Acute Medical Take · ECG library

ECG Atlas

Twenty-nine separately indexed ECG and telemetry categories with real clinical traces, labelled features, specialist management, adult drug doses, monitoring and escalation.

♥⌁⌁╱╲⌁⌁TRACE → PATIENT → ACTION

SEPARATE CLINICAL CATEGORIES

Choose an ECG pattern

Every real trace opens into its own complete acute-care category.

16 individual ECG categories

Real traces with specialist treatment pathways

TRACE → PATIENT → STABILITY → TREATMENT → MONITOR

Safety: Adult UK decision support—not automatic prescriptions. Verify the current BNF, RCUK/NICE/UKKA guidance, allergy, pregnancy, weight, renal/hepatic function, interactions and local cardiology protocols.

ECG ATLAS · CONTINUOUS MONITORING

Assessing telemetry

Confirm the patient, validate the signal, identify the rhythm, measure the event and decide whether it changes care.

Patient → signal → rhythm → event → cause → action

Never diagnose from the alarm label alone.Look at the patient and pulse first. Print the onset, event and offset in more than one lead; check electrodes and gain; obtain a diagnostic 12-lead ECG when the abnormality persists or is clinically important.

1 · Clinical correlation

Symptoms, consciousness, pulse, blood pressure, oxygenation and perfusion. Instability or pulselessness overrides retrospective strip analysis.

2 · Signal quality

Confirm patient identity, time, lead, calibration and electrode contact. Artefact may mimic AF, pauses, VT or VF; lead failure may create a false asystole alarm.

3 · Rhythm framework

Rate and regularity; P waves and P–QRS relationship; PR, QRS and QT; premature beats; pauses; onset/offset; atrial versus ventricular origin.

4 · Quantify the event

State duration, fastest rate, beat count, morphology, frequency/burden, coupling pattern, symptoms and whether it self-terminated.

5 · Search for cause

Ischaemia, hypoxia, K/Mg/Ca disturbance, drugs/QT prolongation, sepsis, pain, volume status, structural heart disease and device malfunction.

6 · Document and escalate

Save the strip with onset and offset, obtain a 12-lead, compare previous ECGs, record the clinical response and communicate urgent findings directly.

Real clinical examples—abnormality clearly labelled

Clinical ECG strip showing a premature ventricular complex followed by a compensatory pause — **Skipped beat: premature ventricular complex (PVC)**James Heilman MD · CC BY-SA 3.0 · source/licence ↗

What the patient may call a “skipped beat”

An early broad, abnormal QRS without a preceding normal P wave is followed by a pause. Confirm whether the ectopy is ventricular or supraventricular with aberrancy; report unifocal/multifocal morphology, couplets, bigeminy/trigeminy and burden.

Escalate

Urgently review ectopy with syncope, chest pain, haemodynamic change, acute ischaemia, prolonged QT, electrolyte disturbance, structural disease, increasing frequency, couplets or runs. Treat the cause—not an isolated monitor label.

Real telemetry monitor strip from a patient showing two sinus pauses — **Sinus pauses: 2.8 seconds and 3.7 seconds**PerpetuallyTachy · clinical telemetry strip · source/licence ↗

Pause: describe the mechanism, not only the seconds

Look through the pause for hidden P waves. No atrial activity suggests sinus pause/arrest; regular P waves without QRS complexes suggest AV block; an early hidden atrial beat may produce a blocked PAC. Confirm the monitor clock/calibration and exclude lead disconnection.

Escalate

Immediate review for symptoms, hypotension, syncope, recurrent/prolonged pauses, high-grade AV block or failure of an escape rhythm. Apply pads and follow the current bradycardia pathway when adverse features are present.

Real clinical ECG showing a run of monomorphic ventricular tachycardia — **Ventricular run: assess as possible NSVT**James Heilman MD · CC BY-SA 3.0 · source/licence ↗

NSVT requires the full event

Three or more consecutive ventricular beats that terminate spontaneously in under 30 seconds are generally described as NSVT. Save onset and offset; note fastest rate, duration, morphology and symptoms. A still frame can show VT morphology but cannot by itself prove that the episode was non-sustained.

