ECG - Think the basic first, then see it

The ECG is a fantastic tool that reveals a great deal of information about the heart to the physiscian. These pages should provide a useful introduction. They can be viewed in any order and the menu on the right allows you to navigate between them.

understanding the ecg

Introduction to cardiac electrophysiology and the way the ECG detects it.

ECG Part 1

understanding the 12 lead ecg

This will probably already be famililar, but just to recap:
The P-wave corresponds to atrial depolarisation.
The QRS complex corresponds to ventricular depolarisation (these are discussed in further detail below).
The T-wave corresponds to ventricular repolarisation.

THE LEADS

A 12-lead ECG shows the heart from various different angles – 6 vertical leads that are arranged around the heart in a coronal plane of section and a further 6 horizontal leads arranged around the heart in a transverse plane of section. As the electrical events in the heart follow specific vectors (directions), a lead placed at a different point will record different electrical activity.
In fact it has 10 leads that you attach to the patient – the ECG machine will then calculate the what it should be seeing from the remaining angles (the term ‘leads' can be misleading here, so remember that a ‘lead' on an ECG trace doesn't always correspond to a lead on a patient!).
Vertical Leads
There are 3 leads that are attached to the patient, from which 6 ECG traces are calculated.
One lead on the right arm (usually red)
One lead on the left arm (usually yellow)
One lead on the left leg (usually green)
An earth lead should also be placed on the right leg (usually black)
This creates Eindhoven's Triangle around the heart:
The three unipolar leads (aVR, aVL and aVF, also known as the limb leads ) show the views of the heart from the leads on the limbs (the three corners of the triangle). The three bipolar leads (I, II and III) are calculated from the differences between points on Eindhoven 's triangle.
This creates the 6 vertical leads:

Horizontal Leads
V1-V6 are the horizontal leads, arranged around the heart in a transverse plane of section (fig 1.9 from ECG made easy). V1 and V2 mainly view the right ventricle, while V3-V6 mainly view the left.

They are placed on the body as follows:
V1 on the 4 th intercostal space, to the right of the sternum.
V2 on the 4 th intercostal space, to the left of the sternum.
V3 inbetween V2 and V4.
V4 on the 5 th intercostal space in the midclavicular line (the apex beat).
V5 inbetween V4 and V6.
V6 in the midaxillary line, on a horizontal level with V4.


 

eindhoven's rules for labelling qrs complexes

The first wave upwards is labelled R (irrespective or whether or not it is preceeded by a downwards wave).
The first downwards wave before R is labelled Q.
The first downwards wave after R is labelled S.
Any upwards wave after S is labelled R` (pronounced R-prime).
 

Vectors of ventricular depolarisation

1.   Depolarisation spreads across the ventricular septum from left to right.
2. The depolarisation then spreads through the mass of the ventricles from inside to outside – as the left ventricle has thicker walls it dominates the vector, which is downwards and to the left.
3.  Finally, the remaining areas of the heart (the posterior aspect) depolarise with a depolarisation running upwards and to the right.
An electrical event coming towards a lead is recorded as a positive (upwards) wave, while one moving away from it is recorded as negative (downwards). If an electrical event is perpendicular to the lead, then no wave is created.
You should hopefully now be able to see how the same electrical event, recorded in different leads may have different letters as these leads are recording the event from different directions. For the electrical events above, viewed from 2 different leads:

Electrical event	Wave created in lead II	Wave created in aVR
1	Q	R
2	R	S
3	S	R`

Look at the diagram showing the arrangement of the leads above and this should make sense to you.

ECG Part 2

Systematic analysis of the ecg trace

When you start looking at ECGs, it's best to have a methodical approach – you can go in any order you like, so long as you make sure you catch all of the following steps. 

1. Identify and standardise

Check the patient name, age, date of birth, hospital number and the time and date at which the ECG were taken. Also check the scale on the ECG is at the standard levels – 1cm = 1mV and speed = 25mm/sec.

2. Check rhythm

Is the rhythm regular or irregular? Look for a change in the R-R interval for ventricular rhythm or P-P interval for atrial rhythm: the easiest way to do this is to lay a piece of paper alongside your ECG trace, mark where about 4 R waves occur then move the paper along the trace and see if waves still line up with marks.

3. check rate

Remember – when calculating times from an ECG trace, 1 small square (1mm) represents 0.04s, 1 large square (5mm) represents 0.2s and 5 large squares (25mm) represent 1 second.

