Adult ECG Interpretation Tool | Dr Josh Emergency Pearl

Red Flag Checklist

🚨

Immediate Red Flags

Tick any that apply before systematic analysis. One tick = senior review now.

Rhythm
Broad complex tachycardia (rate >100, QRS >120ms)

Rhythm
AF with ventricular rate >150 or haemodynamic instability

Ischaemia
ST elevation ≥1mm in ≥2 contiguous leads (or ≥2mm in precordial)

Ischaemia
New left bundle branch block with ischaemic symptoms

Conduction
Complete heart block (third degree AV block)

QT
QTc >500ms or active Torsades de Pointes

Ischaemia
ST depression >2mm especially horizontal or downsloping

Clinical
Any ECG abnormality with syncope, haemodynamic instability, or cardiac arrest

Systematic 12-Step Analysis

1

Rate

Is the ventricular rate between 60 and 100 bpm?

300 ÷ large squares between R-R peaks. 1 large square = ~300 bpm. 5 squares = 60 bpm. For irregular rhythms (AF): count QRS complexes in 10 seconds × 6. Normal: 60–100 bpm. Tachycardia: >100. Bradycardia: <60.

⚡ Tachycardia >150 bpm with regular narrow QRS: consider SVT or atrial flutter (2:1 block). Rate exactly 150 bpm = think flutter until proven otherwise.

2

Rhythm

Is the rhythm regular with consistent R-R intervals?

Mark consecutive R peaks on paper. Regular: R-R varies <10%. Regularly irregular: pattern repeats (e.g. Wenckebach). Irregularly irregular: no pattern (strongly suggests AF). Check Lead II or V1 rhythm strip.

⚡ AF is irregularly irregular with absent P waves. Sinus arrhythmia is regularly irregular — R-R shortens on inspiration, lengthens on expiration. Check: are P waves present?

3

P-Wave Morphology

Is there a normal P wave before every QRS complex?

Normal P: upright in I and II, inverted in aVR. Duration <120ms, amplitude <2.5mm. Every P followed by QRS and every QRS preceded by a P = sinus rhythm. Absent P waves = AF, junctional rhythm, or ventricular rhythm.

⚡ P mitrale (bifid, broad P >120ms in II): left atrial enlargement. P pulmonale (tall, peaked P >2.5mm in II): right atrial enlargement. Retrograde P after QRS = junctional tachycardia. No P = AF or VT/accelerated idioventricular.

4

QRS Axis

Is the QRS axis between −30° and +90° (normal range)?

Quick axis check: if QRS upright in both I and aVF = normal axis. LAD (−30° to −90°): upright in I, inverted in aVF — check II. If II negative = LAD (<−30°). RAD (+90° to +180°): inverted in I, upright in aVF. Extreme axis: negative in both I and aVF.

⚡ LAD + RBBB = bifascicular block (RBBB + LAFB). LAD alone: LAFB, inferior MI, hyperK, Wolff-Parkinson-White. RAD: PE, RVH, lateral MI, LPFB, normal in children. Northwest axis (extreme): VT, hyperkalaemia, dextrocardia.

5

PR Interval

Is the PR interval between 120ms and 200ms (3–5 small squares)?

Measure from P wave onset to QRS onset. Normal: 120–200ms (3–5 small squares). Short PR (<120ms): WPW, junctional rhythm, LGL. Long PR (>200ms): 1st degree AV block. Lengthening PR with eventual dropped beat: Mobitz I (Wenckebach). Fixed dropped beats: Mobitz II.

⚡ WPW: short PR + delta wave + wide QRS. Never give adenosine, digoxin, or verapamil if WPW + AF — risk of precipitating VF by blocking AV node and forcing all conduction via accessory pathway at up to 300 bpm.

6

QRS Duration

Is the QRS duration less than 120ms (less than 3 small squares)?

Normal: <120ms. Incomplete BBB: 110–119ms. Complete BBB (LBBB or RBBB): ≥120ms. Broad QRS differentials: LBBB, RBBB, ventricular pacing, WPW, hyperkalaemia, TCA toxicity, Class Ia/Ic antiarrhythmics. Never assume SVT with aberrancy — treat all broad complex tachycardias as VT.

