How to Read an ECG: Expert Guide

1. The Physiology Behind Every Waveform

"The ECG is a measurement of tiny potential differences on the surface of the body that reflect the electrical activity of the heart." - Costanzo Physiology, 7th Ed.

1. SA node fires → atria depolarize
2. Impulse delays at AV node (allows atrial emptying)
3. Bundle of His → bundle branches → Purkinje fibers → ventricular depolarization
4. Ventricles repolarize

2. The Waveforms, Intervals, and Segments

P Wave

• Represents atrial depolarization
• Normal: upright in leads I, II, aVF; duration < 120 ms; amplitude < 0.25 mV
• Atrial repolarization is "buried" inside the QRS complex, so it's not visible
• Broadened P wave = slowed atrial conduction (e.g., left atrial enlargement, interatrial block)
• Absent P waves = atrial fibrillation

PR Interval

• From onset of P to onset of QRS
• Represents total conduction time from SA node through AV node to the ventricles
• Normal: 120-200 ms (3-5 small boxes)
• Short PR (<120 ms): pre-excitation (WPW syndrome), junctional rhythm
• Prolonged PR (>200 ms): first-degree AV block
• Progressive lengthening then dropped beat: Wenckebach (Mobitz I)
• Fixed prolonged PR with dropped beats: Mobitz II
• No relationship between P and QRS: complete (third-degree) AV block

QRS Complex

• Represents ventricular depolarization
• Q wave: first negative deflection (small Q waves are normal in I, aVL, V5-V6; pathological Q = >40 ms wide or >25% of R height)
• R wave: first positive deflection
• S wave: negative deflection after R
• Normal duration: 60-100 ms (<3 small boxes); >120 ms = bundle branch block
• Despite ventricles being much larger than atria, QRS duration ≈ P wave duration because the His-Purkinje conduction velocity is far faster than atrial conduction

ST Segment

• From end of QRS (J-point) to onset of T wave
• Represents the early ventricular repolarization plateau phase
• Normally isoelectric (flat, on the baseline)
• ST elevation: transmural ischemia/infarction, pericarditis, Brugada, LV aneurysm
• ST depression: subendocardial ischemia, reciprocal changes, digoxin effect

T Wave

• Represents ventricular repolarization
• Normal: upright in I, II, V3-V6; inverted in aVR; may be inverted in III, aVL, V1
• Peaked T waves: hyperkalemia, hyperacute STEMI
• Inverted T waves: ischemia, ventricular hypertrophy strain pattern, pulmonary embolus

QT Interval

• From onset of QRS to end of T wave
• Represents total ventricular depolarization + repolarization time
• Must be corrected for heart rate: QTc = QT / √(RR interval)
• Normal QTc: < 440 ms in men, < 460 ms in women
• Prolonged QTc: risk of torsades de pointes; caused by drugs, electrolyte abnormalities (hypokalaemia, hypomagnesaemia, hypocalcaemia), congenital long QT syndromes

U Wave

• Small, positive deflection after T wave, best seen in V2-V3
• Often normal; prominent U waves = hypokalaemia

3. The 12-Lead System: What Each Lead "Sees"

ECG Paper Calibration

• Horizontal axis: 0.04 s per small box, 0.2 s per large box (5 small boxes)
• Vertical axis: 0.1 mV per mm (standard calibration)
• 5 large boxes = 1.0 second

The 10 Electrodes Produce 12 Views

Lead Groupings by Coronary Territory

4. Systematic Approach: Never Miss Anything

Step 1 - Rate

• 1 box = 300 bpm; 2 = 150; 3 = 100; 4 = 75; 5 = 60; 6 = 50

• Normal: 60-100 bpm
• Bradycardia: <60 bpm
• Tachycardia: >100 bpm

Step 2 - Rhythm

1. Where is the pacemaker? (Is there a P wave before each QRS?)
2. Is conduction normal? (Is PR interval fixed and normal?)
3. Is the rate regular? (Are R-R intervals equal?)

Step 3 - P Wave

• Present? Upright in II? One P per QRS?
• Duration and morphology

Step 4 - PR Interval

• Measure first lead with a clear P wave
• Fixed or variable?

Step 5 - QRS Complex

• Duration (narrow < 120 ms, wide ≥ 120 ms)
• Morphology in each lead group
• Bundle branch block patterns
• Pathological Q waves?

