Most Common ECGs in FRCEM Exams

Topic priority at a glance

ECG interpretation is a core Emergency Medicine skill and a frequent source of marks in MRCEM SBA, FRCEM SBA and FRCEM OSCE stations. In the exam, the task is rarely to provide a perfect cardiology report. The real test is whether you can recognise the dangerous pattern, place it in clinical context, and make the correct immediate Emergency Department decision.

The highest-yield ECGs are those that change management in the first minutes: acute coronary occlusion, unstable tachyarrhythmia, high-grade bradyarrhythmia, hyperkalaemia, toxicological ECG changes, and inherited channelopathy patterns linked to syncope or sudden death. This guide focuses on those patterns, the common mimics, and the next best step expected in UK practice.

Why the Most Common ECGs Matter for FRCEM Exams

ECGs appear across chest pain, collapse, syncope, palpitations, overdose, sepsis, electrolyte disturbance and peri-arrest care. In UK Emergency Medicine, rapid ECG recognition affects:

• Activation of the PPCI pathway
• Immediate ALS-based treatment of unstable tachycardia or bradycardia
• Recognition of STEMI equivalents
• Urgent treatment of hyperkalaemia
• Avoidance of dangerous drugs in pre-excited atrial fibrillation
• Recognition of toxicological patterns such as TCA poisoning
• Identification of high-risk syncope patterns such as Brugada or long QT

Exam questions usually reward recognition plus action. A candidate who says “atrial fibrillation” but does not comment on stability, rate control, cardioversion, anticoagulation relevance, or the underlying cause will often miss the key mark.

Key Definitions

Essential Pathophysiology

The ECG patterns most often tested in FRCEM reflect a small number of pathophysiological processes:

• Coronary occlusion causing transmural or subendocardial ischaemia
• Abnormal impulse generation, for example AF, SVT, VT
• Abnormal impulse conduction, for example AV block, bundle branch block, pre-excitation
• Membrane instability from electrolyte disturbance, especially hyperkalaemia
• Sodium channel blockade in poisoning, especially tricyclic antidepressants
• Inherited or acquired repolarisation abnormalities, for example long QT and Brugada syndrome
• Right ventricular strain from pulmonary embolism

For exam purposes, the key principle is simple: identify the process that changes immediate management. A broad-complex tachycardia is not just a tracing to label. It may represent VT requiring urgent ALS-based treatment. Diffuse ST depression with ST elevation in aVR is not a lesion-specific diagnosis, but it is a high-risk ischaemic pattern requiring urgent senior and cardiology input.

Clinical Presentation

Common stems that should trigger active ECG pattern search include:

• Central chest pain or ongoing ischaemic symptoms
• Syncope or near-syncope
• Palpitations with hypotension or chest pain
• Collapse in a dialysis patient
• Overdose, especially TCA or QT-prolonging drugs
• Fever with syncope or family history of sudden death
• Pleuritic chest pain, hypoxia or unexplained tachycardia
• Sepsis with new AF

In OSCEs and vivas, always integrate the ECG with symptoms, haemodynamics and likely cause. The same rhythm may require very different management depending on whether the patient is stable, shocked, septic, intoxicated or post-MI.

Red Flags and High-Risk Features

• Ongoing chest pain with ST elevation or a STEMI equivalent
• Broad-complex tachycardia, especially if regular
• Any tachyarrhythmia causing adverse features
• Complete heart block or Mobitz II block
• Hyperkalaemic ECG changes
• AF with very rapid broad irregular complexes suggesting pre-excitation
• QTc over 500 ms, especially with syncope or ventricular ectopy
• Brugada type 1 pattern, especially with syncope or fever
• Posterior MI pattern in V1 to V3
• Inferior STEMI with hypotension and clear lungs suggesting RV infarction
• TCA toxicity with QRS widening or terminal R in aVR

Differential Diagnosis

Common exam differentiators are often more important than the primary diagnosis.

Initial ED Assessment

Use a structured approach.

1. ABCDE assessment
2. Identify whether the patient is unstable
3. Attach monitoring, obtain IV access, check capillary glucose
4. Record a 12-lead ECG early and repeat if symptoms continue or evolve
5. Interpret the ECG with a rapid danger-first scan:
   • Rate and regularity
   • QRS width
   • ST elevation or depression
   • T-wave abnormalities
   • PR interval and AV block pattern
   • QTc
   • Conduction delay or pre-excitation
6. Ask the key ED question: what must I do now?

