Here is your complete, professor-pleasing ECG guide - sourced from Harrison's 22e, Goldman-Cecil Medicine, Braunwald's Heart Disease, and The Washington Manual.
π The Complete ECG Guide for Clinical Medical Students
PART 1 - ECG Basics: The Paper, Leads & Waves
The ECG Paper
- Standard speed: 25 mm/sec
- Each small square = 1 mm = 0.04 sec (40 ms)
- Each large square = 5 mm = 0.20 sec (200 ms)
- Amplitude standard: 10 mm = 1 mV
The 12 Leads - What They "See"
| Lead Group | Leads | Territory |
|---|
| Inferior | II, III, aVF | Inferior wall (RCA) |
| Lateral | I, aVL, V5, V6 | Lateral wall (LCx) |
| Anterior (septal) | V1, V2 | Septum (LAD) |
| Anterior | V3, V4 | Anterior wall (LAD) |
| Right ventricular | V1 (+ V3R, V4R) | RV |
- aVR is the "mirror" lead - normally negative
- Precordial lead placement: V1 right sternal border 4th ICS; V2 left sternal border 4th ICS; V3-V6 progressing laterally (see diagram below)
(Harrison's 22e, Fig. 247-5 - Horizontal plane (chest/precordial) lead placement)
The Normal ECG Waveform - A to Z
R
|
P | T U
/\ | /\ /\
--/ \----|--------/ \-------/ \-- (baseline)
|\ /
| \ /
| \ /
| \/
S
|--PR--|--QRS--|--ST--|----QT----|
| Component | What it represents | Normal values |
|---|
| P wave | Atrial depolarization | Duration < 120 ms; amplitude < 2.5 mm; positive in I, II, aVF |
| PR interval | AV conduction time (atria β AV node β His-Purkinje) | 120-200 ms (3-5 small squares) |
| QRS complex | Ventricular depolarization | < 120 ms (< 3 small squares) |
| ST segment | Early ventricular repolarization (isoelectric normally) | Flat at baseline |
| T wave | Ventricular repolarization | Upright in I, II, V3-V6; inverted normally in aVR, V1 |
| QT interval | Total ventricular repolarization | < 440 ms (men), < 460 ms (women); correct with Bazett: QTc = QT/βRR |
| U wave | After-depolarization of Purkinje fibers | Upright, small; prominent in hypokalemia |
Key professor tip: The T wave is normally opposite in polarity to the QRS only in bundle branch blocks (secondary change). If the T wave goes the "wrong way" in a normal QRS, it is a PRIMARY repolarization abnormality (ischemia, electrolytes, drugs). - Harrison's 22e
Heart Rate Calculation
- Regular rhythm: 300 Γ· number of large squares between R-R peaks
- 1 large square = 300 bpm, 2 = 150, 3 = 100, 4 = 75, 5 = 60, 6 = 50
- Irregular rhythm: Count QRS complexes in a 10-second strip Γ 6
QRS Axis (Frontal Plane)
- Normal: -30Β° to +90Β°
- Left axis deviation (LAD): more negative than -30Β° β most common cause is left anterior fascicular block
- Right axis deviation (RAD): more positive than +90Β° β RVH, PE, left posterior fascicular block
- Quick trick:
- Lead I positive + aVF positive = normal axis
- Lead I positive + aVF negative = LAD
- Lead I negative + aVF positive = RAD
- Both negative = "Northwest" / extreme axis
R-Wave Progression (Precordial Leads)
- R wave normally grows from V1 to V5 (transition at V3-V4 where R = S)
- Poor R-wave progression (small r waves persisting through V4) = anterior MI or LVH
- Diagram of ventricular depolarization vectors:
(Harrison's 22e, Fig. 247-6 - Two phases of ventricular depolarization. Phase 1: septal, right to left β small r in V1, small q in V6. Phase 2: LV-dominant, leftward/posterior β deep S in V1, tall R in V6)
PART 2 - The Systematic Approach (14 Steps - Harrison's)
Every ECG should be read in this order - professors love this:
- Standardization/calibration (10mm = 1mV, 25mm/sec)
- Rhythm (sinus vs. non-sinus)
- Heart rate
- PR interval / AV conduction
- QRS duration
- QT/QTc interval
- Mean QRS electrical axis
- P wave morphology
- QRS voltages
- R-wave progression (precordial)
- Abnormal Q waves
- ST segments
- T waves
- U waves
Always compare with prior ECGs when available. - Harrison's 22e, "Clinical Interpretation of the ECG"
PART 3 - Arrhythmias
Bradyarrhythmias
Sinus Bradycardia: Rate < 60 bpm, normal P-QRS-T morphology
AV Blocks
| Block | ECG Feature | Location | Danger |
|---|
| 1st Degree | PR > 200 ms, no dropped beats | AV node | Benign |
| 2nd Degree Mobitz I (Wenckebach) | Progressively lengthening PR β dropped QRS; "group beating"; RR shortens before dropped beat | AV node (proximal) | Usually benign, rarely progresses |
