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I now have comprehensive ECG content and images. Let me compile everything into a thorough, well-structured answer.

ECG Basics & Interpretation

Source: Harrison's Principles of Internal Medicine, 22E (2025) - Chapter 247 Electrocardiography (Ary L. Goldberger)

What is an ECG?

An electrocardiogram (ECG or EKG) is a graphical recording of the electrical activity generated by the heart, detected through metallic electrodes attached to the limbs and chest wall. It is noninvasive, inexpensive, and immediately available. Beyond arrhythmia detection, it reveals conduction disturbances, myocardial ischemia/infarction, metabolic disturbances (e.g., hyperkalemia), drug toxicities, and susceptibility to sudden cardiac arrest.

1. Electrophysiologic Basis

The normal heartbeat begins at the sinoatrial (SA) node, which has spontaneous automaticity. The impulse spreads through the atria, then passes through the AV node and His bundle (together = AV junction), bifurcates into the right and left bundle branches, and reaches the ventricular myocardium via Purkinje fibers.
Cardiac conduction system showing SA node, AV node, His bundle, right and left bundle branches, and Purkinje fibers
The cardiac conduction system. The left bundle branch further divides into left anterior and left posterior fascicles.

2. ECG Waveforms & Intervals

ECG waveforms showing P wave, QRS complex, ST segment, T wave, U wave, and PR/QT intervals
The basic ECG waveform. The J point marks the junction between QRS end and ST segment onset.
Waveform/IntervalRepresentsNormal Value
P waveAtrial depolarizationDuration <120 ms; amplitude <2.5 mm
PR intervalAV conduction time (SA node to ventricular muscle)120-200 ms (3-5 small boxes)
QRS complexVentricular depolarization<100 ms (up to 110 ms in some)
ST segmentVentricular plateau phase (isoelectric)Isoelectric (at baseline)
T waveVentricular repolarization (active recovery)Positive in most leads
QT intervalTotal ventricular depolarization + repolarizationCorrected QTc <440 ms (men), <460 ms (women)
U wavePossibly late ventricular repolarization / Purkinje repolarizationSmall, follows T wave
J pointQRS-ST junctionAt isoelectric line

Paper Speed & Calibration

  • Standard sweep speed: 25 mm/s
  • Smallest box (1 mm) = 40 ms (0.04 s)
  • Larger box (5 mm) = 200 ms (0.20 s)
  • Vertical amplitude: 1 mV = 10 mm at standard calibration

Calculating Heart Rate

  • Count the large boxes between two R waves: HR = 300 ÷ (number of large boxes)
  • Or count small boxes: HR = 1500 ÷ (number of small boxes)

3. The 12 Leads

A standard ECG has 12 leads - each providing a different "view" of the heart's electrical activity.

Limb Leads (Frontal Plane)

LeadView
ILeft lateral
IIInferior (most used for rhythm strips)
IIIInferior
aVRRight shoulder (right atrium) - normally negative
aVLLeft lateral
aVFInferior (foot)

Precordial (Chest) Leads (Horizontal Plane)

Precordial lead placement on the chest wall showing V1-V6 positions
Chest lead positions. V1: 4th ICS right sternal border. V2: 4th ICS left sternal border. V3: between V2 & V4. V4: 5th ICS midclavicular line. V5: anterior axillary line. V6: midaxillary line.
LeadView
V1-V2Right ventricle / septal
V3-V4Anterior LV
V5-V6Lateral LV

4. QRS Complex & R-Wave Progression

Ventricular depolarization phases showing septal and free-wall vectors and their effect on V1 vs V6 morphology
Ventricular depolarization occurs in two phases: (1) septal depolarization left-to-right (producing small r in V1, small q in V6), and (2) free-wall depolarization dominated by the larger LV, directed leftward/posteriorly (producing S in V1, tall R in V6).
Normal R-wave progression: R waves increase in amplitude from V1 through V4/V5. The transition zone (where R and S are equal) is usually at V3 or V4.
  • Poor R-wave progression (small R waves persisting through V4) suggests anterior infarction or other pathology.

5. QRS Axis

The mean QRS axis describes the overall direction of ventricular depolarization in the frontal plane:
AxisDegreesSignificance
Normal-30° to +100°Normal
Left axis deviation (LAD)More negative than -30°LBBB, left anterior fascicular block, inferior MI, LVH
Right axis deviation (RAD)More positive than +90 to +100°RVH, RBBB, left posterior fascicular block, lateral MI, dextrocardia
Quick rule: If QRS is positive in lead I and positive in lead II → normal axis. Positive I, negative II → LAD. Negative I, positive II → RAD.