For arrhythmias, anchor management to Resuscitation Council UK ALS principles. For chest pain, think reperfusion, additional leads, serial ECGs and urgent escalation where indicated.

Investigations

Investigations depend on the pattern and presentation, but common high-yield tests include:

• Repeat 12-lead ECGs if symptoms are ongoing or evolving
• Right-sided leads, especially V4R, in inferior STEMI with possible RV involvement
• Posterior leads V7 to V9 if posterior MI is suspected
• Venous or arterial blood gas for potassium and acid-base status
• Urea and electrolytes, magnesium, calcium
• Troponin according to local ACS pathway
• FBC if anaemia or sepsis is possible
• Toxicology history and drug levels where relevant, for example digoxin
• Pregnancy test where relevant
• Chest radiograph or point-of-care ultrasound if heart failure, tamponade or alternative pathology is suspected
• CT pulmonary angiography if PE is suspected and clinically appropriate

Do not delay reperfusion in clear STEMI or STEMI equivalent while waiting for troponin. Do not rely on machine interpretation.

Management in the Emergency Department

The most useful exam approach is pattern recognition linked to immediate action.

1. STEMI and acute coronary occlusion patterns

Classic STEMI remains one of the commonest ECG themes in FRCEM.

Recognition points:

• ST elevation at the J point in anatomically contiguous leads
• In most leads, at least 1 mm in two contiguous leads
• In V2 to V3, higher thresholds apply:
  • Men aged 40 or over: at least 2 mm
  • Men under 40: at least 2.5 mm
  • Women: at least 1.5 mm
• Reciprocal ST depression supports acute occlusion
• Hyperacute T waves may precede obvious ST elevation

Localisation:

• Anterior: V1 to V4
• Lateral: I, aVL, V5, V6
• Inferior: II, III, aVF

Immediate ED management:

• Activate the local PPCI pathway in a compatible clinical context
• Give aspirin if not contraindicated, according to local ACS protocol
• Continuous monitoring and senior involvement
• Repeat ECGs if symptoms continue and the first ECG is non-diagnostic
• Compare with previous ECGs if available

Exam trap:

• Normal early troponin does not exclude acute coronary occlusion
• Do not dismiss subtle anterior occlusion because ST elevation is modest

2. Inferior STEMI with right ventricular infarction

Recognition points:

• Inferior STEMI in II, III and aVF
• ST elevation greater in III than II suggests RCA occlusion
• ST elevation in V1 may support RV involvement
• Confirm with right-sided leads, especially V4R
• Clinical clue: hypotension, raised JVP and clear lungs

Immediate ED management:

• Urgent reperfusion pathway activation
• If hypotensive and lungs are clear, consider a cautious fluid bolus with reassessment
• Avoid nitrates in hypotension or suspected preload-dependent RV infarction
• Monitor for bradyarrhythmia and AV block
• Manage bradycardia according to ALS if adverse features are present

Exam trap:

• Reflex nitrate use in all chest pain with ST elevation
• Failure to record right-sided leads

3. Posterior MI

Recognition points on the standard 12-lead, usually in V1 to V3:

• Horizontal ST depression
• Tall broad R waves
• Upright T waves

Immediate ED management:

• Record posterior leads V7 to V9
• Treat as a STEMI equivalent in the right clinical context
• Discuss urgent reperfusion rather than defaulting to routine NSTEMI management

Exam trap:

• Mislabelled as anterior ischaemia or generic NSTEMI

4. Wellens syndrome

Wellens syndrome is a high-risk pre-infarction pattern associated with critical proximal LAD disease.

Recognition points:

• Usually pain-free at the time of ECG
• Deeply inverted or biphasic T waves in V2 to V3, sometimes extending to V1 to V6
• Little or no ST elevation
• No significant precordial Q waves
• Recent history of resolved chest pain

Immediate ED management:

• Urgent cardiology discussion
• Admit for further assessment and definitive management
• Do not reassure on the basis of pain resolution or a normal initial troponin
• Do not arrange provocative stress testing from the ED

Exam trap:

• Pain-free patient with normal or minimally raised troponin being discharged

5. De Winter pattern

This is an anterior occlusion pattern and a STEMI equivalent.

