What the ECG is about

What to expect from the ECG 1

The electricity of the heart 2
The shape of the ECG 3
Recording an ECG 7
The shape of the QRS complex 12
How to report an ECG 22
ECG interpretation 23
Things to remember 28

ECG stands for electrocardiogram, or electrocardiograph. In

some countries, the abbreviation used is 'EKG'. Remember:
By the time you have finished this book, you should be
able to say 'The ECG is easy to understand'.
Most abnormalities of the ECG are amenable to reason.

WHAT TO EXPECT FROM THE ECG

Clinical diagnosis depends mainly on a patient's history,

and to a lesser extent on the physical examination. The ECG
can provide evidence to support a diagnosis, and in some
cases it is crucial for patient management. It is, however,
important to see the ECG as a tool, and not as an end in
itself.
The ECG is essential for the diagnosis, and therefore
management, of abnormal cardiac rhythms. It helps with
the diagnosis of the cause of chest pain, and the proper use
of thrombolysis in treating myocardial infarction depends
upon it. It can help with the diagnosis of the cause of
breathlessness.
With practice, interpreting the ECG is a matter of pattern
recognition. However, the ECG can be analysed from
first principles if a few simple rules and basic facts are
remembered. This chapter is about these rules and facts.
nc ~LECTRICITY
OF In c HEAR
The contraction of any muscle is associated with electrical
changes called 'depolarization', and these changes can be
detected by electrodes attached to the surface of the body.
Since all muscular contraction will be detected, the electrical
changes associated with contraction of the heart muscle will
only be clear if the patient is fully relaxed and no skeletal
muscles are contracting.
Although the heart has four chambers, from the electrical
point of view it can be thought of as having only two,
because the two atria contract together and then the two
ventricles contract together.
The wiring diagram of the heart (Fig. 1.1 )
The electrical discharge for each cardiac cycle normally
starts in a special area of the right atrium called the
'sinoatrial (SA) node'. Depolarization then spreads
through the atrial muscle fibres. There is a delay while
the depolarization spreads through another special area in
the atrium, the 'atrioventricular node' (also called the 'AV
Right bundle branch
/
Fig. 1 . I The wiring diagram of the heart
node', or sometimes just 'the node'). Thereafter, the
electrical discharge travels very rapidly, down specialized
conduction tissue: first a single pathway, the 'bundle of
His', which then divides in the septum between the
ventricles into right and left bundle branches. The left
bundle branch itself divides into two. Within the mass of
ventricular muscle, conduction spreads somewhat more
slowly, through specialized tissue called 'Purkinje fibres'.
The rhythm of the heart
As we shall see later, electrical activation of the heart can
sometimes begin in places other than the SA node. The
word 'rhythm' is used to refer to the part of the heart which
is controlling the activation sequence. The normal heart
rhythm, with electrical activation beginning in the SA node,
is called 'sinus rhythm'.
THE SHAPE OF THE ECG
The muscle mass of the atria is small compared with that of
the ventricles, and the electrical change accompanying the
contraction of the atria is therefore small. Contraction of
the atria is associated with the ECG wave called 'P'. The
ventricular mass is large, and so there is a large deflection of
the ECG when the ventricles are depolarized. This is called
the 'QRS' complex. The 'T' wave of the ECG is associated
with the return of the ventricular mass to its resting
electrical state ('repolarization').
The basic shape of the normal ECG is shown in Figure 1.2.
The letters P, Q, R, S and T were selected in the early days
of ECG history, and were chosen arbitrarily. The P, Q, R, S
and T deflections are all called waves; the Q, R and S waves
together make up a complex; and the interval between the
S wave and the T wave is called the ST 'segment'.
Fig. 1.2 Basic shape of the normal ECG
Fig. 1.3 Parts of the QRS complex. (a) Q wave. (b, c) R waves.
(d, e) S waves
The different parts of the QRS complex are labelled as
shown in Figure 1.3. If the first deflection is downward,
it is called a Q wave (Fig. 1.3a).An upward deflection is
called an R wave (Fig. 1.3b)- whether it is preceded by
a Q wave or not (Fig. 1.3~). Any deflection below the
baseline following an R wave is called an S wave (Fig. 1.3d)-
whether there has been a preceding Q wave or not (Fig. 1.3e).
Times and speeds
ECG machines record changes in electrical activity by
drawing a trace on a moving paper strip. All ECG machines
run at a standard rate and use paper with standard-sized
squares. Each large square (5 mm) represents 0.2 seconds
(s), or 200 milliseconds (ms), so there are five large squares
per second, and 300 per minute (min). So an ECG event,
such as a QRS complex, occurring once per large square
is occurring at a rate of 300lmin (Fig. 1.4). The heart rate
1 small square represents 1 large square represents
0.04 s (40 ms) 0.2 s (200 ms)
-
R-R interval:
5 large squares represent 1 s
Fig. 1.4 Relationship between the squares on ECG paper and time.
Here, there is one QRS complex per second, so the heart rate is 60
beatslmin
Table 1 .I Relationship between the number of large squares covered
by the R-R interval and the heart rate
R-R interval (large squares) Heart rate (beatslmin)
can be calculated rapidly by remembering the sequence in
Table 1.1.
Just as the length of paper between R waves gives the
heart rate, so the distance between the different parts of the
P-QRS-T complex shows the time taken for conduction of
the electrical discharge to spread through the different parts
of the heart.
The PR interval is measured from the beginning of the P
wave to the beginning of the QRS complex, and is the time
taken for excitation to spread from the SA node, through
the atrial muscle and the AV node, down the bundle of His
and into ventricular muscle.
PR QRS
0.16s (160 ms) 0.10 s (100 ms)
Fig. 1.5 Duration of the PR interval
PR QRS
0.16s (160 ms) 0.20 s (200 ms)
Fig. 1.6 Duration of the QRS complex
The normal PR interval is 0.12-0.2 s (120-200 ms),
represented by three to five small squares. Most of the
time is taken u p by delay in the AV node (Fig. 1.5). If the PR
interval is very short, either the atria have been depolarized
from close to the AV node, or there is abnormally fast
conduction from the atria to the ventricles.
The duration of the QRS complex shows how long
excitation takes to spread through the ventricles. The QRS
duration is normally 0.12 s (120 ms) (represented by three
small squares) or less, but any abnormality of conduction
takes longer, and causes widened QRS complexes (Fig. 1.6).
RECORDING A N ECG I
The word 'lead' sometimes causes confusion. Sometimes it
is used to mean the pieces of wire that connect the patient
to the ECG recorder. Properly, a lead is an electrical picture
of the heart.
The electrical signal from the heart is detected at the
surface of the body through five electrodes, which are
joined to the ECG recorder by wires. One electrode is
attached to each limb, and one is held by suction to the
front of the chest and moved to different positions. Good
electrical contact between the electrodes and skin is
essential. It may be necessary to shave the chest.
The ECG recorder compares the electrical activity
detected in the different electrodes, and the electrical
picture so obtained is called a 'lead'. The different
comparisons 'look at' the heart from different directions.
For example, when the recorder is set to 'lead I' it is
comparing the electrical events detected by the electrodes
attached to the right and left arms. Each lead gives a
different view of the electrical activity of the heart, and so
a different ECG pattern. Strictly, each ECG pattern should
be called 'lead ...', but often the word 'lead' is omitted.
It is not necessary to remember which electrodes
are involved in which leads, but it is essential that the
electrodes are properly attached, with the wires labelled
'LA' and 'RA' connected to the left and right arms,
respectively, and those labelled 'LL' and 'RL' to the left
and right legs, respectively. As we shall see, the ECG is
made up of characteristic pictures, and the record as a VF
whole is almost uninterpretable if the electrodes are
Fig. 1.7 The ECG patterns recorded by the six 'standard' leads
wrongly attached.

