ECG interpretation

Introduction

• Patient name, DOB, any symptoms (e.g. chest pain)
• ECG date and time and which in series
• Check calibration
  • Standard paper speed: 25mm/s
  • Standard voltage calibration: 10mm/mV (1mV deflection at start/end of trace should be 2 large squares in height)

Rate and rhythm

Use rhythm strip

• Rate: calculate by dividing 300 by number of large squares between R peaks OR, if irregular, total R waves on ECG multiplied by 6 (ECG is 10 seconds long)
  • Sinus bradycardia <60 (physical fitness, hypothermia, hypothyroidism, sinoatrial node disease, β-blockers/digoxin)
  • Sinus tachycardia >100 (exercise/pain/anxiety, pregnancy, anaemia, PE, hypovolaemia, fever/sepsis, thyrotoxicosis) 
• Rhythm
  • Regularity: mark four R wave peaks on a plain piece of paper and move it along the trace to compare regularity against subsequent R waves (irregular: AF, ectopics, 2^nd degree heart block, sinus arrhythmia, atrial flutter with variable block)
  • Sinus rhythm or not? Look for a normal P wave before each QRS complex (no clear P waves and irregular QRS = AF; saw-tooth baseline = atrial flutter; narrow complex tachycardia with abnormal or no discernible P waves = supraventricular tachycardia; broad complex tachycardia with no P waves = VF, VT or rarely SVT/AF with BBB/pre-excitation; bradycardia with no P waves = sinoatrial arrest with junctional or ventricular escape rhythm; P waves present but without constant PR interval = 2^nd degree/complete heart block)

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Axis

Use leads I and II

• Short method: QRS is normally predominantly positive in leads I and II, i.e. both point upwards
  • If QRS is predominantly positive in lead I and negative in lead II (i.e. pointing away from each other), there is left axis deviation – Leaving each other = Left axis (more electricity going to left due to: LV hypertrophy, left anterior hemiblock, LBBB, inferior MI, Wolff-Parkinson-White syndrome, VT) 
  • If the QRS is predominantly negative in lead I and positive in lead II (i.e. pointing towards each other), there is right axis deviation – Reaching towards each other = Right axis (more electricity going to right due to: tall and thin body type, RV hypertrophy (e.g. in PE, lung disease), left posterior hemiblock, lateral MI, Wolff-Parkinson-White syndrome)

P wave

Use rhythm strip

• Height: should be ≤2 small squares (increased in right atrial enlargement, e.g. caused by pulmonary hypertension)
• Morphology
  • Bifid (looks like an ‘m’) = P mitrale (left atrial enlargement – classically caused by mitral stenosis)
  • Peaked = P pulmonale (right atrial enlargement – classically in lung disease)

PR interval

Use rhythm strip

• Length: should be 3-5 small squares
  • Decreased: accessory conduction pathway (look for delta wave in Wolff–Parkinson–White syndrome)
  • Increased in AV node block (‘heart block’) 
    • 1^st degree heart block: PR >5 small squares and regular
    • 2^nd degree heart block
      • Mobitz type 1 (Wenckebach): PR progressively elongates until there is failure of conduction of an atrial beat (then the cycle repeats)
      • Mobitz type 2: constant PR interval in the conducted beats but some of the P waves are not conducted
      • 2^nd degree heart block with 2:1/3:1/4:1 block: alternate conducted and non-conducted atrial beats (P:QRS)
    • Complete heart block: complete dissociation between P waves and QRS complexes. Normal atrial beats are not conducted to ventricles, which results in the ventricles self-depolarising at a much slower rate (a ‘ventricular escape rhythm’).

