Ecg interpretation

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I now have rich content from Harrison's and Kaplan & Sadock's to build a thorough, systematic ECG interpretation guide. Let me compile it all.

Systematic ECG Interpretation - A Guide for Residents

A well-organized approach prevents missed findings. Every ECG should be interpreted in a fixed sequence - never jump straight to the "interesting" part.

The 14-Parameter Systematic Approach (Harrison's, 22e)

Follow this sequence on every ECG:
  1. Standardization & technical features
  2. Rhythm
  3. Heart rate
  4. PR interval / AV conduction
  5. QRS interval
  6. QT / QTc interval
  7. Mean QRS electrical axis
  8. P waves
  9. QRS voltages
  10. Precordial R-wave progression
  11. Abnormal Q waves
  12. ST segments
  13. T waves
  14. U waves
Always compare with a previous ECG when available.

Step 1 - Standardization & Technical Features

Before reading anything, check:
  • Paper speed: standard is 25 mm/s
  • Gain/calibration: standard = 10 mm/mV (1 cm deflection = 1 mV). If the calibration box at the start of the strip is half-height, gain is halved - voltages will appear falsely low
  • Lead placement errors: limb lead reversal (e.g., LA/RA swap) mimics dextrocardia; precordial misplacement distorts R-wave progression
  • Artifact: muscle tremor (Parkinson's, shivering) mimics AF; AC interference gives a 60 Hz wobble

Step 2 - Rate

ECG paper basics:
  • Small box = 0.04 s
  • Large box = 0.20 s
  • 5 small boxes = 1 large box
  • 300 large boxes = 1 minute
Two methods:
MethodUse whenFormula
Rate by squaresRegular rhythm300 ÷ (number of large boxes between R-waves)
QRS complexes per stripIrregular rhythm (e.g., AF)Count QRS complexes in 10-s strip × 6
Quick memorization table (large boxes between R-waves):
BoxesRate
1300
2150
3100
475
560
650
  • Bradycardia: HR < 60 bpm - think medications (beta-blockers, CCBs, digoxin, lithium), hypothyroidism, AV block, sick sinus syndrome, trained athletes
  • Tachycardia: HR > 100 bpm - think pain, sepsis, PE, thyrotoxicosis, anticholinergic drugs, hypovolemia

Step 3 - Rhythm

Ask three questions:
  1. Is the rhythm regular or irregular?
    • Regular: measure R-R intervals (should all be equal)
    • Irregularly irregular (no pattern) = classic AF
    • Regularly irregular = consider Wenckebach, bigeminy
  2. Is there a P wave before every QRS?
    • Normal sinus: upright P in leads I, II, aVF; inverted in aVR
  3. Does every P wave conduct to a QRS?
    • If not: consider AV block
Normal sinus rhythm criteria:
  • Rate 60-100 bpm
  • P wave before every QRS, constant PR interval
  • P wave axis 0-75° (upright in I and II)

Step 4 - PR Interval

  • Normal: 120-200 ms (3-5 small boxes)
  • Short PR (<120 ms): pre-excitation (WPW), junctional rhythm, ectopic atrial pacemaker
  • Long PR (>200 ms): first-degree AV block

Step 5 - QRS Duration

  • Normal: <120 ms (< 3 small boxes)
  • 120-150 ms: incomplete bundle branch block, or subtle intraventricular conduction delay
  • >120 ms: complete bundle branch block (RBBB or LBBB), ventricular paced rhythm, hyperkalemia
Bundle branch block quick rules:
FeatureRBBBLBBB
V1RSR' ("bunny ears")Broad, deep QS or rS
V6Wide S waveBroad, notched R, no S
Clinical hintMay be normal variantAlmost always pathological

Step 6 - QT / QTc Interval

  • Measured from start of QRS to end of T wave (best in lead II or V5)
  • Must be corrected for heart rate because QT shortens as rate increases
  • Bazett formula: QTc = QT / √RR (in seconds) - most common, used by ECG machines; overcorrects at fast rates
  • Normal QTc: <440 ms in men, <460 ms in women
  • Prolonged QTc (>500 ms): high risk for Torsades de Pointes (TdP)
Common causes of QT prolongation:
  • Drugs: antipsychotics, TCAs, amiodarone, sotalol, certain antibiotics (azithromycin, fluoroquinolones)
  • Electrolytes: hypokalemia, hypomagnesemia, hypocalcemia
  • Congenital long QT syndrome
  • Bradycardia, hypothyroidism, acute myocardial infarction

Step 7 - Electrical Axis

The axis represents the net direction of ventricular depolarization. Use leads I and aVF as perpendicular reference points:
Lead IaVFAxis
PositivePositiveNormal (-30° to +90°)
NegativePositiveRight axis deviation (RAD)
PositiveNegativeLeft axis deviation (LAD)
NegativeNegativeExtreme/"northwest" axis
Causes:
DeviationThink of
LADLBBB, left anterior fascicular block, inferior MI, LVH, WPW (right-sided pathway)
RADRBBB, right ventricular hypertrophy, PE, lateral MI, WPW (left-sided pathway), dextrocardia