The 12-lead ECG

ECG interpretation is easy if you remember the directions
from which the various leads look at the heart. The six
'standard' leads, which are recorded from the electrodes
attached to the limbs, can be thought of as looking at the
heart in a vertical plane (i.e. from the sides or the feet)
(Fig. 1.7).
Leads I, I1 and VL look at the left lateral surface of the
heart, leads I11 and VF at the inferior surface, and lead VR
looks at the right atrium.
The V leads are attached to the chest wall by means of a
suction electrode, and recordings are made from six
positions, overlying the fourth and fifth rib spaces as shown
in Figure 1.8.
The six numbered V leads look at the heart in a
horizontal plane, from the front and the left side (Fig. 1.9).
Thus, leads V1 and V, look at the right ventricle, V, and V,
look at the septum between the ventricles and the anterior
wall of the left ventricle, and V, and V, look at the anterior
and lateral walls of the left ventricle. As with the limb leads,
the chest leads each show a different ECG pattern (Fig. 1.10).
In each lead the pattern is characteristic, being similar in
different individuals who have normal hearts.
Fig. 1.8 Positioning of the chest V leads. Note that the rib spaces are
numbered

Fig. 1 . I 0 The ECG patterns recorded by the V leads

Calibration
A limited amount of information is provided by the height
of the P waves, QRS complexes and T waves, provided
the machine is properly calibrated. For example, small
complexes may indicate a pericardial effusion, and tall R
Fig. 1.9 The relationship between the six V leads and the heart
waves may indicate left ventricular hypertrophy (see Ch. 4).
A standard signal of 1 millivolt (mV) should move the stylus
Fig. 1 . I 1 Calibration of the ECG recording
vertically 1 cm (two large squares) (Fig. 1.11),and this
'calibration' signal should be included with every record.
Making a recording
When making a recording:
1. The patient must lie down and relax (to prevent muscle
tremor)
2. Connect u p the limb electrodes, making certain that they
are applied to the correct limb
3. Calibrate the record with the 1 mV signal
4. Record the six standard leads - three or four complexes
are sufficient for each
5. Record the six V leads.
THE SHAPE OF THE QRS COMPLEX
We now need to consider why the ECG has a characteristic
appearance in each lead.
The QRS complex in the limb leads
The ECG machine is arranged so that when a
depolarization wave spreads towards a lead the stylus
moves upwards, and when it spreads away from the lead
the stylus moves downwards.
Fig. 1 .I2 Depolarization and the shape of the QRS complex.
Depolarization moving (a) towards the lead, (b) away from the lead
and (c) at right angles to the lead
Depolarization spreads through the heart in many
directions at once, but the shape of the QRS complex shows
the average direction in which the wave of depolarization is
spreading through the ventricles (Fig. 1.12).
If the QRS complex is predominantly upward, or
positive (i.e. the R wave is greater than the S wave), the
depolarization is moving towards that lead (Fig. 1.12a).
If predominantly downward, or negative (S wave greater
than R wave), the depolarization is moving away from that
lead (Fig. 1.12b).
When the depolarization wave is moving at right angles
to the lead, the R and S waves are of equal size (Fig. 1.12~).
I Q waves have a special significance, which we shall
discuss later.
The cardiac axis
Leads VR and I1 look at the heart from opposite directions.
Seen from the front, the depolarization wave normally
spreads through the ventricles from 11 o'clock to 5 o'clock,
so the deflections in lead VR are normally mainly
downward (negative) and in lead I1 mainly upward
(positive) (Fig. 1.13).
 I11

Fig. 1 . I 4 The normal axis

Fig. 1 . I 3 The cardiac axis

The average direction of spread of the depolarization wave

through the ventricles as seen from the front is called the
'cardiac axis'. It is useful to decide whether tlus axis is in a
normal direction or not. The direction of the axis can be
derived most easily from the QRS complex in leads I, I1 and 111.
A normal 11 o'clock-5 o'clock axis means that the
depolarizing wave is spreading towards leads I, I1 and I11
and is therefore associated with a predominantly upward
deflection in all these leads; the deflection will be greater in
lead I1 than in I or I11 (Fig. 1.14).
If the right ventricle becomes hypertrophied, the axis will
swing towards the right: the deflection in lead I becomes
negative (predominantly downward) and the deflection in
lead I11 will become more positive (predominantly upward)
(Fig. 1.15). This is called 'right axis deviation'. It is associated I11
mainly with pulmonary conditions that put a strain on the Fig. 1 .I5 Right axis deviation
right side of the heart, and with congenital heart disorders.
 Fig. 1 .I7 The cardiac axis is at right angles to this lead since the R
and S waves are of equal size

Fig. 1 . I 6 Left axis deviation

When the left ventricle becomes hypertrophied, the axis

may swing to the left, so that the QRS complex becomes
predominantly negative in lead I11 (Fig. 1.16). 'Left axis
deviation' is not significant until the QRS deflection is
also predominantly negative in lead 11, and the problem is
usually due to a conduction defect rather than to increased
bulk of the left ventricular muscle (see Ch. 2).
An alternative explanation of the cardiac axis
Some people find the cardiac axis a difficult concept, and
an alternative approach to working it out may be helpful.
The cardiac axis is at right angles (90") to the lead in
which the R and S waves are of equal size (Fig. 1.17).
It is, of course, likely that the axis will not be precisely
at right angles to any of the leads, but will be somewhere
between two of them. The axis points towards any lead 1 Limit of the normal
where the R wave is larger than the S wave. It points away cardiac axis
from any lead where the S wave is larger than the R wave. Fig. 1 . I 8 The cardiac axis and lead angle
The cardiac axis is sometimes measured in degrees (Fig. 1.18),
though this is not clinically particularly useful. Lead I is
taken as looking at the heart from 0"; lead I1 from +60; lead
VF from +90; and lead I11 from +120. Leads VL and VR
are said to look from -30" and -150, respectively.
The normal cardiac axis is in the range -30" to +90". For
example, if in lead I1 the size of the R wave equals that of the
S wave, the axis is at right angles to lead 11. In theory, the axis
could be at either -30" or +150". If lead I shows an R wave
greater than the S wave, the axis must point towards lead I
rather than lead 111. Therefore the true axis is at -30" - this is
the limit of normality towards what is called the 'left'.
If in lead I1 the S wave is greater than the R wave, the
axis is at an angle of greater than -30, and left axis
deviation is present. Similarly, if the size of the R wave
equals that of the S wave in lead I, the axis is at right angles
to lead I or at +90. This is the limit of normality towards
the 'right'. If the S wave is greater than the R wave in lead I,
the axis is at an angle of greater than +90, and right axis
deviation is present.
In the normal heart there is more muscle in the wall of
the left ventricle than in that of the right ventricle, and
so the left ventricle exerts more influence on the ECG
pattern than does the right ventricle.
Leads V, and V2 look at the right ventricle; leads V,
and V, look at the septum; and leads V, and V, at the left
ventricle (see Fig. 1.9).
In a right ventricular lead the deflection is first upwards
(R wave) as the septum is depolarized (Fig. 1.19). In a left
ventricular lead the opposite pattern is seen: there is a small
downward deflection ('septal' Q wave) (Fig. 1.19).
In a right ventricular lead (V, and V2) there is then a
downward deflection (S wave) as the main muscle mass is
depolarized (Fig. 1.20) - the electrical effects in the bigger
left ventricle (in which depolarization is spreading away
from a right ventricular lead) outweighing those in the
smaller right ventricle (in which depolarization is moving

Why worry about the cardiac axis?

Right and left axis deviation in themselves are seldom
significant - minor degrees occur in long, thin individuals and
in short, fat individuals, respectively. However, the presence of
axis deviation should alert you to look for other signs of right
and left ventricular hypertrophy (see Ch. 4). A change in axis
to the right may suggest a pulmonary embolus, and a change
to the left indicates a conduction defect.

The QRS complex in the V leads

The shape of the QRS complex in the chest (V) leads is
determined by two things:
The septum between the ventricles is depolarized before v,
the walls of the ventricles, and the depolarization wave Fig. 1 .I9 Shape of the QRS complex: first stage
spreads across the septum from left to right.
 towards a right ventricular lead). In a left ventricular lead
there is an upward deflection (R wave) as the ventricular
muscle is depolarized (Fig. 1.20).
When the whole of the myocardium is depolarized the
ECG returns to baseline (Fig. 1.21).
The QRS complex in the chest leads shows a progression
from lead V,, where it is predominantly downward, to lead
V,, where it is predominantly upward (Fig. 1.22). The

v1
Fig. 1.20 Shape of the QRS complex: second stage

v1
Fig. 1.21 Shape of the QRS complex: third stage Fig. 1.22 The ECG patterns recorded by the chest leads
'transition point', where the R and S waves are equal, ECG INTERPRETATION
indicates the position of the interventricular septum.
The interpretation indicates whether the record is normal
Why worry about the transition point? or abnormal: if abnormal, the underlying pathology needs
If the right ventricle is enlarged, and occupies more of the to be identified. Examples of 12-lead ECGs are shown in
precordium than is normal, the transition point will move Figures 1.23 and 1.24.
from its normal position of leads V3/V4 to leads V4/V5 or
sometimes leads V5/V6. Seen from below, the heart can be
thought of as having rotated in a clockwise direction.
'Clockwise rotation' in the ECG is characteristic of chronic
lung disease.