Recognition points:

• Upsloping ST depression at the J point in the precordial leads
• Tall, symmetrical T waves in the precordial leads
• Often slight ST elevation in aVR
• No classic anterior ST elevation despite acute LAD occlusion

Immediate ED management:

• Treat as acute coronary occlusion
• Urgent senior and cardiology discussion with reperfusion pathway activation according to local practice

Exam trap:

• Called “NSTEMI” because there is no obvious ST elevation

6. Diffuse ST depression with ST elevation in aVR

Recognition points:

• Widespread ST depression in multiple leads
• ST elevation in aVR, sometimes V1

Clinical meaning:

• High-risk global subendocardial ischaemia pattern
• May reflect severe coronary disease, but is not specific for left main stem occlusion
• Can also occur with shock, severe anaemia, tachyarrhythmia or other supply-demand mismatch

Immediate ED management:

• Urgent senior review
• Urgent cardiology input in a compatible ACS presentation
• Treat the underlying cause if this is demand ischaemia rather than primary ACS

Exam trap:

• Overcalling it as a lesion-specific diagnosis

7. LBBB, paced rhythm and Sgarbossa concepts

Recognition points:

• LBBB and ventricular pacing produce secondary ST-T changes that make ACS harder to diagnose
• New LBBB alone is not an automatic STEMI equivalent in modern UK practice
• Concordant ST elevation or concordant ST depression in V1 to V3 is concerning
• Modified Sgarbossa concepts may help in selected cases

Immediate ED management:

• Interpret in clinical context
• Use serial ECGs, symptoms, previous tracings and troponin strategy
• Seek urgent senior and cardiology input if acute occlusion is suspected

Exam trap:

• Automatic activation for “new LBBB” without context

8. Atrial fibrillation

Recognition points:

• Irregularly irregular rhythm
• No organised P waves
• Usually narrow QRS unless aberrancy or pre-excitation is present

Immediate ED management:

• First decide if the patient has adverse features due to the arrhythmia
• If AF is causing haemodynamic instability, perform synchronised DC cardioversion according to ALS guidance
• If stable, treat the underlying cause and consider rate control according to local policy and senior input
• Look for precipitant: sepsis, PE, thyrotoxicosis, alcohol, ACS, heart failure
• Consider anticoagulation implications, though this is rarely the first ED priority in an unstable patient

Exam trap:

• Treating the ECG but ignoring the cause, for example sepsis or PE

9. SVT

Recognition points:

• Regular narrow-complex tachycardia
• P waves absent, retrograde or difficult to see
• Rate often 150 to 250

Immediate ED management:

• If unstable, synchronised DC cardioversion
• If stable and regular narrow-complex, attempt vagal manoeuvres
• If unsuccessful and no contraindication, give adenosine according to ALS guidance
• If uncertain, seek senior help and review the rhythm carefully

Exam trap:

• Giving adenosine to an irregular broad-complex tachycardia or AF in WPW

10. Broad-complex tachycardia and ventricular tachycardia

Recognition points:

• QRS 120 ms or more
• Regular broad-complex tachycardia in an adult should be presumed VT until proven otherwise by an experienced clinician
• Features supporting VT include AV dissociation, capture beats, fusion beats, extreme axis and concordance

Immediate ED management:

• If pulseless, manage as cardiac arrest
• If unstable with a pulse, synchronised DC cardioversion
• If stable monomorphic VT, follow ALS tachycardia guidance and seek senior support
• Correct reversible causes such as ischaemia, electrolyte disturbance or drug toxicity

Exam trap:

• Assuming broad-complex tachycardia is SVT with aberrancy

11. Complete heart block and high-grade AV block

Recognition points:

• AV dissociation in complete heart block
• More P waves than QRS complexes
• Escape rhythm may be narrow or broad
• Mobitz II is also high risk and may progress to complete heart block

Immediate ED management:

• Assess for adverse features
• If unstable, treat according to ALS bradycardia guidance
• Atropine may help in selected cases, especially nodal block, but may be ineffective in infranodal block
• Prepare for transcutaneous pacing if needed and escalate early for transvenous pacing
• Look for reversible causes: MI, hyperkalaemia, drug toxicity

Exam trap:

• Reassurance because the ventricular rate is “not too slow” despite syncope or hypotension

12. Hyperkalaemia

Recognition points:

• Tall tented T waves
• PR prolongation
• P-wave flattening or loss
• QRS widening
• Sine-wave pattern in severe cases

Immediate ED management:

• If ECG changes are present, give IV calcium according to local policy to stabilise the myocardium
• Shift potassium intracellularly with insulin and glucose according to local protocol
• Consider nebulised salbutamol if appropriate
• Arrange definitive potassium removal and treat the cause
• Continuous monitoring, repeat ECG and repeat potassium measurement
• Escalate early if severe, refractory, or in renal failure

Exam trap:

• Waiting for formal laboratory confirmation before treating a dangerous ECG
• Confusing hyperkalaemic T waves with hyperacute ischaemic T waves

13. Pericarditis versus STEMI

Immediate ED management:

• If the diagnosis is uncertain, do not dismiss possible ACS
• Use clinical context, serial ECGs and senior review
• Consider echocardiography if tamponade or significant effusion is suspected

Exam trap:

• Calling all concave ST elevation “benign pericarditis” without considering ACS

14. Pulmonary embolism and right heart strain

Recognition points:

• Sinus tachycardia is the commonest ECG finding
• Right heart strain may produce T-wave inversion in V1 to V4 and inferior leads
• Right bundle branch block may occur
• S1Q3T3 is neither sensitive nor specific

Immediate ED management:

• ECG findings are supportive, not diagnostic
• Interpret with clinical probability, blood tests and imaging pathway
• If shocked or peri-arrest, think massive PE and escalate urgently

Exam trap:

• Diagnosing PE from S1Q3T3 alone

15. WPW and AF in WPW

Recognition points in sinus rhythm:

• Short PR interval
• Delta wave
• Broad QRS due to pre-excitation

Recognition points in AF with WPW:

• Irregular broad-complex tachycardia
• Very rapid ventricular rates
• Beat-to-beat variation in QRS morphology

Immediate ED management:

• If unstable, synchronised DC cardioversion
• Avoid AV nodal blockers in AF with WPW, including adenosine, verapamil, diltiazem, beta-blockers and digoxin
• Urgent senior and cardiology input

Exam trap:

• Giving adenosine or rate-limiting calcium channel blockers to broad irregular tachycardia

16. Long QT and torsades de pointes

Recognition points:

• QTc prolonged, especially over 500 ms
• Polymorphic VT with twisting axis suggests torsades
• Causes include drugs, hypokalaemia, hypomagnesaemia, bradycardia and congenital syndromes

Immediate ED management:

• Stop offending drugs
• Correct potassium, magnesium and calcium abnormalities
• Give IV magnesium sulphate for torsades or marked QT-related ventricular ectopy according to local guidance
• If unstable, immediate defibrillation or cardioversion as appropriate
• Seek specialist input for recurrent episodes; overdrive pacing may be required in selected cases

Exam trap:

• Missing drug-induced QT prolongation in overdose or polypharmacy

17. Brugada pattern

Recognition points:

• Coved ST elevation in V1 to V3 with T-wave inversion in a type 1 pattern
• May be unmasked or worsened by fever
• High-risk context includes syncope, nocturnal agonal respiration or family history of sudden death

Immediate ED management:

• Treat fever aggressively
• Urgent senior review and cardiology discussion if symptomatic or high risk
• Do not dismiss as benign right bundle branch block variant

Exam trap:

• Young patient with fever and syncope being discharged without recognising the pattern

18. Atrial flutter

Recognition points:

• Saw-tooth flutter waves, often best in inferior leads
• Commonly 2:1 block with ventricular rate around 150

Immediate ED management:

• Assess stability first
• Manage unstable patients with synchronised cardioversion
• Stable patients usually need rate control and cause assessment with senior input

Exam trap:

• Calling 2:1 flutter “sinus tachycardia”

19. Mobitz I versus Mobitz II

20. Hypokalaemia

Recognition points:

• Flattened T waves
• ST depression
• Prominent U waves
• Apparent QT prolongation due to QU prolongation

Immediate ED management:

• Replace potassium according to severity and local policy
• Check magnesium
• Monitor if severe or arrhythmogenic

21. TCA toxicity

Recognition points:

• Sinus tachycardia
• QRS widening
• Terminal R wave in aVR
• QT prolongation may occur

Immediate ED management:

• Resuscitation and toxicology support
• Give sodium bicarbonate for significant QRS widening, ventricular arrhythmia or haemodynamic instability according to local toxicology guidance
• Treat seizures promptly
• Continuous cardiac monitoring

Exam trap:

• Missing the significance of aVR changes in overdose

22. Digoxin effect and toxicity

Recognition points:

• Digoxin effect may cause scooped ST depression without toxicity
• Toxicity may produce almost any arrhythmia, classically bradyarrhythmia, AV block or atrial tachycardia with block

Immediate ED management:

• Check potassium, renal function and digoxin level where appropriate
• Seek senior and toxicology advice if toxicity is suspected
• Manage life-threatening arrhythmia and consider digoxin-specific antibody fragments in severe toxicity according to specialist advice

23. Early repolarisation and LVH strain

These are common STEMI mimics.

Early repolarisation clues:

• Young well patient
• Concave ST elevation, often precordial
• J-point notching or slurring
• Stable over time

LVH strain clues:

• Voltage criteria for LVH
• Secondary ST depression and T-wave inversion in lateral leads
• May mimic ischaemia but should fit the overall pattern

Exam trap:

• Overcalling benign or chronic changes as acute STEMI

Immediate versus later care: practical ED summary

Disposition, Referral and Follow-Up

High-risk ECG findings usually mandate admission or urgent specialist review.

• PPCI pathway: STEMI and accepted STEMI equivalents in the appropriate clinical context
• Monitored admission: VT, significant AF/flutter, complete heart block, Mobitz II, hyperkalaemia with ECG changes, long QT with syncope, significant overdose ECG changes
• Urgent cardiology review: Wellens, Brugada with symptoms, suspected ACS in LBBB or paced rhythm, WPW with symptomatic arrhythmia, recurrent syncope with abnormal ECG
• Critical care or resus-level care: unstable arrhythmia, severe hyperkalaemia, massive PE, toxicological instability

Low-risk discharge is uncommon when the ECG is clearly abnormal. If discharge is considered, it should follow senior review, appropriate serial testing where indicated, and a safe follow-up plan.

Special Groups

Paediatrics

• Normal heart rates vary with age; avoid overcalling sinus tachycardia or bradycardia
• Congenital channelopathies and pre-excitation are important causes of syncope
• Use paediatric ALS principles where relevant

Pregnancy

• Do not dismiss chest pain, syncope or palpitations as benign without proper assessment
• PE remains an important differential
• Cardioversion is permissible in pregnancy when indicated

Elderly patients

• More likely to have conduction disease, AF, ACS and polypharmacy-related QT prolongation
• Baseline ECG abnormalities are common; compare with previous tracings

Immunosuppressed or septic patients

• AF may be secondary to sepsis rather than a primary rhythm problem
• Electrolyte disturbance and myocarditis may complicate interpretation

Dialysis and renal failure

• Always think hyperkalaemia in collapse, weakness, bradycardia or broad QRS
• Treat dangerous ECG changes immediately

Common Pitfalls

• Describing the ECG correctly but failing to state the immediate management
• Relying on machine interpretation
• Missing posterior MI because there is no obvious ST elevation
• Forgetting right-sided leads in inferior STEMI with hypotension
• Calling all broad-complex tachycardia SVT with aberrancy
• Giving AV nodal blockers in AF with WPW
• Waiting for blood results before treating hyperkalaemia with ECG changes
• Overcalling aVR elevation as a specific left main stem diagnosis
• Treating “new LBBB” as automatic STEMI without context
• Discharging pain-free Wellens syndrome
• Using simplistic rules to distinguish pericarditis from STEMI
• Diagnosing PE from ECG alone

FRCEM and MRCEM Exam Tips

A safe exam structure is:

1. State the rhythm and whether the patient is stable or unstable
2. Identify the management-changing abnormality
3. Give the immediate ED action
4. Mention one key differential or mimic if relevant
5. State one thing you must not do if it is a classic trap

Useful viva phrasing:

• “This ECG shows a regular broad-complex tachycardia, which I would treat as ventricular tachycardia unless an experienced clinician proves otherwise.”
• “The immediate concern is acute coronary occlusion. I would activate the PPCI pathway and not wait for troponin.”
• “This is an inferior STEMI and I am concerned about right ventricular involvement, so I would obtain right-sided leads and avoid nitrates if the patient is hypotensive.”
• “This irregular broad-complex tachycardia suggests AF with pre-excitation. AV nodal blockers are potentially dangerous.”
• “These ECG changes are consistent with hyperkalaemia. I would give IV calcium immediately and start potassium-shifting treatment.”