Escalate

Assess immediately for instability and ongoing VT. Obtain a 12-lead, K/Mg/Ca, renal function and cause-directed ischaemia/structural assessment. Syncope, frequent/recurrent runs, polymorphic VT, QT prolongation, ACS, heart failure or inherited/structural disease requires urgent senior/cardiology review.

Adverse features or pulseless rhythm

Use the current RCUK tachycardia, bradycardia or cardiac-arrest algorithm immediately; do not wait to complete a telemetry interpretation.

Medication caution

Do not suppress ectopy reflexively. Correct reversible causes and select antiarrhythmic, rate-control or pacing treatment through the rhythm-specific pathway with allergy, QT, interaction and renal/hepatic checks.

Educational adult decision support. Always review the original diagnostic-quality tracing, the patient and local monitoring/escalation policy.

SEPARATE SPECIALIST ECG CATEGORIES

Additional real-life ECG atlases

Each condition is separated rather than hidden inside a combined example.

Atrial rhythm

Atrial fibrillation

Recognise

Irregularly irregular ventricular rhythm without reproducible P waves. Confirm on a diagnostic 12-lead and distinguish artefact, multifocal atrial tachycardia and frequent ectopy.

Specialist management

If adverse features are caused by the tachyarrhythmia, perform synchronised cardioversion. Otherwise define onset, precipitant, rate/rhythm strategy and stroke prevention using current AF guidance.

Monitoring & escalation

Continuous ECG when acute; BP, symptoms, electrolytes, thyroid/cause assessment, echo when indicated and documented anticoagulation ownership.

Specialist medicines and adult doses

1Bisoprolol 1.25–5 mg orally once daily is a common cautious rate-control start; avoid shock, significant block and acute decompensated heart failure.

2Diltiazem immediate-release 60 mg orally three times daily may be used when LVEF is preserved; avoid HFrEF.

3Anticoagulant and dose require renal function, age, weight, valve status, bleeding risk and interaction checks—do not select from ECG alone.

Atrial rhythm

Atrial flutter

Recognise

Organised atrial activity, often best in inferior leads and V1. A regular ventricular rate close to 150/min should prompt a deliberate search for 2:1 flutter.

Specialist management

Synchronised cardioversion for adverse features. Stable flutter needs rate/rhythm and anticoagulation assessment; typical flutter should be referred for cavotricuspid-isthmus ablation consideration.

Monitoring & escalation

Telemetry during acute management; reassess rate, BP and symptoms, and arrange rhythm-service follow-up.

Specialist medicines and adult doses

1Bisoprolol 1.25–5 mg orally once daily may be used cautiously for rate control when appropriate.

2Diltiazem immediate-release 60 mg orally three times daily is an alternative with preserved LVEF; avoid HFrEF.

3Anticoagulation follows the same stroke-risk principles as AF with patient-specific dosing.

Supraventricular tachycardia

Regular narrow-complex SVT

Recognise

A regular narrow-complex tachycardia with abrupt onset/offset suggests AVNRT or orthodromic AVRT. Exclude sinus tachycardia and flutter before AV nodal treatment.

Specialist management

Adverse features: synchronised cardioversion. If stable, use vagal manoeuvres then adenosine with continuous ECG and resuscitation readiness; capture the response diagnostically.

Monitoring & escalation

Continuous 12-lead recording during adenosine; BP, recurrence and electrophysiology referral for recurrent symptomatic SVT.

Specialist medicines and adult doses

1Adenosine 6 mg rapid IV bolus; if unsuccessful give 12 mg, then 18 mg under the current RCUK/local algorithm.

2Use a large proximal vein and immediate saline flush; avoid adenosine in irregular/broad rhythms and use caution/contraindication checks for asthma and transplanted hearts.

3If adenosine fails and the rhythm is confirmed regular narrow-complex SVT, verapamil or a beta-blocker is specialist/protocol directed.

AV conduction

First-degree AV block

Recognise

One P wave before every QRS with a consistently prolonged PR interval. Measure manually and review QRS width and associated fascicular/bundle disease.

