How to read an Electrocardiogram (ECG).

Part
One: Basic principles of the ECG. The normal
ECG
Author(s): Dr Dallas Price
Consultant Cardiologist, St Mary's Hospital, Isle of Wight, UK

Introduction
The electrocardiogram (ECG) is one of the simplest and oldest cardiac investigations available, yet it can
provide a wealth of useful information and remains an essential part of the assessment of cardiac
patients.
With modern machines, surface ECGs are quick and easy to obtain at the bedside and are based on
relatively simple electrophysiological concepts. However junior doctors often find them difficult to interpret.
This is the first in a short series of articles that aim to:

Help readers understand and interpret ECG recordings.

Reduce some of the anxiety juniors often experience when faced with an ECG.

Basic principles
What is an ECG?
An ECG is simply a representation of the electrical activity of the heart muscle as it changes with time,
usually printed on paper for easier analysis. Like other muscles, cardiac muscle contracts in response to
electricaldepolarisation of the muscle cells. It is the sum of this electrical activity, when amplified and
recorded for just a few seconds that we know as an ECG.

Basic Electrophysiology of the Heart (see Figure 1)

The normal cardiac cycle begins with spontaneous depolarisation of the sinus node, an area of
specialised tissue situated in the high right atrium (RA). A wave of electrical depolarisation then spreads
through the RA and across the inter-atrial septum into the left atrium (LA).
The atria are separated from the ventricles by an electrically inert fibrous ring, so that in the normal heart
the only route of transmission of electrical depolarisation from atria to ventricles is through the
atrioventricular (AV) node. The AV node delays the electrical signal for a short time, and then the wave of
depolarisation spreads down the interventricular septum (IVS), via the bundle of His and the right and left
bundle branches, into the right (RV) and left (LV) ventricles. Hence with normal conduction the two
ventricles contract simultaneously, which is important in maximising cardiac efficiency.

After complete depolarisation of the heart, the myocardium must then repolarise, before it can be ready to
depolarise again for the next cardiac cycle.

Figure 1. Basic electrophysiology of the heart

Electrical axis and recording lead vectors (see Figures 2 and 3)

The ECG is measured by placing a series of electrodes on the patients skin so it is known as the
surface ECG.
The wave of electrical depolarisation spreads from the atria down though the IVS to the ventricles. So the
direction of this depolarisation is usually from the superior to the inferior aspect of the heart. The direction
of the wave of depolarisation is normally towards the left due to the leftward orientation of the heart in the
chest and the greater muscle mass of the left ventricle than the right. This overall direction of travel of the
electrical depolarisation through the heart is known as the electrical axis.
A fundamental principle of ECG recording is that when the wave of depolarisation travels toward a
recording lead this results in a positive or upward deflection. When it travels away from a recording lead
this results in a negative or downward deflection.
The electrical axis is normally downward and to the left but we can estimate it more accurately in
individual patients if we understand from which direction each recording lead measures the ECG.

Figure 2. Orientation of the limb leads showing the direction from which each lead 'looks' at the heart
By convention, we record the standard surface ECG using 12 different recording lead directions, though
rather confusingly only 10 recording electrodes on the skin are required to achieve this. Six of these are
recorded from the chest overlying the heart the chest or precordial leads. Four are recorded from the
limbs the limb leads. It is essential that each of the 10 recording electrodes is placed in its correct
position, otherwise the appearance of the ECG will be changed significantly, preventing correct
interpretation.
The limb leads record the ECG in the coronal plane, and so can be used to determine the electrical axis
(which is usually measured only in the coronal plane). The limb leads are called leads I, II, III, AVR, AVL
and AVF. Figure 2 shows the relative directions from which they look at the heart. A horizontal line
through the heart and directed to the left (exactly in the direction of lead I) is conventionally labelled as the
reference point of 0 degrees (0 o). The directions from which other leads look at the heart are described
in terms of the angle in degrees from this baseline.
The electrical axis of depolarisation is also expressed in degrees and is normally in the range from
-30 0 to + 900. A detailed explanation of how to determine the axis is beyond the scope of this article but
the principles mentioned here should help readers to understand the concepts involved.
The chest leads record the ECG in the transverse or horizontal plane, and are called V1, V2, V3, V4, V5
and V6 (see Figure 3).

Figure 3. Transverse section of the chest showing the orientation of the six chest leads in relation to the
heart

Voltage and timing intervals

It is conventional to record the ECG using standard measures for amplitude of the electrical signal and for
the speed at which the paper moves during the recording. This allows:

Easy appreciation of heart rates and cardiac intervals and

Meaningful comparison to be made between ECGs recorded on different occasions or by different

ECG machines.

The amplitude, or voltage, of the recorded electrical signal is expressed on an ECG in the vertical
dimension and is measured in millivolts (mV). On standard ECG paper 1mV is represented by a deflection
of 10 mm. An increase in the amount of muscle mass, such as with left ventricular hypertrophy (LVH),
usually results in a larger electrical depolarisation signal, and so a larger amplitude of vertical deflection
on the ECG.
An essential feature of the ECG is that the electrical activity of the heart is shown as it varies with time. In
other words we can think of the ECG as a graph, plotting electrical activity on the vertical axis against
time on the horizontal axis. Standard ECG paper moves at 25 mm per second during real-time recording.
This means that when looking at the printed ECG a distance of 25 mm along the horizontal axis
represents 1 second in time.
ECG paper is marked with a grid of small and large squares. Each small square represents 40
milliseconds (ms) in time along the horizontal axis and each larger square contains 5 small squares, thus
representing 200 ms. Standard paper speeds and square markings allow easy measurement of cardiac

timing intervals. This enables calculation of heart rates and identification of abnormal electrical
conduction within the heart (see Figure 4).

Figure 4. Sample of standard ECG paper showing the scale of voltage, measured on the vertical axis,
against time on the horizontal axis

The normal ECG

It will be clear from above that the first structure to be depolarised during normal sinus rhythm is the right
atrium, closely followed by the left atrium. So the first electrical signal on a normal ECG originates from
the atria and is known as the P wave. Although there is usually only one P wave in most leads of an ECG,
the P wave is in fact the sum of the electrical signals from the two atria, which are usually superimposed.
There is then a short, physiological delay as the atrioventricular (AV) node slows the electrical
depolarisation before it proceeds to the ventricles. This delay is responsible for the PR interval, a short
period where no electrical activity is seen on the ECG, represented by a straight horizontal or isoelectric
line.
Depolarisation of the ventricles results in usually the largest part of the ECG signal (because of the
greater muscle mass in the ventricles) and this is known as the QRS complex.

