Explain ecg abnormality

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Here is a thorough explanation of ECG abnormalities, drawn primarily from Harrison's Principles of Internal Medicine (22nd ed., 2025).

ECG Abnormalities - A Systematic Overview

The ECG records the heart's electrical activity across time. Abnormalities are classified into six major categories.

1. Cardiac Enlargement and Hypertrophy

Atrial Abnormalities

  • Right atrial overload: Tall, peaked P waves (≥2.5 mm), historically called "P-pulmonale"
  • Left atrial overload: Biphasic P wave in V1 with a broad negative component, OR a broad (≥120 ms), often notched P wave in limb leads ("P-mitrale"). This can also occur with interatrial conduction delays even without true enlargement.

Ventricular Hypertrophy

LVH and RVH ECG patterns vs. Normal
  • Left ventricular hypertrophy (LVH): Increased QRS amplitude directed leftward and posteriorly; ST-segment depression and T-wave inversions in leads with prominent R waves (strain pattern). Common voltage criteria: S in V1 + R in V5/V6 >35 mm.
  • Right ventricular hypertrophy (RVH): Rightward QRS axis; tall R in V1 (R, RS, or qR complex); T-wave inversions in right precordial leads. Associated with pulmonary hypertension, pulmonic stenosis.

2. Bundle Branch Blocks and Intraventricular Conduction Defects

RBBB vs LBBB ECG patterns
Complete bundle branch blocks have QRS duration ≥120 ms; incomplete blocks are 110-120 ms.
FeatureRBBBLBBB
V1 patternrSR' ("rabbit ears")Wide QS (broad negative)
V6 patternqRS (deep S wave)Entirely positive R (no Q, no S)
T waveInverted in V1-V3 (secondary change)Inverted in V5-V6 (secondary change)
Clinical associationsASD, pulmonary embolism, normal variantCoronary artery disease, hypertension, aortic valve disease, cardiomyopathy
Fascicular blocks (hemiblocks) do not widen the QRS but shift the axis:
  • Left anterior fascicular block: axis more negative than -45° (marked left axis deviation) - most common cause of marked left axis deviation in adults
  • Left posterior fascicular block: axis more rightward than +110-120° (rare as isolated finding)
Bifascicular block (RBBB + left anterior or posterior fascicular block) carries ~6% annual risk of progression to complete heart block.
Wolff-Parkinson-White (WPW): Wide QRS due to pre-excitation via an accessory bypass tract, NOT a conduction delay. Shows a delta wave (slurred QRS upstroke) and short PR interval.

3. Myocardial Ischemia and Infarction

Ischemia creates "currents of injury" that manifest as ST-segment deviation:

ST-Segment Elevation MI (STEMI)

  • Transmural ischemia shifts the ST vector toward the epicardium → ST elevation in overlying leads
  • Earliest sign: tall, peaked "hyperacute" T waves
  • Evolution over hours to days: ST elevation → T-wave inversions → Q waves
Localization by leads:
TerritoryLeads with changesArtery
Anterior/ApicalV1-V6, I, aVLLAD
InferiorII, III, aVFRCA or LCX
PosteriorReciprocal ST depression V1-V3LCX or RCA
Right ventricularRight-sided leads (V3R, V4R)RCA

Non-ST Elevation / Subendocardial Ischemia

  • Subendocardial ischemia shifts the ST vector toward the ventricular cavity → ST depression in precordial leads + ST elevation in aVR
  • T-wave inversions without ST elevation

Pathological Q Waves

  • Width ≥40 ms or depth ≥25% of R-wave height indicates prior transmural infarction
  • Exception: septal Q waves in V5-V6 are normal (small, narrow)

4. Arrhythmias and Conduction (Rate/Rhythm Abnormalities)

By Heart Rate

  • Tachycardia (>100 bpm): Sinus tachycardia, SVT, atrial flutter/fibrillation, ventricular tachycardia, ventricular fibrillation
  • Bradycardia (<60 bpm): Sinus bradycardia, sick sinus syndrome, junctional rhythm

