I now have rich content from Harrison's and Kaplan & Sadock's to build a thorough, systematic ECG interpretation guide. Let me compile it all.
Systematic ECG Interpretation - A Guide for Residents
A well-organized approach prevents missed findings. Every ECG should be interpreted in a fixed sequence - never jump straight to the "interesting" part.
The 14-Parameter Systematic Approach (Harrison's, 22e)
Follow this sequence on every ECG:
- Standardization & technical features
- Rhythm
- Heart rate
- PR interval / AV conduction
- QRS interval
- QT / QTc interval
- Mean QRS electrical axis
- P waves
- QRS voltages
- Precordial R-wave progression
- Abnormal Q waves
- ST segments
- T waves
- U waves
Always compare with a previous ECG when available.
Step 1 - Standardization & Technical Features
Before reading anything, check:
- Paper speed: standard is 25 mm/s
- Gain/calibration: standard = 10 mm/mV (1 cm deflection = 1 mV). If the calibration box at the start of the strip is half-height, gain is halved - voltages will appear falsely low
- Lead placement errors: limb lead reversal (e.g., LA/RA swap) mimics dextrocardia; precordial misplacement distorts R-wave progression
- Artifact: muscle tremor (Parkinson's, shivering) mimics AF; AC interference gives a 60 Hz wobble
Step 2 - Rate
ECG paper basics:
- Small box = 0.04 s
- Large box = 0.20 s
- 5 small boxes = 1 large box
- 300 large boxes = 1 minute
Two methods:
| Method | Use when | Formula |
|---|
| Rate by squares | Regular rhythm | 300 ÷ (number of large boxes between R-waves) |
| QRS complexes per strip | Irregular rhythm (e.g., AF) | Count QRS complexes in 10-s strip × 6 |
Quick memorization table (large boxes between R-waves):
| Boxes | Rate |
|---|
| 1 | 300 |
| 2 | 150 |
| 3 | 100 |
| 4 | 75 |
| 5 | 60 |
| 6 | 50 |
- Bradycardia: HR < 60 bpm - think medications (beta-blockers, CCBs, digoxin, lithium), hypothyroidism, AV block, sick sinus syndrome, trained athletes
- Tachycardia: HR > 100 bpm - think pain, sepsis, PE, thyrotoxicosis, anticholinergic drugs, hypovolemia
Step 3 - Rhythm
Ask three questions:
-
Is the rhythm regular or irregular?
- Regular: measure R-R intervals (should all be equal)
- Irregularly irregular (no pattern) = classic AF
- Regularly irregular = consider Wenckebach, bigeminy
-
Is there a P wave before every QRS?
- Normal sinus: upright P in leads I, II, aVF; inverted in aVR
-
Does every P wave conduct to a QRS?
- If not: consider AV block
Normal sinus rhythm criteria:
- Rate 60-100 bpm
- P wave before every QRS, constant PR interval
- P wave axis 0-75° (upright in I and II)
Step 4 - PR Interval
- Normal: 120-200 ms (3-5 small boxes)
- Short PR (<120 ms): pre-excitation (WPW), junctional rhythm, ectopic atrial pacemaker
- Long PR (>200 ms): first-degree AV block
Step 5 - QRS Duration
- Normal: <120 ms (< 3 small boxes)
- 120-150 ms: incomplete bundle branch block, or subtle intraventricular conduction delay
- >120 ms: complete bundle branch block (RBBB or LBBB), ventricular paced rhythm, hyperkalemia
Bundle branch block quick rules:
| Feature | RBBB | LBBB |
|---|
| V1 | RSR' ("bunny ears") | Broad, deep QS or rS |
| V6 | Wide S wave | Broad, notched R, no S |
| Clinical hint | May be normal variant | Almost always pathological |
Step 6 - QT / QTc Interval
- Measured from start of QRS to end of T wave (best in lead II or V5)
- Must be corrected for heart rate because QT shortens as rate increases
- Bazett formula: QTc = QT / √RR (in seconds) - most common, used by ECG machines; overcorrects at fast rates
- Normal QTc: <440 ms in men, <460 ms in women
- Prolonged QTc (>500 ms): high risk for Torsades de Pointes (TdP)
Common causes of QT prolongation:
- Drugs: antipsychotics, TCAs, amiodarone, sotalol, certain antibiotics (azithromycin, fluoroquinolones)
- Electrolytes: hypokalemia, hypomagnesemia, hypocalcemia
- Congenital long QT syndrome
- Bradycardia, hypothyroidism, acute myocardial infarction
Step 7 - Electrical Axis
The axis represents the net direction of ventricular depolarization. Use leads I and aVF as perpendicular reference points:
| Lead I | aVF | Axis |
|---|
| Positive | Positive | Normal (-30° to +90°) |
| Negative | Positive | Right axis deviation (RAD) |
| Positive | Negative | Left axis deviation (LAD) |
| Negative | Negative | Extreme/"northwest" axis |
Causes:
| Deviation | Think of |
|---|
