ECG Interpretation
A systematic, practical guide to reading electrocardiograms for clinical practice — from basic principles to complex arrhythmias.
Contents
Basic Principles
An electrocardiogram (ECG) records the electrical activity of the heart over time using electrodes placed on the skin. Each heartbeat produces a characteristic pattern of electrical changes that can be read to assess heart rate, rhythm, conduction, and evidence of pathology.
Key concept: Electrical depolarisation travelling towards a lead produces a positive (upward) deflection. Depolarisation travelling away produces a negative (downward) deflection. Perpendicular depolarisation produces a biphasic or isoelectric trace.
The Cardiac Conduction System
The normal electrical impulse originates in the sinoatrial (SA) node in the right atrium, travels across both atria (causing atrial contraction), arrives at the atrioventricular (AV) node where it is briefly delayed, then travels rapidly down the Bundle of His, splits into the right and left bundle branches, and fans out through the Purkinje fibres to depolarise the ventricular myocardium.
Cardiac Anatomy & the ECG
Understanding which part of the heart each lead “looks at” is essential for localising pathology. The ECG gives us multiple viewpoints of the same electrical event.
The SA node fires → both atria depolarise → P wave. Repolarisation is hidden within the QRS complex.
The brief physiological delay at the AV node gives the ventricles time to fill — seen as the flat PR segment.
Rapid ventricular depolarisation via bundle branches and Purkinje fibres produces the tall QRS complex.
Recovery of the ventricular myocardium. T-wave changes are sensitive indicators of ischaemia and electrolyte disturbance.
The 12 Leads Explained
A standard 12-lead ECG uses 10 physical electrodes to derive 12 different “views” of the heart’s electrical activity. Each lead represents the electrical potential difference between two points.
Limb Leads
Precordial (Chest) Leads
Electrode placement tip: V1 — 4th intercostal space, right sternal border. V2 — 4th ICS, left sternal border. V4 — 5th ICS, midclavicular line. V3 — midway between V2 and V4. V5 — anterior axillary line. V6 — midaxillary line.
Coronary Territory Localisation
| Territory | Artery (usually) | Leads showing changes |
|---|---|---|
| Inferior | RCA (80%) / LCx (20%) | II, III, aVF |
| Anterior | LAD | V1–V4 |
| Lateral | LCx / OM branch | I, aVL, V5–V6 |
| Septal | Septal branches of LAD | V1–V2 |
| Posterior | RCA / LCx | V7–V9 (reciprocal V1–V3) |
| Right ventricle | RCA | V3R–V4R |
Waves, Intervals & Segments
| Feature | Normal Value | Pathological |
|---|---|---|
| P wave Atrial depolarisation |
<120ms / <2.5mm | Broad (P mitrale), peaked (P pulmonale), absent (AF) |
| PR interval AV node conduction |
120–200ms (3–5 small squares) | Short (<120ms) — WPW; Long (>200ms) — 1° HB |
| QRS duration Ventricular depolarisation |
<120ms (<3 small squares) | Wide (>120ms) — BBB, VT, WPW, hyperkalaemia |
| QT interval Ventricular depolarisation + repolarisation |
QTc <440ms (♂) / <460ms (♀) | Prolonged — drugs, hypoCa, hypoMg, LQTS → TdP risk |
| ST segment Early ventricular repolarisation |
Isoelectric (flat, on baseline) | Elevation — STEMI, pericarditis; Depression — NSTEMI, demand ischaemia |
| T wave Ventricular repolarisation |
Upright in I, II, V3–V6; inverted in aVR | Inversion — ischaemia, PE, BBB, LVH; peaked — hyperkalaemia |
ECG paper speed: Standard recording is at 25mm/s. Each small square = 40ms (0.04s), each large square = 200ms (0.2s). Amplitude: 1mm = 0.1mV at standard calibration (10mm/mV).
Systematic Approach
Always read ECGs systematically. Never jump straight to a diagnosis. A consistent method prevents missed findings and aids pattern recognition over time.
Clinical Context
Age, sex, symptoms, medications, previous ECGs. Always interpret in clinical context.
Calibration & Paper Speed
Check for 1mV calibration mark and standard 25mm/s paper speed. Note any non-standard settings.
Rate
300 ÷ RR interval (large squares). Or count complexes in a 10s rhythm strip × 6.
Rhythm
Regular or irregular? P waves present? Is each P followed by a QRS? Assess the rhythm strip (usually lead II).
