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ECG (Electrocardiogram) — Complete Disease Notes

🔬 ECG Basics: What Each Wave Represents

Wave/Interval	Represents
P wave	Atrial depolarization (SA node → atria)
PR interval	AV node conduction delay (normal: 120–200 ms)
QRS complex	Ventricular depolarization (normal: <120 ms)
ST segment	Isoelectric phase between depolarization and repolarization
T wave	Ventricular repolarization
QT interval	Total ventricular electrical activity

The SA node fires → P wave → AV node delay → PR interval → Bundle of His → Bundle branches → Purkinje fibers → QRS → T wave repolarization. — Miller's Anesthesia, 10e

1. STEMI — ST-Elevation Myocardial Infarction

Diagnostic Criteria

ST elevation ≥ 1 mm in ≥ 2 contiguous limb leads or ≥ 2 mm in ≥ 2 contiguous precordial leads
New LBBB (treat as STEMI equivalent)
Hyperacute T waves (earliest sign — tall, peaked, broad-based)
Q waves develop within hours (pathological = >0.04 s wide, >25% R wave height)
ST morphology in STEMI: flat (horizontal/oblique) or convex/domed upsloping — not concave

Anatomical Localization

Territory	Leads with ST Elevation	Artery
Anterior	V1–V4	LAD (distal)
Anterolateral	V1–V6, I, aVL	LAD (proximal)
Inferior	II, III, aVF	RCA (80%) or LCx
Lateral	I, aVL, V5–V6	LCx
Posterior	ST depression V1–V3 + tall R in V1	RCA / LCx
Right Ventricular	V3R–V6R (right-sided leads)	RCA proximal

Clue for inferior MI from RCA: ST elevation in lead III > lead II + ST depression ≥1 mm in I and aVL.

Right ventricular infarction: Suspect when inferior STEMI is present + ST elevation in V1 or right-sided leads (V3R–V6R). Avoid nitrates/diuretics — depends on preload.

— Tintinalli's Emergency Medicine; Rosen's Emergency Medicine

Reciprocal Changes

Anterior STEMI → ST depression in inferior leads (II, III, aVF)
Inferior STEMI → ST depression in I, aVL
Posterior MI → ST depression V1–V3 (mirror-image)

2. NSTEMI / Unstable Angina

ECG Features

ST depression (horizontal or downsloping ≥ 0.5–1 mm) in ≥ 2 contiguous leads
T-wave inversions — classically narrow, symmetrical, with isoelectric or slightly elevated ST
Normal ECG does NOT exclude NSTEMI (present in up to 6% of patients)

Wellens Syndrome

A critical warning pattern indicating critical LAD stenosis:

Type I (Classic): Deep, symmetrical T-wave inversions in V2–V3 (occasionally V1–V6)
Type II: Biphasic T waves in V2–V3 (positive then negative deflection)
Other features: Minimal or no ST elevation (<1 mm), no precordial Q waves, pain-free at time of ECG
Natural history: Will progress to anterior wall STEMI if untreated
Caveat: T waves may normalize when pain recurs — repeat ECG during pain

— Rosen's Emergency Medicine; Tintinalli's Emergency Medicine

3. Differential Diagnosis of ST Elevation

Multiple conditions mimic STEMI — must differentiate clinically and electrocardiographically:

Cause	Key ECG Differentiator
STEMI	Flat/convex ST, regional leads, evolves with Q waves
Acute Pericarditis	Concave ST elevation, diffuse (all leads except aVR), PR depression (best in inferior leads + V6), PR elevation in aVR
Benign Early Repolarization (BER)	Concave ST, J-point notching, concordant large T waves, V2–V5, stable over time
LV Hypertrophy	ST elevation V1–V2 with strain pattern (asymmetrical T inversion), voltage criteria met
LBBB	Wide QRS, discordant ST changes (ST opposite to QRS direction)
LV Aneurysm	Persistent ST elevation in anterior leads with Q waves; no evolution
Hyperkalemia	Peaked T waves, wide QRS, flattened P, sine wave
Brugada Syndrome	Coved or saddle-back ST elevation V1–V2, RBBB pattern
Pulmonary Embolism	S1Q3T3, sinus tachycardia, new RBBB, T inversions V1–V4
Hypothermia (Osborn wave)	J-point elevation, Osborn (J) wave (positive deflection at J point)
Prinzmetal / Vasospastic Angina	Transient ST elevation during pain, resolves spontaneously
Post-cardioversion	Transient ST changes after electrical shock
Acute cerebral hemorrhage	Deep symmetrical T inversions, QT prolongation

