A structured approach to the ECG

01Purpose and principlesWhat the assessment is for and the core concepts behind it.

A structured sequence prevents premature closure. The RCUK six-stage method is an excellent rhythm core; a full 12-lead then adds calibration, axis, intervals, chamber/QRS morphology and repolarisation.

ECG findings must be interpreted with symptoms and time. NICE explicitly warns that ACS may have a normal initial ECG and that recordings should not delay hospital transfer.

There is no empirical 'ECG medicine'. Drugs below apply only when the tracing plus clinical picture establishes a time-critical pathway.

Key points

Start with context: patient, date/time, symptoms and comparison ECG; then verify calibration (usually 25 mm/s and 10 mm/mV), lead placement and artefact.
RCUK rhythm skeleton: electrical activity, ventricular rate, regularity, narrow/broad QRS, atrial activity, then the P-QRS relationship.
Rate: regular rhythm about 300 divided by large squares between R waves; irregular rhythm count QRS on a 10-second strip and multiply by 6.
Rhythm: name atrial and ventricular rhythms separately when needed; do not call 'sinus' unless each P has appropriate morphology and a consistent relationship to QRS.
Axis: use leads I and aVF as the quick quadrant check, then refine when abnormal; axis is a clue to conduction, hypertrophy or ventricular origin, not a diagnosis alone.
Intervals: measure PR, QRS and QT/QTc; QRS at least 120 ms is broad in the RCUK tachy algorithm, and NICE treats QTc over 450 ms or under 350 ms as a red flag in TLoC.
Inspect P waves, QRS morphology/voltage/R-wave progression/pathological Q waves, then ST segments and T waves in anatomical lead groups with reciprocal changes.
Compare with old and serial ECGs; NICE says a normal resting ECG does not exclude ACS and recommends serial, previous and additional leads when doubt remains.
Finish with one synthesis: rate + rhythm + axis + intervals + key abnormality + comparison + clinical action.
Automated interpretation is a prompt, not the final report; NICE requires competent clinician review.

02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.

Rhythm emergencyRed flag

VF/pulseless VT, sustained VT with adverse features, complete/high-grade AV block with instability, or very rapid irregular broad pre-excited AF. Move from interpretation to RCUK treatment immediately.

Acute ischaemic patternRed flag

New contiguous ST elevation, dynamic ST depression/T inversion, hyperacute T waves, reciprocal change or an occlusion-equivalent pattern with compatible symptoms. A prior ECG helps but must not delay treatment.

Syncope ECG red flagsRed flag

Any heart block, complete RBBB/LBBB, ventricular arrhythmia/ectopy, long QTc over 450 ms, short QTc under 350 ms, Brugada pattern, pre-excitation, pathological Q waves, abnormal T inversion, sustained atrial arrhythmia or paced rhythm under the NICE TLoC framework.

Metabolic/toxic patternRed flag

Progressive peaked T waves, PR prolongation, P-wave loss, QRS widening or sine-wave pattern suggests severe hyperkalaemia; marked QT prolongation suggests torsades risk; sodium-channel blockade can cause broad QRS with terminal rightward axis.

Technical mimic

Unexpected global inversion/positive aVR, poor progression, baseline wander, tremor or isolated impossible morphology may be lead reversal/misplacement or artefact. Repeat correctly, but do not dismiss a plausible emergency as artefact without checking the patient.

