ELECTROCARDIOGRAPHY (III)

THE ANALYSIS OF THE ELECTROCARDIOGRAM

Scridon Alina, erban Rzvan Constantin
Recording and analysis of the 12-lead ECG is part of the basic medical assessment
performed for every patient, providing an invaluable diagnostic tool. Therefore, every
physician is expected to possess a reasonable level of expertise and skill in
electrocardiography, regardless of his/her medical specialty.
As in the case of physical examination, it is desirable to follow a standardized sequence of
steps in order to avoid missing subtle abnormalities in the ECG tracing, some of which may
have major clinical relevance. This chapter presents a systematic, eight-step ECG
interpretation method, based on the analysis of:
1. Cardiac rhythm
2. Heart rate
3. Electrical axis of the heart
4. Rhythm disorders (arrhythmias)
5. Conduction disorders (heart blocks)
6. Myocardial hypertrophy
7. ECG changes in coronary artery disease
8. Other abnormalities
1. The assessment of the cardiac rhythm
The cardiac rhythm is characterized by two main elements: origin and rhythmicity.
1.1. The assessment of the origin of the cardiac rhythm
Since the cardiac rhythm is normally initiated by the sinus node, the normal rhythm is
designated as sinus rhythm.
For the cardiac rhythm to be considered sinus rhythm, all of the following criteria must be
fulfilled:
- P waves must be present in front of each QRS complex if the electrical impulses
originate in the sinus node they first cause the depolarization of the atria (P wave on
the ECG) and only then the depolarization of the ventricles (QRS complex on the
ECG)
- the morphology of the P waves remains constant in each cardiac cycle within the
same ECG lead if the electrical impulses originate in the sinus node they cause an
atrial depolarization that always follows the exact same sequence, generating
identical P waves
- the distance between consecutive P waves is constant the sinus node generates
electrical impulses rhythmically (at a constant rate); however, small irregularities can
occur (See below)
- P waves are positive in leads II and aVF the vector of atrial depolarization points
downwards and leftwards, towards the positive poles of leads II and aVF (See the
Electrocardiography (II) chapter).
If any of these criteria is not fulfilled, the rhythm is not a sinus rhythm arrhythmia is
present.
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1.2. The assessment of the rhythmicity of the cardiac rhythm

Given that the sinus node generates electrical impulses rhythmically (at a constant rate),
the normal cardiac rhythm is regular (heart cycles have equal length).
To determine if the heart cycles are of equal length, one has two options:
- to measure precisely the RR intervals if the RR intervals have equal durations
(duration of RR interval 1 = duration of RR interval 2 = = duration of RR interval n)
the cardiac rhythm is regular
- to use a quick approach mark on a piece of paper the position of 3-4 QRS
complexes; shift the paper to other parts of the ECG trace and compare the position
of the marks with that of the QRS complexes. If the marks correspond to the position
of the QRS complexes, the cardiac rhythm is regular.
If the RR intervals are not equal (the marks do not correspond to the position of the QRS
complexes), the rhythm is irregular arrhythmia is present.
When the cardiac rhythm is irregular, this irregularity can be:
- intermittent (periodic) there are only occasional irregularities in the RR intervals,
but the baseline rhythm is regular (one example of intermittently irregular cardiac
rhythm is due to the presence of premature beats, See below)
- absolute when the RR intervals are completely irregular, on the entire ECG tracing
(one example of absolute irregularity of the cardiac rhythm is atrial fibrillation, See
below).
However, slight variations of the cardiac rhythm can also occur in perfectly healthy
individuals with respiration, causing the so-called physiological respiratory arrhythmia
(shortening of the RR intervals during inspiration and lengthening of the RR intervals during
expiration).
2. The assessment of the heart rate
The normal heart rate, dictated by the discharge rate of the sinus node, is around 70 beats
per minute (bpm), but values between 60 bpm and 100 bpm are considered normal,
depending on the status of the patient at the moment of heart rate measurement (e.g.,
higher heart rate after physical training or in anxious patients; lower heart rate during
sleep).
The physiological variations of the heart rate are defined as:
- sinus tachycardia when the rate of the sinus rhythm is greater than 100 bpm;
occurs most commonly during physical exercise
- sinus bradycardia when the rate of the sinus rhythm is lower than 60 bpm; can be
seen at rest in conditioned athletes.
Three main methods can be used to determine the heart rate: calculating precisely, using
an ECG ruler, or approximating.
1.1. Precise calculation of the heart rate
The heart rate can be calculated precisely starting from the equation of velocity:
v

D
D
t
t
v,

where: v = speed, D = distance, t = time.