The Q wave is the first initial downward or negative deflection

The R wave is then the next upward deflection (provided it crosses the isoelectric line and
becomes positive)

The S wave is then the next deflection downwards, provided it crosses the isoelectric line to
become briefly negative before returning to the isoelectric baseline.

In the case of the ventricles, there is also an electrical signal reflecting repolarisation of the myocardium.
This is shown as the ST segment and the T wave. The ST segment is normally isoelectric, and the T
wave in most leads is an upright deflection of variable amplitude and duration (see Figures 5 and 6).

Figure 5. The major waves of a single normal ECG pattern

Figure 6. Example of a normal 12 lead ECG; notice the downward deflection of all signals recorded from
lead aVR. This is normal, as the electrical axis is directly away from that lead

Normal intervals
The recording of an ECG on standard paper allows the time taken for the various phases of electrical
depolarisation to be measured, usually in milliseconds. There is a recognised normal range for such
intervals:

PR interval (measured from the beginning of the P wave to the first deflection of the QRS
complex). Normal range 120 200 ms (3 5 small squares on ECG paper).

QRS duration (measured from first deflection of QRS complex to end of QRS complex at
isoelectric line). Normal range up to 120 ms (3 small squares on ECG paper).

QT interval (measured from first deflection of QRS complex to end of T wave at isoelectric line).
Normal range up to 440 ms (though varies with heart rate and may be slightly longer in females)

Heart rate estimation from the ECG

Standard ECG paper allows an approximate estimation of the heart rate (HR) from an ECG recording.
Each second of time is represented by 250 mm (5 large squares) along the horizontal axis. So if the
number of large squares between each QRS complex is:

5 - the HR is 60 beats per minute.

3 - the HR is 100 per minute.

2 - the HR is 150 per minute.

This guide demonstrates how to read an ECG in a systematic & effective manner.
Always start by confirming the name and date of birth of the patient to confirm the ECG
belongs to the right person. Also, confirm the date and time the ECG was performed.

Step 1 Heart rate

Heart rate can be calculated simply with the following method:
o

Work out the number of large squares in one R-R interval

Then divide 300 by this number and you have your answer

e.g. If there are 4 squares in an R-R interval 300/4 = 75 beats per minute
.

If the rhythm is irregular:

Count the number of complexes on the rhythm strip (each rhythm strip is 10 seconds long)

Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)

Whats a normal heart rate?

o

Normal = 60 100 bpm

Tachycardia > 100 bpm

Bradycardia < 60 bpm

Hint: If there are obviously P waves present, check the ventricular rate and the atrial rate. The rates
will be the same if there is 1:1 AV conduction.

Step 2 Heart rhythm

The heart rhythm can be regular or irregular.
Irregular rhythms are regularly irregular (i.e. a recurrent pattern of irregularity) or irregularly
irregular (i.e. completely disorganised)
Mark out several consecutive R-R intervals on a piece of paper, then move them along the
rhythm strip to check if the subsequent intervals are the same.
Hint if you are suspicious that there is some atrioventricular block, map out the atrial rate and the
ventricular rhythm separately (i.e. mark the P waves and R waves). As you move along the rhythm
strip, you can then see if the PR interval changes, if QRS complexes are missing or if there is
complete dissociation between the two.

Step 3 Cardiac axis

Cardiac axis describes the overall direction of electrical spread within the heart
In a healthy individual the axis should spread from 11 o clock to 5 o clock
To figure out the cardiac axis you need to look at leads I,II & III
To get a better understanding of cardiac axis read this article

Normal cardiac axis

In normal cardiac axis Lead II has the most positive deflection compared to Leads I & III

Right axis deviation

In right axis deviation Lead III has the most positive deflection & Lead I should be negative
This is commonly seen in individuals with Right Ventricular Hypertrophy

Left axis deviation

In left axis deviation Lead I has the most positive deflection & Leads II & III are negative

Left axis deviation is seen in individuals with heart conduction defects

Step 4 P waves
Next we look at the p waves & answer the following questions:
o

Are P waves present?

If so, is each P wave followed by a QRS complex?

Do the P waves look normal? (check duration, direction and shape)

If not present, is there any atrial activity e.g. sawtooth baseline flutter waves / chaotic baseline
fibrillation waves / flat line no atrial activity at all?

Hint If P-waves are absent & there is an irregular rhythm it may suggest atrial fibrillation.

Step 5 P-R interval

The P-R interval should be between 0.12-0.2 seconds (3-5 small squares)

Prolonged PR interval (>0.2 seconds)

A prolonged PR interval suggests there is atrioventricular delay.
Is the prolonged PR interval fixed or does it vary across the ECG?
o

A fixed prolonged PR interval is a FIRST DEGREE AV BLOCK

First degree heart block

If the PR interval slowly increases then there is a dropped beat, this is MOBITZ TYPE I SECOND
DEGREE AV BLOCK(Wenckebach)

2nd degree AV block (Mobitz Type 1 Wenckebach) 1

If the PR interval is fixed but there are dropped beats, this is MOBITZ TYPE 2 SECOND DEGREE
HEART BLOCK (clarify that by the frequency of dropped beats e.g 2:1, 3:1, 4:1)

Mobitz type 2 (3:1)

If the P waves and QRS complexes are completely unrelated, this is THIRD DEGREE AV

BLOCK (complete heart block)

Complete heart block (3rd degree)

To help remember these degrees of AV block, it is useful to remember the anatomical location
of the block in the conducting system:
First degree AV block:

o
o

Occurs between the SA node and the AV node (i.e. within the atrium)

Second degree AV block:

o
o

Mobitz I (Wenckebach) occurs IN the AV node. This is the only piece of conductive tissue in the heart
which exhibits the ability to conduct at different speeds.

Mobitz II occurs AFTER the AV node in the bundle of His or Purkinje fibres.

Third degree AV block:

o
o

Occurs anywhere from the AV node down causing complete blockage

Shortened PR interval
If the PR interval is short, this means one of two things:
o

Simply, the P wave is originating from somewhere closer to the AV node so the conduction takes less
time (the SA node is not in a fixed place and some peoples atria are smaller than others!)

The atrial impulse is getting to the ventricle by a faster shortcut instead of conducting slowly across the
atrial wall. This is an accessory pathway and can be associated with a delta wave (see below which
demonstrates an ECG of a patient with Wolff Parkinson White syndrome)

Delta wave

Step 6 QRS complex

There are several aspects of the QRS complex to assess.

