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10 classic disease ECG patterns cardiology

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I now have a comprehensive set of information and images. Let me compose the full answer covering 10 classic disease ECG patterns:

ECG Patterns in 10 Classic Diseases

Sources: Harrison's Principles of Internal Medicine 22E; Tintinalli's Emergency Medicine; Goldberger's Clinical Electrocardiography

1. STEMI (ST-Elevation Myocardial Infarction)

Mechanism: Transmural ischemia shifts the ST vector toward the epicardial (outer) surface, producing ST elevation in overlying leads with reciprocal ST depression in mirror leads.
Key ECG findings:
  • Hyperacute T waves - earliest sign; tall, broad, peaked T waves before ST rise
  • ST elevation - convex (domed) or straight, ≥1 mm in limb leads, ≥2 mm in precordial leads (≥1.5 mm in V2-V3 for women)
  • Pathological Q waves - develop within hours-days; indicate necrosis
  • T-wave inversions - follow in the evolving phase
  • Reciprocal ST depression in anatomically opposite leads
Localization:
TerritoryST ElevationReciprocal Depression
AnteriorV1-V4II, III, aVF
InferiorII, III, aVFI, aVL, V1-V3
LateralI, aVL, V5-V6V1-V3
PosteriorNone (mirror image)V1-V3 (tall R + ST depression)
RVV3R-V4R-
Subendocardial vs transmural ischemia - ST vector diagram
Subendocardial ischemia (A) → ST depression. Transmural ischemia (B) → ST elevation.
Anterior wall ischemia - deep T-wave inversions V1-V6
Anterior ischemia: Wellens'-type deep T-wave inversions across V1-V6 indicate severe LAD stenosis.

2. Pericarditis

Mechanism: Diffuse epicardial inflammation causes global ST elevation without reciprocal changes (except aVR).
Key ECG findings (4 stages):
  • Stage 1 - Diffuse saddle-shaped (concave up) ST elevation in most leads; PR depression (most specific finding); ST elevation in aVR is absent or depressed
  • Stage 2 - ST returns to baseline, T waves flatten
  • Stage 3 - Diffuse T-wave inversions
  • Stage 4 - Normalization
Distinguishing from STEMI:
  • Pericarditis: concave (saddle-shaped) ST elevation in all leads except aVR/V1; PR segment depression; no reciprocal depression; no Q waves
  • STEMI: convex (domed) elevation, localized territory, reciprocal changes, Q waves develop

3. Pulmonary Embolism

Mechanism: Acute right heart strain due to pulmonary hypertension.
Key ECG findings:
  • S1Q3T3 pattern - S wave in lead I, Q wave and T-wave inversion in lead III (classic but only ~20% sensitive)
  • Sinus tachycardia - most common finding
  • Right axis deviation
  • New RBBB (complete or incomplete)
  • T-wave inversions in V1-V4 (right heart strain - more sensitive)
  • P pulmonale (tall peaked P in II)
  • Atrial fibrillation (can precipitate)
Note: ECG is not diagnostic for PE alone - it helps support clinical suspicion. Normal ECG does not exclude PE.

4. Hyperkalemia

Mechanism: Elevated extracellular K+ progressively reduces resting membrane potential and slows conduction throughout the heart.
Sequential ECG changes (K+ levels):
  • 5.5-6.5 mEq/L: Peaked ("tented"), narrow, symmetric T waves - earliest sign
  • 6.5-8 mEq/L: PR prolongation → P-wave flattening/disappearance; QRS widening
  • >8 mEq/L: Wide bizarre QRS merges with T wave → sine-wave pattern → asystole
Hyperkalemia progression on ECG
Mild-moderate (peaked T waves) → moderate-severe (P flattening, QRS widening) → very severe (sine-wave pattern).

5. Hypokalemia

Mechanism: Low K+ prolongs ventricular repolarization (phase 3 action potential).
Key ECG findings:
  • Prominent U waves (>1 mm, usually best seen in V2-V3) - hallmark
  • ST depression
  • T-wave flattening or inversion
  • Apparent QT prolongation (actually QU prolongation - U wave merges with T)
  • Risk of Torsades de Pointes (TdP)
Hypokalemia with prominent U wave
Lead II (flat T) and V3 (prominent U wave) in hypokalemia.

