Describing a ECG Rate – number of large squares between R-R divided by 300

Rhythm – regular or irregular (between R-R)

Conduction – PR interval if sinus rhythm

Cardiac Axis – lead I and avF (+ lead II if I +ve and aVF –ve)

QRS complex – width/duration (V1 and V6 (WLM and MRW), height (V1 and V6) and Q

waves

ST segments – depression or elevation

T waves – inversion

Basics Paper speed

o 25mm/sec, large squares = 0.2sec (5mm), small squares = 0.04sec (1mm)

12 leads – 6 standard leads and 6 chest leads

o aVL, I and II look at left lateral heart surface

o aVF and III at inferior heart surface

o aVR looks at RA

o V1-V6 looks at anterior heart surface

o V1 and V2 look at RV

o V3 and V4 at interventricular septum and anterior LV

o V5 and V6 at LV

Standard intervals

o PR interval <0.2sec

o QRS complex <0.12sec

o ST segment <1mm from isoelectric line

Nomenclature for QRS complex

o Q: 1st +ve deflection

o R: 1st -ve deflection

o S: -ve deflection following R wave

Deflections

o When depolarisation wave spreads towards a lead stylus moves upwards and when

it spreads away it moves downwards (for repolarisation wave it is the opposite)

o Depolarisation wave spreads through ventricles in many directions at once but the

QRS complex shape shows the average direction in which the wave spreads through

If QRS predominately upwards (+ve) (i.e. R wave > S wave) depolarisation

moving towards lead

Specific ECG Abnormalities Cardiac axis

Average direction of spread of depolarisation wave through the ventricles as seen from the

front is called the cardiac axis

Direction of axis most easily derived from leads I and aVF

Normal cardiac axis (direction = 11 o’clock to 5 o’clock, range = -30 to +90)

o If both I and aVF have +ve deflections of QRS complexes the normal CA

Right axis deviation – deflection in lead I predominately –ve (downwards) & aVF +ve

(upwards), due to RV hypertrophy (e.g. due to pulmonary hypertension, pulmonary stenosis

or PE)

Left axis deviation – QRS complex predominately +ve in lead I & -ve in aVF but this still may

be normal so need to look at lead II – if its +ve the axis is normal and if –Ve then have left

axis deviation

o LAD more likely due to conduction defect then a increase in LV muscle bulk)

Long thin individuals may have a right axis deviation

Short fat individuals may have a left axis deviation

Heart block

1st degree HB – one P wave per QRS complex but PR interval prolonged (>0.2sec)

2nd degree HB – 3 types

o Mobitz type 1/Wenckebach – progressive PR lengthening then non-conducted P

wave and then repetition of cycle

o Mobitz type 2 – constant PR interval but occasional non-conducted beats

o 2:1/3:1 block – 2 or 3 P waves per QRS complex, with normal P wave rate

3rd degree/complete HB – no relationship between P waves and QRS complexes

o Atrial contraction normal but no beats conducted to ventricles

o When this occurs ventricles excited by a slow escape rhythm

o Acutely may be due to MI (usually transient), chronically may be due to fibrosis of

bundle of his

P wave morphology

P.pulmonale – peaked P wave – due to RA hypertrophy

P.mitrale – broad and bifid P wave – due to LA hypertrophy

QRS Width/Duration (normal <0.12sec)

Relates to time taken for spread of excitation through the ventricles

QRS complex width <0.12sec normal & implies origin of rhythm is supraventricular

QRS complex width >0.12sec implies ventricular rhythm or BBB

o Conduction within ventricles must have occurred by an abnormal and therefore slow

pathway

o In sinus rhythm with BBB normal P waves are present with a constant PR interval,

but this is not the case with rhythms beginning in ventricles

If depolarisation wave reaches interventricular septum normally then PR interval will be

normal, but if there is abnormal conduction through either the R or L bundle branches there

will be a delay in depolarisation in part of the ventricle

o This extra time taken for depolarisation of whole ventricular muscle causes widening

of QRS complex

Block of both bundle branches has same effect as block of bundle of His and causes 3rd

degree/complete HB

RBBB often indicates problems with right side of heart, but RBBB patterns with a QRS

complex of normal duration quite common in healthy people – sometimes called a partial

RBBB, can be considered a normal variant

LBBB always indicates heart disease usually on the left side

Important to recognise BBB present as LBBB prevents further interpretation of the

cardiogram & RBBB makes interpretation difficult

When determining whether left or right BBB evaluate V1 and V6

o In LBBB V1 QRS complex will have a W pattern and V6 a M

o In RBBB V1 QRS complex will have a M pattern and V6 a W

So WLM and MRW

QRS Height

Increase muscle mass in either ventricle will lead to increase electrical activity and to a

increase in height of QRS complex

RV hypertrophy – best seen in V1 (tall R waves) and V6 (deep S waves)