Width
Width can be described as NARROW (< 0.12ms) or BROAD (> 0.12ms)
o

A narrow QRS complex occurs when the impulse is conducted down the bundle of His and the
Purkinje fibre to the ventricles. This results in well organised synchronised ventricular depolarisation.

A broad QRS complex occurs if there is an abnormal depolarisation sequence for example, a
ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle.
In contrast, an atrial ectopic would result in a narrow QRS complex because it would conduct down the
normal conduction system of the heart. Similarly, a bundle branch block results in a broad QRS because the

impulse gets to one ventricle rapidly down the intrinsic conduction system then has to spread slowly across
the myocardium to the other ventricle.

Height
Describe this as SMALL or TALL:
o

Small complexes are defined as < 5mm in the limb leads or < 10 mm in the chest leads.

Tall complexes imply ventricular hypertrophy (although can be due to body habitus e.g. tall slim
people). There are numerous algorithms for measuring LVH, such as the Sokolow-Lyon index or the Cornell
index.

Morphology
This is where you assess the individual waves of the QRS complex.waves
Delta wave
The mythical delta wave is a sign that the ventricles are being activated earlier than normal from a
point distant to the AV node. The early activation then spreads slowly across the myocardium
causing the slurred upstroke of the QRS complex. Note the presence of a delta wave does NOT
diagnose Wolff-Parkinson-White syndrome. This requires evidence of tachyarrhythmias AND a delta
wave.

Delta wave
Q waves
Isolated Q waves can be normal. A pathological Q wave is > 25% the size of the R wave that follows
it or > 2mm in height and > 40ms in width. A single Q waves is not a cause for concern look for Q
waves in an entire territory (anterior / inferior) for evidence of previous MI.

Inferior Q waves (II, III, aVF) with T-wave inversion due to previous MI

R and S waves
Look for R wave progression across the chest leads (from small in V1 to large in V6) with
the transition from S > R wave to R > S wave should occur in V3 or V4. Poor progression (i.e. S > R
through to leads V5 and V6) can be a sign of previous MI but can also occur in very large people
due to lead position.

Poor R wave progression (previous anterior MI)

J point segment
The J point is where the S wave joins the ST segment. This point can be elevated or The ST
segment that follows is then raisedHigh take off (or benign early repolarisation to give its full title)
is a normal variant that causes a lot of angst and confusion as itLOOKS like ST elevation.
o

It occurs mostly under the age of 50 (over age of 50, ischaemia is more common and should be
suspected first) and rarely over 70.

Typically, the J point is raised with widespread ST elevation in multiple territories making ischaemia
less likely

The T waves are also raised (in contrast to a STEMI where the T wave remains the same size and the
ST segment is raised)

The changes do not change! During a STEMI, the changes will evolve in BER, they will remain the
same.

Benign Early Repolarisation (High take off)

Step 7 ST segment
The ST segment is the part of the ECG between the end of the S wave & start of the T wave.
In a healthy individual it should be an isoelectric line (neither elevated or depressed).
Abnormalities of the ST segment should be investigated to rule out pathology.

ST elevation
ST elevation is significant when it is > 1mm (1 small square) in relation to the baseline.
It is most commonly caused by acute myocardial infarction.
The morphology of the ST elevation differs depending on how long ago the MI occurred.

ST depression
ST depression is significant when it is >1mm (1 small square) in relation to the baseline.
ST-depression lacks specificity, therefore you shouldnt jump to any diagnostic conclusions.
It can be caused by many different things including:
o

Anxiety

Tachycardia

Digoxin toxicity

Haemorrhage, Hypokalaemia, Myocarditis

Coronary artery insufficiency

MI

As a result you must take this ECG finding & apply it in the context of your patient.

Step 8 T waves
The T waves represent repolarisation of the ventricles.

Tall T waves
T waves are tall if they are:
o

> 5mm in the limb leads and

> 10mm in the chest leads (the same criteria as small QRS complexes).

Tall T waves can be associated with:

o

Hyperkalaemia (Tall tented T waves)

Hyper-acute STEMI

Inverted T waves
T waves are normally inverted in V1 and inversion in lead III is a normal variant.
Inverted T waves in other leads are a nonspecific sign of a wide variety of conditions:
o

Ischaemia

Bundle branch blocks (V4 6 in LBBB and V1 V3 in RBBB)

PE

LVH (in the lateral leads)

HCM (widespread)

General illness

Around 50% of ITU admissions have some evidence of T wave inversion during their stay.
Comment on the distribution of the T wave inversion e.g. anterior / lateral / posterior leads.
You must take this ECG finding & apply it in the context of your patient.

Biphasic T waves
Biphasic T waves have two peaks and can be indicative of ischaemia and hypokalaemia.

Flattened T waves
Another non-specific sign, this may represent ischaemia or electrolyte imbalance.

U waves
Not a common finding.
The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.
These become larger the slower the bradycardia classically U waves are seen in
various electrolyte imbalances or hypothermia, or antiarrhythmic therapy (such as digoxin,
procainamide or amiodarone).

Prominent U waves in a patient with Hypokalaemia

Summary
Having a system whilst working through ECGs is essential until you gain the experience
required to start using pattern recognition to speed up the process.

ECG scribbles
The following is a basic primer in interpretation of the ECG
(EKG). It is intended solely for teaching purposes, and
should not be relied upon in clinical decision making.
An Approach
ECGs can be very confusing, and there are dozens of
different methods of interpretation. It's perhaps best if
everyone works out their own individual approach, but
here's just one approach you can build upon:
1. Sit back and look - identify the patterns, and write down
what you see!
2. Go through the ECG systematically;
3. Correlate ECG and clinical findings, and if necessary,
go back and do a complete rethink;
4. Try and invalidate your assessment --- look for holes!

Of the above steps, the fourth seems counter-intuitive and

unnecessary. In fact, it's the most important. As in all
medicine, complacence is dangerous. Avoid it!
Now, let's sketch out a systematic approach. Ours is:
1. Check the patient details - is the ECG correctly labelled?
2. What is the rate?
3. Is this sinus rhythm? If not, what is going on?
4. What is the mean frontal plane QRS axis (You may wish at
this stage to glance at the P and T wave axes too)
5. Are the P waves normal (Good places to look are II and V1)
6. What is the PR interval?
7. Are the QRS complexes normal? Specifically, are there:
o significant Q waves?
o voltage criteria for LV hypertrophy?
o predominant R waves in V1?
o widened QRS complexes?
8. Are the ST segments normal, depressed or elevated?
Quantify abnormalities.
9. Are the T waves normal? What is the QT interval?
10.

Are there abnormal U waves?