For MRCEM, focus on basic recognition, narrow versus broad, regular versus irregular, and immediate safe management. For FRCEM, expect more nuance: STEMI equivalents, toxicology, channelopathies, pacing decisions, and management traps.

How This Appears in SBA Questions

Typical question stems:

• “A 58-year-old man with ongoing central chest pain has this ECG. What is the next best step?”
• “A hypotensive patient with inferior ST elevation is given GTN and becomes more unwell. What additional lead would have been most useful?”
• “A dialysis patient collapses. The ECG shows broad QRS complexes and absent P waves. What is the immediate treatment?”
• “A 24-year-old with palpitations has an irregular broad-complex tachycardia. Which drug is contraindicated?”
• “A pain-free patient with recent chest pain has deep T-wave inversion in V2 to V3. What investigation should be avoided?”
• “A febrile patient presents after syncope. The ECG shows coved ST elevation in V1 to V2. What is the most likely diagnosis?”

Key discriminator clues:

• Chest pain plus reciprocal change suggests acute coronary occlusion
• III greater than II in inferior STEMI suggests RCA and possible RV infarction
• ST depression V1 to V3 with tall R waves suggests posterior MI
• Pain-free with anterior T-wave inversion suggests Wellens
• Irregular broad tachycardia suggests AF in WPW until proven otherwise
• Dialysis, weakness or bradycardia suggests hyperkalaemia
• Overdose plus wide QRS and aVR changes suggests TCA toxicity
• Syncope plus QT prolongation or Brugada pattern suggests channelopathy

Common wrong-answer traps:

• Troponin before PPCI activation in clear STEMI
• Nitrates in hypotensive RV infarction
• Adenosine for irregular broad-complex tachycardia
• Rate-limiting calcium channel blocker in AF with WPW
• Stress test for Wellens syndrome
• Observation only for complete heart block with syncope
• Waiting for formal U&Es before treating hyperkalaemia with ECG changes

Key Takeaways

• In FRCEM, ECG questions usually test recognition plus the next best ED action.
• Start by asking whether the patient is unstable and whether the ECG shows a life-threatening pattern.
• Must-not-miss ECGs include STEMI, posterior MI, RV infarction, VT, complete heart block, hyperkalaemia, AF in WPW, long QT, Brugada and TCA toxicity.
• Posterior MI, Wellens and de Winter are classic STEMI-equivalent traps.
• New LBBB alone is not an automatic STEMI equivalent in modern UK practice.
• Diffuse ST depression with ST elevation in aVR is a high-risk ischaemic pattern, not a lesion-specific diagnosis.
• Regular broad-complex tachycardia in an adult should be treated as VT until proven otherwise by an experienced clinician.
• If AF is causing adverse features, synchronised cardioversion is indicated.
• In AF with WPW, avoid AV nodal blockers.
• Hyperkalaemia with ECG changes requires immediate treatment, not delayed confirmation.
• ECG findings in PE are supportive, not diagnostic.
• Do not rely on machine interpretation.

Further Reading

• Resuscitation Council UK. Adult advanced life support guidelines.
• NICE. Acute coronary syndromes guidance.
• NICE. Atrial fibrillation: diagnosis and management.
• RCEM curriculum and relevant clinical learning resources.
• British Cardiovascular Society and local cardiology network STEMI pathways.
• BTS guidance relevant to pulmonary embolism pathways.
• TOXBASE for UK toxicology management, including TCA overdose and digoxin toxicity.

Related on EM Final Exams

• Top 20 Most Examined Topics in FRCEM
• Chest Pain NICE CG95 Simplified for SBA Exams
• Top 15 Paediatric Emergencies for MRCEM
• Top Trauma Topics You Must Know for FRCEM

Authoritative Sources

• NICE guidance
• Royal College of Emergency Medicine (RCEM)

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