⚡ LBBB morphology: no Q in I/V5/V6, broad notched R laterally, discordant ST-T. RBBB: rSR' (M-shape) in V1, wide S in I/V6, T inversion V1–V3. WPW: short PR, delta wave, broad QRS, discordant T changes.

7

QT Interval / QTc

Is the QTc within normal limits (≤450ms men, ≤460ms women)?

Measure QT in V5 or II from QRS onset to T wave end. Use Bazett formula: QTc = QT ÷ √(RR interval in seconds). Normal: ≤440ms. Borderline: 441–499ms. High risk: ≥500ms. At normal rate (60bpm): QT <440ms. At 80bpm: QT <380ms. Rule of thumb: QT >half the RR = prolonged.

⚡ Common QTc-prolonging drugs: antipsychotics (haloperidol, quetiapine), antibiotics (ciprofloxacin, azithromycin, metronidazole), antiemetics (ondansetron, domperidone), antiarrhythmics (amiodarone, sotalol). QTc >500ms + symptomatic: IV MgSO₄ 2g over 10 min.

8

ST Segment — Anterior

Is the ST segment isoelectric (no elevation or depression ≥1mm) in V1–V4?

Measure ST at J-point. Significant STE: ≥2mm in V1–V4 in ≥2 contiguous leads. Significant STD: ≥1mm horizontal or downsloping. STE ≥1mm in V1: RBBB, posterior MI, Brugada, aVR. Upsloping STD at J-point in V1–V6 with tall peaked T = De Winter (LAD occlusion, no STE).

⚡ Wellens syndrome: pain-free with biphasic (Type A) or deep symmetric T inversion (Type B) in V2–V3 = critical LAD stenosis. Do NOT discharge. Do NOT exercise test. This is a pre-infarction state requiring urgent angiography. Serial ECGs during chest pain are essential.

9

ST Segment — Inferior and Lateral

Is the ST segment isoelectric in II, III, aVF, I, aVL, V5–V6?

Inferior STE (≥1mm in ≥2 of II, III, aVF): inferior STEMI (RCA 80%, LCx 20%). A 15-lead ECG is recommended. V4R STE ≥0.5mm = RV infarction: avoid nitrates, use IV fluids. Lateral STE (I, aVL, V5–V6): LCx or diagonal LAD territory. Reciprocal STD in aVL with inferior STE strongly confirms inferior STEMI.

⚡ Isolated ST elevation in aVR ≥1mm with diffuse STD: LMCA or proximal LAD occlusion. ST elevation in aVR ≥ V1 = suspect LMCA. aVL reciprocal change is the most sensitive marker for inferior STEMI in early presentations — look for it first.

10

T-Wave Morphology

Are the T waves normal in polarity and morphology throughout?

Normal T wave: upright in I, II, V4–V6. Inverted in aVR (always). V1 inversion normal in adults. Biphasic T (V2–V3) = Wellens Type A. Deep symmetric T inversion (V2–V3) = Wellens Type B. Diffuse T inversion: PE, subarachnoid haemorrhage, myocarditis, Takotsubo. Tall peaked symmetric T = hyperK or hyperacute STEMI.

⚡ T inversion in V1–V4 in right-sided chest leads = anterior ischaemia or PE. New T inversion in V1–V4 after haemodynamic collapse: consider massive PE (S1Q3T3 is insensitive — 20% specificity). Subarachnoid haemorrhage causes deep widespread T inversions with long QT — always consider in unexplained ECG changes.

11

Q Waves

Are Q waves absent or only septal (small <1mm wide, <2mm deep)?

Septal Q waves (small, narrow) in I, aVL, V5–V6 are normal. Pathological Q: width ≥40ms (1 small square) OR depth ≥25% of QRS amplitude OR ≥2mm deep. Present in ≥2 contiguous leads. Indicates prior full-thickness (transmural) infarction. Q waves in III alone are common and non-pathological.

⚡ In acute STEMI, Q waves may develop within 1–2 hours — they do not exclude an evolving MI. Equivalents: poor R progression (R wave amplitude fails to increase normally V1→V4) without Q waves can indicate prior anterior MI. QS pattern (entirely negative QRS) in V1–V2 with no R wave growth = anterior MI equivalent.