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From this equation, one can obtain:

1
V
I

T RR
T I RR ,
V ,

where: = heart rate, V = speed of the ECG paper (usually 25 mm/s), I RR = RR interval
measured in mm, T = duration of the cardiac cycle (RR interval) measured in sec.
Replacing the constants in the equation, one will obtain:

25 60 1500

I RR
I RR ,

where: IRR = RR interval in mm.

Since the heart rate is measured per minute and not per second, the velocity of the ECG paper
(25 mm/s) will have to be converted into mm/min, hence the 25 x 60 value in the equation.
1.2. Precise determination of the heart rate using ECG rulers (Figure 1)

Figure 1. Electrocardiographic (ECG) ruler. First, the speed of the ECG paper is checked on
the ECG trace. Then, the appropriate marker of the ruler (black arrow) is set on a chosen
ECG element, usually the peak of the R wave. The value corresponding to the 2nd, 3rd, or 4th
R-wave peak, as mentioned on the ECG ruler, is read. This value represents the heart rate
measured in bpm.
1.3. Quick approximation of the heart rate
For this method, one should find a QRS complex situated on (or close to) a thick line of the
ECG paper. If the next QRS complex is situated on the next thick line, the heart rate is 300
bpm (RR interval duration = 5 mm, 1500 / 5 = 300). If this second QRS complex is situated on
the second thick line (RR interval duration = 10 mm), the heart rate is 150 bpm; if it is
situated on the following thick lines, the heart rate is 100 bpm, 75 bpm, 60 bpm, 50 bpm,
and so on (Figure 2).

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START

300

150

100

75

60

50

Figure 2. Quick approximation of the heart rate.

3. The assessment of the electrical axis of the heart
The electrical axis of the heart provides the image of the mean direction of cardiac impulse
propagation through the heart. The term electrical axis of the heart usually refers to the
electrical axis of the QRS complex assessed in the frontal plane, as measured by the limb
leads.
Ideally, the electrical axis of the heart is between +30 and +60, but values between 0 and
+90 are also accepted as normal (known as intermediate axis). Whenever the electrical
axis is outside the 0 to +90 interval, an electrical axis deviation is present (Figure 3). If the
electrical axis of the heart is between +90 and 180, we have a right axis deviation; if the
electrical axis of the heart is between 0 and -90, we have a left axis deviation; when the
electrical axis of the heart is between -90 and 180, we have an extreme axis deviation.

Figure 3. The electrical axis of the heart. N = normal range, LAD = left axis deviation, RAD =
right axis deviation, ED extreme deviation.
The axes of the P and T waves can be defined in the same way as the axis of the QRS
complex.
The electrical axis of the heart can be determined by: performing a precise measurement,
using the quadrant method, or using the method of the equibiphasic waves.
3.1. Precise measurement of the electrical axis of the heart (Figure 4)
The precise measurement of the electrical axis of the heart is performed by using the
hexaaxial system of Einthoven and the calculated amplitude of the waves (amplitude of the
QRS complex).
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For this method, the following steps are made, in order:

- pick any two limb leads (usually leads I and aVF) and represent graphically their axes
- determine the amplitude of the QRS complex in the two limb leads by calculating the
algebraic sum of the amplitudes of the positive and the negative waves of the
complex
- represent the values (the amplitudes of the QRS complexes) in the hexaaxial system
- compute the exact angle (expressed in degrees) of the vector (draw perpendicular
lines on the axes of the two leads through the points representing the amplitudes of
the QRS complexes the cross point of the two lines will give the orientation and
sense of the mean QRS vector).

