How to interpret ecg

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ECG interpretation normal waveform PQRST segments intervals

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I have comprehensive content from Harrison's Principles of Internal Medicine (22nd Ed) and Medical Physiology. Here is a thorough, structured guide to ECG interpretation.

How to Interpret an ECG

An ECG (electrocardiogram) is a graphical representation of the heart's electrical activity recorded via electrodes on the limbs and chest. It is noninvasive, inexpensive, and provides immediate diagnostic information about arrhythmias, conduction disturbances, ischemia/infarction, metabolic disturbances, and drug toxicities.

The Cardiac Conduction System (What the ECG Reflects)

Cardiac conduction system showing SA node, AV node, His bundle, bundle branches, and Purkinje fibers
The normal electrical impulse originates at the SA node → spreads through the atria → passes through the AV node (slows) → travels down the His bundle → splits into right and left bundle branches → activates the ventricles via Purkinje fibers.

ECG Paper & Calibration

ECG paper has a grid of 1 mm small boxes and 5 mm large boxes:
  • Horizontal axis (time): 1 small box = 0.04 s; 1 large box = 0.2 s; 5 large boxes = 1.0 s
  • Vertical axis (voltage): 1 mm = 0.1 mV (standard calibration: 10 mm = 1 mV)
Quick heart rate calculation: Rate = 300 ÷ (number of large boxes between R-R interval)
  • 1 large box → 300 bpm | 2 → 150 | 3 → 100 | 4 → 75 | 5 → 60 | 6 → 50

The 14-Parameter Systematic Approach (Harrison's)

A systematic reading prevents errors of omission. Always analyze all 14 parameters:

1. Standardization & Technical Features

  • Check calibration (standard = 10 mm/mV)
  • Verify lead placement (limb leads: I, II, III, aVR, aVL, aVF; precordial leads: V1–V6)
  • Identify artifacts (muscle tremor, lead displacement, electrical interference)
  • Always compare with prior ECGs

2. Rhythm

Ask three questions:
  1. Where is the pacemaker? (Normal = SA node)
  2. What is the conduction path to the ventricles?
  3. Is it regular and at the correct rate?
Normal sinus rhythm: P wave precedes every QRS, rate 60–100 bpm, regular R-R intervals.
Rhythm FindingClue
No P waves, irregular R-RAtrial fibrillation
Sawtooth P wavesAtrial flutter
Wide, bizarre QRS without PVentricular tachycardia
Regular, slow with no P-QRS relationshipComplete (3rd degree) AV block
Panel A: normal sinus rhythm. Panel B: atrial fibrillation with absent P waves and irregularly irregular rhythm

3. Heart Rate

  • Normal: 60–100 bpm
  • Bradycardia: < 60 bpm
  • Tachycardia: > 100 bpm
  • Use the 300 rule (above) for regular rhythms; count complexes in 6 seconds × 10 for irregular rhythms

4. PR Interval (AV Conduction)

  • Normal: 0.12–0.20 s (3–5 small boxes)
  • Reflects AV node conduction time
PR FindingInterpretation
> 0.20 s (prolonged)1st degree AV block
Progressively lengthening → dropped QRS2nd degree AV block, Mobitz I (Wenckebach)
Constant PR, then suddenly dropped QRS2nd degree AV block, Mobitz II
No relationship between P and QRS3rd degree (complete) AV block
Short PR (< 0.12 s) + delta waveWolff-Parkinson-White (WPW) pre-excitation

5. QRS Duration (Intraventricular Conduction)

  • Normal: < 0.10–0.12 s (< 2.5–3 small boxes)
  • Narrow QRS = normal ventricular conduction
  • Wide QRS (> 0.12 s) = bundle branch block, ventricular rhythm, or pacing
QRS FindingInterpretation
Wide QRS, RSR' in V1, wide S in V6Right Bundle Branch Block (RBBB)
Wide QRS, broad notched R in V5-V6, QS in V1Left Bundle Branch Block (LBBB)
Wide bizarre QRS, no preceding PVentricular ectopic / VT
"WiLLiaM MaRRoW" mnemonic: LBBB → W in V1, M in V6; RBBB → M in V1, W in V6.