| LAD | LBBB, left anterior fascicular block, inferior MI, LVH, WPW (right-sided pathway) |
| RAD | RBBB, right ventricular hypertrophy, PE, lateral MI, WPW (left-sided pathway), dextrocardia |
Step 8 - P Waves
- Normal P: <120 ms wide, <2.5 mm tall, upright in I and II, biphasic or inverted in V1
- Peaked P in II (P pulmonale): >2.5 mm tall = right atrial enlargement (COPD, pulmonary HTN, tricuspid stenosis)
- Broad notched P (P mitrale): >120 ms with double hump in lead II = left atrial enlargement (mitral disease, LVH)
- Absent P waves: AF, sinoatrial block, junctional rhythm
- Retrograde P (inverted in II, III, aVF): junctional or low atrial rhythm
Step 9 - QRS Voltages
LVH criteria (Sokolow-Lyon):
- S in V1 + R in V5 or V6 >35 mm
RVH:
- Dominant R in V1 (R:S ratio >1)
- RAD
- R in V1 + S in V5/V6 >11 mm
Low voltage (QRS <5 mm in all limb leads OR <10 mm in all precordial leads):
- Obesity, emphysema, pericardial effusion, hypothyroidism, amyloidosis
Step 10 - Precordial R-wave Progression
- Normally, R waves grow from V1 (tiny) to V4-V5 (tallest), then decrease to V6
- Poor R-wave progression (PRWP): R waves fail to increase; consider anterior MI, LBBB, RVH, incorrect lead placement
- Transition zone (where R = S) normally at V3-V4; early transition (V1-V2) suggests posterior MI or RVH
Step 11 - Pathological Q Waves
- Normal septal Q waves: small (<40 ms, <25% of R height) in I, aVL, V5, V6
- Pathological Q: >40 ms wide OR >25% of R height in ≥2 contiguous leads
- Indicate prior transmural myocardial infarction
Localization by leads:
| Q waves in | Territory | Artery |
|---|
| II, III, aVF | Inferior | RCA |
| I, aVL | High lateral | Cx or diagonal |
| V1-V4 | Anteroseptal | LAD |
| V4-V6 | Anterolateral | LAD or Cx |
Step 12 - ST Segments
- Normal: isoelectric (at baseline), may have up to 1 mm variation
- ST elevation (STE): >1 mm in limb leads, >2 mm in precordial leads in 2+ contiguous leads
| ST Pattern | Causes |
|---|
| Concave-up elevation in all leads | Acute pericarditis (also PR depression) |
| Convex (domed/tombstone) elevation | STEMI |
| Saddle-shaped | Pericarditis, Brugada |
| ST depression | Ischemia (NSTEMI/UA), digoxin effect ("reverse tick"), reciprocal changes |
| ST elevation V1-V2 with RBBB-like pattern | Brugada syndrome |
Reciprocal ST depression in the leads opposite to the infarct territory is strong evidence for STEMI (not pericarditis).
Step 13 - T Waves
- Normal: upright in I, II, V3-V6; inverted in aVR; may be inverted in III, V1-V2
- Tall peaked T waves: hyperkalemia (early), hyperacute STEMI
- Deep symmetrical T inversion: ischemia (Wellens' syndrome in V2-V3 = critical LAD stenosis), PE (V1-V4), RVH
- Flattened T waves: non-specific but can indicate hypokalemia, digitalis effect, hypothyroidism
Step 14 - U Waves
- Small positive deflection after T wave, best seen in V2-V3
- Prominent U waves: hypokalemia (most common), bradycardia, hypomagnesemia
- Inverted U waves: significant - associated with LVH, ischemia
Key Clinical Patterns to Recognize Immediately
| Pattern | ECG Findings |
|---|
| STEMI | ST elevation + reciprocal depression, may evolve Q waves |
| NSTEMI / UA | ST depression, T inversion, or normal |
| Complete heart block | P waves and QRS with no relation (AV dissociation) |
| Atrial fibrillation | No P waves, irregularly irregular QRS, fibrillatory baseline |
| WPW | Short PR + delta wave + wide QRS |
| Hyperkalemia | Peaked T → wide QRS → sine wave → VF |
| Pulmonary embolism | Sinus tachycardia (most common), S1Q3T3, RBBB, RAD |
| Digoxin effect | Scooped ST ("reverse tick"), short QT, bradycardia |
Practical Tips for Residents
- Never read the computer interpretation uncritically - automated analysis has significant limitations and should always be reviewed
- Always get the clinical context first - a "normal ECG" in a patient with chest pain still warrants repeat ECGs and troponins
- Compare with old ECGs - a new LBBB or new Q wave changes everything
- Leads II, V1, V5 are your workhorses - rhythm in II, conduction in V1, ischemia in V5
- If the ECG looks "weird", check technical quality first - lead reversal and artifact account for many "abnormalities"
Sources: Harrison's Principles of Internal Medicine 22e (2025); Kaplan & Sadock's Comprehensive Textbook of Psychiatry; Tintinalli's Emergency Medicine; ROSEN's Emergency Medicine