Figure 4. Precise measurement of the mean QRS axis (example). First, the amplitude of the
QRS complex is measured in the two leads (I and aVF). Then, the measured values are
marked in the hexaaxial system. Perpendicular lines are drawn on the axes through these
marked points. The cross point of the two perpendiculars will give the orientation and sense
of the mean QRS axis (thick arrow).
3.2. Quick determination of the electrical axis of the heart the quadrant method (Figure
5)
For this method, the following steps are made, in order:
- represent graphically the axes of leads I and aVF
- check if the QRS complex is predominantly positive or negative in these leads
- determine the semicircle in which the axis of the QRS complex lays for each of the
two leads
- overlap the two semicircles this allows you to find the position of the axis with 90
precision.

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Figure 5. Quick determination of the mean QRS axis using the quadrant method (example).
If in lead aVF the QRS complex is predominantly positive (left image), the axis of the QRS
complex lays in the lower semicircle (corresponding to the positive pole of lead aVF); if in
lead I the QRS complex is predominantly positive (middle image), the axis of the QRS
complex lays in the right semicircle (corresponding to the positive pole of lead I). When
overlapping the first two images (right image), one can see that the mean QRS axis lays
between 0 and +90, considered normal.
3.3. Determination of the electrical axis of the heart using the method of the equibiphasic
waves (Figure 6)
The term equibiphasic refers to the QRS complexes for which the amplitude of the
positive waves is equal with the amplitude of the negative waves.
For this method, the following steps are made, in order:
- find a standard or a unipolar limb lead where the QRS complex is equibiphasic (if
there is one). Often this is the lead with the smallest QRS complex.
- the axis of the QRS complex is perpendicular to this lead's orientation and therefore
parallel with the axis of the lead that is perpendicular on this lead
- analyze the QRS complex in the lead that is perpendicular on the lead where the QRS
complex is equibiphasic if the QRS in this lead is predominantly positive, then the
vector of the QRS complex points towards the positive direction of the axis of this
lead; if the QRS in this lead is predominantly negative, then the vector of the QRS
complex points towards the negative direction of the axis of this lead.

Figure 6. Determining the electrical axis of the heart using the method of the equibiphasic
waves (example). If the equibiphasic QRS complex is in lead aVL, the axis of the mean
vector of the QRS complex is perpendicular to the axis of lead aVL, and therefore parallel
with the axis of lead II. If the QRS complex is predominantly positive in lead II, the vector of
the QRS complex points to the positive direction of the axis of lead II, that is 60.
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If there is no lead with an equibiphasic complex, there are usually two leads that are nearly
equibiphasic, and these are always 30 apart. Find the perpendiculars for each lead and
chose an approximate QRS axis within the 30 range.
4. Rhythm disorders (arrhythmias)
Cardiac arrhythmias represent a category of cardiac electrical disturbances that includes a
wide range of abnormalities. This chapter addresses only the arrhythmias most commonly
encountered in clinical practice.
4.1. Premature (ectopic) beats (extrasystoles)
Premature beats represent additional heartbeats that are not initiated by electrical
impulses generated by the sinus node, but arise from ectopic pacemakers. Depending on
the location of the ectopic pacemaker, extrasystoles are classified as:
- atrial extrasystoles when the premature beat arises from an ectopic pacemaker
located in the atria
- junctional extrasystoles when the premature beat arises from the atrioventricular
node (the junction between the atria and the ventricles)
- ventricular extrasystoles when the premature beat arises from an ectopic
pacemaker located in the ventricles.
The non-sinus impulse is generated early, initiating a heartbeat before the next anticipated
sinus beat, and is usually followed by a compensatory period. Thus, the RR interval
between the preceding sinus beat and the premature beat is shorter than normal and the
RR interval between the premature beat and the following sinus beat is longer than normal,
but the 2 x IRR (the RR interval that includes the premature beat) is usually constant (See
Figure 7).
Since the direction of impulse propagation and the mass of myocardium depolarized by
these ectopic impulses varies significantly depending on the location of the ectopic
pacemaker, these premature beats are morphologically different and can be distinguished
using a 12-lead ECG.
In the case of an atrial premature beat the excitation wave generated by an ectopic
pacemaker located in the atria depolarizes the atria prematurely and produces a P wave
that looks different from a sinus node-generated P wave because the direction in which the
atria depolarize is abnormal (Figure 7). The premature atrial impulse is then conducted in a
normal fashion via the atrioventricular node, the His bundle and the bundle branches to
depolarize the ventricles, thus the QRS complex associated with the atrial premature beat
is normal.

