Guide to Reading an ECG

Introduction

The electrocardiogram (ECG) is an indispensable tool in modern medicine, providing a non-invasive window into the electrical activity of the heart. Despite its widespread use, many clinicians and students find ECG interpretation challenging due to the complexity of waveforms, intervals, and axis deviations.

Mastering ECG reading is not about memorizing patterns alone—it requires a structured, systematic approach. A step-by-step methodology ensures that no key feature is overlooked and that the clinical significance of findings is accurately interpreted.

This article provides a complete guide to ECG interpretation, including systematic steps, wave and interval analysis, rhythm identification, axis determination, conduction abnormalities, and clinical correlations.

Section 1: Understanding the ECG Basics

1.1 The Physiological Basis of ECG

The ECG reflects electrical activity generated by cardiac myocytes, recorded at the body surface. Each waveform corresponds to a specific phase of the cardiac action potential:

P wave: Atrial depolarization.
QRS complex: Ventricular depolarization.
T wave: Ventricular repolarization.
PR interval: Conduction through atria and AV node.
QT interval: Total duration of ventricular depolarization and repolarization.

1.2 The Standard ECG Lead System

Limb leads (I, II, III, aVR, aVL, aVF): Measure the electrical activity in the frontal plane.
Precordial leads (V1–V6): Measure activity in the horizontal plane.

Understanding lead placement and orientation is essential for accurate interpretation of wave direction and amplitude.

1.3 ECG Paper and Calibration

Standard speed: 25 mm/s (1 small square = 0.04 s).
Standard amplitude: 10 mm/mV.
Knowing these conventions allows precise measurement of intervals, durations, and voltages.

Section 2: Stepwise Approach to ECG Interpretation

A systematic method prevents errors and ensures a comprehensive assessment. The following steps are recommended:

Step 1: Check ECG Quality

Verify paper speed and calibration.
Check for artifacts: patient movement, tremors, electrical interference.
Confirm all 12 leads are present and correctly labeled.

Step 2: Determine Heart Rate

Method 1: Large-square method
- Count the number of large squares between two consecutive R waves.
- Heart rate (bpm) = 300 ÷ number of large squares.
Method 2: Small-square method
- Count small squares between R waves.
- Heart rate = 1500 ÷ number of small squares.
Method 3: Counting QRS complexes in 6 seconds
- Count QRS in 30 large squares (6 seconds) and multiply by 10.

Step 3: Assess Rhythm

Determine if rhythm is regular or irregular.
Identify P waves:
- Are they present?
- Do they precede every QRS?
- Are they uniform in morphology?
Evaluate PR interval: 0.12–0.20 s normally.
Determine if rhythm is sinus, atrial, junctional, or ventricular.

Common Rhythms:

Sinus rhythm: P wave before every QRS, regular rhythm.
Atrial fibrillation: Irregularly irregular, absent P waves.
Atrial flutter: Sawtooth P waves.
Junctional rhythm: P wave absent, inverted, or after QRS.
Ventricular rhythm: Wide QRS, no preceding P wave.

Step 4: Evaluate P Wave

Duration: 0.08–0.12 s.
Amplitude: <2.5 mm in limb leads.
Morphology:
- P mitrale (broad, notched) → left atrial enlargement.
- P pulmonale (peaked) → right atrial enlargement.
Lead II and V1 are most informative for P wave assessment.

Step 5: Measure PR Interval

Normal: 0.12–0.20 s.
Short PR (<0.12 s): Pre-excitation (WPW).
Prolonged PR (>0.20 s): First-degree AV block.
Variable PR: Second-degree AV block (Mobitz I/Wenckebach, Mobitz II).

Step 6: Analyze QRS Complex

Duration: 0.08–0.10 s (up to 0.12 s).
Assess morphology in all leads:
- Presence of Q waves (pathological if >0.04 s, >25% of R wave amplitude).
- R wave progression in precordial leads (poor progression may indicate anterior MI).
- Bundle branch blocks (wide QRS with characteristic patterns).
Voltage criteria can suggest ventricular hypertrophy.

Step 7: Evaluate the ST Segment

Isoelectric baseline between QRS and T wave.
Elevation: Acute MI, pericarditis, early repolarization.
Depression: Myocardial ischemia, digitalis effect.
Reciprocal changes: Confirms MI location.