Specialist management

Usually no acute rhythm treatment. Identify medicines, ischaemia, myocarditis, electrolyte disease and progressive conduction-system disease; seek review when symptomatic or combined with wider conduction abnormalities.

Monitoring & escalation

Repeat ECG after medication/cause correction; telemetry for symptoms, acute MI or evidence of more advanced block.

Specialist medicines and adult doses

1No medicine is indicated for an isolated asymptomatic prolonged PR interval.

2Review beta-blockers, verapamil/diltiazem, digoxin and antiarrhythmics—do not stop essential therapy without clinical review.

AV conduction

Second-degree AV block—Mobitz I

Recognise

Progressive PR prolongation before a non-conducted P wave, then reset. Confirm the pattern over a long strip and distinguish blocked PACs and 2:1 block.

Specialist management

Treat the patient and cause. Asymptomatic nodal Wenckebach may be observed; adverse features require the bradycardia algorithm, pads and senior/cardiology review.

Monitoring & escalation

Continuous ECG with symptoms or acute disease; document level of block, QRS width and response.

Specialist medicines and adult doses

1Atropine 500 micrograms IV when appropriate; repeat every 3–5 minutes to a maximum total 3 mg.

2If ineffective with adverse features, adrenaline 2–10 micrograms/min or isoprenaline starting 5 micrograms/min may bridge to pacing under protocol.

AV conduction

Second-degree AV block—Mobitz II / high-grade

Recognise

Intermittent non-conducted P waves without progressive PR prolongation. Broad QRS and multiple consecutive blocked P waves increase concern for infranodal/high-grade disease.

Specialist management

Apply pacing pads, obtain urgent cardiology input and arrange definitive pacing assessment. Do not be reassured by a temporarily adequate blood pressure.

Monitoring & escalation

Continuous ECG and perfusion/BP; immediate escalation for syncope, pauses, escape failure or complete block.

Specialist medicines and adult doses

1Atropine 500 micrograms IV may be attempted when appropriate but is often ineffective in infranodal block; repeat to total 3 mg only within the bradycardia algorithm.

2Adrenaline 2–10 micrograms/min or isoprenaline starting 5 micrograms/min may bridge to pacing with monitored specialist care.

Intraventricular conduction

Right bundle branch block

Recognise

Delayed right-ventricular activation produces a wide QRS with terminal right-precordial positivity and broad lateral S waves. Check axis, PR and ST–T changes.

Specialist management

No treatment for RBBB itself. New RBBB with chest pain, syncope, bifascicular disease, bradycardia or suspected PE/myocarditis requires cause-directed urgent assessment.

Monitoring & escalation

Compare prior ECG, telemetry when acute/symptomatic, echo and pacing assessment when clinically indicated.

Specialist medicines and adult doses

1No medicine reverses an isolated RBBB.

2If ACS is suspected, aspirin 300 mg once unless clearly contraindicated; all further antithrombotic treatment follows the ACS pathway.

Pre-excitation

Wolff–Parkinson–White pre-excitation

Recognise

Short PR, delta wave and widened QRS in sinus rhythm. During tachycardia distinguish orthodromic AVRT, antidromic AVRT and pre-excited AF.

Specialist management

Adverse features require synchronised cardioversion. Pre-excited AF is an electrophysiological emergency: avoid isolated AV-nodal blockade and obtain urgent expert help; refer symptomatic WPW for ablation assessment.

Monitoring & escalation

Defibrillator-ready ECG monitoring; document family history, syncope and pathway-risk/ablation plan.

Specialist medicines and adult doses

1For stable regular narrow AVRT, adenosine 6 mg then 12 mg then 18 mg may be used only when the rhythm is confirmed and no pre-excited AF is present.

2In pre-excited AF avoid adenosine, digoxin, verapamil/diltiazem and isolated beta-blockade; use specialist-directed rhythm therapy or cardioversion.

3Flecainide IV dosing is weight- and protocol-specific and should be given only with electrophysiology/cardiology oversight.

Acute coronary occlusion

Inferior STEMI

Recognise

Territorial inferior ST elevation with reciprocal high-lateral change. Obtain right-sided and posterior leads when RV or posterior extension is possible.

