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