03Method and interpretationA systematic approach to the test and its findings.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Identity, indication, date/time, symptoms and comparison tracingFirst step
Why
Anchor the ECG to the correct patient and clinical moment.
Interpretation and limitations
State whether changes are new, old or unknown; a technically identical old abnormality can radically change urgency.
02
Technical check: 25 mm/s, 10 mm/mV, artefact and lead placement
Why
Prevent erroneous rates, intervals, voltage and territory calls.
Interpretation and limitations
At 25 mm/s, one small square is 40 ms and one large square 200 ms; at 10 mm/mV, 10 mm is 1 mV. Recalculate if calibration differs.
03
Rate and regularity
Why
Quantify ventricular rate and decide regular versus irregular.
Interpretation and limitations
Regular: 300/large squares or 1500/small squares. Irregular: count QRS in 10 seconds x6. Use a long strip to avoid sampling error.
04
Atrial activity and P-QRS relationship
Why
Identify sinus rhythm, AF/flutter, ectopic atrial rhythm and AV block/AV dissociation.
Interpretation and limitations
Ask whether P waves exist, their morphology/rate, and whether every P conducts/every QRS has a preceding P with a constant PR. Independent rates indicate AV dissociation.
05
Axis
Why
Screen for fascicular/bundle disease, hypertrophy and ventricular origin.
Interpretation and limitations
I positive/aVF positive is the usual normal quadrant; I positive/aVF negative suggests leftward axis and I negative/aVF positive rightward axis. Refine with lead II and clinical context rather than overcalling borderline values.
06
PR, QRS and QT/QTc
Why
Detect AV delay, pre-excitation, bundle/ventricular conduction and repolarisation risk.
Interpretation and limitations
PR over 200 ms supports first-degree AV block; QRS at least 120 ms is broad. Manually verify QT and use an appropriate correction—Bazett overcorrects at high rates and undercorrects at low rates; NICE TLoC red flags include QTc over 450 or under 350 ms.
07
P waves and QRS morphology
Why
Assess atrial abnormality, hypertrophy, bundle/fascicular block, R-wave progression, pathological Q waves, pacing and pre-excitation.
Interpretation and limitations
Describe what criteria are met and where; avoid diagnosing chamber enlargement from voltage alone without context/imaging.
08
ST segments, T waves and anatomical territories
Why
Find acute ischaemia, pericarditis, strain, electrolyte and CNS/repolarisation abnormalities.
Interpretation and limitations
Look for contiguous and reciprocal changes. Universal MI criteria use J-point ST elevation in at least two contiguous leads with age/sex-specific V2-V3 thresholds; lesser or non-classic changes can still represent occlusion when the clinical picture is strong.
09
Serial ECG, previous ECG and additional right/posterior leads
Why
Expose dynamic or territorially hidden ischaemia and distinguish chronic abnormality.
Interpretation and limitations
NICE recommends these when ACS remains in doubt and explicitly says the results may still be inconclusive; integrate troponin and clinical assessment.

04Clinical next stepsHow the result changes management or prompts escalation.

01Read sequenceA reproducible full 12-lead reportFirst stepEvery ECG, including apparently normal tracings.

11. Context and technical quality: patient, time, symptoms, calibration, lead position, artefact and old ECG.
22. RCUK rhythm core: electrical activity, ventricular rate, regularity, QRS width, atrial activity, P-QRS relation.
33. Axis and intervals: PR, QRS and QT/QTc, manually checking automated values when clinically important.
44. Morphology: P waves, QRS progression/voltage, bundle/fascicular block, Q waves, pacing and pre-excitation.
55. Repolarisation: ST/T changes in territories, reciprocal change and QT context.
66. Synthesis and action: one sentence with comparison and urgency; list uncertainty explicitly.

02Deteriorating patientTreat before completing the essayUnresponsive/abnormal breathing, life-threatening tachy/brady features or a malignant rhythm.

1Switch to ABCDE/ALS, call for help and attach defibrillator/pacing pads.
2VF/pulseless VT: immediate CPR/defibrillation. Unstable monomorphic tachycardia: synchronised cardioversion. Unstable bradycardia: atropine where appropriate and early pacing/chronotrope branch.
3Capture/save the ECG if possible without delaying treatment; document rhythm and timing retrospectively from monitor/defibrillator data.

03Possible ACSECG plus clinical pathwayIschaemic symptoms or dynamic/territorial ST-T changes.

1Obtain a 12-lead as soon as possible, but do not delay transfer. Follow the acute STEMI/local reperfusion pathway for regional ST elevation or a convincing occlusion pattern.
2DefinitiveGive a single 300 mg aspirin loading dose as soon as possible unless there is clear allergy, while arranging definitive ACS care; the ECG finding is not the only diagnostic criterion.
3A normal initial ECG does not exclude ACS. If doubt remains, obtain serial ECGs, review prior recordings and add right/posterior leads as clinically indicated.
4AlternativeInterpret high-sensitivity troponin with symptom timing, serial change, ECG and alternative causes; myocardial injury is not synonymous with type 1 MI.