6. Hypothermia

Mechanism: Cold slows all cardiac electrical activity; abnormal early repolarization creates the Osborn wave.
Key ECG findings:
  • J (Osborn) wave - pathognomonic; a positive deflection at the J point (end of QRS), most prominent in V4-V6 and inferior leads; size correlates with degree of hypothermia
  • Bradycardia (sinus or junctional)
  • PR, QRS, and QT prolongation
  • Atrial fibrillation with slow ventricular rate
  • Muscle tremor artifact (shivering)
Hypothermia - Osborn (J) wave
Osborn wave (arrow) at J point in V5. Core temperature was severely low.

7. Brugada Syndrome

Mechanism: Sodium channel mutation (SCN5A) causes abnormal repolarization in the right ventricular outflow tract.
Key ECG findings (two types):
  • Type 1 (Brugada pattern, diagnostic): Coved (downsloping) ST elevation ≥2 mm with T-wave inversion in V1-V3; resembles RBBB but terminal S waves may be absent
  • Type 2: Saddle-back ST elevation ≥2 mm in V1-V3 (not diagnostic alone; requires pharmacologic challenge)
Clinical significance: Risk of polymorphic VT/VF and sudden cardiac death in structurally normal hearts. Unmasked by fever, sodium channel blockers (flecainide, procainamide challenge used for diagnosis).

8. Wolff-Parkinson-White (WPW)

Mechanism: Accessory pathway (Bundle of Kent) bypasses the AV node, pre-exciting the ventricle before normal conduction arrives.
Key ECG findings (during sinus rhythm):
  • Short PR interval (<120 ms) - AV node bypassed
  • Delta wave - slurred initial QRS upstroke (pre-excitation of ventricle via accessory pathway)
  • Wide QRS (>120 ms) - fusion of delta wave + normal QRS
  • Secondary ST-T changes (discordant to delta wave direction)
Risk: In the setting of AF, impulses can conduct rapidly down the accessory pathway (bypassing AV node) → very fast ventricular rates → VF. Look for irregularly irregular wide-complex tachycardia with varying QRS morphology.

9. Left Bundle Branch Block (LBBB)

Mechanism: Block of the left bundle forces right-to-left ventricular activation instead of normal simultaneous activation.
Diagnostic criteria:
  • QRS duration ≥120 ms
  • Broad, notched (M-shaped) R waves in I, aVL, V5-V6 (lateral leads)
  • rS or QS pattern in V1 (no septal Q wave)
  • Absent septal Q waves in I, V5-V6
  • Secondary discordant ST-T changes (T wave opposite to last QRS deflection)
Clinical note: New LBBB in the context of chest pain is treated as STEMI equivalent. Sgarbossa criteria help detect true STEMI within LBBB: concordant ST elevation ≥1 mm, concordant ST depression ≥1 mm in V1-V3, or excessive discordant ST elevation >5 mm.

10. Subarachnoid Hemorrhage (CNS Injury Pattern)

Mechanism: Massive catecholamine surge from hypothalamic stimulation causes diffuse myocardial injury (neurogenic stunned myocardium).
Key ECG findings:
  • Deep, diffuse T-wave inversions - often wide and symmetric ("cerebral T waves"), most prominent in precordial leads
  • Marked QT prolongation (QTc often >600 ms)
  • Prominent U waves
  • May mimic anterior ischemia or Wellens' pattern
  • Can be associated with troponin elevation (stress cardiomyopathy/takotsubo) without obstructive CAD
Subarachnoid hemorrhage ECG - deep T inversions
Leads III and V3 showing deeply inverted, broad T waves with marked QT prolongation in subarachnoid hemorrhage.

Quick Reference Summary

DiseaseMost Characteristic ECG Finding
STEMILocalized ST elevation + reciprocal depression → Q waves
PericarditisDiffuse concave ST elevation + PR depression (no reciprocal)
Pulmonary EmbolismS1Q3T3, sinus tachycardia, RV strain pattern
HyperkalemiaPeaked T waves → wide QRS → sine wave
HypokalemiaProminent U waves, QU prolongation
HypothermiaOsborn (J) waves + bradycardia
Brugada SyndromeCoved ST elevation V1-V3 (Type 1)
WPWShort PR + delta wave + wide QRS
LBBBBroad notched R in I/V5/V6, rS in V1, ≥120 ms QRS
Subarachnoid HemorrhageDeep, wide T inversions + marked QT prolongation
Sources: Harrison's Principles of Internal Medicine 22E, p. 1916-1918; Tintinalli's Emergency Medicine, Table 49-6; Goldberger's Clinical Electrocardiography 10th ed.
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