Specialist management

Activate the primary-PCI pathway immediately; do not await troponin. Assess bradyarrhythmia, RV involvement, hypotension and mechanical complications.

Monitoring & escalation

Defibrillator-ready telemetry, serial ECG, BP/perfusion, electrolytes and urgent echo for instability.

Specialist medicines and adult doses

1Aspirin 300 mg orally once unless clearly allergic/contraindicated.

2GTN 400 micrograms sublingual only if BP and preload permit; avoid hypotension and suspected RV infarction.

3P2Y12 inhibitor and anticoagulant are selected by the PCI pathway using bleeding and renal risk.

Acute coronary occlusion

Right-ventricular STEMI

Recognise

Inferior infarction with right-sided lead elevation, classically V4R. Look for hypotension, raised JVP and clear lungs; obtain the right-sided ECG early.

Specialist management

Immediate PCI activation. Maintain RV preload without indiscriminate fluid loading; treat bradycardia/high-grade block and escalate shock early.

Monitoring & escalation

Continuous ECG, invasive/close BP and perfusion assessment, urine/lactate and urgent echo.

Specialist medicines and adult doses

1Aspirin 300 mg orally once unless contraindicated; further antithrombotics follow the PCI protocol.

2Avoid nitrates and unnecessary diuretics in hypotensive/preload-dependent RV infarction.

3Small IV crystalloid challenges may be used with repeated haemodynamic/lung reassessment; vasopressor/inotrope choice is critical-care/cardiology led.

Metabolic ECG

Hypocalcaemia with QT prolongation

Recognise

Hypocalcaemia typically prolongs the QT by lengthening the ST segment. Confirm corrected/ionised calcium, magnesium, phosphate, renal function and symptoms.

Specialist management

Seizure, tetany, laryngospasm, arrhythmia or marked QT prolongation requires monitored IV calcium and treatment of the cause; correct magnesium when deficient.

Monitoring & escalation

Continuous ECG when severe; serial ionised/corrected calcium, magnesium and cause-specific monitoring.

Specialist medicines and adult doses

1Calcium gluconate 10% 10–20 mL IV over about 10 minutes with ECG monitoring; repeat according to symptoms, ECG and calcium under the local protocol.

2A continuing calcium-gluconate infusion may be required for persistent symptomatic hypocalcaemia and is calculated/titrated by specialist protocol.

3Avoid rapid calcium administration and confirm compatibility/access; calcium chloride is generally reserved for arrest/peri-arrest or specialist central access.

Drug and toxin ECG

Digoxin/digitoxin effect and toxicity

Recognise

Therapeutic effect may cause scooped ST depression and PR prolongation; toxicity can produce almost any atrial or ventricular arrhythmia, especially with renal dysfunction or low potassium/magnesium.

Specialist management

Stop the glycoside, assess ABCDE, rhythm and haemodynamics, correct electrolytes carefully and discuss urgently with NPIS/TOXBASE and cardiology. Severe ventricular arrhythmia, advanced block or hyperkalaemia may require antibody fragments.

Monitoring & escalation

Continuous ECG, potassium/magnesium, renal function, serial glycoside concentration at interpretable times and post-antibody rebound surveillance.

Specialist medicines and adult doses

1Digoxin-specific antibody fragments are dosed from the amount ingested or post-distribution serum concentration; when neither is reliable, use the current TOXBASE/product protocol—do not guess a universal vial count.

2Atropine 500 micrograms IV may be used for clinically important bradycardia while definitive treatment is arranged; repeat within the bradycardia algorithm.

3Avoid routine IV calcium or cardioversion without toxicology/cardiology guidance; correct K/Mg using serial results and renal function.

Real clinical ECG masterclass

Read every ECG in the same order

Patient → calibration → rate → rhythm → axis → P waves → PR → QRS → QTc → ST–T → comparison → clinical conclusion.

25 mm/s
10 mm/mV

Do not let a picture overrule the patient.These are genuine de-identified clinical traces. Repeat the ECG during symptoms, obtain posterior/right-sided leads when indicated, compare previous traces and urgently escalate ongoing ischaemia, instability, high-grade block or malignant arrhythmia.

