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.
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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.
What do the segments of the ECG represent? P-wave: Atrial contraction 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.
QRS: Ventricular contraction ST segment: Ventricular relaxation T-wave: Ventricular repolarisation Normal duration of ECG segments: • PR interval: 0.12 – 0.2 secs (3-5 small squares) • QRS: <0.12 secs (3 small squares) • 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
• Patient’s name, date of birth and hospital number
• Location
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 When was the ECG done?
• The time • The number of the ECG if it is one of a series
• 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.
Did the patient have chest pain at the time? • 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
• Rate can be calculated in a number of ways:
• Count the number of QRSs on one line of the ECG (usually lead II
– running along the bottom) and multiply by six.
• 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
• Is the rhythm regular or irregular? If it is irregular is it regularly
or irregularly irregular?
• Rhythm can be difficult to assess especially in bradycardia or
tachycardia. It may be helpful to use the ‘paper test’.
• 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 • Axis is the sum of all the electrical activity in the heart. • 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 ).
• As a general rule if the net deflections in leads I and aVF are positive then the axis is normal. • If lead I has a net negative deflection whilst aVF is positive
then there is right axis deviation. • If lead I has a positive deflection and aVF has a negative
deflection then there is left axis deviation
If you want to work it out more precisely you can use the method below:
• 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).
• 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).
• 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.
The axis of the heart – a useful diagram for assessing the cardiac axis using the method above.
6. P-wave and PR interval Can you see a p-wave? If the rhythm is atrial fibrillation, atrial
flutter or a junctional tachycardia you may not be able to. 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.
Assess p-wave morphology 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.
A similar picture can be seen in hypokalaemia (known as
“pseudo p-pulmonale”).
The PR interval may be prolonged in first degree heart block
(described in more detail later).
The PR interval may be shortened when there is rapid
conduction via an accessory pathway, for example in Wolff
Parkinson White syndrome.
PR depression may be seen in pericarditis.
7. Assessing Q-wave and QRS complex
• Q-wave
• 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.
• If q-waves are larger than this or present in other leads they
are pathological.
• QRS complex
• Width
• The QRS complex normally lasts for < 0.12 secs (3 small
squares).
• Causes of a wide QRS:
• Bundle branch blocks (LBBB or RBBB)
• Hyperkalaemia
• Paced rhythm
• Ventricular pre-excitation (e.g. Wolf Parkinson White)
• Ventricular rhythm
• Tricyclic antidepressant (TCA) poisoning
• Shape and height
• The QRS may be small (or low voltage) in pericardial
effusion, high BMI, emphysema, cardiomyopathy and
cardiac amyloid.
• The QRS is tall in left ventricular hypertrophy (LVH)
• 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.
• The QRS can also be tall in young, fit people (especially
if thin).
8. ST segment
• 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.
• ST elevation indicates infarction.
• ST depression is normally due to ischaemia.
• 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 • A mimic of ST elevation is high-takeoff. High-takeoff is also
known as benign early repolarization. • 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.
• The best ways to differentiate it from myocardial infarction are: • 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
• The QT interval is the time between the start of the q-wave and
the end of the t-wave.
• The QT interval is corrected for heart rate giving the QTc.
• As a quick check, if the t-waves occur over half way between
the QRS complexes the QTc may be lengthened
• Not an accurate method but very quick!
• 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.
Drugs Metabolic Familial Other
o Tricyclic
antidepressan
ts (TCAs)
o Terfenadine
o Erythromycin
o Amiodarone
o Phenothiazin
es
o Quinidine
o Hypothermia
o Hypokalaemia
o Hypocalcaemi
a
o Hypothyroidis
m
o Long QT syndrome
o Brugada syndrome
o Arrhythmogenic
RV dysplasia
o IHD
o Myocardi
tis
Causes of long QT:
10. T-wave
The t-wave can be flattened or inverted for a number of reasons:
• Normal variant
• Commonly inverted in aVR and V1 and often in V2 and V3
in people of afro-Caribbean descent.
• Ischaemia
• Ventricular hypertrophy (strain pattern) usually in lateral leads
• LBBB (t-wave inversion in the anterolateral leads)
• Digoxin
• Hypokalaemia (can cause flattened t-waves)
N.B. Hyperkalaemia causes peaked T waves. The classic changes
in hyperkalaemia are:
• Small p-wave
• Tall, tented (peaked) t-wave
• Wide QRS
• 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.
Heart blocks and bundle branch blocks on ECGs (EKGs) In order to understand heart blocks it is important to have an
understanding of the conduction system of the heart:
Passage of current through the heart • The initial signal originates at the sinoatrial node (SAN) • It is conducted through the myocardium of the atria and then
passes via the atrio ventricular node (AVN) to the bundle of His. This bundle then splits into two bundle branches (left and right)
• The left bundle further splits into anterior and posterior fascicles (more on that later)
• Conduction continues through the Purkinjie fibres and finally into the ventricular muscle which contracts in systole which corresponds to the QRS complex
Below we discuss what happens when the conduction system is interrupted. The figure below gives an overview but we will look at each block in more detail.
Significance of type 2 heart blocks Wencheback is a normal variant 2:1 and Mobitz type 2 blocks are pathological; they may precede 3rd degree or complete heart block
3rd degree heart block (complete heart block)
In 3rd degree heart blocks the connections between the atria and the ventricles are
completely lost. The atrial rate continues as normal (as seen by regular p-waves).