Step 8: Analyze T Wave

Amplitude: 0.5–10 mm (limb), 10–15 mm (precordial).
Upright in leads I, II, V3–V6.
Inversion: Ischemia, bundle branch block, LVH, pulmonary embolism.
Peaked T waves: Hyperkalemia.
Flattened T waves: Hypokalemia.
Biphasic T waves: Ischemia or Wellens’ syndrome.

Step 9: Measure QT Interval

From start of QRS to end of T wave.
Corrected QT (QTc) accounts for heart rate using Bazett’s formula: QTc = QT/√RR.
Normal: <440 ms (men), <460 ms (women).
Prolonged QT: Risk for torsades de pointes, drugs, electrolyte disturbances.
Short QT: Hypercalcemia, digoxin.

Step 10: Determine the Cardiac Axis

Frontal plane axis estimated using limb leads.
Normal: −30° to +90°.
Left axis deviation: −30° to −90° → LVH, LBBB, inferior MI.
Right axis deviation: +90° to +180° → RVH, pulmonary hypertension, lateral MI.
Use lead I and aVF to approximate axis quickly:
- Lead I positive, aVF positive → normal.
- Lead I negative, aVF positive → right axis.
- Lead I positive, aVF negative → left axis.
- Lead I negative, aVF negative → extreme axis.

Step 11: Look for Conduction Abnormalities

Bundle branch blocks: Wide QRS, specific R/S patterns.
Hemiblocks: Left anterior or posterior fascicular block → axis deviation with normal QRS width.
AV blocks: First, second, third degree.
Pre-excitation syndromes: Short PR, delta wave (WPW).

Step 12: Identify Chamber Enlargement

Left atrial enlargement: P mitrale.
Right atrial enlargement: P pulmonale.
Left ventricular hypertrophy (LVH): High R wave in V5–V6, deep S in V1–V2 (Sokolow-Lyon criteria).
Right ventricular hypertrophy (RVH): Tall R in V1, right axis deviation.

Step 13: Correlate with Clinical Context

ECG findings should always be interpreted in conjunction with patient history, symptoms, and labs.
Acute chest pain + ST elevation → STEMI.
Dyspnea + S3 gallop + LVH → chronic HF.
Syncope + prolonged QT → risk of torsades.

Section 3: Common ECG Patterns and Clinical Correlation

3.1 Myocardial Ischemia and Infarction

ST elevation: Acute transmural MI.
ST depression/T inversion: Subendocardial ischemia.
Pathological Q waves: Indicate previous MI.
Reciprocal changes confirm infarct location.

3.2 Arrhythmias

Atrial fibrillation: Irregularly irregular, absent P waves.
Atrial flutter: Sawtooth P waves.
Ventricular tachycardia: Wide QRS, regular or slightly irregular.
Supraventricular tachycardia: Narrow QRS, rapid, often paroxysmal.

3.3 Electrolyte Disturbances

Hyperkalemia: Peaked T waves, widened QRS, sine-wave pattern in severe cases.
Hypokalemia: Flattened T waves, U waves, ST depression.
Hypercalcemia: Short QT.
Hypocalcemia: Prolonged QT.

3.4 Drug Effects

Digoxin: Downsloping ST depression (scooped), flattening of T waves.
Antiarrhythmics: Prolonged QT (Class IA/III), wide QRS (Class IC).

Section 4: Tips for Efficient ECG Interpretation

Always use a systematic approach: Skip nothing.
Check rhythm first: Rate and regularity.
Measure intervals precisely: PR, QRS, QT.
Compare with previous ECGs: Identify new vs chronic changes.
Use multiple leads: Confirm findings in more than one lead.
Clinical correlation: Never interpret ECG in isolation.

Section 5: Advanced Interpretation

5.1 Vector Analysis

Understanding electrical vectors explains wave direction and axis deviations.
Depolarization vectors toward positive electrode → positive deflection.
Repolarization vectors toward positive electrode → negative deflection.

5.2 Rate-Dependent Changes

Tachycardia → shortened QT, fusion beats, conduction delays.
Bradycardia → prolonged QT, potential U wave prominence.

5.3 Pediatric and Neonatal ECG

Higher heart rate, shorter PR interval, right axis dominance.