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The basics of reading an ECG

The ECG:

Lead placement:

  • Limb leads:
    • all in a coronal plane & thus can be used to measure the mean frontal axis
  • Chest leads:
    • V1: right sternal edge, 4ICS
    • V2: left sternal edge, 4ICS
    • V3: half-way between V2 & V4
    • V4: pt's apex beat
    • V5: AAL
    • V6: MAL
    • additional leads:
      • V7: PAL
    • NB. all leads subsequent to V4 are horizontal to V4

Paper speed:

  • usually 25mm/sec which results in:
  • each “big” square = 0.2secs
  • each “small” square = 0.04secs
  • can speed paper up to 50mm/sec esp. when interpreting tachycardias looking for P waves, etc.
  • NB. modern ECG machines, record ECG in 5 discrete, sequential time periods so pt's ECG status may have altered during the performance of the ECG and this will be reflected as differences between the ECG sectors:
    • I, II & III are recorded together
    • avR, avL & avF are recorded together
    • V1-3 are recorder together
    • V4-6 are recorded together
    • finally, the rhythm strip is recorded which is usually lead II

Systematic ECG interpretation:

What is the rate?

  • count number of large squares in one RR interval and divide into 300:
    • 1.5 squares = 200 bpm
    • 2 squares = 150 bpm (could this be atrial flutter with 2:1 block)
    • 3 squares = 100 bpm (faster than this is tachycardia)

What is the rhythm & how has the depolarisation been initiated?

  • regular:
    • tachycardias:
      • narrow complex:
        • sinus tachycardia
        • AV nodal reentrant tachycardia
        • atrial tachycardia
        • atrial flutter with fixed AV conduction
      • wide complex (see wide complex tachycardia):
        • VT
        • Torsade de Pointes
        • SVT with BBB or aberrancy
        • atrial flutter with WPW conduction
        • pre-excited (circus movement) tachycardia (WPW anterograde conduction)
    • bradycardias:
      • sinus bradycardia
      • AV block
  • irregularly irregular:
    • AF:
      • narrow complex
      • broad complex if WPW anterograde conduction or intraventricular conduction defect
    • atrial flutter with variable block
    • VF
  • regularly irregular:
    • multifocal atrial tachycardia
    • tachycardia

what is the mean frontal QRS axis?

  • the mean frontal axis is the sum of all the ventricular forces during ventricular depolarisation
  • determined by analysing the 6 limb leads which are in a coronal plane
  • axis directions of the limb leads (NB. 0 degrees is taken here as being the East position of a compass):
    • aVL = -30deg
    • I = 0 deg
    • II = 60deg
    • aVF = 90deg
    • III = 120deg
    • aVR = -150deg (ie. 210deg)
  • normal axis is -30deg to + 120deg
  • left axis deviation (LAD):
  • right axis deviation (RAD):
  • rules of thumb:
    • if there is an isoelectric complex in the limb leads then the axis is 90deg to that lead, check which way by looking at direction in other leads
    • if predominantly +ve in both I & II then it is normal
    • if predominantly -ve in all I, II & III then it is in “no man's land” ie NW quadrant & +ve in aVR:
      • ventricular focus highly likely if leads are correctly placed
  • mathematical determination:
    • create a right angle triangle from 2 resultant vectors:
      • horizontal vector side determined by net sum of lead I complex:
        • length = net sum in mm (ie. subtract height of negatively directed components from height of positively directed components)
        • direction of vector: to right if net sum is +ve
      • vertical side determined by net sum aVF is attached to arrow end of horizontal vector:
        • length = net sum in mm
        • directed downwards if net sum +ve
    • the axis is the angle between the horizontal vector & the hypotenuse:
      • ie. Inverse Tan (net sum aVF / net sum I) (nb. ensure + or - included here)

P wave shape:

  • P waves are best seen in leads II & V1
  • if inverted in lead I and upright in aVR then arm leads are reversed or dextrocardia is present, but in dextrocardia there is loss of R waves in V4-6
  • P mitrale:
    • wide P waves >= 0.12secs
    • notching of wide P wave in lead II with distance b/n peaks > 0.04sec
    • biphasic P wave in V1 - if P-terminal force (depth of inversion x width) > 0.04
  • P pulmonale:
    • tall, peaked P waves:
    • height in lead III > lead I
    • >= 3mm in an inferior lead

