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ECG interpretation

Learn how to perform one too…

Performing an ECG is covered here!

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

Square sizes

1 small square = 40 milliseconds

1 big square = 200 milliseconds

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, 2nd 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 = 2nd degree/complete heart block)

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

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Cardiac conduction circuit
  • 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’
      • 1st degree heart block: PR >5 small squares and regular
      • 2nd 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
        • 2nd 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 – Marro(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 – Willia(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.

ST segment 

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ST-elevation morphology
Upwardly concave (left) and upwardly convex (right) 

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
 LeadsArtery
InferiorII, III, aVFRight coronary
Anteroseptal V1-V4Left anterior descending
Anterolateral V4-V5, I, aVLLeft anterior descending or left circumflex
Lateral I, aVL ± V5-6Left circumflex
Posterior Dominant R wave V1-2, horizontal ST↓ V1-3Left circumflex or right coronary

Other things

Use rhythm strip

  • Corrected QT interval (QTc): 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 QTc interval predisposes to polymorphic VT.
    • Causes of increased QTc 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
Direction from which leads view the heart

Lead traces are deduced from the electric potential differences between certain electrodes. This means they can be said to ‘view’ the heart from different angles. A positive deflection is seen when the overall electric potential is travelling in the direction of that lead’s view, and a negative deflection is seen when the overall electric potential is travelling away from that lead’s view.

Transverse view 

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Coronal view

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Common ECG pathologies you may see

Rhythm abnormalities

  • AF/flutter
    • AF: irregular without P waves
    • Atrial flutter: saw-tooth baseline (fluttering P waves) – may be regular with 2:1, 3:1 or 4:1 block, or irregular with variable block
  • Supraventricular tachycardias 
    • Atrial tachycardia: regular with abnormal P waves
    • AV nodal re-entry tachycardia/AV re-entry tachycardia: regular, usually without discernible P waves
  • VT: regular, organised wavy line (broad complex tachycardia is VT until proven otherwise) – MAY BE PULSED VT OR PULSELESS VT
  • Polymorphic VT (Torsades de pointes): VT with varying amplitude 
  • VF: random wavy line with no discernible P waves or QRS complexes – NO PULSE!
  • Asystole: flat line – NO PULSE!
  • Atrial ectopic: narrow QRS ± preceding abnormal P wave (resets the P wave cycle)
  • Ventricular ectopic: abnormal broad QRS at abnormal time (usually followed by compensatory pause)
  • Ventricular bigeminy (regular ventricular ectopics): abnormal premature ventricular complexes after every normal complex

Perfusion abnormalities

  • Infarction: ST-elevation (first change), T wave inversion, pathological Q waves (signify full thickness MI and develop 8-12 hours after ST-elevation if myocardium is not reperfused)
  • STEMI criteria: ST-elevation in >2 small squares in 2 adjacent chest leads or ST-elevation > 1 small square in 2 adjacent limb leads or new LBBB
  • Ischaemia: ST-depression, new T wave inversion
  • Posterior (wall of LV) infarction: dominant R wave in V1/2 with horizontal ST-depression V1-3. 
  • Previous infarcts: T wave inversion (persists weeks to months), pathological Q waves (permanent) 

Hypertrophy

  • Left ventricular hypertrophy = left axis deviation, dominant S wave in V1, tall R wave (>5 big squares in V5/6), T wave inversion in lateral leads. Sokolow-Lyon voltage criteria: S depth in V1 + tallest R wave height in V5/6 = >7 big squares.
  • Right ventricular hypertrophy = right axis deviation, dominant R wave in V1, dominant S wave in V5/6, T wave inversion in right/inferior chest leads (V1-3, II, III, aVF)

Fascicular blocks

  • Any of the three conduction paths after the bundle of His can become blocked
    • Right bundle branch → RBBB pattern
    • Anterior fascicle of left bundle branch (i.e. left anterior hemiblock) → marked left axis deviation
    • Posterior fascicle of left bundle branch (i.e. left posterior hemiblock; rare) → marked right axis deviation
  • Bifascicular block is RBBB + left anterior/posterior hemiblock → RBBB + left/right axis deviation
  • Trifascicular block is RBBB + left anterior hemiblock + left posterior hemiblock 
    • ‘Incomplete’ may be either of these patterns:
      • Fixed block of 2 fascicles + delayed conduction in remaining fascicle = bifascicular block + 1st/2nd degree heart block 
      • Fixed block of 1 fascicle + intermittent failure of other 2 = RBBB + alternating left anterior/posterior hemiblock
    • ‘Complete’ → complete heart block (escape rhythm shows signs of bifascicular block)

NB: bifascicular block with 1st degree heart block is the most common pattern referred to as ‘trifascicular block’.

Metabolic

  • Hyperkalaemia: wide flat P waves, wide bizarre QRS, tall tented T waves 
  • Hypokalaemia: prolonged PR, depressed ST, flattened/inverted T waves, prominent U wave
  • Hypercalcaemia: short QT interval
  • Hypocalcaemia: prolonged QT interval

Genetic conditions

  • Wolff-Parkinson-White syndrome: slurred upstroke into the QRS complex (delta wave), short PR interval, QRS complexes may be slightly broad, dominant R wave in V1 (if accessory pathway is left-sided, i.e. type A)/dominant S wave in V1 (if accessory pathway is right-sided, i.e. type B)
  • Hypertrophic cardiomyopathy = left ventricular hypertrophy signs + dramatic T wave inversion in lateral leads (maximal in V4 rather than V6)

Other conditions

  • PE – possible changes: tachycardia, right axis deviation, RA enlargement (i.e. P pulmonale), RBBB, RV dilation (i.e. dominant R in V1), RV strain (i.e. T wave inversion in right chest and inferior leads). NB: the ‘classical’ S1Q3Tpattern (prominent S wave in lead I, and Q wave and inverted T wave in lead III) is uncommon.
  • Pericarditis: PR depression, saddle-shaped ST-elevation

Test yourself! What is the rhythm?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm is the above ECG trace?

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What rhythm pathology in green on 1) the left 2) the right?

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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
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