ECG interpretation

Interpretation > Paper traces

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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💡 Conditions

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.

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💡 Conditions

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

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

Interpretation management

Covered in OSCE Stations

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
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One Comment

1. Denise Baillie says:

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   22 August 2023 at 13:34

   Require more ECG examples, e.g. MI of the various locations.

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