6. QT / QTc Interval

  • Measured from start of QRS to end of T wave
  • Normal QTc: < 440 ms in men, < 460 ms in women (Bazett formula: QTc = QT ÷ √RR)
  • Prolonged QTc: Risk of Torsades de Pointes (TdP) → drugs (quinidine, amiodarone, antihistamines), hypokalaemia, hypomagnesaemia, hypocalcaemia, congenital long QT syndromes
  • Short QTc: Hypercalcaemia

7. Mean QRS Electrical Axis

  • Normal axis: −30° to +100° (frontal plane)
  • Quick method: If QRS is mostly positive in leads I and aVF → normal axis
AxisDegrees
Normal−30° to +100°
Left axis deviation (LAD)More negative than −30°
Right axis deviation (RAD)More positive than +90° to +100°
Causes of LAD: Left anterior fascicular block, inferior MI, LBBB, LVH Causes of RAD: RVH, left posterior fascicular block, pulmonary embolism, lateral MI

8. P Waves (Atrial Abnormalities)

  • Normal P wave: Upright in I, II, aVF; < 0.12 s duration; < 2.5 mm amplitude
  • P mitrale (bifid P in lead II, negative terminal deflection in V1): Left atrial enlargement
  • P pulmonale (tall peaked P > 2.5 mm in II, III, aVF): Right atrial enlargement

9. QRS Voltages (Ventricular Hypertrophy)

Left ventricular hypertrophy (LVH):
  • S in V1 + R in V5 or V6 > 35 mm (Sokolov-Lyon criterion)
  • R in aVL > 11–12 mm
  • Often associated with ST-T "strain" changes (downsloping ST depression + T inversion in lateral leads)
Right ventricular hypertrophy (RVH):
  • Tall R in V1 (R > S in V1), right axis deviation
  • Deep S in V5/V6

10. Precordial R-Wave Progression

  • R wave should progressively increase from V1 to V5/V6
  • Transition zone (R = S) normally at V3 or V4
  • Poor R-wave progression (small R waves through V4): Anterior MI, LBBB, RVH, LVH, technical lead misplacement
  • Early transition (tall R in V1/V2): Posterior MI, RVH, WPW

11. Abnormal Q Waves

  • Pathological Q waves: ≥ 0.04 s (1 small box) wide AND ≥ 25% of QRS height, or > 1 mm deep
  • Indicate prior transmural (Q-wave) MI
  • Location of Q waves correlates with territory:
Q wave leadsInfarct territory
V1–V4Anterior (LAD)
II, III, aVFInferior (RCA or LCx)
I, aVL, V5–V6Lateral (LCx or diagonal)
V1–V2 (tall R, no Q)Posterior (reciprocal change)

12. ST Segments

  • Normal: Isoelectric (flat at baseline), or within ±1 mm of the PR baseline
  • ST elevation:
    • STEMI: ≥ 1 mm in ≥ 2 contiguous limb leads, or ≥ 2 mm in ≥ 2 contiguous precordial leads
    • Other causes: Pericarditis (diffuse saddle-shaped elevation), early repolarization, LV aneurysm, Brugada (coved pattern in V1–V2), vasospasm (Prinzmetal's)
  • ST depression:
    • Subendocardial ischemia/NSTEMI, LVH strain, digitalis effect (reverse tick/sagging), reciprocal changes in STEMI

13. T Waves

  • Normal: Upright in I, II, V3–V6; inverted in aVR; variable in III, V1, V2
  • T-wave inversion: Ischemia/infarction, RVH, LVH strain, bundle branch blocks, myocarditis, Wellens' syndrome (deep symmetric T inversions in V2–V3 = critical LAD stenosis)
  • Peaked/hyperacute T waves: Early STEMI, hyperkalaemia
  • Flat T waves: Hypokalaemia, hypothyroidism

14. U Waves

  • Small deflection after the T wave, best seen in V2–V3
  • Prominent U waves: Hypokalaemia, bradycardia, drugs (quinidine)
  • Inverted U waves: LV volume overload, ischaemia

Summary Mnemonic: "Rate, Rhythm, Axis, P-QRS-T"

StepWhat to check
Rate60–100 bpm normal
RhythmRegular? P before every QRS?
Axis−30° to +100° normal
P waveShape, duration, axis
PR interval0.12–0.20 s
QRSWidth, morphology, voltage
QTCorrected for rate
STElevation or depression
T waveUpright, inverted, peaked
U waveProminent or inverted

Common Patterns at a Glance

PatternKey ECG Features
STEMIST elevation in contiguous leads + reciprocal depression
NSTEMI/UAST depression ± T inversion (no elevation)
Atrial fibrillationAbsent P waves, irregularly irregular QRS
Complete AV blockP and QRS independent; broad escape rhythm
LBBBWide QRS, M-shaped R in V5/V6, QS in V1
RBBBWide QRS, RSR' in V1, wide S in V6
PES1Q3T3 (S in I, Q in III, T inversion in III); sinus tachycardia most common
HyperkalaemiaPeaked T → PR prolongation → wide QRS → sine wave
HypokalaemiaFlat T, prominent U, long QU
Digoxin effectSagging ST "reverse tick," shortened QT
WPWShort PR, delta wave, wide QRS

Sources: Harrison's Principles of Internal Medicine, 22nd Ed, Chapter 247 (Goldberger AL); Medical Physiology (Boron & Boulpaep), Chapter 21, Box 21-2
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