UKMLA ECG Interpretation Masterclass: Every Pattern

ECGs are the single most-tested skill in the UKMLA. Cardiology stems lean on them, emergency stems open with them, endocrinology pushes hyperkalaemia traces at you, respiratory questions hide PE in sinus tachycardia, and overdose stems rely on QT prolongation. If you cannot read a 12-lead ECG systematically in under 90 seconds, a double-digit chunk of your AKT score is at risk.

This masterclass is the one pillar that binds pattern recognition to UK guideline-aligned management. Every pattern below is paired with what the UKMLA actually expects you to do next — not just name. It is intentionally long because a single bookmarked reference beats ten scattered ones on exam day.

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1. Why ECGs dominate UKMLA across specialties

The UKMLA content map lists over 430 presentations. ECG interpretation is embedded in at least 40 of them — far more than any other single investigation. Here's the short list of specialties where the AKT will show you a rhythm strip before it shows you a patient:

• Cardiology — ACS, arrhythmias, heart failure, pericarditis, WPW, long QT. Covered in depth in our UKMLA cardiology masterclass.
• Emergency medicine — peri-arrest rhythms, unstable tachyarrhythmias, hyperkalaemic arrest. See the UKMLA emergency presentations pillar.
• Respiratory — pulmonary embolism (sinus tach most common, S1Q3T3 classically tested).
• Endocrinology / nephrology — hyperkalaemia peaked T waves, hypocalcaemia long QT.
• Toxicology — TCA sodium-channel blockade (wide QRS, dominant R in aVR), digoxin reverse-tick.
• Psychiatry — QTc prolongation on antipsychotics (haloperidol, quetiapine) and citalopram.
• Paediatrics — congenital heart disease ECG markers, long QT in syncope.

The takeaway: even specialties where ECGs feel peripheral hide them in SBAs. Systematic reading is non-negotiable.

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2. Systematic approach: rate, rhythm, axis, intervals, morphology

Every ECG — normal or abnormal, complex or trivial — is read in the same six-step sequence. On exam day you should be able to run this in 60–90 seconds per trace.

1. Confirm the trace. Patient name, date, calibration (10 mm/mV, 25 mm/s). Artefact? Lead reversal (tall P in aVR, negative in lead I = right-left arm swap)?
2. Rate. 300 ÷ number of large squares between R–R (regular) or count QRS complexes in 10 seconds × 6 (irregular).
3. Rhythm. Regular or irregular? Is every P followed by a QRS? Is every QRS preceded by a P? Narrow or broad?
4. Axis. Lead I and aVF: both positive = normal. Lead I positive, aVF negative = LAD. Lead I negative, aVF positive = RAD. Both negative = extreme axis (think VT or lead error).
5. Intervals. PR (120–200 ms, 3–5 small squares). QRS (<120 ms). QT (corrected with Bazett: QTc = QT/√RR). QTc >500 ms is a red flag.
6. Morphology. P-wave shape, QRS amplitude, ST segments (elevation/depression), T-wave direction, U-waves, delta waves, pathological Q waves.

Train this sequence until it is automatic. The UKMLA does not penalise slow readers; it penalises inconsistent ones. The students who miss subtle inferior STEMI in an arm-lead artefact trace are the ones who forgot step 1.

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3. Normal values and age-related variation

Common AKT trap: dominant R wave in V1 in adults is abnormal (think posterior MI, RVH, RBBB, WPW, or Duchenne). In children under 7 it is normal — do not over-call it in paeds stems.

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4. Atrial fibrillation — rate vs rhythm, CHA₂DS₂-VASc

ECG features: irregularly irregular, absent P waves, fibrillatory baseline, variable R–R. Rate usually 110–160 bpm if untreated.

UKMLA management you must know (NICE NG196, 2021 update):

• Haemodynamically unstable (shock, pulmonary oedema, syncope, ischaemic chest pain): synchronised DC cardioversion. This is the only time AF goes to the resus room.
• Stable, <48 hours onset: rate OR rhythm control. Rhythm strategy (chemical or DC cardioversion) is reasonable if reversible cause or first episode.
• Stable, ≥48 hours or unknown onset: rate control first (bisoprolol or diltiazem/verapamil; digoxin only if sedentary). Anticoagulate ≥3 weeks before elective cardioversion, or use TOE-guided approach.
• Anticoagulation: calculate CHA₂DS₂-VASc. Men ≥2, women ≥3 → DOAC (apixaban, rivaroxaban, edoxaban, dabigatran). Warfarin only if DOAC contraindicated (mechanical valve, moderate–severe mitral stenosis, antiphospholipid syndrome). HAS-BLED informs bleeding risk modification — it does not override anticoagulation need.
• Reversible causes to screen: thyrotoxicosis (TFTs), sepsis, electrolytes, alcohol, PE, acute MI.

