You are on page 1of 11

ECG (EKG) Interpretation

As with all investigations the most important things are your findings
on history, examination and basic observations. Having a good system
will avoid making errors.

To start with we will cover the basics of the ECG, how it is recorded and
the basic physiology. The 12-lead ECG misleadingly only has 10
electrodes (sometimes also called leads but to avoid confusion we will
refer to them as electrodes).

The leads can be thought of as taking a picture of the heart’s electrical


activity from 12 different positions using information picked up by the
10 electrodes. These comprise 4 limb electrodes and 6 chest electrodes.
When electrical activity (or depolarisation) travels towards a lead, the
deflection is net positive. When the activity travels away from the lead
the deflection is net negative. If it is at 90 degrees then the complex is
‘isoelectric’ i.e. the R and S wave are the same size. This can often be
seen in V4 (see Figure 3).
The areas represented on the ECG are summarized below:

o V1, V2 = RV
o V3, V4 = septum
o V5, V6 = L side of the heart
o Lead I = L side of the heart
o Lead II = inferior territory
o Lead III = inferior territory
o aVF = inferior territory (remember ‘F’ for ‘feet’)
o aVL = L side of the heart
o aVR = R side of the heart

 The ECG can be broken down into the individual components.


For the purpose of this we will look at lead II (see Figure 4). All
boxes are based on the assumption that the paper speed is
running at 25mm/sec, therefore 1 large square is equivalent to 0.2
secs and a small square to 0.04 secs.

What do the segments of the ECG represent?


o P-wave: Atrial contraction
o PR interval: Represents the time taken for excitation to spread
from the sino-atrial (SA) node across the atrium and down to the
ventricular muscle via the bundle of His.
o QRS: Ventricular contraction
o ST segment: Ventricular relaxation
o T-wave: Ventricular repolarisation

 Normal duration of ECG segments:

o PR interval: 0.12 – 0.2 secs (3-5 small squares)


o QRS: <0.12 secs (3 small squares)
o QTc: 0.38 – 0.42 secs

  How to read an ECG

There are many different systems to interpret the ECG. This


system ensures you will never miss anything:

1.  Patient details
2. Situation details
3. Rate
4. Rhthm
5. Axis
6. P-wave and P-R interval
7. Q-wave and QRS complex
8. ST segment
9. QT interval
10. T-wave

These components will now be explained in more detail.

 1. Patient details

o Patient’s name, date of birth and hospital number


o Location
o This becomes important as in the ED or acute medical setting
doctors are often shown multiple ECGs. You need to know
where your patient is in order to ensure that they can be moved
to a higher dependency area if appropriate.

 2. Situation details

o When was the ECG done?


o The time
o The number of the ECG if it is one of a series
o If you are concerned that there are dynamic changes in an
ECG it is helpful to ask for serial ECGs (usually three ECGs
recorded 10 minutes apart) so they can be compared. These
should always be labelled 1, 2 and 3.
o Did the patient have chest pain at the time?
o Or other relevant clinical details. For example, if you are wanted
an ECG to look for changes of hyperkalaemia, note the
patient’s potassium level on the ECG.

 3. Measuring the rate on an ECG

o  Rate can be calculated in a number of ways:

1. Count the number of QRSs on one line of the ECG (usually lead II
– running along the bottom) and multiply by six.
2. Count the number of large squares between R waves and divide
300 by this number (if the patient is in atrial fibrillation it is more
accurate to report a rate range rather than a single value).

 4. Assessing the rhythm on an ECG

o Is the rhythm regular or irregular? If it is irregular is it regularly or


irregularly irregular?
o Rhythm can be difficult to assess especially in bradycardia or
tachycardia. It may be helpful to use the ‘paper test’.
o To do this place a piece of scrap paper over the ECG and mark
a dot next to the top of a QRS complex, draw another dot next
to the top of the next QRS then slide the paper along the ECG.
If the rhythm is regular you should see that your two dots match
to the tops of the QRS complexes throughout the ECG.

 5. Assessing the axis on an ECG

o  Axis is the sum of all the electrical activity in the heart.


o The contraction travels from the atria to the right and left
ventricles. As the left ventricle is larger and more muscular normal
axis lies to the left (at -30 degrees to 90 degrees – see Figure 5).
o As a general rule if the net deflections in leads I and aVF are
positive then the axis is normal.
o If lead I has a net negative deflection whilst aVF is positive then
there is right axis deviation.
o If lead I has a positive deflection and aVF has a negative
deflection then there is left axis deviation
o If you want to work it out more precisely you can use the method
below:
o Count the number of small squares of positive or negative
deflection in aVF and make a dot on the aVF axis (see Figure
5) moving a mm for each small square counted (e.g. x mm up
for negative and x mm down for positive deflections).
o Count the number of small squares of positive or negative
deflection in lead 1 and make a dot on the  lead 1 axis moving a
mm from the centre of the chart for each small square counted
(e.g. x mm right for negative and x mm left for positive
deflections).
o Draw a horizontal line through your lead 1 dot and a vertical line
through your aVF dot then draw a line from this intersection
back through 0 and this will give you the accurate axis.
Figure 5. The axis of the heart – a useful diagram for assessing
the cardiac axis using the method above.