Figure 7. Atrial premature beat (APB). Note the early P wave with different morphology
from a sinus node-generated P wave, the normal QRS complex following the APB and the
compensatory pause.
In the case of a ventricular premature beat (Figure 8) the excitation wave generated by an
ectopic pacemaker located in the ventricles is not conducted to the rest of the ventricles
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along the His bundle and bundle branches, but directly through the ventricular
myocardium, on a cell-to-cell basis (See lecture notes). Thus, conduction of excitation in the
ventricles is slower than normal, producing an abnormally wide QRS complex and a bizarrelooking T wave. Because the premature beat is ventricle-generated, there is no P wave in
front of the QRS complex.

Figure 8. Ventricular premature beat (VPB). Note the early, broad and deformed QRS
complex that is not preceded by a P wave and the bizarre-looking T wave.
4.2. Ectopic tachycardias (tachyarrhythmias)
Tachyarrhythmias define tachycardic rhythms (heart rate >100 bpm) arising from ectopic
pacemakers.
Based on the origin of the rhythm, ectopic tachycardias can be:
- atrial tachycardias when the rhythm arises from ectopic pacemaker(s) located in
the atria
- junctional tachycardias when the rhythm arises from the atrioventricular node (the
junction between the atria and the ventricles)
- ventricular tachycardias (Figure 9) when the rhythm arises from ectopic
pacemaker(s) located in the ventricles.
The morphology of the waves during these tachyarrhythmias is the same as in the case of
single premature beats arising from the same cardiac region (See above Premature beats).
Based on the duration of the episode, ectopic tachycardias can be:
- non-sustained tachycardias when the episode terminates by itself within less than
30 seconds
- sustained tachycardias when the episode lasts more than 30 seconds.
Based on the morphology of the waves during the tachyarrhythmic episode, ectopic
tachycardias can be:
- monomorphic tachycardias when all beats arise form a single ectopic pacemaker,
causing all ectopic P waves (in case of atrial tachycardias) or all ectopic QRS
complexes (in case of ventricular tachycardias) to have the same morphology
- polymorphic tachycardias when there are several ectopic pacemakers that
generate electrical impulses, causing ectopic P waves (in case of atrial tachycardias)
or ectopic QRS complexes (in case of ventricular tachycardias) to have different
morphologies. Torsades de pointes ("twisting of the spikes") is a particular form of
polymorphic ventricular tachycardia giving a characteristic illusion of twisting of QRS
complexes around the isoelectric line.
When ectopic tachycardias have sudden onset and end, the term paroxysmal is used to
describe the arrhythmia. The heart rate in this type of tachycardia is usually between 150
bpm and 250 bpm, and the duration of the run of premature beats is usually more than 30
seconds (sustained).
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Figure 9. Monomorphic non-sustained ventricular tachycardia.

4.3. Cardiac fibrillation
Fibrillation defines a rapid, irregular, and unsynchronized activation of cardiac cells. Based
on the origin of the arrhythmia, fibrillation can be atrial (atrial fibrillation) or ventricular
(ventricular fibrillation).
Atrial fibrillation is the most common cardiac arrhythmia found in clinical practice. The
arrhythmia is due to the genesis of uncoordinated, chaotically electrical impulses generated
by numerous ectopic foci, usually located within the left atrium, causing an absolute
arrhythmia. During such episodes, the contraction of the atria is fibrillatory (quivering).
Because there is no synchronous contraction of the atrial muscle, the ability of the atria to
serve as pumps for the ventricles is abolished, affecting the cardiac output.
During atrial fibrillation, atrial myocytes depolarize rapidly and randomly at a combined
rate that exceeds 400 per minute. P waves are no longer present on the surface ECG, but
the quivering of the atria produces fine f waves on the ECG baseline (Figure 10). The
atrioventricular node is constantly 'bombed' by electrical impulses coming from the atria,
but, because of the long refractory period of the atrioventricular node, only some of these
impulses manage to get through. Thus, the ventricular rate is significantly lower, usually
between 110 bpm and 180 bpm. Because the impulses that manage to pass through the
atrioventricular node are conducted to the ventricles down the His bundle and the bundle
branches, the ventricles are activated normally and the QRS complexes are normal in width
and have the same morphology as during sinus rhythm.