CHA₂DS₂-VASc memory aid: Congestive heart failure (1), Hypertension (1), Age ≥75 (2), Diabetes (1), prior Stroke/TIA/thromboembolism (2), Vascular disease (1), Age 65–74 (1), Sex category female (1).

Four out of five AF questions in the AKT hinge on stroke prevention, not rhythm control. Make that your default instinct.

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5. Atrial flutter — sawtooth, 2:1 block

ECG features: sawtooth flutter waves (best seen in inferior leads II, III, aVF), atrial rate typically ~300 bpm, ventricular rate 150 bpm (2:1 block) — hence the pattern-recognition trap that a regular narrow-complex tachycardia at exactly 150 bpm is flutter until proven otherwise.

Management:

• Unstable: DC cardioversion.
• Stable: rate control (beta-blocker or diltiazem), then consider rhythm control. Catheter ablation of the cavotricuspid isthmus is highly effective and often first-line for typical flutter.
• Anticoagulation: same CHA₂DS₂-VASc rules as AF. Flutter is not a lower-risk rhythm despite the textbook phrasing.

Vagal manoeuvres or adenosine will transiently slow AV conduction and unmask the flutter waves if the diagnosis is uncertain.

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6. Supraventricular tachycardia vs sinus tachycardia

Sinus tachycardia: regular, narrow, rate 100–160, P wave upright in II/III/aVF before every QRS, gradual onset/offset, always a symptom (look for cause: sepsis, PE, bleed, thyrotoxicosis, pain, anxiety).

AVNRT / AVRT (paroxysmal SVT): regular, narrow, rate 150–220, P waves absent or buried in QRS/T, abrupt onset/offset.

AKT management ladder for stable SVT:

1. Vagal manoeuvres — modified Valsalva (legs elevated after strain) superior to standard; carotid sinus massage if no bruit in under-65s.
2. IV adenosine 6 mg rapid bolus with flush → 12 mg → 18 mg if no effect. Warn of impending flushing, chest tightness and transient asystole. Contraindicated in asthma (use verapamil).
3. IV verapamil or beta-blocker if adenosine fails.
4. DC cardioversion if unstable at any point.

Unstable SVT → shock. Do not waste time on drugs.

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7. Ventricular tachycardia vs VF vs torsades

Monomorphic VT: broad complex (>120 ms), regular, rate 120–250, uniform QRS morphology. Think previous MI scar.

Polymorphic VT / torsades de pointes: broad complex, QRS twists around baseline, associated with long QT. Precipitants: hypokalaemia, hypomagnesaemia, hypocalcaemia, methadone, citalopram, haloperidol, macrolides, class Ia/III antiarrhythmics.

VF: chaotic, no discernible QRS, no output. Always pulseless → shock.

Management (Resus Council UK ALS algorithm):

• Pulseless VT / VF → shock → CPR 2 min → reassess. Adrenaline 1 mg IV after 3rd shock, then every 3–5 min. Amiodarone 300 mg IV after 3rd shock.
• Stable VT (patient conscious, BP maintained) → IV amiodarone 300 mg over 20–60 min. Correct K⁺, Mg²⁺. Expert input.
• Unstable VT with pulse → synchronised DC cardioversion.
• Torsades → stop QT-prolonging drug, IV magnesium 2 g, overdrive pacing if persistent, correct electrolytes.

Regular broad-complex tachycardia with history of IHD is VT until proven otherwise. Never assume SVT with aberrancy without clear evidence. The UKMLA loves this distractor.

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8. Heart blocks: 1st, 2nd (Mobitz I/II), 3rd degree

• 1st degree: PR >200 ms, every P conducted. Usually benign.
• Mobitz I (Wenckebach): PR progressively lengthens until a P wave is dropped. Usually AV node, often benign, often drug-induced.
• Mobitz II: fixed PR with intermittent non-conducted P waves. Infranodal — pacemaker territory.
• 3rd degree (complete) AV block: P waves and QRS dissociated; ventricular escape rhythm (narrow 40–50 bpm if junctional, broad <40 if ventricular).

Pacemaker thresholds (UKMLA core): symptomatic 2nd-degree Mobitz II, any complete heart block, symptomatic bradycardia unresponsive to atropine.

Acute management of symptomatic bradycardia (Resus Council UK peri-arrest):

1. IV atropine 500 mcg, repeat to max 3 mg.
2. If no response → transcutaneous pacing or isoprenaline/adrenaline infusion.
3. Transvenous pacing by cardiology.

Atropine is ineffective for infranodal blocks — do not waste time; pace.