— Rosen's Emergency Medicine, Table 64.3

4. Pericarditis

ECG Stages

Stage	ECG Finding	Timing
I	Diffuse concave ST elevation + PR depression	Hours–days
II	ST normalization, PR depression persists	Days
III	T-wave inversions (diffuse)	Weeks
IV	ECG normalizes	Weeks–months

Key features:

ST elevation is concave, diffuse (all leads except aVR, which shows ST depression)
PR segment depression — best seen in II, V6; PR elevation in aVR (pathognomonic when present, but insensitive)
No reciprocal ST changes (unlike STEMI)
No Q waves

5. Pulmonary Embolism (PE)

Classic ECG Pattern — S1Q3T3

S wave in lead I
Q wave in lead III
T-wave inversion in lead III
Sensitivity only ~20% — do not use to rule out PE
Other changes: sinus tachycardia (most common), new RBBB, T-wave inversions V1–V4, P pulmonale, right axis deviation

6. Hyperkalemia

Serum K+	ECG Change
5.5–6.5 mEq/L	Tall, peaked, narrow-based T waves (earliest sign)
6.5–7.5 mEq/L	PR prolongation, P wave flattening/disappearance
7.5–8.0 mEq/L	Wide QRS (>0.12 s), RBBB or LBBB pattern
>8.0 mEq/L	Sine wave pattern, ventricular fibrillation, asystole

Treatment: Calcium gluconate (membrane stabilization), insulin + dextrose, sodium bicarbonate, kayexalate/dialysis.

7. Hypokalemia

ST depression, flattened/inverted T waves
Prominent U waves (positive deflection after T wave, best seen V2–V3)
Prolonged QU interval (may appear as long QT)
Risk of torsades de pointes

8. Hypercalcemia vs. Hypocalcemia

Condition	ECG Change
Hypercalcemia	Short QT interval, short ST segment
Hypocalcemia	Prolonged QT interval (lengthened ST segment), risk of torsades

9. Arrhythmias

Sinus Rhythms

Rhythm	Rate	Key Feature
Normal Sinus Rhythm	60–100	P before every QRS, PR 120–200 ms, QRS <120 ms
Sinus Bradycardia	<60	Same morphology, slower rate
Sinus Tachycardia	>100	Same morphology, faster rate

Atrial Arrhythmias

Arrhythmia	Rate	Key ECG Feature
PAC	—	Premature P wave, different morphology, narrow QRS
Atrial Fibrillation	Ventricular 60–170	No P waves, irregularly irregular narrow QRS, fibrillatory baseline
Atrial Flutter	Atrial 300, Ventricular 150 (2:1)	Sawtooth flutter waves at 300 bpm, best in II, III, aVF
SVT (AVNRT)	150–250	Narrow QRS, P waves hidden in or just after QRS, regular
AVRT (WPW)	Variable	Short PR, delta wave, widened QRS (pre-excitation)
Multifocal Atrial Tachycardia (MAT)	>100	≥3 different P-wave morphologies, irregular

Ventricular Arrhythmias

Arrhythmia	Key ECG Feature
PVC	Wide (>120 ms), bizarre QRS, no preceding P wave, full compensatory pause
Ventricular Tachycardia (VT)	Wide QRS >120 ms at rate >100, AV dissociation, fusion beats, capture beats
Ventricular Fibrillation (VF)	Chaotic, no identifiable complexes — cardiac arrest
Torsades de Pointes	Twisting QRS around baseline, long QT preceding it
Accelerated Idioventricular	Wide QRS at 60–100 bpm, no P waves — seen in reperfusion

Heart Blocks

Block	PR Interval	Key Feature
1st Degree AV Block	>200 ms (>5 small squares)	Every P conducts, just slowly
2nd Degree Mobitz I (Wenckebach)	Progressive lengthening	PR gets longer until a beat is dropped; cycle repeats
2nd Degree Mobitz II	Fixed PR	Sudden non-conducted P without PR lengthening; often progresses to CHB
3rd Degree (Complete) AV Block	No relationship	P waves and QRS dissociated; escape rhythm (junctional = narrow, ventricular = wide)