P-R interval:

  • normally 0.12-0.21sec
  • shortened PR interval:
    • WPW
    • normal variant
    • low atrial or upper AV junctional rhythms
    • accelerated AV conduction
    • phaeochromocytoma
    • glycogen storage disease
    • Fabry's disease
  • prolonged PR interval:
    • no dropped beats ⇒ 1st degree heart block
  • dropped beats:
    • dropped beat after successive increasingly long PR interval ⇒ Wenckebach (Mobitz type I)
    • at least 2 regular, consecutive impulses conducted with same PR ⇒ Mobitz type II
    • no conduction ⇒ complete HB

QRS width:

  • normally < 0.12sec

QRS height:

  • LVH

QRS morphology:

Tall R waves in V1:

  • thin chest wall or normal variant
  • RBBB - NB. slurred S wave in leads I, V5 & V6
  • RVH
  • WPW
  • true posterior infarction - assoc. inf. AMI & no slurred S in V5/6, T wave upright in V1-2
  • HOCM
  • Duchenne's muscular dystrophy
  • low placement of leads V1-2

RSR' or RSr' pattern in V1 or V2 (ie. M-shape):

  • QRS > 0.10sec and slurred S in leads I, V5/6:
    • RBBB:
      • aetiology:
        • normal variant
        • IHD
        • HT
        • RhHD
        • CHD esp. ASD, VSD, Fallot's tetralogy
        • pericarditis, myocarditis
        • PE
        • cor pulmonale
        • cardiomyopathy
        • Chaga's disease
        • endomyocardial fibrosis
        • other conditions
      • unlike LBBB, usually does not interfere with ECG Dx of AMI
      • see RBBB
  • QRS 0.09-0.10sec and slurred S in leads I, V5 or 6:
    • incomplete RBBB:
      • < 1% of normal individuals
      • secundum ASD (90% of these pts have incomplete RBBB)
  • QRS < 0.08sec and no slurred S in leads I, V5 or 6:
    • RSr' variant:
      • aetiology:
        • 5% of normal individuals
        • recording artifacts
        • chest deformities - straight back syndrome, pectus excavatum
        • CHD eg. ASD & rarely VSD or coarctation aorta
        • acquired heart disease - eg. MS
        • RVH
        • RV diastolic or volume overload
        • cor pulmonale
        • pulm. embolism
        • WPW
        • AVNRT - should have pseudo-S wave in leads II, III & avF
        • Duchenne's muscular dystrophy
        • late activation of outflow tract of RV eg. crista supraventricularis


  • ECG:
    • QRS duration > 0.11sec
    • M shape in leads I, V5 or V6
    • QS complex usually present in leads facing RV ie. V1
      • but <50% have small r wave in V1
    • ST elevation common in V1-4 with ST-T waves opposite in direction to terminal QRS direction
  • aetiology:
    • normal hearts but extremely rare in children
    • IHD - these pts have high incidence of LV dysfunction & CCF
    • cardiomyopathy
    • degenerative diseases
  • if present, cannot make diagnosis of LVH & Dx of AMI is difficult - see ECG Diagnosis of AMI
  • see LBBB

Pathologic Q waves:

Q-T interval:

  • the QT interval on the ECG is measured from the start of QRS complex to end of the T wave
  • QTc refers to a QT interval “corrected” for the effect of differing heart rate to give a QT value as if the heart rate is 60bpm
  • if rate 60-100bpm, then QT should be less than half the RR interval
  • Bazett's formula: QTc = QT / square root (RR interval)

prolonged QTc:

  • prolonged QTc represents delayed repolarisation & predisposes to early after-depolarisations, re-entrant tachycardias, especially potentially fatal torsade de pointes VT which is most likely if bradycardia is present too.

shortened QTc:

  • not of significance
  • aetiology:
    • hypercalcaemia
    • hyperkalaemia
    • digoxin intoxication

ST segment:

T wave:

U wave:

  • may be prominent in hypokalaemia but may be present in normal pts
ecg_easy.txt · Last modified: 2018/11/23 12:40 (external edit)