Before we move through the systematic approach outlined

above, we will outline a few basics. More advanced readers
may wish to skip these basics, and move on to the
systematic part of the tutorial.

How the ECG works

When cell membranes in the heart depolarise, voltages change and
currents flow. Because a human can be regarded as a bag of salt
water (with baad attitude), in other words, a volume conductor,
changes in potential are transmitted throughout the body, and can
be measured. When the heart depolarises, it's convenient (and
fairly accurate) to represent the electrical activity as a dipole --- a
vector between two point charges. Remember that a vector has
both a size (magnitude), and a direction. By looking at how the
potential varies around the volume conductor, one can get an idea
of the direction of the vector. This applies to all intra-cardiac
events, so we can talk about a vector (or axis) for P waves, the QRS
complex, T waves, and so on.

In the above picture, the schematic ECG lead on the right

`sees' the (red) vector moving towards it, shown as a
positive deflection in the ECG trace; the lead at 90 degrees
to this sees nothing!
Various events

We assume some knowledge of heart anatomy. Note that the

normal heart has, electrically speaking, only two chambers,
an atrial and a ventricular `chamber'. Propagation of
electrical activity spreads freely within atria and ventricles,
but communication between these two chambers is limited
to the AV node. Everyone knows that the P wave
corresponds to atrial depolarisation, the QRS complex to
ventricular depolarisation, and the T wave to repolarisation
of the ventricle.
The ECG (EKG)

In order to be able to record myocardial activity, the

electrocardiograph needs to be able to detect tiny changes
in potential on the body surface. We are talking about
signals that are often around 1mV, and may be smaller. In
addition, we need some reference point to which we relate
the potential changes.
The 12-lead ECG
Over the years, we have evolved several systems that go to
make up the 12-lead ECG. These are:
Bipolar leads: the reference point is on one limb, the
`sensing' electrode (if you wish) is on another limb. The
leads are termed I, II, and III.

Unipolar leads: The reference point is several leads joined

together, and the sensing lead is on one limb. These leads
are conventionally augmented, in that the reference lead
on the limb being sensed is disconnected from the other
two.

 The V leads, which extend across the precordium, V1 in

the fourth right interspace, V2 4th left, V4 at the apex (5th
interspace, midclavicular line), V3 halfway in between V2
and V4, and V5 & V6 in the 5th interspace at the anterior
and mid axillary lines respectively.

We can visualise the directions of the various leads --- I

points left, and aVF points directly down (in a 'Southward'
direction). The other leads are arranged around the points
of the compass --- aVL about 30o more north of I, II down
towards the left foot, about 60o south of I, and III off to the
right of aVF. aVR `looks' at the heart from up and right, so
effectively it's seeing the chambers of the heart, and most
deflections in that lead are negative.

(a net positive vector in AVR is unusual, and suggests that

lead placement was incorrect. If the leads were correctly
sited, then think dextrocardia, or some other strange
congenital abnormality).
It's usual to group the leads according to which part of the
left ventricle (LV) they look at. AVL and I, as well as V5 and
V6 are lateral, while II, III and AVF are inferior. V1 through
V4 tend to look at the anterior aspect of the LV (some refer
to V1 and V2 `septal', but a better name is perhaps the
`right orientated leads'). Changes in depolarisation in the
posterior aspect of the heart are not directly seen in any of
the conventional leads, although "mirror image" changes
will tend to be picked up in V1 and V2.

Paper

ECG paper is traditionally divided into 1mm squares.

Vertically, ten blocks usually correspond to 1 mV, and on the
horizontal axis, the paper speed is usually 25mm/s, so one
block is 0.04s (or 40ms). Note that we also have "big
blocks" which are 5mm on their side.

Always check the calibration voltage on the right of the

ECG, and paper speed. The following image shows the
normal 1mV calibration spike:

Damping

Note that if the calibration signal is not "squared off" then

the ECG tracing is either over or under-damped, and should
not be trusted.

Heart rate
Knowing the paper speed, it's easy to work out heart rate.
It's also very convenient to have a quick way of eyeballing
the rate, and one method is as follows:
1. Remember the sequence: 300, 150, 100, 75, 60, 50
2. Identify an R wave that falls on the marker of a `big block'
3. Count the number of big blocks to the next R wave.
If the number of big blocks is 1, the rate is 300, if it's two,
then the rate is 150, and so on. Rates in between these
numbers are easy to `interpolate'.
But always remember that in the heart, because we have
two electrically `isolated' chambers, the atria and
ventricles, that we are really looking at two rates --- the
atrial and ventricular rates! It just so happens that in the
normal heart, the two are linked in a convenient 1:1 ratio,
via normal conduction down the AV node. In disease states,
this may not be the case.
Conventionally, a normal heart rate has been regarded as
being between 60 and 100, but it's probably more
appropriate to re-adjust these limits to 50 -- 90/min. A sinus
tachycardia then becomes any heart rate over 90, and

bradycardia, less than 50. Note that you have to look at the
clinical context -- a rate of 85 in a highly trained athlete
may represent a substantial tachycardia, especially if their
resting rate is 32/minute! One should also beware of
agressively trying to manage low rates in the presence of
good perfusion and excellent organ function.
Sinus bradycardia

Apart from fit, but otherwise normal individuals, there's a

long list of situations where sinus bradycardia occurs,
including:
hypothermia;
increased vagal tone (due to vagal stimulation or e.g.
drugs);
hypothyroidism;
beta blockade;
marked intracranial hypertension;
obstructive jaundice, and even in uraemia;
structural SA node disease, or ischaemia.
Sinus tachycardia

Always consider pain as a possible cause of tachycardia.

There's a long list, however:
Any cause of adrenergic stimulation (including pain);
thyrotoxicosis;
hypovolaemia;
vagolytic drugs (e.g. atropine)
anaemia, pregnancy;

 vasodilator drugs, including many hypotensive agents;

FEVER
myocarditis
If the rate is almost exactly 150, always make sure that you
are not mistaking atrial flutter with a 2:1 block for sinus
tachycardia. A common error.

Rhythm
Sinus arrhythmia and heart rate variability

There is normally a slight degree of chaotic variation in

heart rate, called sinus arrhythmia. Sinus arrhythmia is
generally a good thing, and loss of this chaotic variation is
of ominous prognostic significance. Post myocardial
infarction, a metronome-like regularity of the heartbeat is
associated with an increased likelihood of sudden death,
and just before the onset of ventricular tachycardia (or
fibrillation), variability is lost! Absence of any sinus
arrhythmia suggests an autonomic neuropathy.
Atrial extrasystoles

These arise from ectopic atrial foci. Commonly, the ectopic

beat always arises at about the same time after the sinus
beat!

