A Clinician‑Friendly Guide to Mastering EKG Interpretation

Mayta
May 4
4 min read

1. What an ECG Really Records

An electrocardiogram is a time‑stamped graph of the heart’s changing electrical vector as impulses leave the sinus node, traverse the atria, pause in the AV node, sweep the His‑Purkinje network, and depolarise and repolarise the ventricular muscle. Twelve leads—six in the frontal plane (limb leads I, II, III, aVR, aVL, aVF) and six in the horizontal plane (chest leads V1‑V6)—watch that same field from different angles. Whenever the current moves toward a positive electrode, the stylus deflects upward; movement away produces a downward deflection.

2. Recording the Trace Correctly

Electrode placement

Limb leads: right arm, left arm, left leg (right leg is ground).
Chest leads
- V1  4th intercostal space, right sternal edge
- V2  4th intercostal space, left sternal edge
- V3  Midway V2‑V4
- V4  5th intercostal, left mid‑clavicular line
- V5  Same level as V4, anterior axillary
- V6  Same level as V4, mid‑axillary
- Right‑sided leads (V3R, V4R) mirror V3/V4 on the right for suspected RV infarct.

Paper & calibration

Speed: 25 mm/sec → 1 small box = 0.04 s, 1 large box = 0.20 s.
Voltage: 1 mV = 10 mm (two large squares).
Always confirm the calibration pulse and speed before reading.

3. Anatomy of the ECG Waveform

Wave / Segment	What it represents	Normal limits
P	Atrial depolarisation	≤ 0.12 s, ≤ 2.5 mm tall
PR interval	Atria → AV node delay	0.12‑0.20 s
QRS	Ventricular depolarisation	0.06‑0.10 s
ST	Early ventricular repolarisation	Baseline or ≤ 1 mm shift (limb), ≤ 2 mm (chest)
T	Ventricular repolarisation	Upright in I, II, V3‑V6; height ≤ 5 mm limb, ≤ 10 mm chest
QTc	Total depolarisation + repolarisation	≤ 0.44 s
U	Final repolarisation of Purkinje fibres	< 0.2 mV, best in V2‑V4

(Table shown for clarity—no grid formatting is used.)

4. A 10‑Step Reading Sequence

Rhythm – Is it sinus? If P before every QRS and regular, likely yes.
Rate – see Section 5.
P wave – shape, duration, enlargement.
PR interval – prolonged = first‑degree AV block; short ± delta = pre‑excitation.
QRS width – narrow vs wide (BBB, WPW, VT).
QRS axis & morphology – deviation, hypertrophy, pathological Qs.
ST segment – elevation, depression, morphology.
T wave – polarity, height, symmetry.
QT / QTc – prolonged or short.
U wave – prominent in hypokalaemia.

Work systematically every time; it prevents missed diagnoses.

5. Heart‑Rate Calculation—Three Practical Methods

Method 1: 1500 ÷ small boxes

Count the number of small boxes between two adjacent R waves and divide 1500 by that number.

Method 2: “Large‑box sequence”

Starting at an R wave on a heavy line, label the next heavy lines 300, 150, 100, 75, 60, 50.
Where the next R lands gives the approximate rate.
- 1 large box → 300 bpm
- 2 large boxes → 150 bpm
- 3 large boxes → 100 bpm
- 4 large boxes → 75 bpm
- 5 large boxes → 60 bpm
- 6 large boxes → 50 bpm (bradycardia).

Method 3: 5‑second count (the “table method”)

The standard trace marks a 5‑second span every 25 large boxes.
Simply count the number of complete QRS complexes in that 5‑second window and multiply by 12 to yield beats‑per‑minute.
Advantage: works with irregular rhythms such as atrial fibrillation.

6. Normal Waveforms in Detail

P wave

Upright in I, II, V4‑V6 and aVF; inverted aVR; variable III/aVL/V1‑V2.
Left atrial enlargement (P mitrale): broad, notched P ≥ 0.12 s.
Right atrial enlargement (P pulmonale): tall, peaked P ≥ 2.5 mm.

PR interval

Prolonged > 0.20 s: first‑degree block, trifascicular disease, some drugs, hyperthyroidism.
Short < 0.12 s: WPW (with delta wave), LGL, junctional rhythms.