You now know enough about the ECG to understand the

basis of a report. This should take the form of a description,
followed by an interpretation.
The description should always be given in the same
sequence:
1. Rhythm
2. Conduction intervals
3. Cardiac axis
4. A description of the QRS complexes
5. A description of the ST segments and T waves.
Reporting a series of totally normal findings is possibly
pedantic, and in real life is frequently not done. However,
you must think about all the findings every time you
interpret an ECG.
Fig. 1.23 12-lead ECG: example 1
Description
Sinus rhythm, rate 11Olmin
Normal PR interval (140 ms)
Normal QRS duration (120 ms)
Normal cardiac axis
Normal QRS complexes
Normal T waves (an inverted T wave in lead
VR is normal)
Interpretation
Normal EGG
Fig. 1.24 12-lead ECG: example 2
Description
Sinus rhythm, rate 75lmin
PR interval 200 ms
QRS duration 120 ms
Right axis deviation (prominent S wave in
lead I)
Normal QRS complexes
Normal ST segments and T waves
Interpretation
Normal ECG - apart from right axis
deviation, which could be normal in a tall
thin person.
Unfortunately, there are a lot of minor
variations in ECGs which are consistent
with perfectly normal hearts. Recognizing
the limits of normality is one of the main
difficulties of ECG interpretation
 THINGS T O REMEMBER 1
1. The ECG results from electrical changes associated with
activation first of the atria and then of the ventricles.
2. Atrial activation causes the P wave.
3. Ventricular activation causes the QRS complex. If the first
deflection is downward it is a Q wave. Any upward
deflection is an R wave. A downward deflection after an
R wave is an S wave.