The ectopic beat usually discharges the SA node, so

subsequent beats of SA origin are not in synchrony with the
previous sinus rhythm.
If the extrasystole occurs early on, it may find the HisPurkinje system not quite ready to receive an impulse, and
a degree of block may be seen. This is termed `aberration'.
Distinguish between an atrial extrasystole, and an
atrial escape beat, where the SA node falters, and a
subsidiary pacemaker takes over:

(Parenthetically, we didn't draw the P waves very well in the above strip. Don't
let this put you off from indentifying the underlying rhythm).

Supraventricular tachyarrhythmias (SVT)

Irregular SVT

By far the commonest cause of irregular SVT is atrial

fibrillation, where the atrial rate is in the region of 450 to
600/min, and the atria really do not contract rhythmically at
all. The atrium "fibrillates", writhing like a bag of worms.
The conventional view of the pathogenesis of AF is that
there are multiple re-entrant `wavelets' moving through the
atrial muscle, but recent evidence suggests that much AF
actually arises from ectopic activity in the muscular cuff
surrounding the pulmonary veins where they enter the left
atrium. AF is thought to beget further AF through
"electrical remodelling" --- electrophysiological changes that

are induced in atrial myocytes due to fast rates and the

consequent calcium loading.

Note that in the above tracing of AF, the ventricular

response rate seems rather slow, so we suspect that AV
block
has
been
increased
using
pharmacological
manipulation. In uncontrolled AF, rates of about 130 or
more are common.
Other causes of irregular SVT are:
Frequent atrial extrasystoles;
Multifocal atrial tachycardia, where there are three or
more distinct atrial foci, combined with tachycardia. There
is often severe underlying disease (e.g. chronic obstructive
airways disease), and in the ICU setting, MAT has a poor
prognosis.
"Atrial flutter with variable block".

Although it looks like atrial fibrillation, the above image

actually shows multifocal atrial tachycardia. Note how there
are at least three different P wave configurations!
Regular SVT

Atrial flutter is common. The atrial rate is commonly

300/min, and there is usually a 2:1 block, resulting in a
ventricular response rate of 150/min. Other ratios are
possible, and sometimes the ratio varies. This rhythm is
often unstable, and the heart may flip in and out of sinus
rhythm, or there may be runs of atrial fibrillation.

In the above ECG the clue is the rate. A rate of 150

should always engender the suspicion of atrial flutter with
2:1 block.
Probably the commonest cause of regular SVT is AV nodal
re-entrant tachycardia. Here, there are generally two ways
that electrical depolarisation can enter the AV node from
the atrium, a slow and fast `pathway'. A re-entrant
circuit can be set up, with impulses moving in a circular
fashion, and causing depolarisation of the ventricles at fast
rates (up to 200/min or even more).
Other causes of regular SVT include:
1. ectopic atrial tachycardia, due to repetitive discharges
from an ectopic atrial focus;
2. AV re-entrant tachycardia, via an accessory pathway,
discussed next.
Accessory pathways

Abnormal, congenital extra pathways between the atria and

ventricles are common, and can perforate the electrically

insulating fibrous ring that normally separates the atrial

`chamber' and the ventricular one. The most wellcharacterised is the Wolff-Parkinson-White syndrome.
Reasonable (WHO) criteria for the WPW pattern on ECG
are:
1. PR interval under 0.12s
2. A delta wave
3. QRS duration of 0.12s (or more)
4. A normal P-wave axis
Because depolarisation moves `antegrade' from atria to
ventricles, part of the ventricle depolarises prematurely,
and this is responsible for the slurred, initial delta wave. It
should be clear that the PR interval will therefore be short,
and the QRS duration should be prolonged. Note however
that not everyone with an accessory pathway will conduct
all of the time down that pathway. Accessory pathways are
common, estimated to occur in one to three individuals in
every thousand. Symptomatic pathways are far less
common.

The WPW syndrome is a combination of the WPW pattern,

and tachycardias. The tachycardias may be due to impulse
conduction down via the AV node and back up the accessory
pathway (commonest, called orthodromic tachycardia), the
other way around (down accessory pathway, up AV node,
termed antidromic tachycardia), or even related to atrial
fibrillation. This last cause is ominous, as if the accessory

pathway is able to conduct impulses at fast rates, the

ventricle may be driven at rates in excess of 200/min,
causing collapse or even death.
Distinguishing causes of SVT

A few pointers are in order. The important thing to look for

is the P wave:
1. If the P is inscribed before the QRS, it's probably an
ectopic atrial tachycardia;
2. If the P is after the QRS, consider orthodromic AV reentrant tachycardia;
3. If the P is not seen (and probably lost within the QRS) it's
likely to be AV nodal re-entrant tachycardia.
A few other hints:
The baseline ECG is invaluable (may show WPW, for
example);
It's useful if you can capture onset or termination of the
arrhythmia.
Ventricular extrasystoles

Because these arise within an ectopic focus within the

ventricular muscle, the QRS complex is wide, bizarre, and
unrelated to a preceding P wave. There is usually a constant
relationship (timing) between the preceding sinus beat and
a subsequent ventricular beat, because the preceding beat
influences the ectopic focus.

The ventricular beat is not usually conducted back into the

atria. What happens to the atrial beat that occurred, or was
about to occur when the VE happened? Usually, this is
blocked, but the subsequent atrial beat will occur on time,
and be conducted normally.
Rarely, the ventricular beat may be conducted retrogradely
and capture the atrium (resulting in a P wave after the QRS,
with an abnormal morphology as conduction through the
atrium is retrograde). The atrial pacemaker is now reset! In
the following rather complex tracing, we have a ventricular
rhythm (a bit faster than one might expect, perhaps an
accelerated idioventricular rhythm) with retrograde P
waves, and something else --- some of the P waves are
followed by a normal looking `echo' beat as the impulse is
conducted down back into the normal pathways).

Because the intrinsic rate of an ectopic focus often tends to

be slow-ish, extrasystoles will tend to arise more commonly
with slower rates. In addition, if the rate is varying,
extrasystoles will tend to `squeeze in' during long RR
intervals. Some have called this the "rule of bigeminy".

Couplet

Two VE's are termed a couplet.