| 2nd Degree Mobitz II | Fixed PR interval, then sudden dropped QRS with no warning | His-Purkinje (distal) | DANGEROUS - may progress to complete block |
| 3rd Degree (Complete) | P waves and QRS completely dissociated; atrial rate > ventricular rate | AV node or infranodal | EMERGENCY - needs pacing |
(Washington Manual, Fig. 7-5: A=1st degree AVB, B=Mobitz I, C=Mobitz II, D=2:1 block, E=Complete heart block with junctional escape)
Key teaching point: 2:1 block is difficult to classify as Mobitz I vs II. Narrow QRS + concomitant first-degree block = likely Mobitz I (proximal). Wide QRS + bundle branch block = likely Mobitz II (distal, dangerous). - Washington Manual
Tachyarrhythmias
Narrow Complex (QRS < 120 ms) = Supraventricular
| Rhythm | Key ECG Features |
|---|
| Sinus Tachycardia | Rate 100-160, normal P before every QRS, gradual onset/offset |
| Atrial Fibrillation (AF) | Irregularly irregular; NO distinct P waves; fibrillatory baseline; ventricular rate variable |
| Atrial Flutter | "Sawtooth" flutter waves at ~300/min; regular ventricular rate (usually 150 = 2:1 block); most common ratio 2:1 |
| SVT (AVNRT) | Sudden onset/termination; rate 150-250; P waves hidden in or just after QRS |
Professor pearl: AF is the most common sustained arrhythmia after sinus tachycardia. It is an "irregularly irregular" rhythm - no two R-R intervals are the same. - Tintinalli's EM
ECG strip showing sinus tachycardia, rapid AF, 2:1 atrial flutter, AF, and return to sinus rhythm during exercise stress test:
(Braunwald's Heart Disease, Fig. 65.9)
Wide Complex (QRS β₯ 120 ms)
| Rhythm | Key Features |
|---|
| Ventricular Tachycardia (VT) | Rate >100, wide QRS, AV dissociation (P waves march through independently), fusion beats, capture beats |
| VF | Totally chaotic, no identifiable QRS - EMERGENCY |
| SVT with aberrancy | Wide complex SVT (BBB pattern), but history/maneuvers help distinguish from VT |
Rule of thumb: Wide complex tachycardia = VT until proven otherwise.
PART 4 - Bundle Branch Blocks
Diagnosis requires QRS β₯ 120 ms (3 small squares)
Right Bundle Branch Block (RBBB)
- rSR' ("rabbit ears" or M-pattern) in V1
- Wide S wave in I, V5, V6
- T-wave inversion in V1-V3 (secondary change, expected)
- Can be normal variant OR indicate RV strain, PE, congenital heart disease
Left Bundle Branch Block (LBBB)
- Broad, notched R wave ("W"-shaped in V1, "M"-shaped in V5/V6)
- No septal q waves in lateral leads (I, V5, V6)
- T-wave inversion in V5, V6 (secondary, expected)
- LBBB in a chest pain patient = treat as STEMI equivalent (it hides ischemia and is an independent risk marker)
- Isolated LBBB in an otherwise healthy person carries 2Γ increased cardiovascular risk
Mnemonic:
- WiLLiaM MaRRoW: W in V1 = LBBB (Left); M in V1 = RBBB (Right)
- Or: LBBB = "Leave the patient" (more dangerous); RBBB = "Reassure" (usually benign)
(Goldman-Cecil Medicine, "Intraventricular Blocks")
PART 5 - Myocardial Ischemia and Infarction
Mechanism (Why ECG Changes Occur)
Acute ischemia lowers resting membrane potential and shortens action potential duration β voltage gradient between normal and ischemic zones β currents of injury β ST deviation. - Harrison's 22e
Evolutionary Changes in STEMI
| Stage | ECG Finding |
|---|
| Hyperacute (minutes) | Tall, broad, peaked "hyperacute" T waves |
| Early (hours) | ST elevation at J point |
| Established | ST elevation + Q wave formation |
| Old (hours-days) | T-wave inversion; Q waves persist |
| Chronic | Persistent Q waves (scar), T waves may normalize |
Localization of MI by Lead Groups
| Leads with ST Elevation | Territory | Culprit Artery |
|---|
| II, III, aVF | Inferior | RCA (80%) |
| V1-V4 | Anterior/Septal | LAD |
| I, aVL, V5-V6 | Lateral | LCx |
| V1-V2 (tall R + ST depression) | Posterior | RCA / LCx |
| V1 + inferior leads (ST elevation in V3R, V4R) | Right Ventricle | Proximal RCA |
NSTEMI / Unstable Angina
- ST depression (subendocardial ischemia) or T-wave inversion
- No ST elevation, but troponin distinguishes NSTEMI (elevated) from UA (normal)
Wellens Syndrome (professor favourite!)