Step 8 - P Waves

  • Normal P: <120 ms wide, <2.5 mm tall, upright in I and II, biphasic or inverted in V1
  • Peaked P in II (P pulmonale): >2.5 mm tall = right atrial enlargement (COPD, pulmonary HTN, tricuspid stenosis)
  • Broad notched P (P mitrale): >120 ms with double hump in lead II = left atrial enlargement (mitral disease, LVH)
  • Absent P waves: AF, sinoatrial block, junctional rhythm
  • Retrograde P (inverted in II, III, aVF): junctional or low atrial rhythm

Step 9 - QRS Voltages

LVH criteria (Sokolow-Lyon):
  • S in V1 + R in V5 or V6 >35 mm
RVH:
  • Dominant R in V1 (R:S ratio >1)
  • RAD
  • R in V1 + S in V5/V6 >11 mm
Low voltage (QRS <5 mm in all limb leads OR <10 mm in all precordial leads):
  • Obesity, emphysema, pericardial effusion, hypothyroidism, amyloidosis

Step 10 - Precordial R-wave Progression

  • Normally, R waves grow from V1 (tiny) to V4-V5 (tallest), then decrease to V6
  • Poor R-wave progression (PRWP): R waves fail to increase; consider anterior MI, LBBB, RVH, incorrect lead placement
  • Transition zone (where R = S) normally at V3-V4; early transition (V1-V2) suggests posterior MI or RVH

Step 11 - Pathological Q Waves

  • Normal septal Q waves: small (<40 ms, <25% of R height) in I, aVL, V5, V6
  • Pathological Q: >40 ms wide OR >25% of R height in ≥2 contiguous leads
  • Indicate prior transmural myocardial infarction
Localization by leads:
Q waves inTerritoryArtery
II, III, aVFInferiorRCA
I, aVLHigh lateralCx or diagonal
V1-V4AnteroseptalLAD
V4-V6AnterolateralLAD or Cx

Step 12 - ST Segments

  • Normal: isoelectric (at baseline), may have up to 1 mm variation
  • ST elevation (STE): >1 mm in limb leads, >2 mm in precordial leads in 2+ contiguous leads
ST PatternCauses
Concave-up elevation in all leadsAcute pericarditis (also PR depression)
Convex (domed/tombstone) elevationSTEMI
Saddle-shapedPericarditis, Brugada
ST depressionIschemia (NSTEMI/UA), digoxin effect ("reverse tick"), reciprocal changes
ST elevation V1-V2 with RBBB-like patternBrugada syndrome
Reciprocal ST depression in the leads opposite to the infarct territory is strong evidence for STEMI (not pericarditis).

Step 13 - T Waves

  • Normal: upright in I, II, V3-V6; inverted in aVR; may be inverted in III, V1-V2
  • Tall peaked T waves: hyperkalemia (early), hyperacute STEMI
  • Deep symmetrical T inversion: ischemia (Wellens' syndrome in V2-V3 = critical LAD stenosis), PE (V1-V4), RVH
  • Flattened T waves: non-specific but can indicate hypokalemia, digitalis effect, hypothyroidism

Step 14 - U Waves

  • Small positive deflection after T wave, best seen in V2-V3
  • Prominent U waves: hypokalemia (most common), bradycardia, hypomagnesemia
  • Inverted U waves: significant - associated with LVH, ischemia

Key Clinical Patterns to Recognize Immediately

PatternECG Findings
STEMIST elevation + reciprocal depression, may evolve Q waves
NSTEMI / UAST depression, T inversion, or normal
Complete heart blockP waves and QRS with no relation (AV dissociation)
Atrial fibrillationNo P waves, irregularly irregular QRS, fibrillatory baseline
WPWShort PR + delta wave + wide QRS
HyperkalemiaPeaked T → wide QRS → sine wave → VF
Pulmonary embolismSinus tachycardia (most common), S1Q3T3, RBBB, RAD
Digoxin effectScooped ST ("reverse tick"), short QT, bradycardia

Practical Tips for Residents

  • Never read the computer interpretation uncritically - automated analysis has significant limitations and should always be reviewed
  • Always get the clinical context first - a "normal ECG" in a patient with chest pain still warrants repeat ECGs and troponins
  • Compare with old ECGs - a new LBBB or new Q wave changes everything
  • Leads II, V1, V5 are your workhorses - rhythm in II, conduction in V1, ischemia in V5
  • If the ECG looks "weird", check technical quality first - lead reversal and artifact account for many "abnormalities"

Sources: Harrison's Principles of Internal Medicine 22e (2025); Kaplan & Sadock's Comprehensive Textbook of Psychiatry; Tintinalli's Emergency Medicine; ROSEN's Emergency Medicine
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