All ECG Findings

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Here is a comprehensive reference of all major ECG findings, organized systematically for clinical interpretation.

All ECG Findings — Comprehensive Reference

🔬 Systematic Approach to ECG Reading

Always read an ECG in this order: Rate → Rhythm → Axis → Intervals → P waves → QRS → ST segment → T waves → U waves → Special waves

1. RATE

Finding	Value	Significance
Normal sinus rate	60–100 bpm	Normal
Sinus bradycardia	< 60 bpm	Vagal tone, athletes, hypothyroidism, β-blockers, sick sinus syndrome
Sinus tachycardia	> 100 bpm	Pain, fever, sepsis, hypovolemia, hyperthyroidism, PE, anxiety

2. RHYTHM

Normal

Normal Sinus Rhythm (NSR): Regular P waves before every QRS, rate 60–100 bpm, PR 120–200 ms

Atrial Arrhythmias

Rhythm	ECG Features	Causes
Sinus arrhythmia	P-wave morphology normal; R-R varies with breathing	Normal variant (especially young)
Atrial premature complex (APC)	Early P wave with abnormal morphology	Caffeine, stress, structural heart disease
Atrial tachycardia	P waves present, rate 150–250 bpm, abnormal P morphology	Digoxin toxicity, structural disease
Multifocal atrial tachycardia (MAT)	≥3 distinct P-wave morphologies, irregular, rate >100	COPD, electrolyte imbalance
Atrial flutter	Sawtooth flutter waves (~300 bpm) in II, III, aVF; ventricular rate typically 150 bpm (2:1 block)	Structural disease, post-cardiac surgery
Atrial fibrillation (AF)	Absent P waves, irregularly irregular rhythm, fibrillatory baseline	HTN, valvular disease, thyrotoxicosis, alcohol, HF

AV Block (Heart Block)

Block	PR Interval	Dropped QRS?	Notes
1st degree	Fixed, > 200 ms	No	Benign; ↑ vagal tone, inferior MI, digoxin
2nd degree – Mobitz I (Wenckebach)	Progressive lengthening → dropped QRS	Yes, periodically	Usually benign; below AV node
2nd degree – Mobitz II	Fixed PR, intermittent dropped QRS (2:1, 3:1)	Yes	Serious; below Bundle of His → risk of complete block
3rd degree (Complete)	P waves and QRS completely dissociated	Yes (all)	Junctional/ventricular escape rhythm; emergency

Ventricular Arrhythmias

Rhythm	ECG Features	Significance
PVC (premature ventricular complex)	Wide, bizarre QRS, no preceding P wave, compensatory pause	Common; if frequent or R-on-T → malignant
Ventricular tachycardia (VT)	Wide QRS (>120 ms), rate >100, AV dissociation, fusion/capture beats	Life-threatening
Ventricular fibrillation (VF)	Chaotic, irregular deflections; no organized waveforms	Cardiac arrest
Torsades de pointes	Twisting QRS axis around baseline; long QT preceding	Drug-induced, electrolyte disorders
Accelerated idioventricular rhythm (AIVR)	Wide QRS 40–100 bpm, no P waves	Post-reperfusion, benign
Asystole	Flat line; no P waves or QRS	Cardiac arrest

Pre-excitation Syndromes

Finding	Features	Cause
WPW (Wolff-Parkinson-White)	Short PR (<120 ms), delta wave (slurred QRS upstroke), wide QRS	Accessory pathway (Bundle of Kent) → risk of AF with rapid conduction

3. CARDIAC AXIS

Axis	Lead I	Lead aVF	Causes
Normal (-30° to +90°)	Positive	Positive	Normal
Left axis deviation (LAD) (> -30°)	Positive	Negative	LBBB, LAFB, inferior MI, LVH
Right axis deviation (RAD) (> +90°)	Negative	Positive	RBBB, RVH, PE, LPFB, lateral MI
Extreme axis (NW axis)	Negative	Negative	VT, severe RVH, artifact

4. P WAVE ABNORMALITIES

Finding	Features	Cause
P mitrale	Wide (>120 ms), bifid (notched) P in lead II; negative terminal component in V1	Left atrial enlargement (e.g., mitral stenosis)
P pulmonale	Tall (>2.5 mm), peaked P in II, III, aVF	Right atrial enlargement (e.g., COPD, tricuspid stenosis, RVH)
Absent P waves	No visible P waves	AF, junctional rhythm, hyperkalemia (severe)
Retrograde P waves	P negative in II, III, aVF; follows QRS	Junctional tachycardia

5. PR INTERVAL

Finding	Duration	Cause
Normal	120–200 ms	—
Short PR (<120 ms)	<120 ms	WPW, LGL syndrome, junctional rhythm
Prolonged PR (>200 ms)	>200 ms	1st degree AV block, digoxin, inferior MI