There are several ways of calculating rate:
If your ECG is regular, then you may use one of the following equations:
60 divided by R-R interval in seconds
or
300 divided by R-R interval counted in big squares

4. p-wave

Should be smaller than 0.25mV (25mm) and upright in leads II, III and aVF and there should be one P-wave per QRS. An absence of P-waves denotes Atrial Fibrillation or a Junctional/Nodal rhythm.

5. P-R Interval

This is measured from the beginning of the P-wave to the beginning of the Q-wave. The normal range is 0.12 to 0.2s – an interval of greater than 0.2s implies delayed AV conduction.

6. QRS

This is measured from the beginning of the Q-wave to the end of the S-wave. The normal duration is less than 0.12s. A QRS of more than 12s indicates ventricular conduction defects such as bundle branch block.
Low-voltage (smaller than 5mm) QRS complexes can indicate hypothyroidism, chronic obstructive airways disease, myocarditis, pericarditis and pericardial disease.
Normal Q-waves should last less than 0.04 seconds and be less than 2mm deep – they become greater than this approximately 20 hours after MI; if present in lead III consider PE.
Normal axis is between -30 ° and +90 ° (see here for axis estimation)

7. Q-T Interval

Measured from the start of Q to the end of T.
Corrected QT (QT C ) =

QT ÷ vRR

normal is between 0.38 and 0.42
Prolonged in acute MI, myocarditis, bradycardia, head injury, hypothermia, Urea/electrolyte imbalance, congenital disorders, various drugs.

8. ST segment

The section running from the end of ventricular depolarisation (S) to the start of ventricular repolarisation (T).
Elevation of >1mm = infarction.
Depresstion of >0.5mm = ischaemia.

9. T-Wave

Normally inverted in VR and V1, inverted in V2 in some young people and V3 in some black people.
Abnormal if inverted in I/II/V4-V6 – indicates ischaemia/infarction.
T-waves become tall and tented in hyperkalaemia and small in hypokalaemia.

ECG Part 3

Axis determination

The axis is defined as the direction of spread of depolarisation through the ventricles, as seen from the front. It is affected by hypertrophy, conduction defects, etc. 

vertical leads

By knowing the directions in which the leads ‘look' at the heart, the cardiac vector can be ascertained:

• If a lead is predominantly positive (R larger than S), it is close to the vector.
• If a lead is predominantly negative (S larger than R), it is pointing in the opposite direction to the vector.
• If a lead shows little activity (R and S of similar size), it is perpendicular to the vector.

The normal axis is between -30 and +90 – leads I, II and III usually being positive as the vector is in their direction.

• If the axis shifts to the right (greater than 90), lead I becomes predominantly negative.
• If the axis shifts to the left (less than -30), lead III becomes predominantly negative.

Axis deviations of themselves are seldom significant, but when taken with other signs, can be pointers towards right or left hypertrophy; also note that a change to the right may indicate pulmonary embolism, while a change to the left can indicate conduction defects.

Horizontal leads

The QRS complex shows a progression from mainly negative in lead V1 to mainly positive in V6. The transition point is where R and S waves are equal and indicates the position of the septum – usually at V3/V4. However, right ventricular hypertrophy causes clockwise rotation – shifting the transition point to V4/V5 or even V5/V6.
SHORTCUT – if the sum of R in V5 or V6 and S in V1 is greater than 35mm, this indicates left ventricular hypertrophy.

ECG Part 4

pathology

You ought to have a good idea of the sheer depth of information you can gain from an ECG. Pathologies affecting the heart also create characteristic signs in the trace that are useful in clincial diagnosis.

MI

The ECG pathology evolves through 3 stages:

1. 1. T-wave peaking followed by T-wave inversion
2. 2. ST segment elevation
3. 3. Appearance of new pathological Q-waves

Pathological Q-waves

These are Q-waves exceeding 0.04s (one small square) and 2mV (2 small squares). They are created by infarcted or dead tissue, which is electrically inert – forming an electrical ‘hole' or ‘window' with all the electrical activity moves away from this point, so any lead sitting over it records a large pathological Q wave (remember that if the vector of the electrical activity is away from the lead, it records a negative wave) of septal and ventricular depolarisation moving away.

ST Deviation

Due to area of injured tissue surrounding the ‘hole' which is electronegative – may also be caused by pericarditis (in this case, the ST deviation occurs in all leads).

T-waves

Due to ischaemia.

Infarct	Artery involved	Visible in leads
Anterior	Left coronary, anterior descending branch	V1-V6 (Q in V3-V6, T in V4-V6)
Lateral	Left circumflex coronary	I, aVL, V5, V6
Anterolateral		Q: I, II, aVL, V5, V6 ST : V2-V6
Inferior	Right coronary	II, III, aVF (Q in III, aVF, ST in aVL and V6)
Posterior	Right coronary	Reciprocal changes in V1 (ST depression, tall R-waves)

 

pulmonary embolism

• Large S-wave in lead I
• Deep Q-wave in lead II
• Inverted T-wave in lead III

(S1, Q3, T3)
Patients will also demonstrate a pattern of right heart strain and right axis deviation.