4. When the depolarization wave spreads towards a lead,

the deflection is predominantly upward. When the wave
spreads away from a lead, the deflection is
predominantly downward.
5. The six limb leads (I, 11,111, VR, VL and VF) look at the
heart from the sides and the feet in a vertical plane.
6. The cardiac axis is the average direction of spread of
depolarization as seen from the front, and is estimated
from leads I, I1 and 111.
7. The chest or V leads look at the heart from the front and
the left side in a horizontal plane. Lead V1 is positioned
over the right ventricle, and lead V6 over the left
ventricle.
8. The septum is depolarized from the left side to the right.
9. In a normal heart the left ventricle exerts more influence
on the ECG than the right ventricle.
 ..
REglW bundle m h
Remember in all that foUuws that we are assuming
depvlarizatinn begins in the normal way in the SA ntde.
The rhythm of the heart is best interprated from
wtich~verECG l a d .shows the P wave mmt clearly,
This is usually, but not always, lead lead V,. You can
awumr tbat aU t4e 'rhythm stti-' in this h n ~ k T e r e
remrded hem one I I ~these leads
CONUUCTION PROBLEMS IN THE AV NODE AND
HIS BUNDLE
I
The rime taken ~ G Fthe spread of depolarizatinn fr<+rnthe
SA node to the venwkulat husde $Ss b t ~ by ~ qthe PR
intervntl {setrCh. fj, and is not normally greater than 0.2 \
(vqe largr square). ECG rvlVnfsare usually timed in
milliseconds rather than s e m d s , m the limit of the Pft
inftmal is 200 ms. Inlerferenm with the ccmducti<lap r f a s s
causes the ECCl phenomenon called 'heart block'. ,
First h r e e b e d block
If each wave af depolarizaticm that tsri@natesin the SA ncldc
iscc1nducted to the ventricles, but there is delay wmewherr
along the mnduCtion pathway, then the PRintewal is
prolong=i. This is called ' k t degree heart b l ~ &(Fig. 2.2).
Firstdegrm heart Wock k mt in itself implwtant, but it
may be a sign of comnary artery diwaw,srcutr vlwwmatit
carditis, digmin tmicity or ekgFnlyte bistu-bances.
5ec6nd hwrt blork
s exdtaiioncnmp&&ly fails tc>panu throu$h the
s"mr5!r
AV e or the bundle uf His. When thb ocmw
'wcond d q k s heart block' ISmid to cxibt.
irrlr*rr~litfc~#illp,
There are tllree variations of thia:
I. Mtst beats are conducted with a chiwant PR
but vccasicmally the^ is an atrial acontractib~lwitlu
wbsequent ventricular ctmhsrctinn. ThFhis is cal
'Mubitz typ 2 p h n x r r w n
2 There may be progtpive lenkthming of the h w o l
n failure of conduction of an a t r g bmt, fcdlowrd
ndu* beat with a 5rhorker PR tntert'nl a@ thcn
a repetition of khii cycle. This is the 'WcnckcbacR'
phmnmenon (ti%. 2.4).
1.There m y be atternate ccmducted nnd ixm-cttnducte~i
.itrial bcak (tcor t~noconductedatrial be,\t and tlwi two
 ~~~
~ - . ~ -~ ~

me
Twi, P waves per OR6 wmplex ,.,.
r ~ r wand. anwan PFT intew~tin mo mduclael m., . ,,

.
NO@
Progressive IengfiBnQ of PR mnral
Qne riwr-eandw&d beat
a.- '.
.<.., . , . ,
.. .

The underlying mubus of s~vYrnd&+tee hmrt blcrkarc

thc sa* as those offirst degree blnck. The Wenckbacrh
, 8 . ' . . ,. - , ,,,: phenummonis usually lxni~n, but Wt~bitztype2 blcrck
and 2:1 b44d itwy h m l d 'cnm~lrfe.'or 'third drgwc', h e a l
blwk.

T h j r d ~ r o e ~ b b d r
Cnniplcir. Izeirrt bfwk (!ihi.rd delfrer.hkn-k) is %>idto
ottw when jh*l c~rntractb%n but no beat* arc
is m~~rn~al
c o y ~ y $ $ $ ~ . .yg*tric1qr
. k ~ , , ~ ~(Fig. P,7).Whrri thi3 ~>ccvrs
thv
venZaIes a n b e d by a aalow k e s ~ a Wchanism'
~ e (see
Ch. 3), hum a depotatikng focus w*ghim the ventricular
mu&.
Cuinplete blwk is nlat always imniedi&telyobvrous in
a 12-lead ECG, w%erethere may be only a few QRS
complexes per lead (e.g.see Fig. 2.8). You have to ltrok at
the PR interval in all the leads.
Compkte heart b l s k m v mar a5 an acute
phenomenon in patients wiih mymardial infarcti(>n(when
I it is usuaMy transient) ar st may be a chronic state, usually
due to fibroGs around the brYhdle of His. It may elrir be
! caused by the block 30th bundle btdnche*.
 LBBR p m n t s any further interprt'tation of the
~rdi~pmm and, RBBB aul make inte~pwtaric>n difficult
If the drpolanizstiw waue ~et?arhes the interventricular The mechanism underlyiag the ECG patterns of RBBR
septum notmirUy, the interval hetween the of and LBBB can be worked put h m first principle.
the P wave and the fiwt deflection in rhe QRS coqlplex (4he
PR intend) witl bp normal. H w e r e q if there is abnormal
conduction through &her the right or left bundle
.
Remember [weCh.1):

r
The septum is normaEy tydrVrokrrircu-l from left ti) rialit
The left ventricle, llavin the patrrr mu*& nlass M r t s
branches rbundle branch black') there will a delay in
hedepoiarizakn af part of the ventricular muscle. Tht, . more influence on the & &an d m the dght vcntricrirlr.
Excitation spreading @wardsa lead causrs an upward
extra linae taken for depalarization of the whots of the deflection withm the ECG-
v e n t i m k musck causes widenlhg of the QRS romple7c.
In the normal heart. the timFk!n t'nr the depalarizalion Right bundle branch b W
wave to spread fmm the inkrvmtricular srptunl to klir No c<~nduaion~ w r down 5 the right bundle b~anch,
furthest paat of the ventricles is less than 120 m?;, m 16 depoLarized from the left side ar u w l ,
represented b_ythree small squarcs of ECG paper. If the
QRS duration is greater than 121 ms, then condudion
obwt
w ithe =&
n g a R ve in a right ventricular lead (V,)an4 a
s m a i Q wave in a Icfkventticu~lead (Vd (Fig,. 29).
Within the ventricles must have uc~wrredby an abnornlal
and themfore slow pathway.
Although a wide QRS complex can indicate bundle branch
b k ~ kwidening
, also ncolm if depolaoiz.atinn begins within
the vmWkutar muscle itsrlf (stvCh. 3). Rrtnrmbc3r that in
sinus rhythm with bundle branch block, rrormal P wave?:
dnu piesent with a constqnt PB irrtrrval. We shall we that
this 1s not the ease with rhythms beginning in the vnitriclrz.
Block of ktiti bundle branaht.4, has the same effea as
block t)f tthr Hi bundl6, and c a u m complete (third d q t e e )
heart block.
Right bundle branch block (RRBB) often indicates
priblt'nia in the right side of thr heart, bur RRBB patterns
with a QRS cnmplex of normal durdticm an. quite c?>nrrtu*n
in healthy petrple.
Lrft bu~idlebranch block (LBBB) 15always an indication
of heart diseaw, usudlly of the left ride I t is inxpwtant t ~ ,
recngnite that bundle b~anchblock is pprrwnt, b t ~ a ~ l s r

II
 Edtert&Bh@~*hp*ds tothe kft vmhicle, ctlunin,gan
and an R wave In lcad V, (Rig 2.1tO;
heart firr-tion tt~
thq faIIure d H ~ F
r@t ventriefethrr&w
~wo&~@S 8hfl *tho id. a 7wcondR ware (R')in
l a d vg;0ga9 w ~ + ' B M ~ ' & ~ $ u T ~inv ~kKt Vb,(&gi2:11).
An 'RS "'ptteffi,bufw@@q Qpcnmpfex of nt*ml
width (I- than IDrn&: &ern+ c a ~ ~ a' p d g r ~ %~%t
~l
bundie Zlra&Moctc'. 1t &ldrrm of afgqVia~et~,,snd con
be mdderc?dto b~ normal mf. .
, . -
.~.. .,1,
~