Causes of axis deviation

Left axis deviation Right axis deviation

o Can be normal if the o Normal in children or young


diaphragms are raised e.g. thin adults.
Ascites, pregnancy o Right ventricular hypertrophy
o Left ventricular hypertrophy (RVH)
(LVH) o Often due to respiratory
o Left anterior hemiblock (see disease
notes on heart block) o Pulmonary embolism (PE)
o Inferior myocardial infaction o Anterolateral myocardial
o Hyperkalaemia infarction
o Vertricular tachycardia (VT) o Left posterior hemiblock (rare)
o Paced rhythm o Septal defect
6. P-wave and PR interval

o  Can you see a p-wave? If the rhythm is atrial fibrillation, atrial


flutter or a junctional tachycardia you may not be able to.
o At this point you can also assess whether each p wave is
associated with a QRS complex. P-waves not in association
with QRS complexes indicate complete heart block.
o Assess p-wave morphology
o In some cases there can be a notched (or bifid) p-wave known
as “p mitrale”, indicative of left atrial hypertrophy which may be
caused by mitral stenosis. There may be tall peaked p-waves.
This is called “p-pulmonale” and is indicative of right atrial
hypertrophy often secondary to tricuspid stenosis or pulmonary
hypertension.
o A similar picture can be seen in hypokalaemia (known as
“pseudo p-pulmonale”).
o The PR interval may be prolonged in first degree heart block
(described in more detail later).
o The PR interval may be shortened when there is rapid conduction
via an accessory pathway, for example in Wolff Parkinson White
syndrome.
o PR depression may be seen in pericarditis.

 7. Assessing Q-wave and QRS complex

o  Q-wave
o A q-wave is an initial downward deflection in the QRS complex.
These are normal in left-sided chest leads (V5, 6, lead I, aVL)
as they represent septal depolarization from left to right. This is
as long as they are <0.04secs long (1 small square) and <2mm
deep.
o If q-waves are larger than this or present in other leads they are
pathological.
o QRS complex
o Width
o The QRS complex normally lasts for < 0.12 secs (3 small
squares).
o Causes of a wide QRS:
o Bundle branch blocks (LBBB or RBBB)
o Hyperkalaemia
o Paced rhythm
o Ventricular pre-excitation (e.g. Wolf Parkinson White)
o Ventricular rhythm
o Tricyclic antidepressant (TCA) poisoning
o Shape and height
o The QRS may be small (or low voltage) in pericardial
effusion, high BMI, emphysema, cardiomyopathy and cardiac
amyloid.
o The QRS is tall in left ventricular hypertrophy (LVH)
o The criteria suggestive of LVH on the ECG is if the height
of the R wave in V6 + the depth of the S wave in V1. If this
value is >35mm this is suggestive of LVH.
o The QRS can also be tall in young, fit people (especially if
thin).

  8. ST segment

o The ST segment can be normal, elevated or depressed. To be


significant the S-T segment must be depressed or elevated by 1
or more millimeters in 2 consecutive limb leads or 2 or more
millimeters in 2 consecutive chest leads. Look out for reciprocal
changes.
o ST elevation indicates infarction.
o ST depression is normally due to ischaemia.
o ST segment depression may also be seen in digoxin toxicity.
Here the ST depression will be downsloping (sometimes known
as the “reverse tick” sign).

NB: High-takeoff
o A mimic of ST elevation is high-takeoff. High-takeoff is also known
as benign early repolarization.
o High-takeoff is where there is widespread concave ST elevation,
often with a slurring of the j-point (start of the ST segment). It is
most prominent in leads V2-5, is usually in young health people
and is benign.
o The best ways to differentiate it from myocardial infarction are:
o The ST segments are concave; they are most prominent in V2-
5; they have a slurred start (j-point); the ST elevation is usually
minimal compared to the amplitude of the t-wave; there are no
reciprocal changes; the ST segments do not change over time.

 9. QT interval

o  The QT interval is the time between the start of the q-wave and
the end of the t-wave.
o The QT interval is corrected for heart rate giving the QTc.
o As a quick check, if the t-waves occur over half way between
the QRS complexes the QTc may be lengthened
o Not an accurate method but very quick!
o A long QTc interval (known as “long QT”) is especially important
to identify in patients with a history of collapse or transient loss of
consciousness.

 Causes of long QT:

Drugs Metabolic Familial Other

o Tricyclic o Hypothermia o Long QT o IHD


antidepressanto Hypokalaemia syndrome o Myocarditis
s (TCAs) o Hypocalcaemi o Brugada
o Terfenadine a syndrome
o Erythromycin o Hypothyroidis o Arrhythmogeni
o Amiodarone
o Phenothiazine
s m c RV dysplasia
o Quinidine

 10. T-wave

The t-wave can be flattened or inverted for a number of reasons:

o Normal variant
o Commonly inverted in aVR and V1 and often in V2 and V3 in
people of afro-Caribbean descent.
o Ischaemia
o Ventricular hypertrophy (strain pattern) usually in lateral leads
o LBBB (t-wave inversion in the anterolateral leads)
o Digoxin
o Hypokalaemia (can cause flattened t-waves)

 N.B. Hyperkalaemia causes peaked T waves. The classic


changes in hyperkalaemia are:

o Small p-wave
o Tall, tented (peaked) t-wave
o Wide QRS
o Widening of the QRS indicates severe cardiac toxicity

 Summary

Following steps 1-10 above give the ideal system for interpreting
an ECG. If you work through these steps you will be unlikely to
miss anything significant.

You might also like