QRS complex 

Check in all leads

• Q wave: note that small Q waves (<1 small square wide and <2 small squares deep) are normal in I, aVL and V6 (LV leads) due to septal depolarisation
  • Pathological Q waves (established/previous full thickness MI)

Use chest leads

• R wave progression: QRS complexes should progress from mostly negative in V1 (i.e. dominant S) to mostly positive in V6 (i.e. dominant R). Normally the ‘transition point’ (i.e. the lead where R and S are equal) is V3/4.
  • ‘Clockwise rotation’ i.e. transition point after V4 (right ventricular dilatation, usually caused by chronic lung disease)
  • Dominant R wave in V1/2 (right ventricular hypertrophy, posterior MI)

Use rhythm strip (and V1 and V6 if prolonged)

• Length <3 small squares
  • Increased = bundle branch block
    • RBBB: QRS in V1 has M (RSR^’) pattern and QRS in V6 has W pattern – MarroW (may be caused by: right ventricular hypertrophy/cor pulmonale, PE, atrial septal defect, ischaemic disease, cardiomyopathy)
    • LBBB: QRS in V1 has W pattern and QRS in V6 has M pattern – WilliaM (may be caused by: aortic stenosis, ischaemic disease, hypertension, anterior MI, cardiomyopathy, conduction system fibrosis, ↑K⁺)
    • NB: the W pattern is often not fully developed; the RSR^’ pattern may be seen with a normal QRS length – this is partial (incomplete) bundle branch block and is of no clinical significance

Use V1 and V5/V6

• Height: look for ventricular hypertrophy
  • S wave depth in V1 + tallest R wave in V5/6 = >7 big squares (left ventricular hypertrophy, e.g. hypertension, AS, AR, MR, coarctation of aorta, hypertrophic obstructive cardiomyopathy)
  • Dominant R wave in V1 + dominant S wave in V5/6 (right ventricular hypertrophy, e.g. pulmonary hypertension, MS, PE). If this is present, look for other signs too, e.g. T wave inversion in right chest leads (V1-V3) and right axis deviation.

A patient presents to ED with chest pain and this trace. What would you do?

Interpretation management

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ST segment 

Check in all leads – ST-elevation/depression is measured from the ‘J point’ (start of ST segment)

• Elevation ≥1 small square (infarction; or pericarditis or tamponade if in every lead)
• Depression ≥0.5 small square (ischaemia; or reciprocal change in posterior MI) 
• Morphology – ST segment is normally upwardly concave
  • Convex or straight ST-elevation (infarction)
  • Concave ST-elevation (usually other causes, e.g. early repolarisation, LVH)
  • Saddled ST-elevation (pericarditis, tamponade)
  • Downward sloping ST/‘reverse tick’ (digoxin toxicity)

T wave

Check in all leads

• Inversion: note it can be normal in III, aVR and V1 (right leads) due to the angle from which they view the heart (also in V2-3 in Afro-Caribbean patients). It’s almost always inverted in aVR.
  • Causes: ischaemia/post-MI, PE, right/left ventricular hypertrophy (right chest or lateral leads respectively), bundle branch block, digoxin treatment
• Morphology
  • Tented (hyperkalaemia) or flat (hypokalaemia)
  • Biphasic (ischaemia → up then down; hypokalaemia → down then up)

ST lead changes by infarct territory

	Leads	Artery
Inferior	II, III, aVF	Right coronary
Anteroseptal	V1-V4	Left anterior descending
Anterolateral	V4-V5, I, aVL	Left anterior descending or left circumflex
Lateral	I, aVL ± V5-6	Left circumflex
Posterior	Dominant R wave V1-2, horizontal ST↓ V1-3	Left circumflex or right coronary

Other things

Use rhythm strip

• Corrected QT interval (QT_c): usually <450ms. It may be calculated by the ECG machine; if not, an online calculator can be used. It is likely prolonged if T waves extend beyond midpoint of RR interval. An increased QT_c interval predisposes to polymorphic VT.
  • Causes of increased QT_c interval: congenital syndromes, antipsychotics, sotalol/amiodarone, tricyclic antidepressants, macrolides, hypokalaemia/hypomagnesaemia/hypocalcaemia
• U waves – can be normal or seen in hypokalaemia, hypothermia, or with antiarrhythmics

Common ECG pathologies you may see

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Test yourself! What is the rhythm?

Try some OSCE stations with ECGs in!

1. STEMI
2. Cardiovascular examination – atrial fibrillation
3. HAP data interpretation
4. Hyperkalaemia
5. Diabetic ketoacidosis
6. Find lots more stations here