1. Orientate yourself on a real 12-lead ECG

First confirm the patient identifiers on the original, recording date/time, speed, gain and lead placement. Then read each lead and the rhythm strip systematically.

A genuine twelve-lead clinical electrocardiogram — **Clinical 12-lead ECG**Peter H Charlton, CC BY 4.0 · source and licence ↗

2. Axis made simple

Look at lead I and aVF

The main QRS deflection points toward the lead’s positive electrode. This teaching wheel explains the calculation; confirm it on the real 12-lead.

Lead I +aVF +Normal
−30° to +90°Left axis
I + / aVF −Right axis
I − / aVF +Extreme
I − / aVF −

I +, aVF +Normal quadrant.

I +, aVF −Check lead II: a negative QRS supports true left-axis deviation.

I −, aVF +Right-axis deviation: consider RVH, acute right-heart strain, lateral MI, dextrocardia or normal variant.

I −, aVF −Extreme axis: consider ventricular rhythm, severe RV disease or lead error; confirm placement.

3. Hypertrophy

Left ventricular hypertrophy with secondary repolarisation change

Real clinical ECG showing left ventricular hypertrophy and secondary repolarisation abnormalities — **LVH with strain pattern**James Heilman MD, CC BY-SA 4.0 · source and licence ↗

What the labels show

High QRS voltage plus a lateral “strain” pattern—down-sloping ST depression and asymmetric T-wave inversion. Voltage criteria are screening tools, not proof of anatomical LVH.

Keep it simple

Large left-sided voltage suggests increased LV muscle mass. Repolarisation then travels abnormally, producing ST–T changes that can resemble ischaemia.

Do not miss

LVH does not exclude acute coronary occlusion. Compare previous ECGs, look for disproportionate or dynamic change and correlate with echocardiography.

4. Electrolytes

Real patient traces: potassium disorders

Real ECG from a patient with severe hyperkalaemia showing peaked T waves — **Severe hyperkalaemia (K 8.2 mmol/L)**Agbayani & Gonzales, CC BY 4.0 · source and licence ↗

Hyperkalaemia can progress from peaked T waves to PR prolongation/P-wave loss, QRS widening and a sine-wave pattern. The sequence is unreliable: treat the patient and biochemical severity, not the picture alone.

Real ECG showing severe hypokalaemia with ST depression, T inversion and large U waves — **Severe hypokalaemia (K 1.1 mmol/L)**James Heilman MD, CC BY-SA 3.0 · source and licence ↗

Hypokalaemia produces ST depression, flattened/inverted T waves and prominent U waves, with apparent QT prolongation that is often a long QU interval. Arrhythmia risk increases with low magnesium or QT-prolonging medicines.

Calcium and magnesiumHypocalcaemia typically lengthens the QT (mainly ST); hypercalcaemia shortens it. Severe magnesium disturbance can alter PR/QRS/QT and provoke arrhythmia, but these appearances are nonspecific—confirm the blood result and clinical context.

5. Acute coronary syndromes

Real STEMI tracing and an NSTEMI reading approach

Real twelve-lead ECG showing anterior ST elevation myocardial infarction and reciprocal depression — **Anterior STEMI with reciprocal change**Displaced, public domain · source and licence ↗

STEMI: look for ST elevation in anatomically contiguous leads with reciprocal change, hyperacute T waves and dynamic evolution. A convincing occlusion pattern requires immediate pathway activation—do not wait for troponin.

NSTEMI

The ECG may show ST depression, T-wave inversion, transient elevation—or be normal

Repeat ECGs during pain and after symptom change.
Compare with previous traces.
Look for new horizontal/down-sloping ST depression or dynamic symmetrical T inversion.
Diagnose NSTEMI from a troponin rise/fall plus clinical evidence of ischaemia—not from ECG alone.

Septal V1–V2Anterior V3–V4Lateral I, aVL, V5–V6Inferior II, III, aVFPosterior V7–V9 / reciprocal V1–V3Right ventricle V3R–V4R

6. STEMI mimics

Compare real clinical examples

A mimic can coexist with MI. Use symptoms, serial ECGs, troponin, echo and urgent expert review.

