Structured Approach to ECG Interpretation

Basic Principles of the 12-Lead ECG

An electrocardiogram (ECG) captures the electrical activity of the heart from multiple viewpoints to help identify, localize, and quantify pathology. A so-called “12-lead” ECG actually uses 10 adhesive electrodes placed on the patient’s limbs and chest; the ECG machine combines pairs of these electrodes electrically to produce 12 graphical leads on paper/screen.

Anatomy of a Normal ECG Cycle

P wave – atrial depolarization (atrial contraction). A healthy tracing shows one P wave before every QRS.
PR interval – onset of P to onset of Q; reflects atrioventricular (AV) conduction time.
- Normal: $120\,\text{–}\,200\,\text{ms}$ (3–5 small squares).
QRS complex – ventricular depolarization; appears as Q, R, and S deflections.
- Normal width: <0.12\,\text{s} (3 small squares).
ST segment – isoelectric line from end of S to start of T; reflects early ventricular repolarization.
T wave – ventricular repolarization; normally a modest upright deflection after QRS.
QT interval – start of QRS to end of T; time for full ventricle depolarization → repolarization.
U wave – small, infrequent upright deflection after T; accentuated in severe bradycardia, electrolyte imbalance, hypothermia, or certain anti-arrhythmic drugs.

Pre-Interpretation Safety Checks

Verify patient name and date of birth match the ECG.
Note date & exact time of recording.
Confirm calibration (standard paper speed $25\,\text{mm s}^{-1}$ and amplitude $10\,\text{mm mV}^{-1}$ unless stated otherwise).
Clarify clinical context: Why was the ECG obtained? Symptoms (chest pain, dyspnoea, palpitations, syncope) guide interpretation priorities.

Step 1 – Heart Rate

Normal resting rate: $60\text{–}100\,\text{beats·min}^{-1}$ .

Tachycardia > $100\,\text{b·min}^{-1}$ .
Bradycardia < $60\,\text{b·min}^{-1}$ .

Two calculation methods:

RR-interval method (regular rhythms):
\text{HR} = \frac{300}{\text{# large squares between successive R peaks}}
• Example: 7 large squares → $\text{HR}=\tfrac{300}{7}\approx48\,\text{b·min}^{-1}$ .
10-s rhythm-strip method (irregular rhythms):
• Standard rhythm strip = 50 large squares = $10\,\text{s}$ .
• \text{HR} = (\text{# QRS complexes in 10 s}) \times 6.
• Example: 11 complexes → $11\times6=66\,\text{b·min}^{-1}$ .

Step 2 – Rhythm Regularity

• Regular? Spacing of RR intervals constant.
• Regularly irregular (predictable pattern) vs Irregularly irregular (totally disorganized, e.g., atrial fibrillation).
• Practical assessment: mark three consecutive RR distances on scrap paper, “march” along strip to see if spacing recurs.

Step 3 – Cardiac Axis

The axis describes the net direction of ventricular depolarization in the frontal plane.

Normal: $-30^{\circ}\text{ to }+90^{\circ}$ .

Interpretation shortcut:

Lead I positive & Lead II positive ⇒ Normal axis.
Lead I negative, aVF positive / Lead III positive ⇒ Right axis deviation (RAD) $+90^{\circ}\text{ to }+180^{\circ}$ .
- Common cause: right-ventricular hypertrophy (e.g., pulmonary hypertension); may be normal in very tall people.
Lead I positive, Lead II negative & Lead III negative ⇒ Left axis deviation (LAD) $-30^{\circ}\text{ to }-90^{\circ}$ .
- Causes: left-ventricular hypertrophy, left anterior fascicular block, inferior MI.

Conceptual rules:
• Depolarization toward a lead → tall positive R.
• Depolarization away from a lead → predominantly negative (QS).

Step 4 – P Waves (Atrial Activity)

Questions:

Are P waves present?
Is every P followed by a QRS?
Morphology: duration, amplitude, shape, polarity.
If absent, is there alternative atrial activity?
- Saw-tooth baseline ⇒ atrial flutter.
- Chaotic baseline ⇒ atrial fibrillation.
- Flat baseline ⇒ sino-atrial arrest or junctional rhythm.

Step 5 – PR Interval & AV Conduction Blocks

Normal $120\text{–}200\,\text{ms}$ .

5.1 First-Degree AV Block

PR consistently > $200\,\text{ms}$ .
Each P still followed by QRS.
Usually benign incidental finding.

5.2 Second-Degree AV Block

Type I (Mobitz I, Wenckebach)

Progressive PR prolongation → non-conducted P (dropped QRS) → cycle repeats.
Usually arises in AV node; seldom symptomatic.