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9. WPW and pre-excitation patterns

ECG features: short PR (<120 ms), delta wave (slurred QRS upstroke), widened QRS (>110 ms), possible ST/T changes.

Clinical relevance:

• Orthodromic AVRT (narrow complex re-entry) — usual SVT management but avoid AV-nodal blockers (adenosine, verapamil, digoxin, beta-blockers) if AF develops — they can accelerate conduction down the accessory pathway.
• AF in WPW → pre-excited AF — irregular, broad, very fast (often >250 bpm). Synchronised DC cardioversion. If drugs needed, flecainide or procainamide.
• Definitive management: catheter ablation of accessory pathway.

AKT trap: WPW + palpitations SBA offering adenosine vs DC cardioversion — always check if AF is present. If irregular, shock.

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10. LBBB and RBBB criteria

RBBB (MaRRoW):

• QRS >120 ms
• RSR′ pattern in V1 (M-shape)
• Wide slurred S wave in V6, I, aVL (W-shape)

LBBB (WiLLiaM):

• QRS >120 ms
• Broad monomorphic R (no Q) in V6, I, aVL
• Dominant S (or QS) in V1
• Secondary ST/T changes opposite to QRS direction

Key rule: new LBBB with chest pain = STEMI-equivalent (activate primary PCI pathway per NICE NG185). Old LBBB obscures ST analysis — use Sgarbossa criteria to catch superimposed MI (concordant ST elevation ≥1 mm, concordant depression V1–V3, discordant elevation ≥5 mm).

RBBB is common and often benign. LBBB is almost always pathological — screen for structural heart disease.

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11. STEMI localisation by lead — territories and reciprocal changes

Diagnostic criteria: ≥1 mm ST elevation in ≥2 contiguous limb leads, or ≥2 mm in V1–V3 (≥1.5 mm in women, ≥2.5 mm in men <40).

Inferior STEMI → ALWAYS do a right-sided ECG. Up to 40% have RV infarction. GTN in RV infarction causes catastrophic hypotension (preload-dependent).

Management (NICE NG185): aspirin 300 mg chewed + ticagrelor 180 mg / prasugrel 60 mg + morphine + oxygen only if SpO₂ <94% + GTN (unless RV) + primary PCI within 120 min of diagnosis. Thrombolysis only if PCI unavailable within that window.

Deeper on ACS in our cardiology masterclass and emergency presentations pillar.

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12. NSTEMI / ischaemic changes

NSTEMI ECG features: ST depression ≥0.5 mm, T-wave inversion ≥1 mm, or normal ECG with elevated troponin.

High-risk features:

• Wellens' syndrome — biphasic or deeply inverted T waves in V2–V3; indicates critical proximal LAD stenosis. Do NOT stress-test; refer for urgent angiography.
• De Winter T waves — upsloping ST depression at J-point with tall symmetric T waves V1–V6; STEMI-equivalent.
• aVR ST elevation + diffuse depression — left main / three-vessel disease. Urgent angiography.

Management: fondaparinux (or LMWH), aspirin 300 mg + ticagrelor/clopidogrel, nitrate, beta-blocker. Risk-stratify with GRACE score: high risk → angiography within 72 h (or 24 h if very high risk).

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13. Pericarditis and PE-related ECGs (S1Q3T3, sinus tach)

Acute pericarditis:

• Widespread concave (saddle-shape) ST elevation — not territorial.
• PR depression (best seen lead II) — highly specific.
• PR elevation in aVR.
• Evolves through four stages (Spodick): ST↑/PR↓ → normalisation → T inversion → resolution.

Differentiating from STEMI: reciprocal changes absent (except aVR), diffuse ST elevation, PR changes present, pleuritic chest pain relieved by sitting forward, pericardial rub.

Pulmonary embolism:

• Sinus tachycardia — most common ECG finding (up to 40%).
• S1Q3T3 — deep S in I, Q wave in III, inverted T in III (classic but present in only ~20%).
• Right bundle branch block, right-axis deviation, T-wave inversion V1–V4 (right heart strain).

Clinical pathway: Wells score → D-dimer (if unlikely) or CTPA (if likely). Submassive PE with RV strain → thrombolysis consideration. Fuller algorithm in our respiratory masterclass.

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14. Electrolyte ECGs: hyperK, hypoK, hyperCa, hypoCa

Hyperkalaemia (progressive as K⁺ rises):

1. Tall, peaked T waves (>5.5 mmol/L)
2. P-wave flattening and PR prolongation (>6.5)
3. QRS widening (>7.0)
4. Sine-wave pattern → VF/asystole (>8.0)

Management ladder (UK Kidney Association 2023): IV calcium gluconate 10 mL 10% → insulin 10 units + 25 g dextrose → salbutamol nebuliser → Lokelma/Patiromer → dialysis. Detailed in the UKMLA nephrology pillar.

