ECG Changes in Myocardial Infarction (MI)

Pathophysiological Basis

The "Current of Injury" Concept

• Transmural ischemia (full-thickness): ST vector shifts toward epicardium → ST elevation in overlying leads, with reciprocal depression in opposite leads.
• Subendocardial ischemia: ST vector shifts toward endocardium/cavity → ST depression in overlying leads (with ST elevation in aVR).

Chronological Evolution of ECG Changes

Four Key ECG Features of MI

1. Hyperacute T Waves (earliest sign, minutes)

• Tall, broad, peaked T waves
• Appear within minutes of occlusion
• Often missed as they are transient

2. ST Segment Elevation (STEMI) or Depression (NSTEMI)

• STEMI criteria: ST elevation ≥1 mm in 2 contiguous limb leads, or ≥2 mm in 2 contiguous precordial leads
• Convex (coved/"tombstone") upward morphology is the classic STEMI shape
• ST depression indicates subendocardial ischemia or posterior MI (as a reciprocal change)

3. T Wave Inversion

• Follows ST elevation as infarct evolves
• Deep symmetric T-wave inversions in V1-V4 (Wellens sign) indicate severe LAD stenosis

4. Pathological Q Waves (irreversible necrosis)

• Q wave duration >40 ms, depth >25% of R wave height
• Represent electrically silent dead myocardium
• "Failure of R-wave progression" is an equivalent finding in anterior MI
• May develop as early as 1-2 hours or take 24-48 hours to appear

Localization by Lead Distribution

Real 12-Lead ECG Examples

(Rosen's EM Fig 64.22A - Baseline paced rhythm)

(Rosen's EM Fig 64.22B - Evolution showing concordant ST elevation in I and aVL consistent with lateral STEMI)

STEMI vs NSTEMI on ECG

Special Patterns and Pitfalls

• LBBB masking MI: New LBBB with acute chest pain is treated as STEMI equivalent (Sgarbossa criteria help)
• Posterior MI: No direct leads face the posterior wall; look for ST depression + tall R in V1-V2 (mirror image); confirm with posterior leads V7-V9
• Wellens syndrome: Biphasic or deeply inverted T waves in V2-V3 indicate LAD critical stenosis, even between episodes of pain
• De Winter T waves: ST depression with tall symmetric T waves in precordial leads - equivalent to proximal LAD occlusion, requires immediate cath

ECG Patterns of Myocardial Infarction - Complete Guide

Understanding the Normal ECG First

• P wave - atrial depolarization
• PR interval - AV node conduction
• QRS complex - ventricular depolarization
• ST segment - early ventricular repolarization (should be isoelectric)
• T wave - ventricular repolarization

The Three Zones of MI and Their ECG Signatures

Phase-by-Phase ECG Evolution

(Ganong Fig 29-17: Diagrammatic serial ECG patterns in anterior MI - A=Normal, B=Hyperacute, C=Early evolving, D=Established, E=Chronic)

Phase 1: Hyperacute T Waves (Minutes after occlusion)

• Tall, broad, symmetric, peaked T waves
• Often also called "hyperacute T waves"
• ST may already begin to rise

Phase 2: ST Segment Elevation (Hours - the hallmark of STEMI)

• ST elevation ≥1 mm in ≥2 contiguous limb leads, or ≥2 mm in ≥2 contiguous precordial leads
• Convex upward (coved/tombstone) morphology - the most specific shape for STEMI
• Reciprocal ST depression in opposite leads

1. Rapid repolarization - current flows out of infarct
2. Decreased resting membrane potential (K⁺ loss from cells) - TQ segment depression, recorded as ST elevation
3. Delayed depolarization - infarct still positive when normal tissue has repolarized

Morphology key:

(Rosen's Fig 64.2: Row A = STEMI morphology - flat/convex ST-T. Row B = Non-AMI causes of STE (BER, pericarditis) - concave morphology. Row C = STEMI may also show concavity - serial ECGs are essential)

The ST segment in STEMI is classically flat or convex upward (unlike pericarditis or BER where it is concave/saddleback). However, this is a guideline, not a rule - serial ECGs are needed.

Phase 3: T-Wave Inversion (Hours to days)

• Symmetric, deep T-wave inversions in leads overlying the infarct
• ST segment begins to return toward baseline

Phase 4: Q Waves Appear (Hours to days - indicates irreversible necrosis)

• Pathological Q waves: duration >40 ms (1 small square wide), depth >25% of R wave height, or any Q in V1-V3
• "Failure of R-wave progression" in anterior leads (R waves fail to grow from V1→V6)

Phase 5: Chronic/Resolved Pattern (Weeks to months)

• Q waves may persist permanently (marker of old infarct) or gradually shrink
• ST segment normalizes (persistent ST elevation >6 weeks suggests LV aneurysm)
• T waves normalize or remain inverted

Leads and Localization: Which Territory is Infarcting?