Type II (Mobitz II)

PR interval normal or constant; intermittent dropped QRS (e.g., 3:1 or 4:1 pattern).
Pathological (His-Purkinje disease). High risk of progression to complete block → warrants investigation ± pacing.

5.3 Third-Degree (Complete) AV Block

No relationship between P waves & QRS complexes; atria & ventricles beat independently (AV dissociation).

5.4 Shortened PR & Pre-Excitation (Wolff-Parkinson-White)

Accessory pathway (bundle of Kent) bypasses AV node → premature ventricular activation.
ECG triad:
1. Short PR.
2. Slurred delta upstroke of QRS.
3. Wide QRS.
Predisposes to paroxysmal tachyarrhythmias (AVRT, AF with rapid conduction).

Step 6 – QRS Complex Assessment

Parameters to scrutinize:

Width: Broad > $0.12\,\text{s}$ suggests aberrant conduction (bundle branch block, ventricular ectopy).
Height:
- Small: <5 mm in limb leads OR <10 mm in precordial leads (may reflect obesity, COPD, effusion).
- Tall: can indicate ventricular hypertrophy (but also common in tall, thin habitus).
Morphology: delta wave? Fragmentation? Pathological Q waves (≥1 mm wide & ≥2 mm deep or >25 % of ensuing R – suggest prior MI).

6.1 Bundle Branch Blocks – “William–Marrow” Mnemonic

Inspect V1 and V6:

Left BBB (WiLLiaM) – V1 shows “W” (deep/notched S), V6 shows “M” (broad notched R).
Right BBB (MaRRoW) – V1 shows “M” (RSR′), V6 shows “W” (broad/slurred S).
Both produce QRS ≥ $0.12\,\text{s}$ .

Step 7 – ST Segment Abnormalities

• In health, ST is isoelectric.

7.1 ST Elevation

Clinically significant:
- ≥1 mm (1 small square) in ≥2 contiguous limb leads OR
- ≥2 mm in ≥2 contiguous precordial leads.
Commonest cause: acute transmural MI (ST-elevation MI, STEMI).
Benign early repolarization (“high take-off”) is a normal variant—usually concave, widespread, stable.

7.2 ST Depression

≥0.5 mm in ≥2 contiguous leads implies ischemia (e.g., non-STEMI, demand ischemia) or reciprocal change.

7.3 Territory Localisation

Inferior: II, III, aVF (right coronary or circumflex).
Anterior: V3–V4 (LAD).
Septal: V1–V2.
Lateral: I, aVL, V5–V6.
Linking ST elevation pattern to coronary anatomy guides acute reperfusion therapy.

Step 8 – T Wave Analysis

• Tall / peaked – hyperkalaemia, early STEMI hyper-acute phase.
• Inversion – may be normal in aVR & V1 (± III, V2, V3). New widespread inversion → consider ischemia, myocarditis, pulmonary embolism.

Step 9 – U Waves

>0.5 mm deflection after T (seen best V2–V3).
Accentuated with bradycardia, hypokalaemia, hypothermia, anti-arrhythmics (digoxin, amiodarone).

Documentation Checklist

Patient ID, DOB.
Time & date of ECG.
Objective findings: rate, rhythm, axis, intervals, morphology, ST/T/U changes.
Impression (diagnosis) & immediate plan (e.g., “Irregularly irregular AF at 102 bpm – anticoagulation work-up”).

Case Study Walkthrough

Given strip (10 s): 17 QRS complexes → $17\times6 = 102\,\text{b·min}^{-1}$ (mild tachycardia).

Rhythm: irregularly irregular with no pattern; absent P waves.

Axis: leads I & II positive ⇒ normal.

Intervals/morphology: QRS narrow, ST/T normal.

Synthesis: Atrial fibrillation with ventricular rate ≈102 bpm.

Practical, Ethical & Exam Tips

• Always correlate ECG findings with clinical presentation—never treat the tracing in isolation.
• An incorrect ECG label can lead to treatment of the wrong patient; verify identity before acting.
• In exams, vocalise the structured steps; it earns “method” marks even if final diagnosis is wrong.
• For ABG, CXR, echo, and serial ECG correlation, consider timeline of MI evolution (hyperacute T → ST elevation → Q wave formation).
• Recognise normal variants (early repolarization, athlete’s heart) to avoid over-diagnosis.

Quick Reference Formulae

$\text{HR} = \frac{300}{\text{No. large squares}}$ (regular)
$\text{HR} = (\text{No. QRS in 10 s}) \times 6$ (irregular)

PR normal: $120\text{–}200\,\text{ms}$
QRS normal: <120\,\text{ms}
QT normal (rough rule): QT_c < 440\,\text{ms (male)}, <460\,\text{ms (female)} (Bazett-corrected).