b1 9 bundh brand G k ' ,I

If con$uaic.)n.dn(he te$ tqurdlc?.@@bfait&:+&&kptum
becmea deplrladwd h q ribkt to I& caudng:a Q
Lin tqd
: I V*,pi&.
wave in lead V,! . , I R .yaw
, ~ .: , 1..X,?. " 8 .., ,. $,%
. - . ...
~
 3UNDLE BFIANCH BLOCK

The hght ventricle is d~polariwdWfnre the k'ft,so

despite the snaller muscle inas tirere is an R wave in hid
V, and an S wave (,&fenappedng ant?.as a m c h ) in
lead V++(Fig.213). --c
Subsequent depaladzation d #hehe leftwentrick cwses an
S wave in lead V , and anothe~R w ~ w e

A
. . I.
. '
~
-
m Sead V, (Fig. 2.14).
W3B k ass~eistedwi% T ware inv&b h the lateral
, .

, ,
Fig,.2.fi
 , I
' . - G$f i . 7 , , .;
. ,
;+l.~~~,:::! ';J,~;~ ..
,...$r?$dk,
'. >*;,<&:%r
P . .
.<, .,
..#~.;:$;.,',~::(i
8

.'
:;~,;t;*'~
:-
.~..
$1 , ; ,, , &;

Wcae
. S W S , ~ &, ' $ ~ n
wm?lpRk,@~
&WarrrrkDc*
* w w m&.conIpleue(IBOg M)
Paasm i n h d V, and w,wide

- a kr,18gc1
6
Nomurl ST segments and T waves
CONWCllON AND ll!3 PROMEMS PROBLEMS IN ME DISTAL PARTS OF M E LEFT BUNDLE B W H .
-
2
.,
If the anterior fascirte of the left bundle branch fails hr !eftbundk: ili;w)t crfit.n. ;
I!,* pos~~ri$?k,{aJxia!q.yf~pq
~ n & f &the left ventride has to be deplerized thrnu& sek$i$ety.b\~g&4,~~ if ihiq dpp.mw.rtb >FCCs h w q ,
the posterior Fascicle and w the a r d ' i axis mhks ri&t .wir;d+$@k)&
,. . ,. . * ,.;,.
upwards (Fig. 2,19). bpe<jb.rt@t.~k
w&+4;thr:.cprdit?c~xh
Left *Xis doriation is thrrebre due to left anterior usually noml, b , tk?~ iti nurni%ldap~1ariL;lWbi
fascicular b1ack, or 'left anterior hemiblack' (Fig. U 3 f . of the I& venbiclr. *th itS ls%ernuwIt+q i s s (Fig.2.21).

Fig,2.19 Etfeot at ldt an.nterior fsssiouhr black ou the eardisc axla

-
[ION AND ITS PROBLEI

Lefl axis deviation

, .

(RSR pa~tefn
in MV,. BM deep

Jm8
 -
>NDUCTiONAND ITS PROBLEMS

h.lk%i@;hr+niw.rthaf.k iu thS+k.&f:ivhc, khluuiL+& ~ ,

tt&t@; hiit Em. ReriU,~i p p ~ i i na t~h i p &&-''

first ~owrve;sntn~ge~riaipoi~&s $mihi! fit*
aitioq that nii&ht be taken if the ECG sherwx ctrnductitm
abnornmlitie%:
., '7 i
LeHorois~d*h.dseaekbbh
Fist d . e g e Mork %. , ...

Often wm in n n r r n a b ~ i .l
Think ahlut amtc* t n y c ~ n rnfarc-h~m
t
, ,
md acutr
,: '

.
IndEcs~stl~~maludbylissae~
No specific h h n m t Dseded
~lcerrequ~Sthepmtifntb5TepPIE
rhrunlatic A w as P~sdM%&us+. ...,,, '.. -dimem%kMaarplfdckprtbbdf
No s,gwifis nreded.
., -,.%,
'..
Second degree block ,: :
U.%uaUyindicirtr- he&? di'why;1rftc17-vmin acutt-
-.
tny c~.iudialinf'~rc~<.in?'--~
r M!?t?i@ &W.,:.2 md ,Vdgrt.lp+kach Irl<*Jl&*,~ua\,~i spcctfic
trciltnirnt.
3: 1 block may i!vikitl+tc
a need for temprrary t)r pernl.$nc*nt
plcin# +?+pqci.?lly ifthe vcnhicwler rat^ is dew.

Thinj &$tee
Alwoyr indicates rrrnductin~tissue disrp~@ eften
fib& thah i@%&emic.
Cm- . ,. ps .pwn?amiu p;letinokr.
f,ky3e*r+!ry
.

Right hebrancfi bf& , :,

* Tbipnkhtrt an et&l *@I &f&.
No specific treacmml.
..
--
Leftbxlmilebrpnchbloct
Think ~hrulmr%icictentxis anti i h ~ h . w ~ k $ i & q w .
. -.
If the patient i s ahymptuillatic no acticm is 11nrk.d.
stylus moyps npwaNk
 ,
M...,xw
THE RHYTHM OF THE hEART lNTRlNSlC RHMHMlClTY OF THE HEAR
. ~~~ --

Atrial cuntrarti~ini i .is~cxhtrdwith tl>i3P wiivr- uf thr. ECG.

M.nlricular contr~ztiunis a*st>ciatc~l with the QRS
wmpkrx.
.%&I eb%ntraai*m 1-rBrmeUpp f e ~ g @venk@whr
~(3cthk'Fiic*l, aod th@ie,4srie1n.ormily@$ p t r i f i l ~ , p ~ a t ~ ~ ~ t i t m
~rvewbrieadareonti&~tti frs.tlrere gbcuI,db.g *as,bwvy
'P'wa\n* as th,r?e a:ce Q,Eu ~ n l p i @ ~ ~ , ~

I
Mnat parts of thv heart can depnlarite .ipc~ntati@ously .ind
rhythmically, dnd thc rate ot contrwticln of Lhe venhic1.w
will be controlled by the part of the herir't thal is R5 3.1 Sinus m $ m m i s
drpolaricing nimt frequently.'Thc SA n n f e nc>miallyhas
the hi#hrsl fr.equt.n~cyof discharge. Thi.ref<>rv the rate of
mntracfion of tht vrritrirlrs ww equal Ehr rzl,tr rlf 8 i s l i i i r p
..w
ewr *.get @g'fom*
copt*ld Fa:-1
ttf khe S.A no~tc. * ~ b m m -rn R-R b t w ~
'l'hr rate cif clischai~e(if ihr 5 A nodc it. intlucnced by thr The star in this ard WIer flguns in thls chepfer indicpcas tm part of the
vagus nrrvcx, and reflexes i,riginaFing in t hc. lung sl?;~ hlwt wnem ihB actmation soqrance began
affect thc heart ratc. Chenges in l m r t ratras%ida'ted with
rcspiratiun are normally see11in younR people, and this is
called 'sitius nrrhytkmia' (Fig. 3.1).
A slow s i t i ~ rhytlim
~s CsinuJ bradycardia') is aa7inciatect
with athletic traimns, kinring atkircks,hypothrrmia and
myxoedema, ~ n itd is oAen seen immediately sflrr a ]wart
attack. A &?,st sinus rhythm ('sinus tnih~m~rdia') is assrxirltld
with exercise, fea.r, pain, knemorrhigr o ~ i dthyr~b~xicr,sis.
l'hrrr is nu particular rate thal is edlkfd 'bradycardia' or
'tachycardia'- Ihwe are merely descriptive terms.
Abnormal cardiac rhythms can bel;jn in threk p1aci.s -
the atrial muscle; the rigign around the AV nilde (this
rhythtii is called 'nodal' 06 more properly, 'junctional');
or the ventricular muscle. In F i ~ u r 3.2
e the ,stars s u g ~ c ~ k
I within the ahiat and ventnmlar mu&
rrcfivatios might W n , M & o m t

w a initiated by the SA nude. the atrial ahid.a lhe

juncticmal region.
In ventricular rhythm. an the other hand, tba
dup~larizakiottwave +s ahwcgh the b n k d d e s b y
abnormal,and thedune &we& pathway tbm@ ttm
Purkinje tibrPs(Rpc 35). The QRS is Wmfuw
wide and ~~~. Rcpdarizat&rnis a h dbWmd, 90
the T warn? is of abrulwal shape.
Ranember:
I. Supmventricubr ~hythmsha- aamw QS r e ? %
2. Venhicuhr rhydrms have wide QRS rwnpbrtrs
3. The mly exceptinn to this rule accurr when ba
supmventricuCar rhythm with rigfit wkft bonllrbmrd,
blc~k.

A b w r i d rhythmsaMng in the a t d a h m s k the

~unFtiwal~cinurtk~m~lnusdranbr~rd
sunbined (bradywdii); r they c s o~ w !as aaty

r;
hid- - .-
wlhrca~ed d i t r U ~ ~ d a u a
.ndawb%miua*-ddIbeMaBr
m & i s ~ a i s & ~ ' ~ % - ~
 Vrntrirularescaperhyfhmrrmnrur~~*a
heart tdndc ~ ~ escape brats
b canrk (Fia 3.%
Therhythmoftheheartwn~be~hy
a venhicubrfauswithmiatrillskfreplprryd~~
fasterthaq thatsqxnkmmplekhemtbkdr7hrmhyLhmir
called 'a-krated idiovenbiarhr Aythsi (Fig. 3.111). This h
<&enassciated with r u t e r n y a c d d idawtha.
Although the appearance ofthe K G is similar h~that of
vmhicular tach- ( d ~ ~ LIer),
d d accekabd
idi~wmhknlbrrhythm is benign rd s h m i d tw* br tw*h.rl.
Ventricular tachycardia rhaold nm be diaffmcd u d e s the
hrart raw cxareds 1Wmin.
W
 A ~ Q&t offhe h@crln d@pgl'rul&i! e3JW tt&mit,shdt~ld,
8.2 the & p ~ p n + # g h e a P l b t t$ c8B.d an @?asystr)lt..
The term 'eckppic'h ~ g e H . m & usLid
S to in$i@tr that
11e~Iar'~vion iyiejiriaW ia an abqorn-d3Ib@iti@i, ,&in8
fh*
term 'pm&tut.c.&fiftj%?Wn'@ensfbe W$thitig.
Thp EGG appearance of an o ~ ~ @ i c ~ s i b f n~irhw giti - .
#[rea ~ a mu&;thl.
l fuWondokno;&l re@n,W the
vcntricql&t ~ R S E Iis~the
, s&r a$ that al the c@rrrt.~p.rmdSng
Wt-'th@,diffmn@& @a%an m s y s t o l e comI(S