However, the actual heart rate is slow reflecting a ventricular escape rhythm which
is generated from a focus within the ventricular muscle its self. Each p-wave is not
associated with a QRS complex and the QRS complex is wide reflecting its
ventricular origins.
Bundle branch blocks (BBBs)
Refer back to the figure below as you read about the different blocks:
How RBBB works • From first principles RBBB occurs as left ventricular
contraction happens just prior to right ventricular contraction (as the R bundle is not working) where they would normally contract together.
• Remember that the positive deflection is caused by depolarization travelling towards that lead. Therefore: • Initially there is septal depolarization (left to right)
causing a small R wave in V1 and Q wave in V6 • Then LV contraction causes an S wave in V1 and R wave in
V6 • Then RV contraction causes an R wave in V1 and a deep S
wave in V6
Left bundle branch block (LBBB)
This is always pathological and relates to left heart disease. If acute it may
indicate acute myocardial infarction and is one of the indications for
thrombolysis or transfer for PCI. This is one of the situations that illustrates
How LBBB works • In LBBB you will see wide complexes with a negative
(sometimes W shaped) complex in V1 and an M pattern in V4 -V6 and T wave inversion in the anterolateral leads.
• The T wave inversion is due to abnormal repolarization (after abnormal depolarization) rather than ischaemia.
• From first principles: • The septum depolarizes from R to L causing a Q wave in V
1 and a R wave in V6 • The R ventricular contraction occurs first causing an R
wave in V1 and a S wave in V6 • Then LV contraction causes an S wave in V1 and a further
R wave in V6
Right bundle branch block (RBBB) Left bundle branch block (LBBB)
o Normal in young, tall thin people
o Idiopathic
o Right ventricular strain (PE or
chronic respiratory disease)
o Ischaemic Heart Disease
o Myocarditis
o Ischaemic Heart Disease (MI)
o Hypertension
o LVH
o Aortic valve disease
o Post aortic valve replacement
o RV pacemaker
o Myocarditis
o Cardiomyopathy
Causes of bundle branch blocks (BBBs)
Fascicular blocks • The left bundle can also be split into anterior and posterior fascicles (as
shown in the figure above) and block can affect either of these. • Anterior fascicular block
• If the anterior fascicle is blocked the cardiac axis swings round to the left causing left axis deviation.
• This is known as left anterior hemiblock • It is often caused by LVH
• Posterior fascicular block • Uncommonly the left posterior fascicle is exclusively blocked in
which case there is right axis deviation. • Bifascicular block
• If the left anterior fascicle (or left posterior fascicle but this is much less common) and the right bundle are blocked you will see both right bundle branch block and left axis deviation, this is known as bifascicular block.
• This is clinically important as the patient may intermittently go into complete heart block as they are solely relying on the posterior fascicle for ventricular contraction.
Trifascicular block If there is bifasicular block with a prolonged pr interval (i.e. first degree block) this is known as trifasicular block as there is block in 2 fasicles and a delay in the 3rd As with bifasicular block it should be treated urgently as it may deteriorate into complete heart block
ECG (EKG) examples and quiz For each of the questions below a short clinical scenario is given followed by the 12-lead ECG. Review the ECG (EKG), present it according to the structure in ECG interpretation and attempt a diagnosis before clicking on the plus symbol to see the answer.
Answer We will not go through the ECG as the most important information is in the clinical history. This is pulseless electrical activity (PEA). It is the most extreme example of why you should look at the patient in conjunction with the ECG! There are no specific ECG changes in PEA – the most important thing is to recognize that this patient is in cardiac arrest and to start chest compressions and Advanced Life Support (ALS) immediately. However, the ECG may help you ascertain the underlying pathology. In this case there are low voltage QRS complexes which may simply due to large body habitus or could indicate pathology ‘interrupting’ the signal between the heart and the electrode. This can include pericardial fluid or pneumothorax. This is worth thinking about as tamponade and tension pneumothorax are both reversible causes of PEA.
Diagnosis: This is a normal ECG. There are many variants of normal and it is worth looking at as many ECGs as possible to get exposed to the common variants. It is crucial to remember that a very sick patient can have a normal ECG so always use all the information available to you and don’t rely on the ECG alone.
Question 6
A 65 year old man with a history of ischaemic heart disease is found
unresponsive. He has no central pulse and is making no respiratory effort.
This is his ECG. What is the diagnosis and what will you do?
Diagnosis: This is acute posterior MI. What we see in the anterior leads is the equivalent of ‘upside down’ ST elevation. Imagine flipping the ECG paper over and looking at it from behind or looking at the ECG in a mirror held along the inferior border. You would see ST elevation (the deep ST depression reversed), t-wave inversion (upright t-waves seen upside down) and this represents what is going on in the posterior region of the heart. Another clue is the bradycardia seen in this case: the vessels supplying the posterior of the heart also supply the ‘pacemaker’ region of the SA node.
Question 16
A 29 year old presents with central chest pain. She has a history of recent flu-like
illness but no significant past medical history. This is her ECG. What is the
Diagnosis: The diagnosis is pericarditis. Pericarditis often presents in young people after a history of viral illness. He you can see the characteristic widespread saddle-shaped ST elevation and PR depression.
Question 17
A 70 year old woman presents with sudden onset of chest pain. The pain is crushing
in nature and radiates up to her jaw. This is her ECG. Present your findings and give