LV hypertrophy – V5 or V6 (tall R waves (>25mm)) and V1 (deep S waves)

Q waves

May be physiological or pathological and can be due to 3 reasons:

o Axis – Q wave may be seen in a lead with a overall –ve QRS complex (e.g. aVR, III, V1)

o Small (septal) Q waves - appear in LV leads (I, aVL and V6) as result from

depolarisation of septum from left to right

o Previous MI - Q waves > 1 small square in width and >2mm in depth are

pathological and indicates a MI, with the leads in which these Q waves appear giving

some indication as to the part of the heart that has been damaged

Presence of a Q wave does not give a indication of the age of an infarction because once a Q

wave has developed it is usually permanent

ST segment

ST segment should be isoelectric

Elevation of the segment (in a lead with a upright QRS) is a indication of acute myocardial

injury – due to recent infarction or pericardiits

o Leads in which elevation occurs indicate part of heart which is damaged, and as

pericarditis is not usually a localised affair it causes ST elevation in most leads

Depression of ST segment associated with a upright T wave, generally non-specific but is

usually a sign of ischaemia as opposed to infarction (other causes hypokalaemia,

hypokalaemia, digoxin (down-sloping, as opposite to horizontally depressed ST segments

usually due to treatment with digoxin))

o When a ECG at rest is normal ST segment depression may appear during exercise

particularly when exercise induces angina

T waves

Polarity – the T wave should follow the QRS (be upright is QRS upright and negative if QRS is

negative)

o T wave inversion may be seen in following circumstances:

Normality – normally inverted in VR and V1, and in V2 in young people and

V3 in some black people

Ischaemia

Infarction

Ventricular hypertrophy – in leads looked at hypertrophied ventricle

BBB – the abnormal path of depolarisation in BBB is usually associated with

a abnormally path of repolarisation and therefore inverted T waves

associated with widened QRS complexes have no significance in themselves

Digoxin treatment – get T wave inversion with characteristic sloping

depression of ST segments. May be helpful to record to ECG before giving

digoxin to save later confusion about significance of T wave changes

Size

o Small – hypokalaemia

o Large – hyperkalaemia, ischaemia

Myocardial Infarction

Sequence of ECG chances

o Normal ECG

o ST segment elevation (hours)

o Appearance of Q waves (hours – permanent)

o Normalisation of ST segment

o Inversion of T waves (hours – weeks)

Rhythms

Supraventricular Rhythms

o Constitutes sinus rhythm (one P wave per QRS complex), atrial rhythm and

junctional rhythm

o Depolarisation wave spreads to ventricles normally via bundle of His and its

branches and hence QRS complex is normal (narrow)

Ventricular Rhythms

o Depolarisation wave spreads through ventricles by an abnormal and therefore

slower pathway and hence QRS complex is wide and abnormal

o Repolarisation also abnormal so T wave is of abnormal shape

Supraventricular tachyarrhythmias

o Supraventricular extrasystole

Premature P wave followed by normal QRS with normal or lengthened PR

interval

Treatment – nil

o Supraventricular tachycardia

Rapid atrial rate >100/min, regular

Normal rapid QRS, P waves may be present in QRS

o Atrial flutter

Rapid P wave rate (250-350/min), sawtooth pattern on ECG

Normal P waves, normal QRS but slower and often regular

Treatment – acute attack: digoxin, cardioversion

Prophylaxis – sotalol, amiodarone

o Atrial fibrillation

Rapid P wave rate (>350/min) but none identifiable – completely irregular

baseline

Irregular P waves, normal but irregular QRS 50-160/min

Treatment – acute attack: digoxin, cardioversion

Prophylaxis – sotalol, amiodarone

Chronic – digoxin, warfarin to prevent thrombo-embolism

Ventricular tachyarrhythmias (wide QRS complexes)

o Ventricular extrasystole

Premature abnormally shaped QRS but no P (as did not arise in atrial region)

Treatment – usually nil, B-blocker

o Ventricular tachycardia

Rapid QRS rate (100-250/min)

Regular but abnormal QRS, P waves typically dissociated

Treatment – acute attack: cardioversion

Prophylaxis – amiodarone

If QRS complex

rapid & there are

no P waves:

a wide QRS

indicates VT &

a narrow QRS

indicates

supraventricular

tachycardia

o Ventricular fibrillation

Rapid QRS rate (>350/min)

Irregular and abnormal QRS, no P waves

Treatment – cardioversion (immediately)

Prophylaxis – amiodarone