Figure 10. Atrial fibrillation. Note the complete absence of P waves, the presence of small
f waves on the ECG baseline, the normal morphology of QRS complexes and the absolute
irregularity of the cardiac rhythm.
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When the same phenomenon occurs at the ventricular level, the arrhythmia is called
ventricular fibrillation. This can occur due to the genesis of uncoordinated, chaotically
electrical impulses generated by numerous ectopic foci located within the ventricles. In
ventricular fibrillation ventricular myocytes depolarize rapidly and randomly at a combined
rate of at least 400 per minute. Instead of the normal ECG trace, no baseline (i.e. no
isoelectric line) can be seen and there are no clear and reproducible waves (i.e. no P, Q, R, S,
T waves). During such episodes, the contraction of the ventricles is fibrillatory (quivering).
Because there is no synchronous contraction of the ventricular muscle, the ability of the
ventricles to pump the blood into the circulatory system is abolished, resulting in cardiac
arrest. If the arrhythmia is not treated immediately (within a few minutes), ventricular
fibrillation results in sudden cardiac death.
4.4. Cardiac flutter
Literary, the term flutter means to flap or to vibrate. Based on the origin of the
arrhythmia, flutter can be atrial (atrial flutter) or ventricular (ventricular flutter).
Ventricular flutter is only rarely seen in clinical practice and difficult to distinguish from
other ventricular arrhythmias based on a surface ECG.
Atrial flutter originates in the atria (usually the right atrium) and is caused by a special
circuit in which the wave of depolarization moves in a loop in the atrial wall. The atria are
activated at a rate of about 300 per minute. Each atrial depolarization produces a triangular
wave on the ECG trace, giving it a saw tooth appearance (F waves), best seen in the
inferior leads (Figure 11). Due to its longer refractory period, the atrioventricular node
exerts a protective effect on the heart rate, blocking some of the atrial impulses. Thus,
ventricular rate is usually a submultiple of 300 150 bpm in case of 2:1 conduction, 100 bpm
in case of 3:1 conduction, 75 bpm in case of 4:1 conduction, etc. Once atrial flutter impulses
pass the atrioventricular node, they depolarize the ventricles by passing down the His
bundle and bundle branches, thus the accompanying QRS complexes are normal.

Figure 11. Atrial flutter. Note the complete absence of P waves, the saw tooth
appearance of the ECG baseline, given by the presence of F waves. QRS complexes have
normal morphology. Atrioventricular conduction is variable (6-7:1).
5. Conduction disorders (heart blocks)
Heart blocks define an abnormal delay or a complete block of electrical impulses at various
levels of the electrical conduction system of the heart. Most commonly, conduction
disorders occur at the level of the atrioventricular node or in the bundle branches.
5.1. Atrioventricular conduction blocks
In atrioventricular blocks there is a pathological delay in the conduction of electrical
impulses within the atrioventricular node. The analysis of the PQ (PR) interval and of the P
QRS relationship allows us to differentiate between the different types of atrioventricular
block.
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In first-degree atrioventricular block the cardiac rhythm originates in the sinus node and
the atrioventricular node conducts each electrical impulse to the ventricles, but slower than
normal. Thus (Figure 12):
- each P wave of atrial depolarization is followed by a QRS complex of ventricular
depolarization
- the time from the initial depolarization of the atria to the initial depolarization of the
ventricles is abnormally delayed the PQ (PR) interval is longer than normal (above
its upper limit of 210 msec).