- Deeply inverted or biphasic T waves in V2-V3 in a pain-FREE patient
- Indicates critical LAD stenosis - do NOT stress test!
De Winter T Waves
- ST depression + tall peaked T waves in V1-V6 = proximal LAD occlusion equivalent (STEMI variant - needs cath lab)
PART 6 - Other High-Yield ECG Patterns
LVH (Left Ventricular Hypertrophy)
- Sokolow-Lyon criteria: S in V1 + R in V5 or V6 β₯ 35 mm
- R in aVL β₯ 11 mm (Cornell criterion)
- Often associated with "strain pattern" (ST depression + T inversion in lateral leads)
RVH (Right Ventricular Hypertrophy)
- Tall R in V1 (R > S in V1)
- Right axis deviation
- ST depression + T inversion in V1-V3
Pericarditis
- Diffuse ST elevation (saddle-shaped, concave upward) in multiple lead groups (not fitting one territory)
- PR depression (reciprocal PR elevation in aVR) - pathognomonic early sign
- No reciprocal ST depression (vs. STEMI)
Pulmonary Embolism (PE)
- Sinus tachycardia (most common, ~44%)
- S1Q3T3 pattern: deep S in lead I, Q wave + T inversion in lead III
- New RBBB, right axis deviation
- T inversions in V1-V4 (RV strain)
Hyperkalemia
- Peaked/tented T waves (early)
- Wide QRS (later)
- Flat/absent P waves
- Sine-wave pattern β VF (severe)
Hypokalemia
- Prominent U waves (larger than T in same lead)
- T-wave flattening
- Prolonged QT
- Risk of torsades de pointes
Hypercalcemia / Hypocalcemia
- Hypercalcemia: Short QT (short ST segment)
- Hypocalcemia: Long QT (prolonged ST segment)
Long QT Syndrome
- QTc > 440 ms (men), > 460 ms (women)
- Risk of torsades de pointes (polymorphic VT) β VF β sudden death
- Causes: congenital channelopathies, drugs (amiodarone, sotalol, quinolones, antipsychotics), electrolyte disturbance (βK, βMg, βCa)
Wolff-Parkinson-White (WPW)
- Short PR interval (< 120 ms)
- Delta wave (slurred upstroke of QRS)
- Wide QRS
- Due to accessory pathway (Bundle of Kent) bypassing AV node
Brugada Syndrome
- Coved-type ST elevation in V1-V2 (right chest leads)
- RBBB pattern
- Risk of sudden cardiac death - important channelopathy
PART 7 - The "Things That Impress a Professor" Checklist
When presenting an ECG to your professor, say ALL of these:
- "I will use a systematic approach..." (then use the 14-step Harrison's method)
- Always state rate, rhythm, axis, intervals first
- Describe P waves: "present/absent, morphology, relation to QRS"
- Know the difference between primary vs. secondary ST-T changes
- In any wide-complex tachycardia: "This is VT until proven otherwise"
- In any new LBBB with chest pain: "This is a STEMI equivalent"
- Know reciprocal changes (ST depression in leads opposite to ST elevation) - confirms STEMI
- State the "territory and likely culprit artery" for any ischemic pattern
- Mention QTc (corrected QT), not just QT
- With AV blocks: always classify (1st/2nd Mobitz I or II/3rd) and state the clinical risk
Quick-Reference Summary Card
| Normal Value | Number to Know |
|---|
| PR interval | 120-200 ms |
| QRS duration | < 120 ms |
| QTc (men) | < 440 ms |
| QTc (women) | < 460 ms |
| Normal axis | -30Β° to +90Β° |
| LVH (Sokolow) | S-V1 + R-V5/6 β₯ 35 mm |
| STEMI threshold | β₯ 1 mm ST elevation in 2 contiguous leads (β₯ 2 mm in V1-V3) |
| Complete BBB | QRS β₯ 120 ms |
| AF flutter rate | ~300/min atrial, ~150/min ventricular (2:1) |
Sources: Harrison's Principles of Internal Medicine 22e (2025) - "Clinical Interpretation of the ECG"; Goldman-Cecil Medicine International Edition, 2 Vol Set - "Conduction Abnormalities" & "Intraventricular Blocks"; Braunwald's Heart Disease, 2 Vol Set - "Resting Electrocardiogram"; The Washington Manual of Medical Therapeutics - "AV Conduction Disturbances"; Tintinalli's Emergency Medicine - "Atrial Fibrillation/Flutter"