A Clinician‑Friendly Guide to Mastering EKG Interpretation
- Mayta
- 13 minutes ago
- 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.
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