Fusion beat

Occasionally, a VE occurs just after a sinus beat has started

to propagate into the His-Purkinje system. This results in a
`fusion beat', which combines the morphology of a normal
sinus beat and that of the extrasystole.
Parasystole

Rarely, the ectopic focus is protected from other influences,

and does its own merry thing. This is termed `parasystole',
and is detected by noting the unvarying coupling between
extrasystoles, and the lack of coupling between the
extrasystole and sinus beats! In the following trace, note
the fusion beats as the normal rhythm and parasystolic
rhythm transiently coincide...

We've put in the above unusual ECG more as a mnemonic

than for any other reason. We want you to remember that
even with extrasystoles, there is flow of information from
the normal rhythm to the ectopic focus. The ectopic focus is
therefore modulated by the normal rhythm, and usually
occurs at about the same interval from the normal events.
Parasystole is unusual.
Ventricular tachycardia

Three or more ventricular extrasystoles are a bad sign, and

are termed ventricular tachycardia (VT). There is usually
severe underlying myocardial disease. Sustained VT (more
than about 30 beats) often degenerates into ventricular
fibrillation, resulting in death.

The above strip shows several `characteristic' features of

VT. Apart from the regular fast rate and wide complexes, we
have a few more clues ... clearly, the atrial rate is different
from the ventricular rate, and there is dissociation between
atria and ventricles --- the P waves occur at any time in
relation to the QRS complexes. Even more characteristic of
VT is the presence of a fusion beat at the start of the trace
--- a QRS complex which is something in between the VT
morphology and normal morphology. There is also acapture
beat later on, where the P wave has managed to sneak
through and transiently take over, resulting in a normallyshaped QRS complex and T wave.
VT vs SVT+aberration

Distinguishing between VT, and SVT with aberration is

tricky. When in doubt, one should apply synchronised DC
countershock, and agonize later. This is especially the case
if the patient is haemodynamically unstable. If the patient is
haemostable, the rate is slowish (under about 150), then
one may have more time. A variety of algorithms have been
proposed - Brugada's approach may have merit --- you can
explore a web-based version of his algorithm here.
Ventricular fibrillation

This is a chaotic ventricular rhythm that rapidly results in

death. It is often precipitated by a critically timed
extrasystole, that occurs during the relative refractory
period of the myocardial fibres. Conventional wisdom has it
that this results in chaotic, unco-ordinated wavelets of
depolarisation moving through the ventricular mass.

VF is a dire emergency. If unsynchronised DC countershock

is applied within 30s of the onset of VF, there is an
approximately 97% chance that sinus rhythm will be
restored, and the person will survive. Survival decreases
exponentially thereafter, with every minute of delay.
Ventricular flutter

Ventricular 'flutter' is a bizarre sine-wave like rhythm, and

usually degerates into ventricular fibrillation. You won't see
it often (or for long).

Axis
The peculiar system we use in electrocardiography is nonCartesian, and rather arbitrary! We measure the direction
of vectors in degrees, and zero is indeed facing `East', but
+90o is South, instead of North as it would be in a Cartesian
system. You can work out that 180 o is 'West', and that
minus 90o is 'North'.
We can talk about the `axis' of any ECG depolarisation, but
most people when they are talking 'axis' are referring to
the mean frontal plane QRS axis. There is a number of ways
of determining this, but the following method has the merit
of simplicity:

1. Estimate the overall deflection (positive or negative, and

how much) of the QRS in standard lead I;
2. Do the same for AVF;
3. Plot the vector on a system of axes, and estimate the
angle, thus:

Note in the above picture that the (abnormal) axis

illustrated is negative ("towards the left") because AVF is
negative.
People tend to faff quite a lot about QRS axis deviations, but
they are a fairly blunt-edged tool. Marked right axis
deviation (e.g. +150o) may signify significant `right-sided'
heart disease. Left axis deviation is not uncommon in
inferior myocardial infarction, and if this is absent, the most
likely `diagnosis' is left anterior hemiblock. (There are
several other cause of left or right axis deviation, for
example depolarisation via accessory pathways).
Where the axis is up and to the left (eg. -135 o)*, this is
termed a "north west axis". It is commonly seen in
congenital heart disease, dextrocardia, and sometimes in
severe chronic obstructive airway disease.
The T wave axis is much neglected, and may be of value. If
the T wave axis is more than about 45 to 60 o different from
the QRS axis, this is abnormal. Schamroth gives a super

mnemonic --- "the T-wave axis moves away from the `region
of mischief'".
Even the P-wave axis is of use. The normal axis is about +40
to +60o, moving right with chronic obstructive disease. The
axis may move left with congenital heart disease, even up to
-30o (especially Ebstein's anomaly). One can also spot an
ectopic atrial focus low down in the atrium (`coronary sinus
rhythm') due to the `northern' shift in axis.
*{Footnote:

One reader pointed out that an axis of -135 o could just as well be

regarded as being `markedly to the right'. This is a reasonable argument. }

The P wave
Normal atrial activation is over in about 0.10s, starting in
the right atrium. A good place to look at P waves is in II,
where the P shouldn't be more than 2.5mm tall, and 0.11
seconds in duration.
A tall P wave (3 blocks or more) signifies right atrial
enlargement, a widened bifid one, left atrial enlargement:

In V1, another good place to look, depolarisation of the

right atrium results in an initial positive deflection, followed
by a vector away from V1 into the left atrium, causing a
negative deflection. The normal P wave in V1 is thus
biphasic. It's easy to work out the corresponding
abnormalities with left or right atrial enlargement:
There are a few other tips:

 A qR in V1 suggests right atrial enlargement, often due

to tricuspid regurgitation! (Observed by Sodi-Pallares).
If the overall QRS amplitude in V1 is under a third of the
overall QRS amplitude in V2, there is probably RA
enlargement! (Tranchesi).
A P wave originating in the left atrium often has a `dome
and dart' configuration.

The PR interval (and PR segment)

The PR interval extends from the start of the P wave to the
very start of the QRS complex (that is, to the start of the
very first r or q wave). A normal value is 3 to 5 `little blocks'
(0.12 to 0.20 seconds). It's convenient at this point to
discuss blocks...
SA node block

This is a diagnosis of deduction, as no electrical activity is

seen. An impulse that was expected to arise in the SA node
is delayed in its exit from the node, or blocked completely. A
second degree SA block can be `diagnosed' if the heart
rate suddenly doubles in response to, say, administration of
atropine. If the SA node is blocked, a subsidiary pacemaker
will (we hope) take over, in the atrium, AV node, or
ventricle!
AV nodal blocks

There are three "degrees" of AV nodal block:

1. First degree block:

simply slowed conduction. This is manifest by a prolonged PR

interval;

2. Second degree block:

Conduction intermittently fails completely. This may be in a

constant ratio (more ominous, Type II second degree block),
or progressive (The Wenckebach phenomenon, characterised
by progressively increasing PR interval culminating in a
dropped beat --- this is otherwise known as Mobitz Type I
second degree heart block)*.
*{Footnote: Thanks to the reader who pointed out the typo}

3. Third degree block:

There is complete dissociation of atria and ventricles.