mrty and an q p e beat cmt& let*.
Atr~nlexhyy&jlus b v u abnamal P w m . ( P k 3.11)'.In
r n ,ir~llC~M @xFFasys9@k
i either there is mi Pwatrc at all, r)r
it appeaw i m M i 6 k l y be&e or ifliin&iaty after the
QRS qomplepl (Pip 3.11). llie Q&,emp!- at athJ aand
junctional ~ t i d $ y ~ &al ~~&
&, ttit.. illmt' ~ ffi k<if ~
sinus rhythm. r ,' "
, . # ', .
 k n t r i n r b r ~ ~ a b m m d QleE
,whkharptypi@i(rridrbutwhafllwat
(Fig. 3.12). V m k i e u l p r ~ a ~ . ~
?nd ate usually ofno .hpbme. H m e w , w h thtyl
cwwt earlyintheTwaw?ofapoxBngberrthe)rran
jnduce ventricular 6brl&tim ( d e w herband am thPI
patentiarty dangerous ,
Itmay, h o w e v e r . A o t k a s e u s y a s U S 8 , ~ i T a
beat of supraventriculsr &gin $ onoduEeedl abnamal(y
kt; the ventrides h w & branth i*rf seeCh Zi It h
advisable to get &to the habit d &hg fivp
~.
- ~

-r]
tinre an ECC is being analysnl:
1, alesan arly QRS cum* ft~llnw an rarEy P -7 ifrra.
it mud be yl atrial exbwptde-
ZCan a P wive teseen anyruhem? A ju-
.. e x t m s y s w b r ~ c a u a e t k ~ p p s e r a n c p d a P w p r r n q
d w hr, and .even aftm f b QRS ~ ~ arnpla bxrRap
encitation is n~nduEtedbnth tcl the at& and lu h
KM*.
3.IstheQ~camp the-shapethmclghouteha
~
the 8am* initial d i h dddkcthn w the b & r
e l
an2 hfrit the same d u e ? -kg
leak thr s m r , ~ ~ beats ladtlWmtt.
h r
4. b t h r T w a v e ~ k s u t r p w e y u p e v m t h e m r r r v l ~ ? l m
supfaventricularbea&.it fs fhe spmr way m
Wtinrlar brats,it is inwrtett
5.Qxs t h e n e x t P w a w e a H c r t t a r e r ~ a p p t a r a t m
r'xpcrct~.time? In bath m w m b i a d a r and ~nhiruhr -
rxlmsystola them is= ~ & p e m t a v ~ kfnm t k
next k%nbmt,but a a r p a &mptak ~ ~
upet9 t h e n m a l p e r i u f i c i t y o f t h e t r U . ~ ) f h p t U y .
next SA mdr dischargy(4 P caw] cmffstat&
The rffiw-tsofsupwvnrtriLubrand vmhknbr
rxtrasystt*es en thr frrlltwvin~:
P warn am & hrllrmws
 rH KAOClCNtDlS - THE F m RMYlWW

Fmiin be* thc jmwtbud (AV nodal) region, and

\*enhide -
, caOsin5 a sustained
~'Ilra%terbPbsrdydcsnibrdcanbeusedto
d e d d c t h e ~ d ~ a d + r & , a n d k s b e b r e the most
importanttIdngkaitrytryLoidentIfyaPwavr.

theahirm)
in ahial tdyadb, the abia &polarize faskr than
-DS&* . 8 '

.I' . , 8

. I, I . i - . r
. .
 The AV nodeanmt conduct atial rates.of 4isctuaw Wlren Btrinl kathylcqdin or airbl fluttgr is,awx$ai& wit),,
peaDn)Aan a h t i t 2W/min. If the atrial rate is faster than 3 1 bkirk, tLh r e i - i t l ' y k ettfi
d I8nkrarefully~
njiea E
this, 'aMoventrEctdar block' acrurs, with mn1e I' w a w nut P w.;w~Ls~'@$$; 3Jj), & WYftlWmmpkX taei-iy&r@$$ Wifh 0
f~nowedby QRS c o t n p b The di&emce this v u n t h i & rake of 2lWmin s%aldal.w*ye alert to t h ~
ssrt datiovrntricular block and s&md degrect hean
@Yity 6f oM& fhttt* with &I M&.
block iS that h atriovcnhfculw Wo& asssefatnd with a a~rhgilhmmsheuld bpidmtlfird fmm &l d irr
, AY node is m ~ i n p-IgF
t a c h ~ r d i athe - it is w h i P wave? an d emily b~ WI*.Full l%lead E C A
pfcW~tingthe ventrictc~from being asWuakd at a fast 4rt? ttpe.rmb.vc t&er than 'ihyihm strip'. In the WE(W$ in
(and therefore inefficient)I&. h kt, or tfiird Figure 818,nttiaJ flutter is most easily men in lead I!,. htri 'it
degrtic blwk assmiatpd wfth sinw rhytllm the AV nrde is oWmi&h.lea& VR Wd~VE
and/or the Hisbundle are not conduding normally.

Atrial flutter
When the atrial rake is p n t e r than w m i n , and t h m -* ncl
flat baseline between the P waves, 'atrial flutter' is pwhent
(Fig. 3.16).

-- -. ,. .in- : . .
. .~
...-,'A:'
i

%na?i~ t r ~ s l m w i m ' P : t ~ + '.

r*ra,
At& fluperwith an alrial rate ol300mdn is present, and M e is ?:I
b k d i g w r ( ~ g a ~ ~ d ~ ~ . ~ i ~ ~ a f f h e w u P w v
wEM@A@ Wh sach MfS em be rnisleken lor the T W e of
Wa persadinp beel, But P w a W can bs idamiliedby lheir regularity. In
Wk m.T waws csmm ba dearly identirm
, .
id. ,

, . . "
 CSP

Note
In Ihiscass. ,!atatid si+ presgure (applidrjuringhe &Mica
Bv ttre amwe) has MMt f i ~he @weanatrk an@ vmmm

'. .
, , .
C a a i d sinus prrswrr mav {lave a 1~wktl thcrram~tic
* '

s , is always w
t.fWo n s ~ ~ m v ~ n t r i r ubl~ahr y v n r ~ i aand
trying bcuuue it may make the nature of %c arrhvthnli~
mere obuiobs (Fig.3.19). Carotid sinu3 plessure activakx
a reflex that leads tt>vagal stimulntion of the A and
AV ncrdes. Tltk b:u>usesa reduction 1st the ftlrquenc of
tlischa~mof the SA node, and an in0~t.win the &YV
of rnn&ction in the AW nude, It k the latter which ip.'
inip(irtaat in t h diagntasie
~ and traa'tnvmt nf errhythmias.
Carotid sinus ptmsure $lows the ventriculmt rske in aimq
.supraventriculor arrhythmias and compktrly nbilishe$
nthars, hut it has no effect e n ventTIcu4ar arrllythniiac;.

1
Juncfjonol fnodolj fachycordio
Ifthe area around the AV node drpolari~rrfrcyuently, the I'
wavtli niay be wen very clcne to the QRS complaxvb (ah with
the curms~~onding extmsystole8),or may not bc wen at all
(Fig. 321). The QRS amtplrk is of ntwnul shape h ~ a u xa:.,
1. Find* m e s and m 5- hnw they r&e w Phe
m p b i s a b a p the b y to t O & n 8 ~ ~ ~ $. c .
h I ~ M - ~ m ~ ~ a1 2t h; d~ cG,& I : . ,

-
,..

2. W pdbk, compare theW ,wmptpadudig W,

tilahyeawdh with &&d-.sinus r h y h p #ft&*r. -
:
&*
--,W,wkin
: ', siws &$q thp Q B
wMa &a haw*'&
dd't$y@
as durift&<p&,B &$hkd.: ?
:
&p
3. iff the Q@ ivwi&r *an &II~UBWS .'
(160oa3,the m - M , , p K o b s b l ybe~ve&&uhrin
4. Left &a dev&km du- t k tilchye
indkgiesa yentclmhrr migin. as docs
covgared with 4 wad taken durirrp,
. "
t iQ
5. if dwhg,,th@f e c ~ ~ ~ wthe a W . n 4 8 + . vmp.
@&uliQthe&#kip i8 p&&Iy ~ ~ 1 : W a e e y i d k . k
b d 'M. ~ block i(@ %Wj.

%. 8.26 AtrW tWIWun

N6 P ww$s- Irrd$uiar bmeflne
Nole

lnegular QFiSronplaRBs
N o W J h q w i QRS o o m p l s ~ ~
tmmm In
fn lea4 W, w i w s OMI be SBen W* t h e membbq~eo
atrial Ruber - thisB
common in a t r t librillation

arr irreylss and the ventricles thertifl+tucctntraet

~rrcgdady.-use conductinn inko and thrtx~tghthe
ventricles is by the normal route, mrh QRS complex is of
normal s h o p .
In a 1Llead record, fibrill tion waves cpn t>ftenbe s e n
much better in some leads than clthrrs (Fig. 3.20),
 Flg 3 s Awn1 IlbrUlation

..
Nofe
MoPYrsv&i
basaline
lmgular QRS cmebx80, rate warring
- llswwmB%and1mbl
~ o w C ) f + S r n ~ ~ ~ ~ o
Depress@ST sagm& in leads VS-Ve
WormalT v a w s
-

When the ventricular muscle f i b m cc~ntract

independently, no QR5 complex can be identified and tlic
ECO h rotally dir~rganized(Fig.3-27).
As tlie patient will usually have tost consctt%usntwsby kk
time y ~ Rave
u rcaliaed that the change in the ECC, pattern
is not just due to a lnme cr~nnrctim,the diagniwis is vaby.

Tlleonly normal ektrlral cr>nncrcti&?n hctwccn Ehc .rtrw

dnd vcntriclcs i\ thc His bundk. Smir pcopli: hi~wever,
havean extra or 'acceswry' ci~nductinfibundle. A c c c w ~ r y