04Long/short QT or syncope abnormalityPrevent malignant arrhythmiaQTc over 450 ms or under 350 ms in TLoC, Brugada/pre-excitation, ventricular arrhythmia or conduction abnormality.

1Treat as a NICE TLoC red flag and arrange urgent specialist cardiovascular assessment within 24 hours where applicable.
2Review QT-prolonging drugs and potassium/magnesium/calcium; if torsades occurs give magnesium 8 mmol IV over 10 minutes and shock if unstable/pulseless.
3Do not use a single automated QTc to diagnose inherited disease: manually confirm, repeat when rate/electrolytes normal and obtain specialist/family assessment.

05Procedure and medicine safetyRelevant preparation, treatment and contraindications.

Immediate NICE therapy when ACS is suspected, alongside transfer/reperfusion/risk pathway.

Aspirin for suspected ACS

300 mg PO as a single loading dose as soon as possible unless there is clear allergy; document if given before hospital arrival.

Do not give for every nonspecific ST-T change; consider active major bleeding and true hypersensitivity. Other antiplatelet/antithrombin choices are pathway-specific and usually hospital-led.

Long-QT polymorphic VT while correcting the cause; shock first if unstable or pulseless.

Magnesium sulfate for ECG-confirmed torsades context

8 mmol magnesium (approximately 2 g magnesium sulfate) IV over 10 minutes.

Avoid amiodarone in torsades. Monitor BP/respiration and renal function; magnesium does not replace defibrillation.

RCUK treatment when the ECG plus adverse features indicate an atropine-responsive bradyarrhythmia.

Atropine for symptomatic bradycardia where appropriate

500 micrograms IV, repeat every 3-5 minutes to maximum total 3 mg.

Do not use after cardiac transplant or in high-grade broad-QRS AV block per RCUK; prepare pacing and do not let atropine delay it.

06Risks, monitoring and follow-upComplications, safety checks and further assessment.

Repeat ECG when symptoms change, after treatment/conversion and when correcting potassium/QT or lead-placement concerns.
Use continuous monitoring for unstable arrhythmia, high-grade block, marked QT abnormality/torsades risk or suspected dynamic ischaemia.
Compare automated and manual rate/interval/QTc; document the correction formula when it could change management.
For suspected ACS, serial ECG and troponin timing follow the local validated pathway; do not use one normal tracing to discharge a high-risk presentation.
Save pre-treatment and diagnostic adenosine/cardioversion tracings for specialist review.

07Special situationsVariants, exceptions and circumstances that change the usual approach.

The six-stage rhythm core scales well

Electrical activity, rate, regularity, width, atrial activity and P-QRS relation can safely describe almost any rhythm before a precise label is available.

Calibration is clinical information

At 50 mm/s or 5 mm/mV, familiar square-counting and voltage criteria change. A technically correct interpretation starts before the P wave.

QTc is a model, not a measured truth

Automated Bazett QTc can mislead at extreme rates. Manually verify the end of T and consider another correction while still treating obvious torsades risk urgently.

Contiguous plus reciprocal beats isolated

Territorial clustering and reciprocal change make acute coronary occlusion more persuasive than a single noisy lead, but clinical context and serial evolution remain essential.

The final sentence should change care

'Sinus rhythm 48/min, broad complete AV block with shock—pacing pathway now' is safer than a page of measurements without urgency or comparison.

08Common pitfallsFrequent interpretation and management errors.

01
Reading the automated diagnosis before checking patient, calibration and lead quality.
02
Calling a rhythm sinus because P waves exist without proving consistent P-QRS conduction.
03
Using a normal ECG to exclude ACS or intermittent arrhythmia.
04
Applying standard square formulas when paper speed is not 25 mm/s.
05
Overcalling an isolated ST change without contiguous/reciprocal/context review—or undercalling a convincing occlusion pattern because it misses a simplistic threshold.
06
Giving an antiarrhythmic from the ECG label without checking stability, QRS regularity and pre-excitation/QT.