Hypokalaemia:

• ST depression
• T-wave flattening/inversion
• U waves (after T, most visible V2–V3)
• Prolonged QT → torsades risk
• VE, VT, VF if severe (<2.5)

Replace potassium; always check and replace magnesium — hypokalaemia rarely corrects without it.

Hypercalcaemia: shortened QT (short ST segment), Osborn (J) waves if severe, arrhythmias.

Hypocalcaemia: prolonged QT (prolonged ST segment), risk of torsades especially with concurrent QT-prolonging drugs.

Exam pattern: abnormal T waves + renal failure + AKI on bloods = hyperkalaemia ladder. Abnormal U waves + diuretics + vomiting = hypokalaemia + magnesium. The ECG finding usually appears before the bloods do.

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15. 15 exam-pattern ECGs with annotated interpretation

Rapid-fire recognition pairs — the ECG feature, the likely diagnosis, and the UKMLA action.

1. Irregularly irregular, no P waves, rate 140 → AF with RVR → rate control + CHA₂DS₂-VASc.
2. Sawtooth in inferior leads, ventricular rate 150 → atrial flutter 2:1 → cardiology referral + anticoagulation.
3. Regular narrow complex at 180, no visible P → SVT → modified Valsalva then adenosine.
4. Broad regular complex at 180 in 70-year-old post-MI → VT until proven otherwise → amiodarone if stable, shock if not.
5. Polymorphic VT, QT prolonged → torsades → IV magnesium 2 g + correct electrolytes.
6. PR progressively lengthens, dropped beat → Mobitz I → observe; pace only if symptomatic.
7. Fixed PR, intermittent dropped beats → Mobitz II → pacemaker.
8. P and QRS dissociated, ventricular escape 35 → complete heart block → atropine, pace.
9. Short PR, delta wave, palpitations → WPW → ablation referral; avoid AV-blockers if AF occurs.
10. M in V1, W in V6, QRS 140 → RBBB → often benign; look for underlying cause.
11. Broad monomorphic R in V6, QS in V1, new onset with chest pain → STEMI equivalent → primary PCI.
12. ST elevation II/III/aVF + reciprocal depression I/aVL → inferior STEMI → right-sided ECG, PCI, avoid GTN if RV involvement.
13. Widespread saddle ST elevation + PR depression → pericarditis → NSAIDs + colchicine.
14. Sinus tach + S1Q3T3 + hypoxia in a post-op patient → PE → Wells + CTPA, anticoagulate if high pre-test probability.
15. Tall peaked T waves + broad QRS in AKI → hyperkalaemia → calcium gluconate immediately.

Rehearse these until every feature triggers a reflex management plan. The UKMLA rewards pattern-recognition speed paired with a first-line action.

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Exam technique — the 90-second ECG read

On exam day you will not have time for a textbook-perfect reading. Compress it:

1. Glance: is the rhythm regular? Narrow or broad? Rate rough?
2. Scan: any obvious ST change, block, peaked T, delta, tombstones?
3. Verify: check intervals, axis if relevant, compare with prior if given.
4. Commit: name the rhythm, name the pathology, name the next action.

Most SBAs test the action more than the name. Identifying AF is worth one mark; picking apixaban over warfarin for a CHA₂DS₂-VASc of 3 is worth the stem. Train yourself to move from pattern → management in one breath.

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How this post fits your revision

• Foundation — use this alongside the UKMLA cardiology masterclass as a paired read; cardiology gives pathophysiology, this gives trace-reading.
• Acute application — cross-reference the emergency presentations pillar for peri-arrest algorithms.
• Systemic integration — respiratory for PE traces; nephrology for hyperkalaemia and hypocalcaemia patterns.
• Skills triad — upcoming ABG and CXR masterclasses will complete the clinical-skills cluster; together they handle >90% of the investigation-interpretation questions in the AKT.

Bookmark this page. Re-read section 15 the week before the exam. Then the morning of, skim sections 4–7 and 11–14 — the highest-density territory.

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Summary

If you can only remember five things from this masterclass:

1. Read every ECG the same way, every time — rate, rhythm, axis, intervals, morphology.
2. Unstable rhythm = shock, not drugs. This single rule saves multiple AKT marks.
3. Inferior STEMI → right-sided ECG. Never give GTN until RV infarct is excluded.
4. New LBBB + chest pain = STEMI-equivalent. Activate primary PCI.
5. Peaked T waves + AKI = hyperkalaemia → calcium gluconate first, before anything else.

The UKMLA will reward you for speed and ladder-step-first reflexes. Practise the 15 patterns until each one triggers its management plan automatically. That is the difference between a borderline pass and a confident one.