Clearly a bad thing, requiring temporary or even

permanent pacing.

The QRS complex

The nomenclature is mildly arcane --- small deflections are
reflected using lower case, and larger deflections UPPER
CASE. An initial downwards deflection is a Q (or q), any
negative deflection after this is an S. An upward deflection
is an R. Note that we refer to a second deflection in the
same direction by adding a prime, so we have R', R'', S' and
so on. We might thus refer to an rSR' morphology, or
whatever.
Normally, the septum depolarises before other parts of the
left ventricle. This is seen as a small initial vector, which in
the `septal leads' (V1 and V2) is a positive deflection, and in
lateral leads (e.g. V6) is seen as a small q. This observation
is of relevance, as in conditions such as left bundle branch
block, where the septum cannot depolarise normally, the
lateral (septal) q is conspicuously missing.
Something of some importance is the time it takes the
ventricle to depolarise, often termed the ventricular
activation time. We can estimate this from the surface ECG
by looking at the time from the onset of the QRS to the
sudden downstroke of the QRS. (The fancy name for this
sudden downstroke is the `intrinsicoid deflection'). In right
orientated leads, a normal VAT is 0.02s, and on the left (e.g.
V6) the duration should not exceed 0.04s.

Q waves - myocardial infarction

Many people who have had a prior

MI will have an ECG that appears
normal. There may however be
typical features of previous MI, and
the most conspicuous of these is Q
waves. A simplistic explanation of
these prominent Q waves is that an
appropriately placed lead "sees
through" the dead tissue, and
visualises the normal depolarisation
of the viable myocardial wall
directly opposite the infarcted area.
Because, in the normal myocardium,
depolarisation moves from the
chamber outwards, this normal
depolarisation is seen as a Q wave!
Another feature of previous MI is
loss of R wave amplitude. It's easy to
imagine that if muscle is lost,
amplitude must be diminished.
(Having a pre-infarction ECG for
comparison is invaluable).

One can get some idea of the site of infarction from the lead
in which abnormalities are seen - inferior, lateral, or
anterior.
Hypertrophy and chamber enlargement

Because of the thin-walled nature of the atria, from an ECG

point of view, one cannot talk about "atrial hypertrophy" but
only about enlargement. Conversely, thickening of the
ventricle may result in increased voltages seen on the
surface ECG, and we can then discuss "ventricular
hypertrophy".
Left ventricular systolic overload/hypertrophy (LVH)

The absence of LVH on ECG means nothing, as the features

are insensitive. If however they are present, LVH is very
likely. Because the criteria were formulated on white males,
they are very insensitive in e.g. black women.

Systolic overload results in increased QRS deflections, with

the sum of the S in V1 and the R in V5 or V6 over 35mm
indicating hypertrophy. (In the above picture, also note the
predominantly negative deflection of the P wave in V1,
suggesting left atrial enlargement). A host of other criteria
have been proposed. Useful are:
R in I over 15mm
R in AVL over 11mm
Sum of all QRS voltages under 175mm (!)
T wave axis changes can be predicted knowing Schamroth's
rule .
LV diastolic overload

Features of LVH may be present (as above). Enormous R

waves may be seen in left-sided leads, especially with aortic
or mitral regurgitation. In contrast to systolic overload,
where septal q waves in the lateral leads are often
diminished or absent, in diastolic overload, prominent
lateral Qs are noted. Unlike systolic overload (where the T
waves are often inverted), T waves are usually upright, very
symmetrical, and somewhat pointed.

Inverted U waves in V4-6 suggest either systolic or diastolic

LV overload.
RV hypertrophy

A number of ECG abnormalities have been associated with

right ventricular hypertrophy. These include:
right axis deviation;
A tall R wave (bigger than the S) in V1;
A `little something' in V1 (an initial slur of the QRS, a
small r, or a tiny q).
Increased VAT in V1
left-sided RS or rS complexes, partial or complete RBBB,
or RS complexes in the mid-precordial leads.

Whenever you see a tall R in V1, consider the following

differential:
posterior myocardial infarction
RV hypertrophy
Right bundle branch block
Wolff-Parkinson-White syndrome (with an appropriately
placed accessory pathway)
Other rare causes such as dextrocardia, Duchenne
muscular dystrophy, and so on

 and, of course, incorrect lead placement!

Bundle branch blocks

A broadened QRS complex suggests a bundle branch block,

although there are other causes:
RBBB

Diagnostic criteria for right bundle branch block are

somewhat empiric, but useful. Here they are:
1. Tall R' in V1;
2. QRS duration 0.12s or greater (some would say, >= 0.14);
In addition, there is usually a prominent S in the lateral
leads (I, V5, V6).

RBBB is sometimes seen in normal people, or may reflect

congenital heart disease (e.g. atrial septal defect),
ischaemic heart disease, cardiomyopathy, or even acute
right heart strain.
LBBB

Diagnose this as follows:

1. No RBBB can be present;

2. QRS duration is 0.12s or more;

3. There must be evidence of abnormal septal depolarization.
The tiny q waves normally seen in the left-sided leads are
absent. (And likewise for the normal tiny r in V1).
In addition, the VAT is prolonged, and tall, notched R waves
are seen in the lateral leads (RR' waves). There is usually a
notched QS complex in V1 and V2.

Fascicular blocks

Left anterior hemiblock (LAHB) is interruption of the thin

anterosuperior division of the left bundle. Suspect it if there
is left axis deviation (past -45o) without another cause (such
as inferior myocardial infarction, or some types of
congenital heart disease or accessory pathways).
Other features of LAHB include an initial QRS vector which
is down and to the right, a long VAT, and several other
minor changes.
LAHB may indicate underlying heart disease, but is much
more worrying when associated with other abnormalities
(such as PR interval prolongation or RBBB).

The diagnosis of left posterior hemiblock is mentioned only

to be avoided!

The ST segment
The junction between QRS and ST
Hypothermia

Besides sinus bradycardia, the most common finding is a

prominent J wave.

