — the dead tissue produces no electrical signal, so the opposite wall's depolarization dominates (away from the necrotic lead = Q wave)

Anterior MI ECG showing pathological Q waves in V1–V2, ST elevation V1–V3, and T-wave inversion — evolving anteroseptal infarction

C. T-Wave Inversion

Develops after ST elevation begins to resolve
Deep symmetrical T-wave inversions in V1–V4 with minimal ST elevation = Wellens' sign (critical LAD stenosis)

Wellens' syndrome pattern: ST elevation resolving with deep T-wave inversions in anterior leads V2–V5, typical of LAD reperfusion

4. Localizing the Infarct by Lead

Territory	Culprit Artery	Leads with Changes
Anterior	LAD	V1–V4
Anteroseptal	LAD (proximal)	V1–V3
Lateral	LCx or diagonal	I, aVL, V5–V6
Inferior	RCA (or LCx)	II, III, aVF
Posterior	RCA or LCx	Tall R wave in V1–V2; reciprocal ST depression V1–V3
Right ventricular	Proximal RCA	ST elevation in right-sided leads (V3R–V4R)

Severe anterior wall ischemia — Wellens T wave pattern with deep T inversions V1–V4 and leads I/aVL, indicating proximal LAD obstruction (Harrison's Fig. 247-12)

5. Reciprocal Changes

Reciprocal ST depression appears in leads electrically opposite to the infarcted territory. These are an important clue and increase diagnostic confidence:

Inferior STEMI (ST ↑ in II, III, aVF) → reciprocal ST ↓ in I, aVL
Anterior STEMI → reciprocal ST ↓ in II, III, aVF
Lateral STEMI → reciprocal ST ↓ in inferior leads

6. STEMI vs NSTEMI Classification

Feature	STEMI	NSTEMI
ST elevation	Present (≥2 contiguous leads)	Absent
Q waves	Often develop	May or may not
Coronary occlusion	Usually total	Usually partial
Reperfusion urgency	Immediate (PCI/thrombolysis)	Risk-stratified
Troponin	Elevated	Elevated

Note: Q-wave MI vs. non-Q-wave MI has been replaced by STEMI/NSTEMI in modern classification, as ECG-pathologic correlations are imperfect. MRI studies show Q wave development depends more on volume of infarcted tissue than transmurality. — Harrison's, 2025

7. Real 12-Lead Examples

Massive STEMI — anterior + inferior involvement with tombstoning:

12-lead ECG showing acute STEMI with tombstone ST elevation in inferior leads II/III/aVF and precordial leads V1–V5, with pathological Q waves in limb leads — multivessel occlusion pattern

Acute lateral STEMI with reciprocal changes:

12-lead ECG showing acute lateral STEMI with ST elevation in I and aVL (~4mm), reciprocal ST depression in inferior leads II/III/aVF, and anterior Q waves

8. Important Limitations

The ECG has significant limitations:

A single normal ECG does not exclude acute MI
LBBB, ventricular pacing, and WPW can mask or mimic ischemic changes (Sgarbossa criteria help with LBBB)
Posterior MI produces no Q waves in conventional leads — diagnosed by tall R in V1–V2 and reciprocal ST depression
ST elevation can persist weeks after Q-wave MI → suggests ventricular wall motion disorder (not necessarily aneurysm)

Sources: Harrison's Principles of Internal Medicine 22E (2025), Ch. 247 & 286; Guyton and Hall Textbook of Medical Physiology, Ch. 12

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ECG strip ST elevation myocardial infarction STEMI anterior inferior

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ECG strip pathological Q wave T wave inversion myocardial infarction evolution

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Here are real ECG strips showing each key MI pattern:

🫀 ECG Strips: MI Findings

1. Inferolateral STEMI (Acute Phase)

ST elevation in II, III, aVF + V4–V6 (green circles) with reciprocal ST depression in I, aVL, V2–V3 (yellow arrows)

Inferolateral STEMI — ST elevation circled in green in inferior leads II, III, aVF and lateral V4-V6; reciprocal ST depression marked with yellow arrows in I, aVL, V2-V3

What to see: Convex ST elevation inferolaterally + reciprocal depression anteriorly. Culprit: RCA or LCx

2. Inferior STEMI (Acute Phase)

ST elevation in II, III, aVF with reciprocal ST depression in V1–V6 and aVL

Acute inferior STEMI — convex ST elevation in II, III, aVF with widespread reciprocal ST depression in precordial leads V1-V6 and high lateral aVL

What to see: Classic inferior ST elevation + anterior reciprocal depression. Culprit: RCA

3. Anterior STEMI (LAD Occlusion)

Tombstone ST elevation V1–V6 with reciprocal ST depression in II, III, aVF

Acute anterior STEMI — tombstone ST elevation across precordial leads V1-V6 with T-wave changes and reciprocal ST depression in inferior leads II, III, aVF — LAD occlusion

What to see: Extensive precordial tombstoning — highest risk pattern. Culprit: proximal LAD

4. Post-Reperfusion / Evolving MI (Subacute Phase — 12 hrs post-PCI)

Pathological Q waves in II, III, aVF + deep symmetrical T-wave inversions V2–V6

Subacute MI post-reperfusion — pathological Q waves in inferior leads II/III/aVF and deep symmetric T-wave inversions V2-V6, consistent with post-PCI Wellens-like evolution

What to see: ST elevation has resolved → now shows Q waves (necrosis) + T inversions (reperfusion/evolving). This is the subacute phase.

5. Old/Subacute Inferior MI with Posterior Extension

Q waves + T inversions in II, III, aVF; tall R wave + ST depression in V1–V3 (posterior MI pattern)

Subacute inferior MI with posterior extension — pathological Q waves and T-wave inversions in II/III/aVF; prominent R wave and ST depression in V1-V3 indicating posterior wall involvement

What to see: Posterior MI is a "silent" territory — no Q waves in standard leads; instead look for tall R + ST ↓ in V1–V3 as a reciprocal mirror image.

Quick Summary Table

ECG Strip	Territory	Key Finding	Culprit Artery
Strip 1	Inferolateral	ST ↑ II/III/aVF/V4–V6 + reciprocal ↓ I/aVL	RCA or LCx
Strip 2	Inferior	ST ↑ II/III/aVF + widespread reciprocal ↓	RCA
Strip 3	Anterior	Tombstone ST ↑ V1–V6	Proximal LAD
Strip 4	Evolving (post-PCI)	Q waves + deep T inversions	Any
Strip 5	Inferior + Posterior	Q waves + tall R/ST ↓ in V1–V3	RCA

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