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Hussam Ro

on 13 February 2013

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Transcript of The ECG

The ECG Hussam Rostom Principles of the ECG Cardiac physiology The limb leads Chest leads V1-V4 - 'anterior'
V5-V6 - 'lateral'

V1-V2 look at RV
V3-V4 look at septum
V5-V6 look at LV Technical aspects "This is the 12-lead electrocardiogram of (name), taken on (date) at (time) for (indication, e.g. chest pain).

The electrocardiogram is calibrated to run at 25mm/s with a deflection of 1cm/mV. "
(This should be the case for all ECGs! The rectangle at the start should be 5mm wide and 10mm tall.)

1 big square = 0.2s (200ms)
1 small square = 0.04s (40ms) Rate 2 methods:

1) 300 divided by R-R interval Rhythm 1) Regular Axis 2) Total QRS complexes multiplied by 6 2) Regularly irregular 3) Irregularly irregular (=AF) Consistency of R-R interval "Average spread of depolorisation through ventricles"

Normal axis vs left axis deviation vs right axis deviation

Different ways of determining axis Axis Method 1
(Tim L's method - plot I vs aVF) Method 3
(the easiest) Method 2
(my method - compare I, II and III) LAD RAD Normal (-30 to +90) I aVF I - positive
aVF - positive I - positive
aVF - negative I - negative
aVF - negative I - negative
aVF - positive I II III Extreme RAD
I - negative
II - negative RAD
I - negative
II - positive
III - positive Normal
I - positive
II - positive LAD
I - positive
II - negative I and II Leaning away = Left

I and II Reclining towards = Right Causes LAD
Physiological (with age)
Mechanical (abdo pressure)
Sometimes LVH (look for other signs)
Inferior MI
Left anterior hemiblock
Physiological (children and young adults)
Mechanical (e.g. emphysema)
RV strain (pulmonary HTN)
Anterolateral MI
Left posterior hemiblock
Some WPW P waves 1) Are P waves present? No = AF 2) If present, what is relationship between P and QRS? a) P before every QRS = supraventricular rhythm

b) Complete atrioventricular dissociation = ventricular rhythm (VT/VF if fast, complete heard block if slow)

c) Relationship present, but not every P followed by QRS (e.g. second degree heart block, atrial flutter) PR interval Start of P wave to start of QRS complex

Normal = 120-200ms (3-5 small sq)

Increased PR interval - 1st degree heart block, hyperkalaemia
Decreased PR interval - Accessory pathway 3) What do the P waves look like? Either too tall or too wide

Too tall (>2.5mm in II or V1) = P pulmonale (R atrium enlarged)

Too wide (>0.11s) or bifid = P mitrale (L atrium enlarged) Heart block 1st degree PR interval > 200ms

Not important in itself - common in athletes
May signify coronary artery disease, digoxin toxicity, electrolyte disturbance, rheumatic fever 2nd degree - Mobitz type I (Wenckebach) Progressive increase in PR interval, followed by dropped beat

Usually benign - seen in athletes
May signify coronary artery disease, digoxin, myocarditis 2nd degree - Mobitz type II or 2:1 block PR interval constant, but some P waves not followed by QRS

Usually ischaemic heart disease - may lead to 3rd degree heart block

Requires pacemaker 3rd degree Complete A-V dissociation with bradycardia

Causes: fibrosis, ischaemic heart disease, aortic valve disease, myocarditis, post cardiac surgery

Always needs a pacemaker QRS complex If first deflection downwards = Q wave
If first deflection upwards = R wave
Any downward deflection after R wave = S wave

QRS complexes can be normal, too broad, too tall or have an abnormal Q wave

Look for:
1) QRS duration (normal is <120ms) - broad vs narrow
2) Chest leads - R wave progression or evidence of LVH
3) Any pathological Q waves Broad complex (duration >120ms) Either bundle branch block or ventricular rhythm Bundle branch block 'William Marrow'
Left BBB - WiLliaM - 'W' in V1, 'M' in V6'
Right BBB - MaRroW - 'M' in V1, 'W' in V6' LBBB RBBB Distinguishing VT from SVT+BBB If any doubt, assume ventricular tachycardia (VT) - especially if e.g. post MI Causes:
Aortic stenosis
Primary disease of conducting system Causes
Normal heart
ASD/congenital defect
Pulmonary embolism
Primary disease of conducting system ECG findings in favour of VT (but not always seen!):

Positive QRS concordance in chest leads
A-V dissociation
Marked left axis deviation
Fusion beats or capture beats Abnormalities of QRS height Normal R wave progression In other words:
S>R in V1
R>S in V6 Right ventricular hypertrophy R>S in V1 with poor R wave progression Left ventricular hypertrophy Biggest R wave in V1/V2
Biggest S wave in V5/V6
>35mm Q waves 'Septal' Q waves may be seen in I, aVL, V5, V6
Note: these are <1mm wide and <2mm deep

Pathological Q waves due to 'electrical window' because of transmural infarction.
Q waves, when formed, tend to be permanent.

Therefore location of a previous infarct can be determined by location of Q waves:
anterior: V2-V4
lateral: I, aVL, V5, V6
inferior: II, III, aVF
posterior: may see permanent R wave in V1 ST segment Isoelectric vs Elevated vs Depressed Elevation:
MI (convex upwards) - territory
Pericarditis (concave upwards/saddle shaped) - widespread

High take off
Ventricular aneurysm
Prinzmetal's angina Depression:
Ventricular strain/hypertrophy
Digoxin (downsloping/reverse tick)
Other: e.g. hypokalaemia Note:
Depolarization towards a lead - +ve deflection
Septum depolorizes from left to right
--> septal Q waves (see later)
LV normally exerts more electrical activity than RV T wave Normal vs Tall vs Inverted vs Flat Tall (>2/3 height of R):
MI Inverted/flat:
Ventricular hypertrophy
PE (lead III) T waves usually inverted in aVR
May be inverted in V1 (and V2), and in III (if isolated) QT interval Start of QRS to end of T wave

Need to adjust for heart rate
QTc = QT/√(R-R interval)
Normal QTc - <450ms Causes:
Genetic: e.g. Brugada syndrome
Acquired: heart disease (e.g. ischaemic), drugs, electrolyte disturbance, hypothermia Common ECG abnormalities MI First few hours: peaked T waves, ST elevation ('tombstoning')
24 hours: ST resolution, T wave inversion (may persist)
Days: Q waves (usually persist) PE Most commonly a normal ECG
Sinus tachycardia most common abnormality
Others: RAD, RBBB, RV strain
Rarely: SI QIII TIII Metabolic/drug Hyperkalaemia:
tall tented T wave, wide QRS, P wave flattening
later, 'sine wave' appearance
eventually VT Hypokalaemia: small T waves, prominent U waves
Hypercalcaemia: short QT interval
Hypocalcaemia: long QT interval

Digoxin: ST depression and inverted T ('reverse tick') Pericarditis Widespread saddle-shaped ST elevation
Other features: PR depression, sinus tachycardia WPW Wolff-Parkinson-White syndrome
due to presence of accessory pathway
features: short PR interval, slurred upstroke to QRS

patients present with SVT (AVRT), pre-excited AF, or pre-excited atrial flutter Abnormalities of rhythm Not covered here, but consider:


Supraventricular rhythms
Ventricular rhythms
Full transcript