bundlcs ftirrn ,idirect rt~nnectii~n L w ~ w e ratriuni
~i otict
ventricle, usuallv crn the Itmfl 5ide iif the Iicort, and i t r th~.
 ,,.I .+%*It,., '.;,; .,.
I,, : ,:;;:;.,,;,; <; ,.,. \..:17. -:.

:I
I
/ ; . . .i , . . >

acsrssory bundle thew is nr,AV nrde todelay cdnducti(m.

A dcpnlarization w w e thrrefgte reiuc'hc%tkr *nttide li.,t>+ , . ...-i.,l,71,,..I
. , ik'l. 'C.Y,! T$'
~ ~ 'pre-exeitatism'
n d aecurs,The PR intrml is rlttlrt and
tile URS complex showv m rady 8- uostntke r.nl1ed ~t
'~ieltawave' (Fig3.28).The? second p ~iaft the QRS cim~pb~x
a
-i ctinducti.on throqsh the His bundle catches tap
with the prere-excitation.
The onty clintbd inr@ortancrof1h2s snaWmic;rl
'~hnohnalityla t k t i t - cause paxixpmal tachycardia.
L3~polarMoOn criri spread down the His bun& and beck
upthe accesse~typathway, and so wctiwatc the atrium. A
'wentry' circuit is thus set u p and a sitstained t<$chyrordi.~
viccurs (Fig. 329),

"e
 :t

Accurate i~+iera&h UF ~WECCis an g ~ ~ ~ ~ . f i ~d::,, f , t

'

th@h@.id
~f arrhythmia ~ ~ e . m & t - i ' i ' h ~ O ~Ch & ,.
intend& ttl d'mss. thwapy ih any d&&$, .,
a.pp~(~p&de to sylii~eswnt?simple appmwt+bpat&*n
management rhat'b~ieailyfallow intrrpMEglii~nrrf an EC<;
.
recording; ..,, ,

- Atrial RuW-carotid sinw m e usually c a m a

temporary inuease m block (eg. fmm 21 to 33:)
- -
Atrid fibrillation and ventricular tachvcardia carohd
 BNORMALITIESOF THE P WAVE
41

.. . . .

.s-.,:.-&%$: :
4. The T wave can only be G right way up or the wrong,:,,
"y up.

~-
,..,..,.,,
(.. ,.
*
1i \:.:
Apart from slteratiollr,of the shape of fhe P pGave awwiated
,tws--imm , ,

I.,.,. . , "..' '.

. :3srt;
I1.h-gth.t ihpripiht?a* t O m r :,.; r
hyperimphied (suchas t&u+ .tm .
*Pigh. ~
2. M ehial
h-on)-rheP
$11.. . . . .~.
p e ~ ~ ~ ~ ~ ~ ~ h a t :
waye.t$.-
" ,

,, h d and b&l P waw (Rg. M). .Y5

.s;i;n.a'. Ztii; - 1 . 2 r - 8 s:.,;+. 'J - W n ~ r ~ ! 4
When hderp-gan ECG, &dnntEfg .hythm firs
.-. # f i r u + ~ I I ~ 9~s..&e,.r..!*~rn,,~
137.2-yrq .~,i!
'

, i?

-
%-ten ?sk the following question% atway8 in the %aw
sequence:
1. An? thanyabnannatities of theP w e ?
2. What is the c a r d i a%&?{Loadc at the QRS complmin
leads 1,11,111 -and at Chapter I if neeesurrry) , ,
3. Is thv QR5 complex of normal dutatinnP .: I i
L.
:8
4. Are then any other abnannaljtim in the Q&%
complex - partieulady, arc there any&yrttid Q W ~ V W ?
5. Is the.STsegment r a i d or W : M ?'-. ''7:: "1 2.
6.Is the T wave nor&?
 SNQRMALITIES OF THE QRS COMPLEX

~ ~ 1 W Q n ~ k p s ~ d u u a e t n k t i * r
, - . . r , , rr ..I-+ - . , . . A . !:, :,I, . - . , ~,.,,.,
, ;A
~.,*fi?~iG'ra&
E '-
2.in a rrghtVd?knh kaqf,), the S
ttre,Rwape . L
 -4.7 AmBe-Im,
and prdt.b%lold hhrrW i n t s d n (.a
Fig. 4.1s)

~ & m v i n g e t 4 a y f m w V , ) . T h e d i s adominant
S a r w e h h d V , [seeh. I).Withinfaz&i~ofthe
ura af the ventrlde, &eph+tim of the
xi&t ventlldc is less q+wed by lelt WnMnaIar forces, and
ss becomes mwe obvious and a dominant R prave develops
Sn kd V,. Thc aO -P of the ECG is similar to that of
rjght .r~ntrieuk hypertrophy,though the other changes
of dght v e n t r h k hypertrophy (& above) do not appear.
Z"be presence of a Q wave does not give any indication
of theageofan~,infirrction,useeuseaQwwavehas
&doped it isnsuayl pffnanent
 ..
. N o m a I O R S ~
RW ST s a g ~ n t lin
l 11.111, M
~,~,~~r~s~ri~inleadVLandtnV;.
vtrimbmrmal

~ ~ u r S T ~ ~ ~ e s b e h y e s n t h e ~ a o n ( p l ~ ~ ~ t ~ ~ y ST segment
wave(Fig. 4.10)).
"~hddbe'~~'-tErati~atthe-~r*,~~~
partbetweefltfteTyayeaftd thene*tFwa*-butitmay
be elorated (Rg.4.lla) or depressed 4.11w.
Elevation of the 511 segment isan in&& of
myocardial injury, u- due eithR to a Rcent infhtrtion
or to perlcadi%. The leads in which h t b n
indicate the part of the he& that is danragpd--
d m @ slums inthe V I d s , and inferior da- in w.
Q*11 t.)Eb"'md~.~gmi~)-=~-
IB and VF (see Figs 4.749). M m d i is n o t . M ya
localized &ir, and so it causes ST elevatbn in most
QF
 W T l E S OF P WAVES, QRS COM

ABNOR
ninq !a : ~:. ;<> . . d ' ,,.;,
~ ., ,

T *aye jnmm&n is seen in the foBmw@ :- . ,~

- ,

i, s i
?~ - :,-
i n v d d n @is MR @ & W 1 , 1 ~ i n
vz*m.&apb, and elaaiakod V s S n ~ ~
peopl@. , ' . , ,
,'.iI . ' IU, ~2
4
a my-
-r.~-~?%,r
infarctinn, the kst abnowality setir
..C:x: ,k

om &e &CG fs eleMltlanof the ST w e n t +I%. m.

Fw.WF.$lel@y Q UfB* appear,
Holizantul dep-n af the ST segmonL asm&t& ..m&.*.Q"vt
with an upright T wave, isb y a sign ofkhasmir as p&ess~a~etimeYNt
oppospdtoinf~.WhmthECGntrr.tis~I, a f ~ ~ . T ~ e ~ ~ i & o f t a n
ST segment depmion may appear dwing aercise,
partidarly when e m induces angina (Fig.4.U). win-, there will bP
i Pwpve izbrdonwno
hwnslopln&as opposed tu horizonfdy - , Q wavm @%@. 414). This is called a 'non-Q'wm inttmth'
ST sepmts are usually due to treatment witfc +xin pat&n. The tar08 'subendcadd idamidp a m is
(dcsuibed later). sometktm wed, but il is &h liot p8thobgi& W X d .
 . d 'I
ABNORM
ABNORMALITIES OF P WAVES, QRS COMPLEX AND
1 ;/I
rHER ABNORMALITIES OF THE ST SEGMENT
W l l F W I.,
.I.\
IVES
L"".F'~~A.
~ ~ o a w e p l a a m a ~ o f p ~ ~ ~,,; , *
&,"
~$

and m&ndum.a3kct the WG, thou@ dran$psin &

plasmg sodium level do not The T wave md QT interval
( m ~ d ~ t h e ~ o C ~ Q R S m ~ p l e x t o L h e ~ o f
&e.,bwsve),.awmw& cmm@y afkted.
4b
' mvpotsssium level c@pmT w v e RattPning ;arkithe
&or*.?.~ave~&!I&~,.~Ip
l ' ~ ~ ~ ~ ! ~ ~ ~ e p . ~ & ,
.m.b ,QM,W*.
or4tmormal lmela
.,., ><.'',?i ~

hhw&na+ii,levp1 c a ~ p o b q p t i & q fthe

~T~&~@.%*,pbma calaiuraipvel shoEw it.
-
-
. . .. , ,-,..,

ofMb&&&&
t'
..,, ~ ,,,,,.,.,,,

T~ & a h & & & &

wave &attenin&etc.)are usually of no great significance,
,,

and are best reported as 'mn9peciacST-T changes'.

QAT TO LQQK FOR IN THE E
 . , LC.. .

-kdm I i.. -., '.

-w m

w - i P e Q E 5 q h

f1-* ME.
= -
~ j ~ - s e a L * c a ~ i p
-.,- ---
-
mn-m%ad P

-
a1 ptl]bltrlr
and thCn lepetition of the

rwa (or 4 h e ) P1YBv$$ per Qmts.

~*,-
c m q # I r x . w i t h ~ r w a w n r t e . If..
 'I
ysrbundbbtorrhblock
Q y m$a&tion greater than 120nta.

..- ~~
tvfpa~inleadVwand80~esmleadsiV~ stnZ,s'rhh.
AhjalextmqSwfea
Juhclional(AvnbdaIl exkq4tUea
Ei&l&uhkk Aclipihtter.
~eftantedmh~(i.e.d@adswitkdeep$ *Atdalf?mJMom
w m in leads I1 and Im. 0 Jrm&imd (AV nodal) &*.
Jllmmmi(kV W)e3W4F.e'

.
~-*~clqrthcm
l
- -m
n ~
QBg m n p 1 ~ c e ~ than 120 ms)
- -@QRScompkeaasksinwrhythm
- nmdT waves.
E.w@,m
a ~ v a i W c u h e bavewldaQl6
h ~
eo@em wiih Siriuu rhythm:
- bun& branch block - me P wave per QRScomplex
-~ ~ W h i t e s p t d m n r e . - P-P intewal v&zs with rspiratlon (sinusWhFhfiia).
a snpnven* iMmy6bh
VeMrkulrrr mylhmr - - early QRS c a p l a
* In general: - noP~~~e~(~:abnam&yahapad(atdal)Bwavs
-wideWuntlpb&eakrk1Mnts)
-
amwmwplexesba~re-inb - MuOwandmrmalm~t)~tex
rhrn
- n o w T wave
- ntlt P waw is '4.
.-

I
- abnmmal T werea
Atrial tnch*

-
Wrn mbnonnulilk.