12

Voltage / LVH

Is the voltage within normal limits without features of LVH?

LVH criteria (Sokolow-Lyon): SV1 + RV5 or RV6 >35mm. Cornell: SaVL + RV5 >28mm (men) / >20mm (women). LVH with lateral strain (downsloping STD + asymmetric T inversion in I, aVL, V5–V6) increases cardiovascular risk and may mimic lateral ischaemia. Low voltage (<5mm all limb leads): pericardial effusion, obesity, COPD.

⚡ LVH strain pattern: downsloping ST depression with asymmetric T inversion in lateral leads (slow descent, rapid ascent). This differs from ischaemia (horizontal/downsloping STD + upright/symmetrically inverted T). LVH + LBBB: Sgarbossa criteria for diagnosing STEMI. New LVH pattern in clinical context = consider hypertensive emergency.

Disposition Matrix

Flag

Abnormalities

Symptoms

Disposition

✓

Any

Immediate senior review. Activate pathway now.

✗

0

Low risk

Clinically correlate. Discharge if appropriate.

✗

1

Any

Senior review. Serial ECG + troponin.

✗

≥2

Any

Cardiology advice. Admit for monitoring.

✗

Any

STEMI pattern

PPCI activation. Dual antiplatelet + anticoagulation.

16-Pattern Clinical ECG Library

Real clinical ECG examples from reputable open-access sources. Each pattern includes key diagnostic features, immediate ED action, and verified source links. LITFL content used under CC BY-NC-SA 4.0 (non-profit educational, credited, linked back). Cross-referenced against ESC 2023, NICE CG167, RCEM 2019, and AHA/ACC 2022 guidance.

OMI / NOMI Open the full OMI / NOMI Occlusion MI module →

Quick Navigation — Select Pattern

Normal ECG Values

Heart Rate

60–100 bpm. Tachycardia >100. Bradycardia <60.

PR Interval

120–200 ms (3–5 small squares). Prolonged >200 ms = 1° AV block.

QRS Duration

<120 ms. 110–119 ms = incomplete BBB. ≥120 ms = complete BBB or VT.

QTc (Bazett)

Men ≤440 ms. Women ≤460 ms. Alert at >500 ms (Torsades risk).

P-wave

<120 ms duration, <2.5 mm amplitude. Upright in I, II. Inverted in aVR.

ST Segment

Isoelectric at J-point ±0.5 mm (1 mm in V2–V3 in men, ≥0.5 mm in women).

Sokolow-Lyon

SV1 + RV5 or RV6 ≤35 mm. Cornell: SaVL + RV5 ≤28 mm (men) ≤20 mm (women).

QRS Axis

Normal: −30° to +90°. LAD: <−30°. RAD: >+90°. Extreme: <−90° or >+180°.

Governing Guidelines

ESC 2023Updated 2023

ESC Guidelines for Acute Coronary Syndromes (ACS)

STE ≥1mm in ≥2 contiguous limb leads or ≥2mm in V2–V3 defines STEMI requiring immediate reperfusion. New LBBB with symptoms = STEMI equivalent. Target door-to-balloon ≤60 min primary PCI (PPCI) from first medical contact. Apply Sgarbossa criteria for STEMI in pre-existing LBBB or paced rhythm. De Winter pattern, Wellens syndrome, and posterior MI (STD V1–V3) qualify as occlusion MI equivalents requiring PPCI pathway activation.

NICE CG167Updated 2023

Myocardial Infarction with ST-elevation (NICE CG167)

Offer immediate PPCI if available within 120 min of when fibrinolysis could have been given. Dual antiplatelet therapy: aspirin 300 mg + ticagrelor 180 mg (or prasugrel or clopidogrel). Give unfractionated heparin before PPCI. Offer serial ECGs if diagnosis uncertain. Perform 15-lead ECG for inferior STEMI to identify RV MI (V4R) and posterior extension (V7–V9).