Metabolic abnormalities

Hyperkalaemia

•  Tall, tented T-waves
•  Widened QRS
•  Prolonged PR
•  Arrhythmias

Hypokalaemia

•  Small T-waves
•  Prominent U-waves (occur after T-wave)
•  ST depression
•  Arrythmias

Hypercalcaemia

•  Short QT interval

Hypocalcaemia

•  long QT
•  Small T-waves

ECG Part 5

identifying ecg patterns

Author's note - yes, I know the image links are broken! Sorry about that, I will fix them when I get the time...

An abnormality of the cardiac rhythm is called a cardiac arrhythmia – of which there are two main types:
Bradycardia, where the heart rate is slow (<60 b.p.m.)
Tachycardia, where the heart rate is fast (>100 b.p.m.) 

SINUS RHYTHMS:

  Sinus denotes that the rhythm of the heart is still being generated by the sinuatrial node, so the P-wave and QRS complex are generally normal.
  Sinus Bradycardia:Slower than 60bpm, otherwise normal.
Causes: Hypothermia, hypothyroidism, drugs ( b -blokers, digitalis and other antiarrhythmic drugs), acute ischaemia and infarction of the sinus node.
Sinus tachycardia: Faster than 60bpm, otherwise normal.
Causes: Fever, exercise, emotion, pregnancy, anaemia, thyrotoxicosis.
  Sinus arrhythmia: During inspiration, parasympathetic tone falls and the heart rate quickens, and on expiration the heart rate falls. This variation is normal, particularly in children and young adults. There is still one P wave per QRS complex and a constant P-R interval, but a progressive beat to beat change in R-R.

PATHOLOGICAL BRADYCARDIAS:

  Atrioventricular Blocks

These are problems in conducting between the Sinuatrial node and the Atrioventricular node.
  First Degree AV Block: Where the PR interval > 0.22 sec but there is still one P-wave per QRS.

 
Second degree AV Block: The Mobitz blocks are types of Second degreee AV block
Mobitz I Block (Wenckebach phenomenon): Here there is progressive PR interval prolongation until a P wave fails to conduct.

Mobitz II Block: This is a special type of second degree block that occurs when an absent QRS complex is not preceded by progressive PR interval prolongation - i.e. PR remains constant. Look for a P-wave not followed by a QRS.

2:1 or 3:1 Block: Occurs when every second or third P wave conducts to the ventricles. P-R interval remains normal in the conducted beats.

Third degree (complete) AV Block: Occurs when no P waves conduct to the ventricles. There will be no relationship between P-wave (atrial) rate and QRS complex (ventricular) rate. QRS complexes tend to be abnormally shaped due to abnormal spreading of depolarisation across the ventricles.

PATHOLOGICAL TACHYCARDIAS

  Atrial tachyarrhythmias

Here, ‘atrial' denotes that the electrical activity begins in the atria (i.e with a P-wave).
Atrial ectopic beats (extrasystoles): Appears as early and abnormal P waves, followed by normal QRS complexes.


Atrial tachycardia: High rate of atrial depolarisation (e.g. around 150/min). P-waves can be seen superimposed ontop of T-waves.

Atrial Flutter: Atrial rate around 300 b.p.m. regular sawtooth-like P-waves (known as F waves) between QRS complexes (the ventricular rate becomes independent of the atrial rate and remains much slower).

Atrial Fibrillation: Continuous rapid >400 b.p.m. activation of atria, irregular QRS complexes.

Junctional (Nodal) Tachyarrhythmias

Here, the depolarisation originates from around the AV node.
  Junctional ectopic beats (Extrasystoles): Appears as early normal QRS complex, without a preceeding P wave, followed by a compensatory pause.

Junctional (nodal) tachycardia: No visible P waves, normal QRS complexes, rhythm is rapid 140-280 b.p.m.

Ventricular Tachyarrythmias

Note that the depolarisation originates in the ventricles here. Consequently, the QRS is much wider, as it takes longer for the electrical activity to spread.
Ventricular ectopic beats (extrasystoles): No P wave, broad (>0.12 sec) QRS complex

Ventricular tachycardia: Rapid ventricular rhythm with broad (>0.14 sec) QRS complexes at a rate of 120 b.p.m. or more

Ventricular Fibrillation: Very rapid and irregular ventricular activation with no mechanical effect.