Axis
Normal: –30° to +90°. Use leads I and aVF as a quick guide. If both positive → normal axis.
P Wave Morphology
Present and upright in II? Consistent shape? Duration <120ms? Amplitude <2.5mm?
PR Interval
120–200ms? Consistent? Variable PR (2° HB type I) vs fixed prolongation (1° HB)?
QRS Complex
Width <120ms? Morphology (BBB patterns)? Voltage (LVH/RVH)? Pathological Q waves?
ST Segment
Elevation or depression? In which leads? Localises territory. Degree and morphology matter.
T Wave
Expected direction in each lead? Inverted, flattened, or peaked? Symmetrical or asymmetrical?
QT Interval
Measure QTc (Bazett: QT ÷ √RR). >500ms associated with increased TdP risk.
Overall Interpretation
Synthesise all findings. Correlate with clinical picture. Compare with previous ECGs where available.
Rate & Rhythm
Calculating Heart Rate
Regular rhythm: Divide 300 by the number of large squares between consecutive R waves.
Irregular rhythm: Count R waves in the 10-second rhythm strip, multiply by 6.
Memory aid — 300, 150, 100, 75, 60, 50 for 1, 2, 3, 4, 5, 6 large squares.
Sinus Node Dysfunction
| Arrhythmia | Rate | Key Feature |
|---|---|---|
| Normal sinus rhythm | 60–100 bpm | Upright P in II, 1:1 P:QRS, regular |
| Sinus bradycardia | <60 bpm | Normal P morphology, slow rate |
| Sinus tachycardia | >100 bpm | Normal P, find the cause |
| Sinus arrhythmia | 60–100 bpm | Rate varies with respiration — normal variant |
Electrical Axis
The cardiac axis describes the overall direction of ventricular depolarisation in the frontal plane.
Leads I and aVF are both positive. The most common finding.
Lead I positive, aVF negative. Causes: LBBB, LVH, inferior MI, LAFB.
Lead I negative, aVF positive. Causes: RVH, PE, RBBB, lateral MI.
Both I and aVF negative. Often VT or lead reversal.
Quick trick: If the QRS is most positive in lead I and most negative in aVF, think LAD. Opposite for RAD. Check aVL and II to refine.
Chamber Hypertrophy & Enlargement
Left Ventricular Hypertrophy (LVH)
Increased myocardial mass leads to larger QRS voltages. Multiple criteria exist — no single criterion is highly sensitive.
S in V1 + R in V5 or V6 ≥ 35mm
Also look for: ST depression + T-wave inversion in lateral leads (“strain pattern”), LAD, broad notched P wave.
Right Ventricular Hypertrophy (RVH)
Dominant R wave in V1 (R>S), right axis deviation (>+90°), ST depression + T-wave inversion in V1–V3, P pulmonale (peaked P >2.5mm in lead II).
Atrial Enlargement
| Type | ECG Feature | Typical Cause |
|---|---|---|
| Left atrial enlargement (P mitrale) | P wave ≥120ms, bifid “M-shaped” P in II | Mitral stenosis, LVH |
| Right atrial enlargement (P pulmonale) | Peaked P >2.5mm in II, III, aVF | COPD, pulmonary hypertension |
Conduction Blocks
Heart Blocks (AV Blocks)
Delayed AV conduction but all impulses conducted. PR interval >200ms, every P is followed by a QRS.
Progressive PR prolongation until a P wave is not conducted (dropped QRS). The pattern then resets. Usually at the level of the AV node.
Sudden, unpredictable drop of QRS without preceding PR prolongation. Below the level of AV node. Risk of progression to complete heart block.
Complete AV dissociation. P waves and QRS complexes are independent. Ventricular escape rhythm (40–60 bpm if junctional; 20–40 if ventricular — wide QRS).
Bundle Branch Blocks
QRS >120ms, RSR’ in V1–V2, wide S in I, V5–V6. Causes: PE, RHD, congenital, normal variant.
QRS >120ms, broad/notched R in I, aVL, V5–V6, no septal Q waves. New LBBB with chest pain = STEMI until proven otherwise.
New LBBB in the context of acute chest pain should be treated as a STEMI-equivalent and triggers the same pathway. Refer immediately for primary PCI assessment. Sgarbossa criteria can help identify concurrent STEMI in LBBB.