RCEM 2019RCEM Guideline

RCEM ECG Interpretation Standards for Emergency Physicians

All ED physicians should systematically review rate, rhythm, P wave, PR, QRS, axis, ST, T wave, and QTc on every ECG. Formal documentation of ECG interpretation required. Serial ECGs at 0 and 3 hours mandatory in undifferentiated chest pain. Junior clinicians must escalate any ECG with: new conduction defect, ST change, arrhythmia causing haemodynamic compromise, or QTc >500 ms. ECG must be reviewed by a senior clinician within 10 minutes of acquisition in suspected ACS.

ESC 2022Updated 2022

ESC Guidelines for Ventricular Arrhythmias and Sudden Cardiac Death

All broad complex tachycardias: treat as VT until proven otherwise. Criteria supporting VT: QRS >160 ms, AV dissociation, fusion or capture beats, NW axis, concordance in precordial leads. IV amiodarone 300 mg over 20–60 min for stable VT. Synchronised DC cardioversion for haemodynamically compromised VT. Adenosine and verapamil are contraindicated for broad complex tachycardias of uncertain origin.

ESC 2020Updated 2020

ESC Guidelines for Atrial Fibrillation

New-onset AF: rate control with beta-blocker or rate-limiting CCB. CHA₂DS₂-VASc ≥2 (men) or ≥3 (women): initiate anticoagulation (DOAC preferred over warfarin). AF onset <48 h: consider cardioversion after LMWH bolus. AF >48 h or unknown onset: 3 weeks therapeutic anticoagulation before elective cardioversion, or TOE-guided cardioversion. Emergency cardioversion (DC) for haemodynamically unstable AF regardless of duration.

AHA/ACC 2022Updated 2022

AHA/ACC Guideline on QT Prolongation and Drug-Induced Arrhythmia

Baseline QTc should be documented before starting QTc-prolonging agents. QTc >500 ms: discontinue offending agents, correct electrolytes (K+ target >4.0 mmol/L, Mg²⁺ >0.8 mmol/L), IV MgSO₄ 2g for active Torsades. Avoid isoproterenol in congenital long QT. Electrical overdrive pacing for recurrent Torsades refractory to magnesium.

Immediately Actionable Patterns

Pattern

ECG Hallmark

Action

Anterior STEMI

STE ≥2mm V1–V4, hyperacute T, loss of R progression

Activate PPCI

Inferior STEMI

STE ≥1mm II/III/aVF, reciprocal STD aVL/I

Activate PPCI + right-sided leads

Posterior OMI

STD V1–V3 (mirror), tall R V1–V2, STE V7–V9

Activate PPCI + posterior leads

New LBBB + symptoms

QRS ≥120ms, no septal Q laterally, discordant ST-T

Activate PPCI (STEMI equivalent)

De Winter Pattern

Upsloping STD J-point + tall T in V1–V6. No STE.

Activate PPCI (occlusion equivalent)

Wellens Syndrome

Biphasic or deep T inversion V2–V3. Pain-free. No STE.

Admit cardiology urgently. No discharge.

3rd Degree AV Block

P and QRS independent rates, no PR relationship

Atropine → TCP → TVP

VT (broad complex)

Rate >100, QRS >120ms, AV dissociation

Amiodarone / DC cardioversion

Torsades de Pointes

Polymorphic VT, undulating QRS, long QTc

MgSO₄ 2g IV, stop QTc drugs

Secondary Patterns Requiring Assessment

Pattern

ECG Hallmark

Consider

RBBB (new)

rSR' V1, broad S I/V6, T inversion V1–V3

PE, anterior MI, Brugada

Atrial Fibrillation

No P waves, irregular R-R, fibrillatory baseline

Rate control, CHA₂DS₂-VASc, DOAC

WPW

Short PR, delta wave, wide QRS

No adenosine/digoxin/verapamil. EP referral.

Prolonged QTc

QTc >450ms men / >460ms women

Drug review, electrolytes, MgSO₄

LVH + Strain

Tall R, downsloping STD + asymmetric T inv. V5–V6

Rule out ACS, ECHO, BP control

Hyperkalaemia

Peaked narrow symmetric T, PR prolongation

Ca gluconate, insulin/dextrose, salbutamol

1° AV Block

PR >200ms, consistent

Check drugs (digoxin, beta-blockers)

Adult ECG Manual Interpretation

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