Common pathological ecg finding

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pathological ECG findings ST elevation STEMI Q wave bundle branch block

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left bundle branch block right bundle branch block ECG pattern

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atrial fibrillation ECG ventricular hypertrophy PR interval prolonged

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Common Pathological ECG Findings

A systematic ECG review covers: rhythm, rate, PR interval, QRS duration, QT interval, axis, P waves, voltages, R-wave progression, Q waves, ST segments, T waves, and U waves. Below are the major pathological findings organized by category.

1. Ischemia & Infarction

ST-Segment Elevation (STEMI pattern)

  • Transmural (full-thickness) ischemia shifts the ST vector toward the epicardium → ST elevation in leads overlying the ischemic zone
  • Earliest sign: tall, broad hyperacute T waves (before ST elevation develops)
  • "Tombstoning" / "shark fin" morphology = massive ST elevation merging with T wave → high-risk, often proximal LAD or multi-vessel occlusion
  • aVR elevation with diffuse ST depression = left main or proximal LAD occlusion
Acute STEMI with tombstoning pattern in anterior leads

ST-Segment Depression / Subendocardial Ischemia

  • Subendocardial ischemia shifts the ST vector toward the endocardium → ST depression in overlying leads (e.g., anterior precordial leads)
  • Typically horizontal or downsloping ≥1 mm

Pathological Q Waves

  • Represent myocardial necrosis (transmural scar)
  • Criteria: duration ≥40 ms (1 small square) OR depth >25% of the R wave in that lead
  • Persist after healed infarction as a permanent marker
  • Location indicates infarct territory:
    • Q in II, III, aVF = inferior (RCA)
    • Q in V1–V4 = anterior (LAD)
    • Q in I, aVL, V5–V6 = lateral (LCx)
Post-STEMI: persistent Q waves in inferior leads, residual ST elevation

T-Wave Inversion

  • Deep, symmetrical T-wave inversion in anterior leads (V2–V5) = Wellens' syndrome (critical proximal LAD stenosis, reperfused STEMI pattern)
  • Diffuse T-wave inversion = may indicate pericarditis (after initial ST elevation), myocarditis, cardiomyopathy, or PE (right precordial leads)
Wellens' pattern: terminal T-wave inversion V2–V5 with resolving ST elevation

2. Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

  • QRS ≥120 ms
  • rSR' ("rabbit ears") in V1 — M-shaped wide complex
  • Wide, slurred S wave in I and V6
  • Secondary T-wave inversions in V1–V3 (discordant with last QRS deflection)
  • Causes: PE (acute), RV pressure overload, CAD, congenital heart disease, normal variant

Left Bundle Branch Block (LBBB)

  • QRS ≥120 ms
  • Broad, notched R wave in V5–V6, I, aVL (no preceding Q)
  • Deep, wide S wave in V1
  • Secondary T-wave inversions in lateral leads
  • Always pathological — associated with CAD, hypertensive heart disease, aortic valve disease, cardiomyopathy
  • New LBBB + chest pain = treat as STEMI equivalent
RBBB vs LBBB QRS-T patterns in V1 and V6

Fascicular Blocks

  • Left Anterior Fascicular Block (LAFB): QRS axis more negative than −45° (marked left axis deviation); most common cause of left axis deviation in adults
  • Left Posterior Fascicular Block (LPFB): axis >+110°; rare, must exclude other causes
  • Bifascicular block (RBBB + LAFB): broad S wave in I/V6 + left axis deviation

3. Arrhythmias

Atrial Fibrillation (AF)

  • Irregularly irregular R-R intervals
  • Absent P waves replaced by chaotic fibrillatory baseline (best seen in V1)
  • Narrow QRS (unless aberrant conduction)
  • Associated with LVH, structural heart disease, thyrotoxicosis, alcohol
Atrial fibrillation with rapid ventricular response and LVH voltage criteria