QRS complex

Axis
- Lead I + and aVF + → normal (0° to +90°)
- Lead I – / aVF + → right axis (> +90°)
- Lead I + / aVF – with lead II – → left axis (< −30°)
- Lead I – / aVF – → indeterminate
Voltage: > 5 mm limb and > 10 mm chest leads is normal.
R‑wave progression: R roughly equals S in V3‑V4 (transition zone).

ST segment

Should be flat. Up‑ or down‑sloping ≥ 1 mm suggests injury or ischemia. Concave elevation in many leads with PR depression suggests pericarditis.

T wave

Normally concordant with QRS polarity in that lead.
Tall symmetrical T: hyperkalaemia, early MI, early repolarisation.
Deep symmetrical inversion: ischaemia, intracranial bleed, LVH strain.

QT interval

Corrected (QTc) = QT / √RR (seconds).
Prolonged predisposes to torsades.
Shortened (< 0.30 s) seen with hypercalcaemia, digitalis, rare congenital syndromes.

U wave

Prominent, same polarity as T in hypokalemia.

7. Abnormalities Every Clinician Must Recognise

Low‑voltage QRS

Limb amplitudes < 5 mm or chest < 10 mm can signal effusion, obesity, COPD, amyloidosis, myxoedema.

Chamber hypertrophy

LVH
- S in V1 + R in V5/6 > 35 mm, or R in aVL > 11 mm.
- “Strain” pattern: ST depression/T‑wave inversion in lateral leads.
RVH
- Tall R in V1 (> S), right axis.
Biventricular
- LVH voltage plus RVH criteria or right axis deviation.

Bundle branch blocks

RBBB
- rSR′ (“rabbit ears”) in V1‑V2, slurred S in I/V6, QRS ≥ 0.12 s.
LBBB
- Broad notched R in I/V6, deep S in V1‑V2, secondary ST‑T inversion.

Axis deviation

Left (> −30°): LVH, inferior MI, LAFB, LBBB, hyperkalaemia.
Right (> +90°): RVH, pulmonary disease, LPFB, RBBB, dextrocardia.

Acute coronary syndromes

ST‑elevation MI (transmural)
- Hyperacute T ➜ convex ST elevation ➜ Q waves and T inversion ➜ ST returns to baseline, Q persists.
- Location by leads:
  - Septal V1‑V2
  - Anterior V3‑V4
  - Anterolateral V3‑V6 + I, aVL
  - Inferior II, III, aVF
  - Posterior: reciprocal tall R in V1‑V2 plus ST depression.
Reciprocal changes: ST depression and tall T opposite the infarct area.

Pericarditis

Diffuse concave ST elevation plus PR depression, no reciprocal depression, no Q.

Early repolarisation

Young adults: J‑point notch and mild concave elevation, stable over time.

Digitalis effect

“Scooped” sagging ST depression with flattened T in leads that have tall R.

Electrolytes

Hyperkalaemia: tall peaked T, then widened PR/QRS, sine wave, asystole.
Hypokalaemia: flat T, ST depression, prominent U.
Hypercalcaemia: shortened QT.
Hypocalcaemia / hypomagnesaemia: prolonged QT.

QT syndromes

Prolonged QT: congenital, many drugs, electrolyte deficits, MI, CNS events.
Short QT: congenital, hypercalcaemia, digitalis toxicity, severe hyperkalemia.

8. Miscellaneous Pitfalls to Avoid

Electrode misplacement (e.g., swapping V1 & V2) can mimic septal MI or T‑wave inversions.
Pseudo‑infarct Q waves appear in LBBB, WPW, hypertrophic cardiomyopathy, pulmonary embolism.
“Tall R in V1” differential: RBBB, RVH, WPW, posterior MI, normal variant.
S1Q3T3 pattern plus sinus tachycardia suggests acute pulmonary embolism.

9. Putting It All Together – A Mental Checklist

Clinical context first – ECG changes mean little without the story.
Apply the 10‑step sequence – never skip steps even if the tracing looks normal.
Compare with old ECGs – new LBBB in chest‑pain patient is an emergency.
Repeat if odd – many “abnormal” findings vanish after re‑attaching leads.
Act on life‑threats immediately – wide‑complex tachycardia, STEMI, hyperkalaemia.

Final Thought

Every ECG is a three‑second physiology lesson. Reading it well comes from pattern recognition built on systematic analysis anchored in sound electrophysiology. Follow the sequence, correlate with the patient, and practise daily—you will soon interpret tracings with speed, safety, and confidence.