In addition, there may be delayed VAT , QRS prolongation,

and nonspecific T wave abnormalities, with QT
prolongation. Eventually, blocks, ventricular extrasystoles,
and finally ventricular fibrillation occurs, below 30oC.
Ischaemic heart disease - ST changes

One should always remember that more than a quarter of

people presenting with an acute myocardial infarction will
have no ECG evidence of ischaemia or infarction! The ECG
on its own is a blunt-edged tool in the detection of coronary
artery disease. Exercise testing to elicit ischaemia is also
not very sensitive in detecting this common disease.
Acute myocardial infarction --- the `hyperacute phase'

There are four main features of early myocardial infarction

(as per Schamroth):
1. increased VAT
2. increased R wave amplitude (!)
3. ST elevation which is sloped upwards!

4. Tall, widened T waves (The ST segment often merges with

these)

Note that Q waves are not seen early on.

Established acute myocardial infarction

We now lay great emphasis on ST

segment elevation in diagnosing acute MI
(In the past, Q waves were remarked on,
but as noted above, these are often
absent, early on). The features of `full
blown' MI may be:
1. prominent Q waves;
2. elevated ST segments;
3. Inverted `arrowhead' T waves.
Remember our previous warning, that a
significant proportion of people having an
acute MI will have a normal ECG, so do
not rely on any of these features to
exclude MI.
Posterior MI

The trick in diagnosing this is to realise that posterior wall

changes will be mirrored in the leads opposite to the lesion

--- V1 and V2. S we'll see a tall R (corresponding to a Q), ST

depression, and upright arrowhead T waves:
Right ventricular infarction

This occurs in about 1/3 of patients with inferior MI, but is

often missed. It would be distinctly unusual in the absence
of inferior MI. Sensitivity can be improved by looking
atV4R --- V4, but put the lead on the right side of the chest!
Look for ST elevation which is higher than that in V1 -- V3.
Another suggestive feature is lack of ST depression in V1
with evidence of MI in the inferior leads (look for ST
depression in V2 under 50% of the ST elevation in AVF).
Non-ST elevation MI

There are no reliable correlates of "subendocardial" or nonST elevation MI, and the diagnosis is based on the
combination of clinical and laboratory criteria (troponin
elevation being important). There may be no ECG changes,
or even ST segment depression and/or T wave
abnormalities.
Angina and stress testing

The most important component of an effort ECG that

indicates the presence of coronary artery disease is where
exercise reproduces the patient's chest discomfort or pain.
Other findings may be:
ST segment depression (It is customary to apply
the Sheffield criteria, that is, 1mm (0.1mV) ST depression
0.08s after the J point;
failure of suppression of ventricular ectopy, or (especially)
development of ectopy in the recovery period;
Failure of the blood pressure to rise with exercise (an
ominous finding);
ST segment elevation
T-wave changes (which may be rather nonspecific)

 Development of inverted U waves, which, although subtle,

is said to be specific for the presence of ischaemia!
Did you notice the ST segment depression in our section on
voltage and timing, above?

Prinzmetal's angina

The simple (and possibly even correct) explanation of why

you see ST segment elevation with this variant form of
angina is that the predominant area of ischaemia is
epicardial. This disorder is thought to be related to vascular
spasm, and angiography shows coronaries without a
significant burden of atheroma. Many other morphological
abnormalities have been described with this disorder.
Other morphological abnormalities
'Early repolarisation'

This is common --- ST segment elevation is conspicuous,

often with a prominent J wave. It has been remarked upon
in athletes, particularly. It's important to relate the ECG to
the clinical context, as always, as otherwise one might
inappropriately suspect serious underlying heart disease.

T waves
T wave abnormalities are common and often rather
nonspecific. T-wave changes that suggest ischaemia are a
very sudden junction between the ST segment and the T
wave, and very symmetrical T waves. A variety of changes
may
be
seen
with
cardiomyopathies,
intracranial
haemorrhage and so on. Symmetrical deep T-wave changes

most prominent in V3 and V4 suggest ischaemia in the

territory of the left anterior descending artery (LAD T0waves). We should all know the features of hypo- and hyperkalaemia.
Hyperkalaemia

Initial features are tall "tented" T waves. Later, despite the

continuation of sinus rhythm, the P waves disappear, and
finally, the QRS complexes broaden and become bizarre, the
ST segment almost vanishes, and the patient dies from
ventricular arrhythmia or cardiac standstill.
For features of hypokalaemia, see below .
Measures - QT

This is the time from onset of QRS to end of T wave.

Because QT varies with rate, it is common to apply a
correction, usually using Bazett's formula:
QTc =

QTmeasured
--------------------SQRT (RR interval)

SQRT refers to the square root. A normal value is about

0.39s 0.04s (slightly larger values are acceptable in
women). Be particularly concerned if the value is over 0.5,
as may be seen in poisoning with tricyclic antidepressants,
congenital QT syndromes, hypocalcaemia, and toxicity from
a variety of other drugs (quinidine, procainamide,
amiodarone, sotalol, erythromycin, etc). Other cause have
been reported, including hypothermia, head injury, acute
myocardial infarction (!), and hypertrophic cardiomyopathy.

U waves
Hypokalaemia

The T waves flatten, U waves become prominent (this may

be falsely interpreted as QT prolongation), and there may
even be first or second degree AV block.

Several syndromes
Myocarditis

Common findings are tachycardia, heart blocks (first

degree, LAHB), and increased VAT . A variety of ST changes
may be seen, including those of myopericarditis. Atrial and
ventricular extrasystoles are common.
Myopericarditis

Pericarditis is usually associated with a degree

contiguous myocarditis. The major manifestation
widespread ST segment elevation.

of
is

There is also usually sinus tachycardia, and T wave

abnormalities are common.
Pericardial effusion

The most common finding here is simply diminished

amplitude of the ECG deflections. There may also be T wave
inversion, and sometimes one sees electrical alternans .
Pulmonary thromboembolism

Apart from sinus tachycardia, ECG abnormalities are not

common. The `classical' S1Q3T3 syndrome occurs in under
10%. Other features may be those of right atrial
enlargement, RV hypertrophy or ischaemia, RBBB and atrial
tachyarrhythmias.
Digoxin effect

ST segment changes are pretty characteristic, with their

"reverse tick" conformation. These changes are not
indicative of toxicity, but merely the presence of digitalis.
With toxicity, practically any arrhythmia can be seen,
although certain arrhythmias are highly suggestive, for
example, the presence of both increased irritability and AV
nodal block (such as paroxysmal atrial tachycardia with a
2:1 AV nodal block).
Electrical alternans

Here, there is no rhythm disturbance, but the QRS

amplitude alternates --- tall one beat, shorter the next (and
so on...). At fast rates, this is said to be of little significance,
but at slower rates usually signifies severe heart disease, or
pericardial effusion.