AV Blocks

DegreeECG Feature
1st degreePR interval >200 ms; every P conducts
2nd degree Mobitz I (Wenckebach)Progressive PR lengthening → dropped QRS
2nd degree Mobitz IIFixed PR, sudden dropped QRS (no warning) — higher risk
3rd degree (Complete)P waves and QRS dissociated; junctional or ventricular escape rhythm

Pre-excitation (Wolff-Parkinson-White)

  • Short PR (<120 ms) + delta wave (slurred upstroke of QRS) + wide QRS
  • Due to accessory pathway bypassing AV node

4. Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

  • Sokolow-Lyon criteria: S in V1 + R in V5 or V6 ≥35 mm
  • Cornell criteria: R in aVL + S in V3 ≥28 mm (men) / ≥20 mm (women)
  • Associated strain pattern: ST depression + T-wave inversion in lateral leads (I, aVL, V5–V6)
  • Causes: hypertension (most common), aortic stenosis, HCM

Right Ventricular Hypertrophy (RVH)

  • Right axis deviation (>+90°)
  • Dominant R wave in V1 (R > S in V1)
  • Deep S waves in V5–V6
  • ST depression + T-wave inversion in right precordial leads (V1–V3)
  • Causes: pulmonary hypertension, mitral stenosis, tetralogy of Fallot

5. Electrolyte & Drug Effects

CauseECG Finding
HyperkalemiaPeaked T waves → widened QRS → sine-wave → VF
HypokalemiaFlattened T waves, prominent U waves, QTc prolongation
HypercalcemiaShort QT interval
HypocalcemiaProlonged QT interval
Digoxin"Reverse tick" ST depression (scooping), PR prolongation
Class I antiarrhythmics / TCAsWide QRS (sodium channel blockade)
Class III agents / QT-prolonging drugsProlonged QTc → risk of Torsades de Pointes

6. QT Prolongation

  • QTc >440 ms (men) / >460 ms (women) = pathological
  • Predisposes to Torsades de Pointes (polymorphic VT) → VF → sudden death
  • Causes: congenital long QT syndrome, drugs (antiarrhythmics, antipsychotics, antibiotics), hypokalemia, hypomagnesemia, hypothyroidism

7. Pericarditis

  • Saddle-shaped ST elevation in multiple leads (diffuse, not territory-specific)
  • PR segment depression (pathognomonic early finding)
  • T-wave inversions develop after ST elevation resolves
  • No pathological Q waves

8. Right Heart Strain (Acute PE — "S1Q3T3")

  • S wave in lead I + Q wave in III + T-wave inversion in III
  • Sinus tachycardia (most common ECG finding in PE)
  • New right bundle branch block
  • T-wave inversions V1–V4

9. Brugada Pattern

  • RBBB morphology + ST elevation in V1–V3 (coved or saddle-back pattern)
  • Predisposes to sudden cardiac death from polymorphic VT/VF
  • Exacerbated by fever, sodium-channel blocking drugs

Summary Table

FindingKey FeatureKey Causes
ST elevationCoved ≥1mm in ≥2 contiguous leadsSTEMI, pericarditis, Brugada, vasospasm
ST depressionHorizontal/downsloping ≥1mmSubendocardial ischemia, digoxin, LVH strain
Pathological Q wave≥40ms wide or >25% R wave depthOld MI, LBBB, HCM
LBBBWide QRS + notched R in V5–V6CAD, HTN, cardiomyopathy
RBBBrSR' in V1 + slurred S in V6PE, CAD, normal variant
AFIrregularly irregular, no P wavesValvular disease, HTN, alcohol
LVHHigh voltage + strain patternHypertension, aortic stenosis
Long QTQTc >440/460 msDrugs, electrolytes, congenital
AV blockProgressive/dropped P-RIschemia, drugs, fibrosis
Pre-excitationShort PR + delta waveWPW accessory pathway
Source: Harrison's Principles of Internal Medicine 22E (2025, McGraw Hill Medical), Chapter 247 — ECG section
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