Ischaemia, Injury & STEMI
Spectrum of Ischaemic Change
| Phase | ECG Findings | Significance |
|---|---|---|
| Hyperacute ischaemia | Tall, peaked (hyperacute) T waves | Very early STEMI — can be missed. May precede ST elevation. |
| STEMI (injury) | ST elevation ≥1mm in ≥2 contiguous limb leads, or ≥2mm in ≥2 contiguous precordial leads | Complete occlusion — emergent reperfusion required |
| NSTEMI / UA | ST depression >0.5mm, T-wave inversion, or dynamic changes | Partial occlusion or demand ischaemia — urgent management |
| Established infarction | Pathological Q waves (≥40ms wide, ≥25% QRS height) | Completed infarction, may persist permanently |
| Ischaemia | T-wave inversion (symmetrical, deep), ST depression | Demand ischaemia or post-STEMI reperfusion changes |
STEMI Localisation
| STEMI Location | Leads with ST Elevation | Artery | Reciprocal Changes |
|---|---|---|---|
| Inferior | II, III, aVF | RCA | ST depression in I, aVL |
| Anterior | V1–V4 | LAD | Reciprocal depression II, III, aVF |
| Lateral | I, aVL, V5–V6 | LCx | Inferior leads |
| Posterior | V7–V9 (or tall R + ST↓ in V1–V2) | RCA/LCx | ST depression V1–V3 |
| Anterolateral | I, aVL, V1–V6 | Proximal LAD | aVR, inferior leads |
STEMI equivalent patterns to recognise: New LBBB, De Winter T waves (upsloping ST depression with tall T waves in V1–V6 → proximal LAD occlusion), Wellens pattern (T-wave changes in V2–V3 indicating critical LAD stenosis), posterior STEMI with ST depression V1–V3 only.
Common Arrhythmias
Chaotic atrial activity replaces organised P waves. The irregularly irregular ventricular response is the hallmark. Rate varies 100–180 bpm in uncontrolled AF.
Re-entrant circuit in the right atrium produces “sawtooth” flutter waves at ~300 bpm. Commonly presents with 2:1 block (ventricular rate ~150 bpm — always suspect flutter at rate of 150).
Narrow complex regular tachycardia, typically 150–250 bpm. Usually AVNRT or AVRT. P waves often buried in or immediately after QRS. Responds to vagal manoeuvres or adenosine.
Wide complex tachycardia (>120ms QRS), rate typically 120–250 bpm. AV dissociation confirms VT. Fusion and capture beats are pathognomonic. If haemodynamically unstable — DC cardioversion immediately.
Chaotic ventricular activity with no coordinated contraction — cardiac arrest. Immediate CPR and defibrillation. Follow ALS algorithm.
Polymorphic VT with twisting QRS axis around the isoelectric line. Associated with prolonged QTc. Causes: drugs (antiarrhythmics, antipsychotics, antibiotics), hypokalaemia, hypomagnesaemia, congenital LQTS. Treat with IV magnesium 2g over 10 minutes.
Wide Complex Tachycardia — VT vs SVT with Aberrancy
Apply sequentially — answer YES = VT. Answer NO = proceed to next step.
- Absence of RS complex in all precordial leads? → YES = VT
- RS interval >100ms in any precordial lead? → YES = VT
- AV dissociation present? → YES = VT
- Morphology criteria for VT in V1 and V6? → YES = VT
- All above criteria absent → SVT with aberrancy
Remember: If in doubt, treat as VT. It is safer to treat SVT as VT than VT as SVT.
Further Resources
ECG interpretation improves with practice. The following resources are well-regarded for self-directed learning and clinical reference.
Comprehensive free ECG library with hundreds of annotated examples covering every pattern and pathology.
A detailed educational reference with systematic tutorials and example strips.
Recognition and management reference for resuscitation-relevant arrhythmias.
Official ALS guidelines including arrhythmia management algorithms.
In-depth educational content on ECG interpretation, echo, and exercise testing.
ESC clinical guidelines on arrhythmias, ACS, and heart failure.
Recommended Reading
- 📘 Dale Dubin — Rapid Interpretation of EKG’s — Classic introductory text. Clear and systematic.
- 📗 Hampton — The ECG Made Easy — Excellent UK-focused primer for clinical practice.
- 📙 Grauer — A Practical Guide to ECG Interpretation — Detailed, evidence-based reference.
- 📕 Wagner — Marriott’s Practical Electrocardiography — Comprehensive advanced reference.
This tutorial is provided for educational purposes. Clinical decisions should always be made in conjunction with appropriate senior review, clinical guidelines, and the full clinical context of the individual patient. For emergencies, follow your local resuscitation protocols.