Real ECG showing acute pericarditis with widespread ST elevation — **Acute pericarditis**James Heilman MD, CC BY-SA 3.0 · source and licence ↗

Widespread rather than territorial ST elevation, often with PR depression; reciprocal ST depression is usually limited to aVR/V1.

Real ECG showing a type one Brugada pattern in V1 to V3 — **Type 1 Brugada pattern**PeaBrainC, CC BY-SA 4.0 · source and licence ↗

Coved ST elevation followed by T-wave inversion in the right precordial leads. Fever and medicines can unmask it; syncope or arrhythmia requires urgent specialist review.

Real twelve-lead ECG showing left bundle branch block — **Left bundle branch block**CardioNetworks/ECGpedia, CC BY-SA 3.0 · source and licence ↗

Wide QRS with secondary discordant ST–T change. Use validated occlusion criteria and clinical context; ongoing ischaemia still needs urgent review.

Real ECG showing LVH voltage and strain that can mimic ischaemia — **LVH strain—a common mimic**James Heilman MD, CC BY-SA 4.0 · source and licence ↗

Large voltage with lateral ST depression/T inversion and sometimes discordant anterior elevation. Compare old traces; LVH does not rule out ACS.

Other mimics to remember: benign early repolarisation, ventricular aneurysm, hyperkalaemia, paced rhythm, takotsubo syndrome and myocarditis.

About these ECGs

All clinical traces are de-identified educational examples hosted by Wikimedia Commons. Labels are explanatory overlays added by Acute Medical Take; the original files remain unchanged. Attribution and licence links are shown beneath every image.

Educational examples—not a substitute for assessment of the original diagnostic-quality 12-lead ECG, clinical presentation, local ACS pathway and senior/cardiology interpretation.

Choose an ECG pattern

Foundations & artefact

Rhythm & conduction

Ischaemia & mimics

Metabolic & repolarisation

High-risk patterns

Normal sinus rhythm

Specialist medicines and adult doses

Atrial flutter / atrial arrhythmias

Specialist medicines and adult doses

Ventricular tachycardia

Specialist medicines and adult doses

Ventricular fibrillation

Specialist medicines and adult doses

Complete heart block

Specialist medicines and adult doses

Long QT and torsades

Specialist medicines and adult doses

Pulmonary embolism / RV strain

Specialist medicines and adult doses

Type-1 Brugada pattern

Specialist medicines and adult doses

Pacemaker ECG

Specialist medicines and adult doses

Lead reversal

Specialist medicines and adult doses

Anterior STEMI

Specialist medicines and adult doses

Acute pericarditis

Specialist medicines and adult doses

Left bundle branch block

Specialist medicines and adult doses

Left ventricular hypertrophy with strain

Specialist medicines and adult doses

Severe hyperkalaemia

Specialist medicines and adult doses

Severe hypokalaemia

Specialist medicines and adult doses

Real clinical examples—abnormality clearly labelled

What the patient may call a “skipped beat”

Pause: describe the mechanism, not only the seconds

NSVT requires the full event

Atrial fibrillation

Specialist medicines and adult doses

Atrial flutter

Specialist medicines and adult doses

Regular narrow-complex SVT

Specialist medicines and adult doses

First-degree AV block

Specialist medicines and adult doses

Second-degree AV block—Mobitz I

Specialist medicines and adult doses

Second-degree AV block—Mobitz II / high-grade

Specialist medicines and adult doses

Right bundle branch block

Specialist medicines and adult doses

Wolff–Parkinson–White pre-excitation

Specialist medicines and adult doses

Inferior STEMI

Specialist medicines and adult doses

Right-ventricular STEMI

Specialist medicines and adult doses

Hypocalcaemia with QT prolongation

Specialist medicines and adult doses

Digoxin/digitoxin effect and toxicity

Specialist medicines and adult doses

1. Orientate yourself on a real 12-lead ECG

Look at lead I and aVF

Left ventricular hypertrophy with secondary repolarisation change

Real patient traces: potassium disorders

Real STEMI tracing and an NSTEMI reading approach

The ECG may show ST depression, T-wave inversion, transient elevation—or be normal

Compare real clinical examples