ECG changes

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ECG changes electrocardiogram ST elevation T wave inversion MI ischemia

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ECG Changes: A Comprehensive Overview


1. Acute Myocardial Infarction (STEMI)

The classic ECG evolution in acute ST-elevation MI passes through three overlapping phases:

Phase 1 — Early Acute (minutes to hours)

  • Hyperacute T waves: tall, peaked, widened T waves are the earliest sign — can precede ST elevation
  • ST elevation: ST segment evolves from concave → straightened → convex upward ("tombstone" appearance)
  • Reciprocal ST depression in leads opposite the infarct zone; associated with larger infarcts and worse prognosis but greater benefit from reperfusion

Phase 2 — Evolved Acute (hours to days)

  • ST elevation begins to regress
  • T-wave inversion develops in leads with prior ST elevation
  • Pathologic Q waves appear (diagnostic of transmural MI)

Phase 3 — Chronic/Stabilized

  • Persistent Q waves (often permanent)
  • ST segments return to baseline
  • T-wave inversions may persist or resolve
"When typical ST-segment elevation persists for hours and is followed within hours to days by T-wave inversions and Q waves, the diagnosis of acute MI can be made with virtual certainty." — Goldman-Cecil Medicine
STEMI diagnostic thresholds:
LeadCriteria
V2–V3 (men)ST elevation ≥2 mm at J point
V2–V3 (women)ST elevation ≥1.5 mm
All other leadsST elevation ≥1 mm in ≥2 contiguous leads
Pathologic Q wave criteria:
  • V2–V3: Q wave ≥0.02 s or QS complex
  • Other leads: Q wave ≥0.03 s and ≥0.1 mV deep in ≥2 contiguous leads
STEMI evolution ECG — Goldman-Cecil

2. Non-ST-Elevation ACS (NSTEMI / Unstable Angina)

  • ST-segment depression (≥0.5 mm) — subendocardial ischemia
  • T-wave inversion — may be symmetric and deep (Wellens' pattern in LAD territory = V1–V4)
  • "Dynamic" ECG changes — new or worsening ST-T changes vs prior ECG strongly suggest ACS
  • A normal ECG does not exclude ACS

3. Pericarditis

Classic four-stage ECG evolution:
StageECG Finding
IDiffuse ST elevation (saddle-shaped/concave) + PR depression in I, II, III, aVF; PR elevation in aVR
IIST returns to baseline; T waves flatten
IIIDiffuse T-wave inversion
IVNormalization
Distinguishing pericarditis from STEMI:
  • ST elevation in pericarditis is diffuse (not territory-specific) and concave
  • PR depression is characteristic of pericarditis (not STEMI)
  • No reciprocal ST depression (except aVR/V1)
  • ST:T-wave ratio in V6 >0.25 favors pericarditis over early repolarization
Pericarditis ECG stages A (Stage I), B (Stage II), C (Stage III) — Tintinalli's Emergency Medicine

4. Electrolyte Abnormalities

Hyperkalemia (progressive sequence):

  1. Peaked (tented) T waves — narrow, tall, symmetric (earliest change)
  2. Prolonged PR interval, diminished P-wave amplitude
  3. Widened QRS
  4. Sine-wave pattern → asystole
Hyperkalemia ECG progression: mild-moderate → moderate-severe → very severe (sine wave) — Harrison's Principles

Hypokalemia:

  • Prolonged ventricular repolarization
  • Prominent U waves (most characteristic)
  • Flattened or inverted T waves
  • Prolonged QU interval (often mistaken for QT prolongation)

Hypocalcemia:

  • Prolonged QT interval (prolonged ST segment specifically)

Hypercalcemia:

  • Shortened QT interval

5. Drug-Induced ECG Changes

Drug/ClassECG Effect
Digoxin"Scooping" of ST-T complex; shortened QT; PR prolongation
Class IA (quinidine, procainamide)QT prolongation; wide QRS
Class III (amiodarone, sotalol)QT prolongation
TCAs, phenothiazinesQT prolongation; wide QRS
CocaineST elevation (vasospasm)

6. Pulmonary Embolism

Classic (but insensitive/non-specific) pattern:
  • S1Q3T3: deep S in I, Q wave + T inversion in III
  • Right heart strain: sinus tachycardia, RBBB, T inversion in V1–V4
  • Right axis deviation
  • Most common finding is simply sinus tachycardia or a non-specific change

7. Left Ventricular Hypertrophy (LVH)

  • High-voltage QRS (tall R in V5–V6, deep S in V1–V2)
  • "Strain" pattern: ST depression + T inversion in lateral leads (I, aVL, V5–V6)
  • Can mimic ischemia

8. Bundle Branch Blocks

BlockQRSKey Features
LBBB≥120 msBroad notched R in V5–V6, I, aVL; deep S in V1
RBBB≥120 msRSR' ("rabbit ears") in V1–V2; broad S in I, V5–V6
New LBBB in the setting of chest pain may represent STEMI equivalent; use Sgarbossa criteria:
  • ST elevation ≥1 mm concordant with QRS → 5 pts
  • ST depression ≥1 mm in V1–V3 → 3 pts
  • ST elevation ≥5 mm discordant with QRS → 2 pts (≥3 pts = STEMI likely)

9. Other Notable Changes

ConditionECG Finding
HypothermiaOsborn (J) waves (convex hump at J point); bradycardia; prolonged intervals
Subarachnoid hemorrhageDeeply inverted, wide T waves ("CVA T waves"); prolonged QT
Brugada syndromeCoved ST elevation in V1–V2; RBBB morphology
Cardiac tamponadeElectrical alternans (P-QRS-T beat-to-beat alternation) + sinus tachycardia + low voltage
Pericardial/pleural effusionLow QRS voltage
Posterior MITall R + ST depression in V1–V2; confirmed with posterior leads V7–V9

Differential Diagnosis of ST Elevation (Non-STEMI Causes)

CardiacOther
Prior MI with aneurysmPulmonary embolism
Pericarditis/myocarditisHyperkalemia
LVH/aortic stenosis (strain)
Hypertrophic cardiomyopathy
Coronary vasospasm / Prinzmetal
Early repolarization (normal variant)
Brugada syndrome
(Washington Manual of Medical Therapeutics; Goldman-Cecil Medicine)

Sources: Goldman-Cecil Medicine (9780323930345) | Harrison's Principles of Internal Medicine 22E (9781265977061) | Tintinalli's Emergency Medicine (9781260019933) | Washington Manual of Medical Therapeutics (9781975190620) | Swanson's Family Medicine Review (9780323698115)
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