6. ST Segment & T Wave Abnormalities

ST Elevation - Key Causes

CausePattern
STEMIRegional (follows coronary territory), convex/tombstone shape
PericarditisDiffuse, saddle-shaped; PR depression
Early repolarizationBenign variant, notch at J point, common in young males
Brugada syndromeCoved ST elevation V1-V3, RBBB-like morphology
LVH/LBBBDiscordant ST changes (opposite to main QRS deflection)
HyperkalemiaMay cause V1-V3 elevation

ST Depression - Key Causes

  • Subendocardial ischemia (horizontal or downsloping)
  • Digoxin effect (reverse tick / "sagging")
  • Reciprocal changes in STEMI
  • LVH strain pattern

T Wave Changes

  • Inversion: Ischemia, ventricular hypertrophy, bundle branch block, pulmonary embolism (right heart strain), pericarditis
  • Peaked/tall T waves: Hyperkalemia (early), posterior MI (prominent T in V1-V2)
  • Flat T waves: Hypokalemia, hypothyroidism

QT Prolongation

Prolonged QTc (>500 ms) increases risk of Torsades de Pointes:
  • Drugs: antiarrhythmics (amiodarone, sotalol), antipsychotics, fluoroquinolones, azithromycin
  • Electrolytes: hypokalemia, hypomagnesemia, hypocalcemia
  • Congenital long QT syndrome

7. Systematic 14-Step Interpretation (Harrison's Approach)

A systematic approach is mandatory to avoid errors of omission. Analyze every ECG for:
  1. Standardization & calibration (1 mV = 10 mm, paper speed)
  2. Lead placement & artifacts
  3. Rhythm (sinus vs. ectopic)
  4. Heart rate
  5. PR interval / AV conduction
  6. QRS interval
  7. QT/QTc intervals
  8. Mean QRS electrical axis
  9. P waves (morphology, axis)
  10. QRS voltages (hypertrophy criteria)
  11. Precordial R-wave progression
  12. Abnormal Q waves
  13. ST segments
  14. T waves & U waves
Compare with any previous ECGs - this is invaluable.

8. P Wave Abnormalities

FindingMeaning
Peaked P >2.5 mm in II ("P pulmonale")Right atrial enlargement
Notched/broad P >120 ms in II ("P mitrale")Left atrial enlargement
No P wavesAtrial fibrillation (irregularly irregular), junctional rhythm
Retrograde P (after QRS)Junctional rhythm
P waves not related to QRSComplete (3rd degree) AV block

9. Ventricular Hypertrophy

LVH Voltage Criteria (Sokolow-Lyon)

  • S in V1 + R in V5 or V6 >35 mm (age >35 years)
  • R in aVL >11-13 mm
  • Often accompanied by "strain pattern" (ST depression + T wave inversion in lateral leads I, aVL, V5-V6)

RVH

  • Dominant R wave in V1 (R > S)
  • Right axis deviation
  • ST depression + T wave inversion in V1-V3 (strain)

10. Clinical Correlations at a Glance

ConditionKey ECG Finding
Anterior STEMIST elevation V1-V4, Q waves
Inferior STEMIST elevation II, III, aVF
Lateral STEMIST elevation I, aVL, V5-V6
Posterior MITall R + ST depression V1-V2 (mirror image)
Atrial fibrillationNo P waves, irregularly irregular RR
Complete heart blockP-QRS dissociation, slow ventricular rate
LBBBBroad QRS, notched "M" in V5-V6, QS in V1
RBBBBroad QRS, RSR' ("bunny ears") in V1, wide S in I and V6
HyperkalemiaPeaked T → wide QRS → sine wave
PE (S1Q3T3)S wave in I, Q wave in III, T inversion in III
PericarditisDiffuse ST elevation + PR depression
Digoxin effectSagging ST depression ("reverse tick")

Source: Harrison's Principles of Internal Medicine, 22E (2025), Chapter 247 - Electrocardiography (pp. 1911-1918), by Ary L. Goldberger. Also based on Goldberger's Clinical Electrocardiography: A Simplified Approach, 10th ed. (Elsevier, 2024).

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