Competency-based and progressive: foundational electrophysiology through advanced clinical pattern recognition, weighted toward the conditions where reading the tracing right changes what happens to the patient. Recommended training volume: ≥500 ECG interpretations (COCATS 4 Level I). Tap any module to expand.
The ECG is the sum of millions of action potentials projected onto the skin. One rule explains every deflection: depolarization toward a lead reads up, away reads down.
Action potential — 5 phases
- 0 — rapid depolarization: Na⁺ influx in working myocytes; Ca²⁺ influx in nodal cells.
- 1 — early repolarization (K⁺ efflux).
- 2 — plateau (Ca²⁺ in balances K⁺ out); the long refractory period unique to cardiac cells — stops tetany.
- 3 — repolarization (K⁺ efflux dominates).
- 4 — resting −90 mV; pacemaker cells slope upward here (automaticity).
Conduction hierarchy (intrinsic rates)
Fastest pacemaker wins (overdrive suppression); lower sites are backups. The AV node's built-in delay = the PR segment, and it's your drug target in narrow-complex SVT. Sympathetic → ↑rate/conduction/contractility; vagal → ↓SA rate, ↓AV conduction.
Standardize before you interpret. Wrong paper speed, bad calibration, or a swapped lead manufactures pathology that isn't there.
Grid & calibration
Intervals to own
Limb leads (I, II, III, aVR, aVL, aVF) view the frontal plane; precordials (V1–V6) the horizontal. Einthoven: lead II = lead I + lead III. P = atrial depolarization (upright II, inverted aVR); QRS = ventricular depolarization; T = repolarization; U = late repolarization (tall in hypokalemia).
Normal variants that fake disease
Early repolarization (concave ST elevation, notched J point, young/healthy), persistent juvenile T inversions, vagal effects.
Run the same five steps on every tracing, every time. The disciplined read is how you catch the quiet killer hiding behind the obvious finding.
1 · Rate
Count big boxes between R waves: 300 – 150 – 100 – 75 – 60 – 50. Slow/irregular → QRS in a 6-second strip ×10.
2 · Rhythm
Regular? A P before every QRS and a QRS after every P? An upright P in lead II = sinus origin.
3 · Axis — read leads I and aVF
| Pattern | Lead I | aVF |
|---|---|---|
| Normal | up | up |
| LAD (confirm w/ II) | up | down |
| RAD | down | up |
| Extreme | down | down |
4 · Intervals · 5 · Morphology
Intervals: PR, QRS, QT. Morphology: chamber size, ST/T changes, pathologic Q waves.
A bigger chamber writes a bigger, odder deflection. Read the P wave in II and V1 for the atria; read QRS voltage for the ventricles.
Atria
- Left (LAA) — wide notched "M" P ≥120 ms in II = P mitrale; deep, wide (≥1 mm, ≥40 ms) negative terminal in V1.
- Right (RAA) — tall peaked P >2.5 mm in II = P pulmonale; initial positive >1.5 mm in V1.
Ventricles — voltage criteria
LVH strain: asymmetric ST depression / T inversion in lateral leads (I, aVL, V5–6). RVH: R>S in V1, right axis deviation, RAA, ± RV strain (V1–3) — think pulmonary HTN / cor pulmonale.
Low-voltage differential — "fat, fluid, air, infiltrate": obesity, pericardial effusion, COPD, hypothyroidism, amyloid.
Supraventricular = narrow QRS. The P wave — its shape, count, or absence — is the entire diagnosis.
- Sinus rhythm — upright P in II, one per QRS, 60–100. Sinus arrhythmia (rate varies with breathing) is normal in the young.
- AFib — irregularly irregular, no organized P waves, fibrillatory baseline. The #1 board buzzword.
- Atrial flutter — sawtooth F waves (~300/min), usually 2:1 → ventricular ~150. A regular SVT at exactly 150? Suspect flutter.
- MAT — ≥3 distinct P-wave morphologies, rate >100, irregular. Classic in COPD/hypoxia.
- Atrial tach with AV block — think digitalis toxicity.
When the SA node fails or a re-entry circuit fires, the junction runs the show: narrow QRS with P waves absent, inverted, or retrograde.
| AVNRT | AVRT | |
|---|---|---|
| Circuit | within AV node | accessory pathway (WPW) |
| Frequency | most common SVT (~60%) | orthodromic 90% (narrow) / antidromic 10% (wide, mimics VT) |
| Clue | pseudo-r′ in V1, pseudo-S inferiorly | retrograde P after QRS (short RP) |
Narrow-complex workup: regular or irregular first (irregular → AFib / MAT / flutter with variable block). For regular SVT, vagal maneuvers / adenosine either break AVNRT/AVRT or transiently block the node to unmask flutter.
Wide QRS (≥120 ms) from a ventricular focus. The safe default: assume VT until proven otherwise.