Figure 12. First-degree atrioventricular block. Note the excessive duration of the PR
interval (240 msec) and the normal morphology of the QRS complex.
In second-degree atrioventricular block the cardiac rhythm originates in the sinus node,
but the transmission of the depolarizing impulse from the sinus node through the
atrioventricular conduction system is interrupted intermittently. Thus, the P wave of atrial
depolarization is not always followed by a QRS complex.
Depending on the changes that occur in the PQ (PR) interval, two major types of second
degree atrioventricular block are described: Mobitz I and Mobitz II.
Mobitz I type second-degree atrioventricular block (with Wenkebachs phenomenon) occurs
when the PQ (PR) interval prolongs progressively with each beat (Figure 13) until an
electrical impulse is completely blocked by the atrioventricular node (occasionally, some P
waves are not followed by QRS complexes). The gradually increasing PQ (PR) intervals are
called Wenkebachs intervals and the process of gradual increase in PQ (PR) intervals is
called Wenkebach phenomenon.

Figure 13. Second-degree atrioventricular block type Mobitz I. Note the progressive
prolongation of the PQ interval until a P wave (arrow) is completely blocked (not followed
by a QRS complex). When present, QRS complexes have normal morphology.
Mobitz II type second-degree atrioventricular block occurs when electrical impulses coming
from the sinus node are occasionally blocked by the atrioventricular node (occasionally,
some P waves are not followed by QRS complexes), but there is no progressive
prolongation of the PQ (PR) interval. The PQ (PR) interval can be normal or prolonged, but
remains constant.
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In third-degree (complete) atrioventricular block (Figure 14), all electrical impulses arising
from the sinus node are blocked in the atrioventricular conduction system and none of
them is conducted to the ventricles (none of the P waves is followed by a QRS complex). In
the absence of an alternative pacemaker, ventricular contraction comes to a standstill and
the patient dies. However, an ectopic pacemaker below the block usually takes over
ventricular pacing, generating an escape rhythm. The lower pacemaker can be part of the
conduction system of the heart or an ectopic focus located in the ventricular wall. Since the
sinus node and the ectopic pacemaker stimulate the atria and the ventricles independently,
there will be no relationship between the P waves and the QRS complexes (situation called
atrioventricular dissociation). If the block is high in the atrioventricular node and the
ventricular pacemaker is located lower in the atrioventricular junction, then the QRS
complex is normal in width, because ventricular activation occurs via the bundle branches.
If the block is located low in the atrioventricular junction, the ventricles are paced by a
ventricular pacemaker, and the QRS complexes will be wide.

Figure 14. Third-degree (complete) atrioventricular block. Note the lack of any relationship
between the P waves (normal arrows) and the QRS complexes (dashed arrows). The atrial
rhythm is regular (PP intervals are constant), as well as the ventricular rhythm (RR intervals
are constant), but there is no relationship between the two rhythms.
5.2. Bundle branch blocks
In bundle branch blocks the conduction defect is in one of the two bundle branches. If the
two bundle branches exhibit a block simultaneously, the progress of activation from the
atria to the ventricles is completely inhibited; this is regarded as a third-degree
atrioventricular block.
In case of a bundle branch block the activation of one ventricle (the ventricle serviced by the
non-affected bundle branch) is normal, occurring through the normal conduction system of
the heart (atrioventricular node His bundle bundle branches), while the other ventricle
(the ventricle serviced by the blocked bundle branch) must await initiation from the
normally depolarized ventricle. The activation of the ventricle serviced by the blocked
bundle branch in this case is done entirely on a cell-to-cell basis and is therefore
significantly delayed compared to the activation of the non-affected ventricle. Thus, the
normal synchrony of right and left ventricular depolarization is lost.
In right bundle branch block (Figure 15) the electrical impulse cannot travel through the
right bundle branch to the right ventricle. The depolarization of the left ventricle occurs
normally, but the depolarization of the right ventricle is done on a cell-to-cell basis after the
depolarization of the left ventricle and the septal muscle mass. This progress is slower than
46

that through the conduction system so that the activation of the right ventricle is so much
delayed, that it occurs after the activation of the left ventricle.
This produces a number of abnormalities on the ECG tracing:
- QRS complexes with abnormally long duration (above the upper limit of 120 msec)
- tall, broad, and usually notched (M-shaped) R waves or rSR-shaped QRS complexes
in the right precordial leads (V1 and V2)
- deep and broad S waves in the lateral leads (I, aVL, V5, V6)
- right axis deviation due to the abnormal terminal QRS vector that is directed towards
the right ventricle (i.e., rightward and anteriorly)
- T wave inversion in the right precordial leads (V1 and V2) due to the abnormal spread
of depolarization, which alters the pattern of repolarization.