6. QRS COMPLEX

Duration / Width

Finding	Duration	Features	Cause
Narrow QRS	< 120 ms	Normal conduction	—
RBBB (Right Bundle Branch Block)	≥ 120 ms	RSR' (M-shape/"bunny ears") in V1; wide S in I, V6	Pulmonary embolism, RVH, congenital, ischemia
LBBB (Left Bundle Branch Block)	≥ 120 ms	Broad, notched R in I, aVL, V5–V6; deep S/QS in V1; T-wave discordance	IHD, cardiomyopathy, hypertension; may mask STEMI
LAFB (Left anterior fascicular block)	Normal	LAD, small Q in I/aVL, small R in III	Common; usually benign
LPFB (Left posterior fascicular block)	Normal	RAD, small R in I/aVL, small Q in III	Rarer; associated with extensive MI

Amplitude / Morphology

Finding	Features	Cause
Low voltage	QRS amplitude < 5 mm in all limb leads, < 10 mm in precordial leads	Pericardial effusion, obesity, COPD, amyloidosis, hypothyroidism
Electrical alternans	Alternating QRS axis/amplitude	Large pericardial effusion/tamponade
Pathological Q waves	> 25% of R wave height, ≥ 40 ms wide	Prior MI (transmural infarction), LBBB, WPW
Poor R-wave progression (PRWP)	Failure of R wave to grow V1→V4	Anterior MI, LBBB, RVH, COPD
LVH (Left ventricular hypertrophy)	S in V1 + R in V5 or V6 ≥ 35 mm (Sokolow-Lyon); tall R in aVL ≥ 11 mm	Hypertension, AS, HCM
RVH (Right ventricular hypertrophy)	R > S in V1; RAD; deep S in V6	Pulmonary HTN, COPD, PS, ASD
Delta wave	Slurred initial QRS upstroke	WPW
Epsilon wave	Small positive deflection at end of QRS in V1–V3	Arrhythmogenic right ventricular cardiomyopathy (ARVC)
J wave (Osborn wave)	Positive deflection at J-point (junction of QRS and ST)	Hypothermia (pathognomonic), Brugada
Fragmented QRS (fQRS)	Notching/slurring of QRS in ≥2 contiguous leads	Myocardial fibrosis/scar, prior MI

7. ST SEGMENT

Finding	Features	Cause
ST elevation (STE)	Convex (tombstone) morphology in contiguous leads ≥1 mm	STEMI, vasospasm (Prinzmetal), LV aneurysm
Inferior STEMI	STE in II, III, aVF + reciprocal STD in I, aVL	RCA or LCx occlusion
Anterior STEMI	STE in V1–V4	LAD occlusion
Lateral STEMI	STE in I, aVL, V5–V6	LCx, diagonal branch occlusion
Posterior MI	STD in V1–V3 (= reciprocal); tall R in V1–V2	LCx/RCA (posterior territory)
ST depression (STD)	Horizontal or downsloping ≥ 0.5 mm	Subendocardial ischemia/NSTEMI, digoxin effect (reverse tick), LVH strain
Saddle-shaped (concave) STE	Diffuse, saddle-shaped ST elevation in most leads (not just contiguous)	Pericarditis
Brugada pattern	Coved-type (type 1) STE with RBBB morphology in V1–V2	Brugada syndrome (VF risk)
Early repolarization	Concave STE + J-point notching, most prominent V2–V5	Normal variant (young, athletic males); occasionally malignant
de Winter T waves	Upsloping STD + tall, symmetric T waves in V1–V6 (without STE)	Proximal LAD occlusion equivalent

8. QT INTERVAL

Finding	QTc	Cause
Normal QTc	350–440 ms (♂), 350–460 ms (♀)	—
Prolonged QT (QTc > 440/460 ms)	> 440 ms ♂, > 460 ms ♀	Drugs (amiodarone, sotalol, haloperidol, azithromycin, quinolones, TCA), hypokalemia, hypomagnesemia, hypocalcemia, congenital LQTS → risk of Torsades
Short QT (QTc < 360 ms)	< 360 ms	Hypercalcemia, hyperkalemia, acidosis, hyperthermia, Short QT syndrome, digoxin

9. T WAVE ABNORMALITIES

Finding	Features	Cause
Normal T wave	Upright in I, II, V3–V6; inverted in aVR; variable in III, aVL, V1–V2	—
Tall/peaked T waves	> 5 mm in limb leads, > 10 mm in precordial	Hyperkalemia (early/tent-shaped), hyperacute MI, vagotonia
Inverted T waves	Downward deflection (in leads where normally upright)	Ischemia/NSTEMI, PE (V1–V4), RVH (V1–V3), cardiomyopathy, CNS events (deep symmetric inversion), RBBB, digoxin
Wellens syndrome T waves	Deep symmetric T inversions (type A: biphasic) or (type B: deeply inverted) in V2–V3	Critical proximal LAD stenosis (pre-infarction pattern)
Flat T waves	Non-specific	Ischemia, hypokalemia, LVH strain
Biphasic T waves	Two-phase deflection	Ischemia, hypokalemia, Wellens