AV Conduction Blocks

DegreePR IntervalQRSNotes
1st degree>200 ms (prolonged)NormalBenign
2nd degree - Mobitz I (Wenckebach)Progressive lengthening → dropped beatNormalUsually at AV node; relatively benign
2nd degree - Mobitz IIFixed PR, sudden dropped QRSNormal or wideBelow the AV node; higher risk
3rd degree (complete)No relationship between P and QRSEscape rhythm (wide or narrow)Full AV dissociation

Atrial Fibrillation

  • Absent P waves, irregularly irregular rhythm, fibrillatory baseline
  • Narrow QRS unless aberrant conduction

Ventricular Tachycardia

  • Wide QRS (>120 ms), rate >100 bpm, AV dissociation
  • Fusion beats and capture beats are diagnostic

5. Metabolic and Drug-Induced Changes

CauseECG Change
HyperkalemiaPeaked (tented) T waves → widening QRS → loss of P waves → sine-wave → asystole
HypokalemiaFlattened T waves, prominent U waves, prolonged QU interval
HypercalcemiaShortened QT interval
HypocalcemiaProlonged QT interval (ST portion lengthened)
HypothermiaOsborn (J) waves, bradycardia, prolonged QT
Digoxin"Scooped" ST-T depression, shortened QT, AV block at toxic levels
Class IA/III antiarrhythmicsProlonged QT → risk of torsades de pointes
Intracranial hemorrhageDeep, wide T-wave inversions ("CVA T waves"), especially with SAH

6. Other Notable Abnormalities

Brugada Pattern

  • Right bundle branch block morphology + ST elevation in V1-V3 (coved or saddleback type)
  • Associated with sudden cardiac death risk; inherited channelopathy

QT Prolongation

  • QTc >440 ms in men, >460 ms in women (Bazett formula)
  • Risk of torsades de pointes and sudden death
  • Causes: congenital LQTS, drugs, electrolyte disturbances, hypothermia

Pericarditis

  • Diffuse ST elevation (concave/"saddle-shaped") in multiple leads + PR depression
  • No reciprocal changes (unlike MI), no Q waves

Low QRS Voltage

  • Peak-to-trough QRS ≤5 mm in all limb leads and/or ≤10 mm in chest leads
  • Causes: pericardial effusion, pleural effusion, COPD, cardiac amyloid, anasarca

Electrical Alternans

  • Beat-to-beat alternation in QRS amplitude (and sometimes T waves)
  • Classic finding in large pericardial effusion with cardiac tamponade

Pulmonary Embolism (Acute Cor Pulmonale)

  • Sinus tachycardia (most common)
  • S1Q3T3 pattern (deep S in I, Q and inverted T in III)
  • Right axis deviation, new RBBB, atrial fibrillation

Summary Table of Key ECG Abnormalities

CategoryPatternKey LeadsClinical Significance
LVHIncreased voltage + strainV5-V6, I, aVLHypertension, aortic stenosis
RVHTall R in V1, right axisV1, III, aVFPulmonary HTN, RV pressure overload
RBBBrSR'V1, V6Can be normal; also PE, ASD
LBBBWide QS, broad RV1, V6Usually significant heart disease
STEMIST elevationLocalizes by territoryEmergency reperfusion needed
NSTEMIST depression, T invDiffuseSubendocardial ischemia
HyperkalemiaPeaked T → sine waveAllLife-threatening
Long QTQTc >440/460 msAllRisk of torsades de pointes
AFNo P waves, irregularAllStroke risk, rate control needed
BrugadaRBBB + V1-V3 ST elevV1-V3Sudden cardiac death

Sources: Harrison's Principles of Internal Medicine, 22nd ed. (2025), Chapter 247 (Electrocardiography); Fuster and Hurst's The Heart, 15th ed.

I need an complete comparison between Mitra, tricuspid, aortic, pulmonary stenosis and regurgitation

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