Step 6 - Axis

Step 7 - ST Segment

• Elevation or depression?
• Which leads? (Localizes territory)
• Shape: concave (pericarditis/early repol) vs convex/tombstone (STEMI)?
• Reciprocal depression in opposite leads strongly supports STEMI

Step 8 - T Waves

• Upright or inverted?
• Symmetric inversion = ischemia or Wellens pattern
• Peaked T waves = hyperkalemia or hyperacute MI

Step 9 - QT Interval

• Calculate QTc
• Prolonged? (risk of arrhythmia)

5. Key Patterns You Must Know

Bundle Branch Blocks

• QRS ≥ 120 ms
• RSR' ("rabbit ears") in V1
• Wide, slurred S wave in I, aVL, V5-V6
• Remember: "WiLLiaM MaRRoW" (LBBB: W in V1, M in V6; RBBB: M in V1, W in V6)

• QRS ≥ 120 ms
• Broad, notched R in I, aVL, V5-V6 (M-shaped)
• No Q in V5-V6
• Secondary ST and T wave changes opposite to QRS
• New LBBB with chest pain = treat as STEMI equivalent

ST-Segment Elevation MI (STEMI)

"Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential. When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone."

1. Hyperacute T waves (minutes)
2. ST elevation (hours)
3. Q wave formation + T wave inversion (hours to days)
4. ST normalizes; Q waves persist (days to weeks)
5. Permanent Q waves = marker of old infarct

Hypertrophy Patterns

• Sokolow-Lyon: S in V1 + R in V5 or V6 > 35 mm
• Cornell: R in aVL + S in V3 > 28 mm (men) or > 20 mm (women)
• Left axis deviation
• Strain pattern: ST depression and T wave inversion in I, aVL, V5-V6
• Cause: hypertension (most common), aortic stenosis, HOCM

• Right axis deviation
• R/S > 1 in V1
• R/S < 1 in V5-V6
• Strain pattern in right precordial leads
• Causes: pulmonary hypertension, PE, congenital heart disease

Arrhythmia Recognition

• Absent P waves replaced by irregular fibrillatory baseline
• Irregularly irregular QRS
• Ventricular rate typically 100-180 if uncontrolled

• Sawtooth flutter waves at ~300 bpm in II, III, aVF
• Usually 2:1 conduction → ventricular rate ~150 bpm
• Regular or regularly irregular rhythm

• Narrow QRS tachycardia, rate 150-250 bpm
• P waves either absent or retrograde (after QRS)
• Abrupt onset and termination

• Wide QRS (>120 ms) tachycardia, rate >100 bpm
• AV dissociation (P waves independent of QRS) = definitive for VT
• Fusion beats and capture beats = pathognomonic of VT
• If wide complex tachycardia: assume VT until proven otherwise

• P waves and QRS complexes at different, regular rates
• P-P interval regular; R-R interval regular; NO relationship between them
• QRS may be narrow (junctional escape) or wide (ventricular escape)

Pulmonary Embolism Pattern: S1Q3T3

• S wave in lead I
• Q wave in lead III
• T wave inversion in lead III
• Also: sinus tachycardia (most common), RBBB, right axis deviation, right heart strain

Pericarditis

• Diffuse (saddle-shaped) ST elevation in multiple territories simultaneously
• PR depression (characteristic)
• No reciprocal ST changes (unlike STEMI)
• No Q waves

Hyperkalemia (Potassium Toxicity)

6. Normal Intervals and Values Reference

7. R Wave Progression in the Precordial Leads

8. Expert Tips

1. Always confirm lead placement - misplaced electrodes are the #1 cause of diagnostic errors
2. Compare with prior ECGs - change over time is often more informative than a single tracing
3. Never read an ECG in isolation - always correlate with clinical context
4. Wide complex tachycardia = VT until proven otherwise - never assume SVT with aberrancy in an undifferentiated patient
5. New LBBB with chest pain = STEMI equivalent - call the cath lab
6. Check for Brugada - coved ST elevation in V1-V2 can be easily missed; look for it in syncope and resuscitated cardiac arrest
7. Wellens syndrome - biphasic or deep symmetric T wave inversions in V2-V3 in a pain-free patient = critical LAD stenosis, do NOT stress test
8. Rate-correct your QT - a "normal" QT at slow rates may be dangerously prolonged at faster rates

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