10. U WAVES

Finding	Features	Cause
Normal U wave	Small positive deflection after T wave, best in V2–V3	Purkinje fiber repolarization
Prominent U waves	Tall U waves > T wave	Hypokalemia (classic), hypomagnesemia, bradycardia, digoxin, amiodarone
Inverted U waves	Negative U	Ischemia, LVH

11. ELECTROLYTE & METABOLIC PATTERNS

Condition	ECG Pattern
Hyperkalemia	Peaked T waves → widened QRS → sine-wave pattern → asystole/VF
Hypokalemia	Flattened T waves, prominent U waves, ST depression, long QU interval
Hypercalcemia	Short QT interval, shortened ST segment
Hypocalcemia	Long QT (prolonged ST segment)
Hypomagnesemia	Long QT, Torsades de pointes
Hypermagnesemia	Prolonged PR, widened QRS, heart block
Hypothyroidism	Sinus bradycardia, low voltage, prolonged QT, flat T waves
Hypothermia	Osborn (J) waves, sinus bradycardia, slow AF, long QT
Digoxin effect	Reverse-tick (scooped) ST depression, short QT, flat T waves
Digoxin toxicity	PAT with block, bidirectional VT, AV block, junctional tachycardia

12. SPECIAL CONDITIONS / SYNDROMES

Syndrome	Hallmark ECG Finding
Brugada syndrome	Type 1: coved STE ≥ 2 mm in V1–V2 with RBBB pattern; fever-induced
ARVC	Epsilon wave in V1–V3, T inversions in right precordial leads, LBBB-morphology VT
Long QT syndrome (LQTS)	QTc > 500 ms; Torsades de pointes
Short QT syndrome	QTc < 320 ms; peaky symmetric T waves; AF/VF risk
Brugada pattern type 2 & 3	Saddle-back STE in V1–V2; diagnostic only with Na-channel blockers
HCM (hypertrophic cardiomyopathy)	LVH, deep narrow Q waves in I, aVL, V5–V6, T inversions
Acute pericarditis	Widespread saddle-shaped ST elevation + PR depression (especially II, aVF); reciprocal ST/PR changes in aVR
Pulmonary embolism (PE)	Sinus tachycardia (most common); S1Q3T3 pattern; RBBB; T inversions V1–V4; RAD
Cardiac tamponade	Low voltage + sinus tachycardia + electrical alternans
Prinzmetal angina	Transient STE with normal baseline ECG
Wellens syndrome	Biphasic or deeply inverted T waves in V2–V3 during pain-free interval → critical LAD stenosis
de Winter pattern	Upsloping STD + tall T waves V1–V6; no STE → LAD STEMI equivalent
LQTS type 1	Broad-based T waves
LQTS type 2	Notched/biphasic T waves
LQTS type 3	Long isoelectric ST, late-peaking T wave

13. PACEMAKER ECG FINDINGS

Finding	Features
Ventricular pacing	Pacing spike → wide LBBB-morphology QRS
Atrial pacing	Pacing spike → normal QRS (if AV conduction intact)
Dual-chamber pacing	Two spikes: before P and before QRS
Failure to pace	No pacing spike when expected
Failure to capture	Pacing spike present but no QRS follows
Failure to sense	Pacing spike fires when it shouldn't (e.g., during intrinsic rhythm)
Pacemaker-mediated tachycardia (PMT)	Regular tachycardia at upper rate limit in dual-chamber pacemakers

14. LOCALIZATION OF MI BY LEADS

Territory	Leads with STE	Artery (usual)
Inferior	II, III, aVF	RCA (80%), LCx (20%)
Anterior	V1–V4	LAD
Anteroseptal	V1–V3	Septal branches of LAD
Anterolateral	V4–V6, I, aVL	LAD / LCx
Lateral (high)	I, aVL	LCx / Diagonal
Posterior	STD in V1–V3 (reciprocal) + tall R/T in V1	LCx / RCA
Right ventricular	V1 + V4R	RCA (proximal)

Lateral STEMI ECG with reciprocal changes

Quick Reference Summary

RATE        → Normal 60–100 bpm
RHYTHM      → Sinus? AF? Flutter? Block? VT?
AXIS        → Normal / LAD / RAD / extreme
P WAVES     → Present? Morphology? PR interval?
PR          → 120–200 ms; short = WPW; long = heart block
QRS         → Width (BBB); voltage (LVH/RVH); Q waves; delta/epsilon/J waves
ST SEGMENT  → Elevation (STEMI/pericarditis/Brugada) or depression (ischemia/digoxin)?
T WAVES     → Peaked (hyperK/hyperacute), inverted (ischemia/PE/Wellens), flat (ischemia/hypoK)
QT          → Prolonged = Torsades risk; short = hyperCa/short QT syndrome
U WAVES     → Prominent = hypokalemia

Sources: Tintinalli's Emergency Medicine, Braunwald's Heart Disease, Goldman-Cecil Medicine, StatPearls (NBK549803), GeekyMedics ECG Guide

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