(Rosen's Fig 64.24: 15-lead ECG showing inferior + lateral + posterior + right ventricular MI simultaneously)

Reciprocal Changes - Why They Matter

(Rosen's Fig 64.12: Inferior MI showing ST elevation in II, III, aVF with reciprocal ST depression in leads I and aVL)

• Larger infarct size
• More extensive coronary artery disease
• Greater degree of pump failure
• Higher mortality - the more leads showing changes, the worse the outcome

Anterolateral STEMI - Real ECG Example

(Rosen's Fig 64.10: Anterolateral STEMI - ST elevation in V1-V4 anteriorly plus I, aVL, V5, V6 laterally. Proximal LAD occlusion confirmed at PCI)

High Lateral MI (I, aVL elevation with reciprocal depression in III, aVF):

(Rosen's Fig 64.11: High lateral MI from LAD/D1 bifurcation stenosis - ST elevation in I and aVL)

Distinguishing STEMI from NSTEMI on ECG

Special ECG Patterns and Pitfalls

Diagnostic Criteria Summary (STEMI)

• ST elevation ≥1 mm (0.1 mV) in ≥2 contiguous limb leads (I, II, III, aVL, aVF)
• ST elevation ≥2 mm in ≥2 contiguous precordial leads (V1-V6)
• New or presumably new LBBB
• Posterior MI pattern (ST depression V1-V3 + tall R, confirmed by V7-V9 STE)

• Single ECG: sensitivity ~60%, specificity ~90%
• Serial ECGs (20-minute intervals) significantly increase sensitivity for STEMI detection (~16% additional diagnoses)

The "Current of Injury" - Visual Summary

(Harrison's Fig 247-11: The injury current concept - Panel A: Subendocardial ischemia → ST vector points inward → ST depression in overlying leads. Panel B: Transmural ischemia → ST vector points outward → ST elevation in overlying leads)

Normal ECG vs MI ECG - A Complete Comparison

Part 1: The Normal ECG - Building Blocks

Normal ECG Diagram

(Costanzo Physiology Fig 4.17: The normal ECG measured from lead II - all waves, intervals, and segments labeled)

What Each Component Means

Key Features of a Truly Normal ECG

• P wave present before every QRS, with constant PR interval
• QRS narrow (<100 ms), no pathological Q waves
• ST segment sits exactly on the isoelectric baseline
• T waves upright and asymmetric (gentle upslope, steep downslope) in most leads
• R-wave progression in precordial leads: R wave grows progressively from V1 → V5/V6
• No reciprocal changes between lead groups

Part 2: How MI Disrupts the Normal ECG

1. Rapid repolarization (accelerated K⁺ channel opening) - current flows out of infarct
2. Loss of resting membrane potential (K⁺ leaks out of dying cells) - TQ depression, displayed as ST elevation
3. Delayed depolarization (necrotic cells can't fire) - electrical silence creates Q waves

(Harrison's Fig 247-11 - Panel A: subendocardial ischemia - ST vector inward → ST depression. Panel B: transmural ischemia - ST vector outward → ST elevation in overlying leads)

Part 3: Side-by-Side Comparison - Normal vs MI ECG

The Three Zones and Their ECG Signatures

Normal heart:     Uniform depolarization/repolarization → balanced ECG

MI heart:
  ┌─────────────────────────────────────────────────────┐
  │ Outer zone (ISCHEMIA)    →  T-wave inversion        │
  │   Middle zone (INJURY)   →  ST elevation            │
  │     Inner zone (NECROSIS)→  Pathological Q wave     │
  └─────────────────────────────────────────────────────┘

Feature-by-Feature Comparison Table

Part 4: The Five Stages of MI ECG Evolution

(Ganong Fig 29-17: Serial ECG patterns in anterior MI across all leads)

Part 5: Visual Comparison of ST Segment Morphology

(Rosen's Fig 64.2: ST morphology analysis)

Part 6: Real MI ECG - Anterolateral STEMI

(Rosen's Fig 64.10: Real anterolateral STEMI - proximal LAD occlusion confirmed at emergency PCI)

• V1-V4: marked ST elevation where it should be flat; large tombstone morphology in V3-V4
• Lead I, aVL: ST elevation (lateral involvement)
• V5, V6: ST elevation continuing laterally
• aVR: reciprocal ST depression
• This is an emergency requiring immediate catheterization

Part 7: Concise Summary Card

┌──────────────────────────────────────────────────────────────────────┐
│           NORMAL ECG          │           MI ECG (STEMI)             │
├──────────────────────────────────────────────────────────────────────┤
│ P wave:    Normal, upright    │ P wave:    Unchanged (usually)       │
│ PR:        120-200 ms         │ PR:        Unchanged (usually)       │
│ Q wave:    Absent/small       │ Q wave:    PATHOLOGICAL - wide+deep  │
│ R wave:    Normal progression │ R wave:    Reduced/absent (lost)     │
│ ST segment: FLAT, isoelectric │ ST segment: ELEVATED, convex upward  │
│ T wave:    Upright, asymmetric│ T wave:    Hyperacute → INVERTED     │
│ Reciprocal: None              │ Reciprocal: ST DEPRESSION opposite   │
└──────────────────────────────────────────────────────────────────────┘

Quick Memory Aid

• Q - Pathological Q waves (necrosis/dead tissue)
• S - ST elevation (injury current)
• I - T-wave Inversion (ischemia)
• T - Tall hyperacute T waves (earliest sign)
• E - Evolutionary changes over time