Bundle Branch Blocks:

RBBB: Wide QRS + RSR' ("rabbit ears") in V1 + wide S in I, V6 — can be normal variant
LBBB: Wide QRS + broad notched R in V5/V6, no septal Q in I/V6, ST-T discordant — always pathological when new

10. WPW (Wolff-Parkinson-White) Syndrome

Short PR (<120 ms)
Delta wave (slurred upstroke of QRS)
Wide QRS (>120 ms)
Risk of rapid conduction to ventricles in AF → VF
Avoid AV nodal blockers (digoxin, verapamil, adenosine) in WPW + AF — may accelerate accessory pathway conduction → VF

11. Brugada Syndrome

Type 1 (diagnostic): ≥2 mm coved (downsloping) ST elevation in ≥1 of V1–V2 with RBBB pattern
Type 2: Saddle-back ST elevation (may convert to Type 1 with Na-channel blockers)
Risk of sudden cardiac death (VF) — treat with ICD
ECG may be dynamic — unmasked by fever, flecainide, ajmaline

12. Long QT Syndrome

QTc (corrected) > 440 ms (men), >460 ms (women) — at risk for torsades de pointes
Congenital: Romano-Ward (AD), Jervell-Lange-Nielsen (AR + deafness)
Acquired causes: Drugs (class Ia/III antiarrhythmics, macrolides, antipsychotics, antihistamines), hypokalemia, hypomagnesemia, hypocalcemia

13. Right Ventricular Hypertrophy (RVH)

Right axis deviation (>+100°)
Tall R in V1 (R > S in V1)
Deep S in V5/V6
T-wave inversion in V1–V3 (strain pattern)
P pulmonale (peaked P >2.5 mm in II) — suggests right atrial enlargement

14. Left Ventricular Hypertrophy (LVH)

Voltage criteria (most common):

Sokolow-Lyon: S in V1 + R in V5 or V6 > 35 mm
Cornell: R in aVL + S in V3 > 28 mm (men) / 20 mm (women)
Associated strain: ST depression + asymmetrical T inversion in lateral leads (I, aVL, V5–V6)

15. Pulmonary Hypertension

ECG changes develop late in the course of disease:

RVH pattern (see above)
Right axis deviation
P pulmonale
RBBB
ST-T changes in right precordial leads

— Murray & Nadel's Respiratory Medicine

16. Hypothermia

Osborn (J) wave: Positive deflection at the J-point (junction of QRS and ST), best seen in II and V5–V6 — pathognomonic
Sinus bradycardia, AF, prolonged PR/QRS/QT
Muscle tremor artifact
Asystole/VF risk at <28°C

17. Digoxin Toxicity / Effect

Feature	ECG Finding
Digoxin effect (therapeutic)	"Scooped"/sagging ST depression, T-wave changes, shortened QT
Digoxin toxicity	Bradycardia, AV blocks (any degree), accelerated junctional, bidirectional VT (classic)

18. Tricyclic Antidepressant (TCA) Overdose

Wide QRS (>100 ms = significant toxicity, >160 ms = severe — VT/seizure risk)
Tall R in aVR (>3 mm) — sensitive for toxicity
Sinus tachycardia (anticholinergic), QT prolongation
Treatment: Sodium bicarbonate (narrows QRS by alkalinizing)

Quick Summary: "The Big 5" ECG Emergencies to Recognize

Emergency	Key ECG Sign
STEMI	Regional ST elevation with flat/convex morphology
Hyperkalemia	Peaked T waves → wide QRS → sine wave
VT	Wide regular tachycardia with AV dissociation
Complete Heart Block	P-QRS dissociation with slow escape
WPW + AF	Irregular rapid wide-complex tachycardia

Sources: Rosen's Emergency Medicine, 9e; Tintinalli's Emergency Medicine; Miller's Anesthesia, 10e; Murray & Nadel's Respiratory Medicine; Goldman-Cecil Medicine, 27e; Harrison's Principles of Internal Medicine, 22e; Fuster & Hurst's The Heart, 15e

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