- PVCs — wide, bizarre, early, no preceding P, usually a full compensatory pause. Bigeminy / trigeminy / couplets; unifocal vs multifocal.
- AIVR — regular wide rhythm at 50–100; classic during reperfusion after MI — benign and self-limited.
- VT — ≥3 consecutive ventricular beats >100. Monomorphic (scar) vs polymorphic (ischemia/channelopathy). Sustained ≥30 s or unstable.
- Torsades — polymorphic VT on a long QT, twisting around baseline → magnesium.
- VF — chaotic, no QRS → defibrillate.
VT vs SVT-with-aberrancy → favors VT
AV dissociation, capture beats, fusion beats, precordial concordance, QRS >160 ms, prior MI. Vereckei: an initial R wave in aVR → VT.
The PR interval and the pattern of dropped beats tell you where the block sits and how dangerous it is. Location decides urgency.
| Block | Signature | Level / Risk |
|---|---|---|
| 1st degree | PR >200 ms, every P conducts | Benign |
| Mobitz I | PR lengthens → drop (PR after drop is shortest) | AV-nodal · benign |
| Mobitz II | Constant PR → sudden drop, often wide QRS | Infranodal · pace |
| 3rd degree | P's and QRS's independent, atrial > ventricular | Pace |
2:1 block can't be typed from one strip: narrow QRS → likely nodal (I); wide QRS → likely infranodal (II). 3rd-degree escape sets survival — junctional (narrow, 40–60) vs ventricular (wide, 20–40).
A wide QRS (≥120 ms) from a slow detour through the ventricle. Look at V1 and V6 to name the block.
| RBBB — MaRRoW | LBBB — WiLLiaM | |
|---|---|---|
| V1 | rSR′ "rabbit ears" (M) | deep QS (W) |
| V6 | wide slurred S (W) | broad notched R, no septal Q (M) |
| Meaning | often benign | always pathologic; discordant ST-T |
Fascicular blocks: LAFB → left axis (−45° to −90°), qR in aVL, rS inferiorly, QRS <120; LPFB → right axis (rarer). WPW: short PR (<120 ms), delta wave, wide QRS, secondary ST-T changes.
The ST segment is the headline: elevation = injury/occlusion, depression and T-inversion = ischemia. Localize by lead group and always hunt for reciprocal change.
Ischemic cascade
Hyperacute T (tall, broad, symmetric) → ST elevation (convex / "tombstone") → T-wave inversion → pathologic Q (>40 ms wide or >25% of R height).
STEMI criteria (4th Universal Definition) — STE in ≥2 contiguous leads
| Territory | Leads | Artery |
|---|---|---|
| Anterior/septal | V1–V4 | LAD |
| Lateral | I, aVL, V5–V6 | LCx / diagonal |
| Inferior | II, III, aVF | RCA (85%) / LCx |
| Posterior | ST↓ V1–V3 (mirror); STE V7–9 ≥0.5 mm | RCA / LCx |
| Right ventricle | STE in V4R | proximal RCA |
Equivalents not to miss
- Wellens — biphasic (Type A) or deep symmetric (Type B) T inversions in V2–V3 while pain-free → critical proximal LAD. Do NOT stress test; cath.
- de Winter — upsloping ST depression >1 mm with tall symmetric T waves (± STE in aVR) → acute LAD occlusion. Treat as STEMI.
- Posterior MI — isolated ST↓ V1–V3; get V7–V9.
Sgarbossa (MI in LBBB / paced)
Concordant STE ≥1 mm (most specific) · concordant ST↓ ≥1 mm V1–3 · discordant STE ≥5 mm. Modified: replace the 5 mm rule with ST/S ratio ≥25% (sensitivity 52% → 91%).
Pericarditis vs STEMI
| Pericarditis | STEMI | |
|---|---|---|
| ST shape | concave "smiley" | convex / straight |
| Distribution | diffuse | regional (territory) |
| Reciprocal | absent (except aVR) | present |
| PR segment | depressed | normal |
The ECG is a window onto chemistry and drug levels. A handful of these patterns are genuinely can't-miss.
Electrolytes
- Hyperkalemia (progressive): peaked narrow T (5.5–6.5) → PR prolongation, P flattening, QRS widening (6.5–7.5) → loss of P, sine wave (7+) → VF/asystole. QRS widens at both ends (unlike BBB).
- Hypokalemia — ST depression, flat T, prominent U waves (V2–3), long QU; risk of torsades.
- Calcium — high Ca → short QT; low Ca → long QT. Calcium tweaks the ST segment; potassium tweaks the T wave.