~ b s s &de&y
e+sk&t
; beas ~ u ~ t t t e n e x t
-w
QBgcornplexzate~terthMl5Qhh
- abnoraMlPwavps,~yw&hshartPRintds
aUy one P wave pa QBS complax, brrt somimes
* &$ape hegk Bbsenceofstnus beat f ~ b w e by
d single
P wave tate XXl-Wrnin, 621blQdL
beat. '

rn'
 - 2:1,+3 1 or A:%Mock
.-
- Neck in- d
Ahial'&&,tio~:
by m d &us

~ m c d t ~ r h y t h w d ~
p m . .
.
- QRS Complex tab W a c t e r i s w over 161Ymin
withaw WaWent, b@can be slower
- rro P waves iden&abk, but t h e is a varyins
completety inegular?7%a&ne.
J u n c W d (AYW)ta&y*ndia:
- cmmodq, but ~ p p r g ~ rc?&dy , ' S W
rawnairuhrtach+dia) . .. .

- mte m y zsa-matin
- -tia sinw F- may a= mersim tb sinu$
Ihythm.
. Facape rhythkw:
:
- bradydas. ofherwisec h r a c t e r f ~ag %except
t k t atrial %&attondew .notstcur a$ :m e g a p
rhythm.

VentrkIder rhyhw
Mnbic&t~.er~les:
- early QRSc~rnplex
- no P Wave
- QEcomplex wide k t e r &n la0 ms)
- abnormally shaped QRS c~111pIex
- abnamally shaped T wave
- ~ e xPt wave is ffn W.

I
Wentriculartachycardia:
- no P waves
- QRS minplex rate greater than -1
- accelerated idiowtrt&uh rhythm: as for v-
Mchycqdia, but QRS comp1ex rate less &an -1
I
. REMINDERS
1
- DII

YPERTROPHY OF THE HEART 3. If the QRS co@= rate is repq$yVi>Ww,w''jyw,

a w i i s QRS mmplaindicates vs?- tach- and
arwmw~RSca&kx~bpafonol(AV~~)

. .
RQR5 Baorr hl r l
IfyarataseemaePwsves
-*,'d ~.
.

t h e f o w . ~.
,
. ,~
. : .2 .

DIFFERENTIAL DIAGNOSIS OF ECG CHANGI

Q*naM
-sP&,,&q:*.,,.: ' . ' . .

.
(sepbllQ -ate normalin leads I, VL andVb.
,! *&he,..,' . . . V ~ &FQW cbf?plk,cbr;sidir
If yau cannot see @neP P
,
' ,. ,.
.,
w Qwaueinle&8jtWeotWisa~filvuiaFa
~inriipahinbncthnii~hrmorethnnona
1. P wavep~sentbutnot ewkyvi9jble:look- st
leads u a d vl.
2. t ~ a w ~ w at hre rel l ~ i s ' m o &w
fibdlktion and w M seem to be P wavesadru(yl are nOL
REMINDERS

:'

Normal $i leads Dl, U,,V, ond VzV, in Milrrk Gke

.
Now test yourself
V e n ~ i t h ~ ,. . ... . . . , ~ ., .. .. ,
. . & d e branch bhk
Mosa& *&& ..
IIight or left v. - e n .'-~hypertroph~
t
-iSV'
i
~,~
me lbu should h~rr be able to ne~ognkethe c.mmon ECG
, ..-
,- paltmw, and this hischapter mntedns kn 12lead W d s
.
.
--
,
,
, . , , for ~ Q U
to inteTpret Whem rqxlrthg an KG,rememk.
. . .
, , . , . I . _ . IheECGiseasy.
A m p ' t has Wo pmts - a dewriptionand an
, , . i . . , , ' . , , , , . ,
, . . hnwBoIL
L m k at &'the leads, and descriBe tke ECG the same
... ., , ,
onlereverytlme;
). .. .. ., . ,: .. . . ,
, , .. _,.:.
I
, .. ,. - FomduC&t?a -PR iweval if ~ h u rh-
e
--ads
- Q w ~ ~
dludim
9

heightofUsndSwaves
-s r ~ e n t s
-Twrrves,
Remember what csm be nmd, espedally which had8
csm show an hv&d T wave.
TIUSI, and d y the& mala?a diagnosis.
Iheten FXXs here are in no par@cularsequen*, but
hsre been desPibdl earlier in book. Their -@ions
and inkpbttomare giwn aftenvards, on p. 140.
-
.6 NOW TEST YQUBSZLF
 11 ;I
'I '

':I I

'I! I
''1
, I 8

,I
:'I
'8

' 8

/
I
'1
ll'
, '; ,I .~C

I
1'.
1 'J.
I
ECG 9
F
OW TEST YOURS

- -=-
,=a1
This k G sh~ws:
Sinus rhythm; rhythm ship (lead tl)shows sinus
arrhythmia I.

Norm1 pR i n t e e ms
Nor& axis Get this one wrong? Read pages 95-102 again.
QRS dw&on 80 rns, narmal height
ST m p s ~i tm e W c in dl all&
T i n ~ e r ~h
i ~ n VR but no ather h d This ECG shows:
Interpretnticnz
Norm& r e c d A i t m t e conducted and nonconducted beats
you did not $et this right, Lwk again et pcy:es 25-27.
EGO i
This ECG shows:
%us rhyShm ahd irght bundle branch block, indieating severe
M o m 1 PR interval coflducting tissue disease
NmmdaxiP
Wide QRS duration, at 169 as This was expained on page 32..
RSR pattern in lead V,
Wide and notched S wave in lead V,
ST segment isolelechic
T inverdon in leads VR ( n o d ) . ,V1-Vz .
The ECG shows:
At+ial &&tion

lntefpdfattion
Right bundle branch block .
i.
Downsloping ST segments, best seen in leads V4-V,
U waves, best seen in lead V,
h y pnoblems7 If if,look at pages 3739 and 43.
143
iiu
 JOW TEST YOURSELF

I* #Q&
b m-tim
tal , ~
uiwaajn iaw with di.gitaG,,eEecti This ECG shows:
U Vaves wggest hyp&lae& Bmad complex tirchqcardiaat 16Qhin
If you made a miSfake with this one, readp a p 1W-1&. 4 Nb P waves BfsIble
., .
Left axis
QRS duration a00 ms
TWs ECC shhvhvs: a QRS complexes an point downwards in the chest leads
(NB: lead V, shows &facts)
Narrow cori\5,1ex (i,.e.QRS duration Ii-s than 120 ms)
&yc&& at 2aa/min Inierpetalion
No Whle P WLI.W&S ,...: . ) . Ventricular tachycardia
* QRS rampkw ggmd The diagngsis of tachycardiag iS covered on pasea 74-78,
ST s o g n i d ahow a little depression in leads II, III, VF
T waves normal except in lead W , ... .
. ,
- , i s ECG 9
r I~lte?prct~tirm ... . . This ECG shows
suprav.m&iCular(junctional)tachycardia Sinus rhythm
In ease of -9, lbbk at eges 72-74, r Bifid P waves
-.
K;O ,. a:'
f.
<:**
,-.

,,
.
, <.., -< , ..,,,
:;, .
r
9
Normal conducting inW&
Normal axis
Thii ECG shows:
,,.< I. ',! ; ~? ,
L, . r Tall R wave in lead V, aMf deep S wave in lead Vz
Small (septa!) Q wave inleads I, VL,vrv6
r S . i ~ ~rhyulm
wi r Inverted T waves in leads I, V L VsK
n Normal PR ihterval
r N e d mb IntcrpretaMon
Wide QRSI complex at &Ims ,.. . . ., b f t atrial and left ventricular hyperhiphy
8
;+ "M"p a e m in l&ds li VL, V5-Vh If you needed he$ with this one, re-md p a p 90and 93.
Deep Fo waves in leads Vy V5
Downslaping ST segment i n leads'l, Vli, WCV6 ECO 10
Biplysic or inverted T waves i'nleads I, VI. VrV6 This ECG shows: ..
Sinus rhythm

.
r Mormd condticting intervals
Normal axis
Q wave in lead V,
. .
Raised ST segmentsin h d s I, W, V&
r N e d T waves
 -m~durtionfdkm and AV
nodm 3Q-5

Heart MI& 3B-5

aeamem&M.
udxlarrtrd MkMmwlqbl.
escnpespgz . ..
nQla154,r)qB :".:,. :: . ,
... . ~ .
Vcnfinr$rM&&.
iw*w , . .
En; mMder 7-G?, no41 ~usU,X73 .'
lWad H,s.PO,lZ,ZM, 26-7 wlthM.amdh*w ?6
c a l i b m l h 11-12.1? supravc11- *z, s6
n
i -13 u e n W r 5 4 57,F
repmngn Ri@ aria dw&+ 14,15,.pI
-.adsgnds5-7,5#6 B&ht bymila i w y h bk~?+,@-9~
BctO@beata JT,.~. 4.m,we,+s
W y t a hmndfwmad T amIMW~apvkg,@
wave 1i.X
snh3ocedmItmddty84
-fipUmtWlls
ama154,59
funeiiwa68.W
*Wk&&3-% 61.a

-*-
exacroclmai6zke+3l#a,1PZ

atrial 61W
jmbbnel %a64

*'
I

siwbwm)nodeLJ,irl Guiginrs4
~ a S ~ S o , g $ , -m
shwaW#Ymldiase #nus% S3
$mtr hstkntsk 3.n& w m w ~ w 7 cnl
~ W s f t u i s ~ 1 6 -, fh3 tine Ek-7
~ h f t ~ b m ~ J 1 ~mLdollar7J.%76~W-8,tl(r
~ 7 6
wntlsIshm%s TWutegPeaEWjMW
n 10s W ,z% 61
lW33 mz 1
s Tisrd&, K G -5-7
de&li\ion 322 'Gwi170npeintaZ
subm-hrfamknIm
ktpnvm- &wwtvk blb.
66,it5
kp4vetUY4llat rh* %Y, 56,
f&L4
-5 116
77 *YmBM URkkUkfphmbhZl Sf), 116
M ~ - ~ @ Y
TW112 left%&%
@lt %a,91,92
nbmmla- lW %sa !S wwe 14%
Mnhieulmrh* 6 57,57,114,
a d asesldn 16% m 116
and--M1m %1entdcula~&14,15,~6,
diadWmwW
awl V e R W l a r h w h y 106 n-$
i~
'brhpardkm-78
atrialcV-B,W, I @ W e & s k S h p h e ~ t ~ ~ 3%
1,
' r-veIl?&Aw -.eJectw94
eZZ2tibn Y Y a U f - (WPW) ~ ~ ~
1s wndre-m-a,u