Figure 15. Right bundle branch block. Note the broad QRS complex (160 msec), with a
broad, tall, and notched R wave in lead V1, the inverted T wave in lead V1, and the deep and
broad S wave in lead V6.
In left bundle branch block (Figure 16) the electrical impulse cannot travel through the left
bundle branch to the left ventricle. The depolarization of the right ventricle occurs
normally, but the depolarization of the left ventricle is done on a cell-to-cell basis after the
depolarization of the right ventricle and the septal muscle mass. This progress is slower
than that through the conduction system so that the activation of the left ventricle is so
much delayed, that it occurs after the activation of the right ventricle.
This produces a number of abnormalities on the ECG tracing:
- QRS complexes with abnormally long duration (above the upper limit of 120 msec)
- disappearance of the normal septal q waves in the lateral leads because the
activation of the interventricular septum no longer occurs from left to right
- tall, broad, and usually notched (M-shaped) R waves in the lateral leads (I, aVL, V5,
V6)
- deep and broad S waves in the right precordial leads (V1 and V2)
- left axis deviation due to the abnormal terminal QRS vector that is directed towards
the left ventricle (i.e., leftwards and posteriorly)
- T wave inversion in the lateral leads (I, aVL, V5, V6) due to the abnormal spread of
depolarization, which alters the pattern of repolarization.

Figure 16. Left bundle branch block. Note the broad QRS complex (160 msec), with a
broad, tall, and notched R wave in lead V6, the inverted T wave in lead V6, and the deep and
broad S wave in lead V1.
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6. Myocardial hypertrophy
The term hypertrophy defines an increase in the volume of an organ or tissue due to an
increase in the size of its component cells. In contrast, an increase in the number of cells,
but with constant cell size is called hyperplasia. Dilation refers to the enlargement of a
cardiac chamber.
Hypertrophy can affect either of the two atria or of the two ventricles, separately or in
various combinations. Atrial and ventricular hypertrophy can occur as a result of pressure or
volume overload.
6.1. Atrial abnormality
Since atrial hypertrophy and atrial dilation cause similar changes on the surface ECG, the
term atrial abnormality is used to define both conditions. Signs of atrial abnormalities can
normally be found in the leads in which the P wave is most prominent: usually lead II, but
also leads III, aVF, and V1. Normally, right atrial depolarization precedes the depolarization
of the left atrium, the sum of the two generating the normal P wave on the surface ECG.
Right atrial abnormality (Figure 17, A) is a consequence of right atrial overload. In such
cases, the depolarization of the right atrium lasts longer than normal, its terminal phase
overlapping the left atrial depolarization. The amplitude of the right atrial depolarization
vector remains unchanged, but its maximal value now falls on top of that of the left atrial
depolarization vector. Thus, a number of changes will be present on the surface ECG:
- P wave taller than normal (>2.5 mm) and sharp, but with normal duration (shorter
than 100 msec). Since this characteristic tall and sharp P wave usually appears in
patients with pulmonary disorders, this P wave is called P pulmonale.
- tall, biphasic P wave in lead V1, with the initial positive portion of the biphasic P wave
(depicting right atrial depolarization) larger than the terminal negative portion
(depicting left atrial depolarization)
- right axis deviation of the P wave.
Left atrial abnormality (Figure 17, B) is the consequence of left atrial overload. Left atrial
depolarization lasts longer than normal, prolonging the total duration of atrial
depolarization, but the amplitude of the left atrial depolarization vector remains
unchanged. Thus, a number of changes will be present on the surface ECG:
- usually notched P wave, with duration longer than normal (>100 msec), but with
amplitude within the normal limits (< 2.5 mm). Since this characteristic notched and
prolonged P wave usually appears in patients with mitral valve disorders, this P wave
is called P mitrale.
- deep, biphasic P wave in lead V1, with its terminal negative deflection (depicting left
atrial depolarization) more than 40 msec wide and more than 1 mm deep
- left axis deviation of the P wave.