Drugs
Digitalis effect = scooped "Salvador Dalí" ST sagging (therapeutic); toxicity = atrial tach with block, bidirectional VT, accelerated junctional. QT-prolongers (class IA/III, macrolides, fluoroquinolones, antipsychotics, methadone) → torsades. TCA overdose → sinus tach, wide QRS, terminal R in aVR >3 mm.
Disease patterns
Pericarditis: diffuse concave STE + PR depression, Spodick sign (downsloping TP). PE / cor pulmonale: sinus tach is most common; classic S1Q3T3, RV strain (TWI V1–4). Brugada: Type 1 coved STE ≥2 mm V1–3. Long QT: QTc >500 = high torsades risk (LQT1 exercise, LQT2 auditory, LQT3 sleep). HCM: LVH + deep narrow "dagger" Q waves. Hypothermia: Osborn (J) waves. CNS/SAH: deep "cerebral" T inversions + long QT. Dextrocardia: inverted P/QRS in I, reverse R progression.
Find the pacing spikes, then ask two questions: is each spike producing a beat (capture), and is the device seeing the heart (sensing)?
NBG code
Position 1 chamber Paced · 2 chamber Sensed · 3 Response (I/T/D) · 4 rate modulation (R). VVI = ventricle paced+sensed, inhibited. DDD = dual everything. CRT/BiV = biventricular for HF with LBBB. A paced ventricular beat looks like LBBB (RV apical pacing).
Malfunction
- Failure to capture — spike present, no complex follows.
- Undersensing — spikes fire despite native beats (doesn't "see" them).
- Oversensing — inappropriately inhibited by T waves / myopotentials → pauses.
- Failure to pace — no spike when one is needed.
Ambulatory monitoring (match duration to symptom frequency)
A real 12-lead appears — make the call. You get the answer and the one-line teaching point after each, then your score at the end. Same patterns, fresh order every time.
Inferior = bottom leads = floor of the heart = RCA feeds there
Reciprocal: I and aVL go DOWN when II/III/aVF go up · V4R = get it every time
Anterior leads V1-V4 = LAD territory = anterior wall of LV = highest mortality
Proximal LAD → huge territory → cardiogenic shock risk · Watch for new LBBB
Pain-free patient + deep inverted T waves in V2-V3 = reperfused critical LAD stenosis
Type A = biphasic · Type B = deep symmetric inversion (more common, ~75%)
Upsloping ST depression + tall symmetric T waves = static pattern = active proximal LAD occlusion
No ST elevation ever · aVR may show STE · Immediate cath lab activation
No P waves + chaotic baseline + variable R-R = AFib every time
Rate control vs rhythm control · CHA₂DS₂-VASc drives anticoagulation · DOAC preferred
Atria beat at ~75 bpm · Ventricles escape at ~30–40 bpm · No relationship between them
Junctional escape = narrow QRS (40–60) · Ventricular escape = wide QRS (20–40, worse prognosis)
MaRRoW: In RBBB — M-shape in V1, W-shape in V6
New RBBB in anterior STEMI = proximal LAD occlusion, worse prognosis · Isolated RBBB may be normal
LBBB: W-shape in V1 (QS pattern), M-shape in V6 (broad notched R) · Always pathologic
Discordant ST changes expected in LBBB — use Sgarbossa criteria to identify superimposed STEMI
Pericardial effusion → heart swings like a pendulum → electrical axis rotates each beat → alternating QRS height
Sinus tachycardia + electrical alternans = tamponade until proven otherwise · Give fluids, call surgery
The reflex reads, the can't-miss moves, and the buzzword associations — the points-per-minute payoff of any ECG review, pulled into one place.
- Irregularly irregular, no P waves → atrial fibrillation
- Regular narrow tachy at ~150 → atrial flutter (2:1)
- Regular narrow tachy 150–250, abrupt → AVNRT
- Wide-complex tachycardia → VT (esp. prior MI / structural disease)
- Peaked T waves in a renal patient → hyperkalemia
- Electrical alternans + sinus tach → effusion / tamponade
- Inferior STEMI → V4R before nitrates (RV infarct)
- New LBBB + ischemic pain → Sgarbossa; STEMI-equivalent
- AFib + WPW → procainamide / cardiovert; no AV-nodal blockers
- Torsades → IV magnesium
- Mobitz II / complete block → pacing
- Wellens → no stress test, urgent cath
- de Winter → treat as acute LAD occlusion
- Hyperkalemia w/ ECG changes → IV calcium first
- Sawtooth waves → atrial flutter
- Short PR + delta wave → WPW
- S1Q3T3 → pulmonary embolism
- Osborn (J) waves → hypothermia
- Scooped "Salvador Dalí" ST → digitalis effect
- Deep narrow "dagger" Q waves → HCM
- Coved ST elevation V1–V3 → Brugada
- Prominent U waves → hypokalemia
The highest-priority patterns every PA/MD student must recognize on sight. The ones in red are the can't-miss, time-critical reads.