Figure 17. (A) Right atrial abnormality. Note the tall (3.5 mm), sharp P wave. (B) Left atrial
abnormality. Note the broad (120 msec), notched P wave (P mitrale).
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6.2. Ventricular hypertrophy

Ventricular hypertrophy is characterized by unusually tall R waves and unusually deep S
waves in the left or right precordial leads, depending on the affected ventricle (See below).
To determine the presence of ventricular hypertrophy, the Sokolov-Lyon index is calculated,
as follows:
- for the right ventricle: RV1 + SV5 = amplitude of the R wave in lead V1 + amplitude of
the S wave in lead V5 should normally be (in the absence of right ventricular
hypertrophy) 10.5 mm
- for the left ventricle: RV5 + SV1 = amplitude of the R wave in lead V5 + amplitude of
the S wave in lead V1 should normally be (in the absence of left ventricular
hypertrophy) 35 mm.
Right ventricular hypertrophy is a consequence of right ventricular overload. The increase
in the muscle mass of the right ventricle produces an increase in the ventricular electrical
forces directed towards the right ventricle (rightwards and anteriorly).
This causes a number of changes on the surface ECG:
- predominantly positive QRS complexes with unusually tall and narrow R waves in
leads V1 and V2
- unusually deep and narrow S waves in leads V5 and V6
- Sokolov-Lyon index for the right ventricle >10.5 mm
- right axis deviation
- signs of right atrial abnormality are often present because the right atrium is forced
to pump blood into a thick-wall, non-compliant, hypertrophied right ventricle
- T wave inversion in the right precordial leads (V1 and V2) due to increased oxygen
consumption by the hypertrophied ventricle causing myocardial ischemia.
Left ventricular hypertrophy (Figure 18) is the consequence of left ventricular overload.
The increase in the muscle mass of the left ventricle produces an increase in the ventricular
electrical forces directed to the left ventricle (leftwards and posteriorly).
This causes a number of changes on the surface ECG:
- predominantly negative QRS complexes with unusually deep and narrow S waves in
leads V1 and V2
- unusually tall and narrow R waves in leads V5 and V6
- Sokolov-Lyon index for the left ventricle >35 mm
- left axis deviation
- signs of left atrial abnormality are often present because the left atrium is forced to
pump blood into a thick-wall, non-compliant, hypertrophied left ventricle
- characteristic ST segment depression and T wave inversion in the lateral leads (I,
aVL, V5, V6) known as ventricular strain due to increased oxygen consumption by the
hypertrophied ventricle causing myocardial ischemia (See below).

Figure 18. Left ventricular hypertrophy. Note the tall, narrow R wave in lead V5 and the
deep, sharp S wave in lead V1. The Sokolov-Lyon index for the left ventricle is 36.5 mm.
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7. Electrocardiographic changes in coronary artery disease

Whenever there is a significant stenosis (abnormal narrowing) of one or several of the
coronary arteries, the transport of oxygen to the cardiac muscle is impaired, leading to
myocardial ischemia. Ischemia causes changes in the resting potential and in the
repolarization of muscle cells, leading to various T wave changes on the ECG (Figure 19):
- T wave inversion (negative T waves in leads where they should be positive) or
pseudonormalization (return of abnormal T waves back to the normal pattern during
an episode of myocardial ischemia)
- symmetrical T waves
- sharp-tall T waves.

Figure 19. Myocardial ischemia. Note the negative and symmetrical T waves.
More severe abnormalities in coronary circulation can lead to ECG abnormalities described
under the electrocardiographic term of lesion. These abnormalities involve ST segment
deviations. The ST segment can be:
- elevated - usually this is the ECG mark of acute myocardial infarction (See below) or
- depressed - by more than 1 mm in leads V1-V2, and/or more than 2 mm in the other
leads. The ECG term of lesion is only used for horizontal or descendent ST segment
deviations (Figure 20).

Figure 20. Three types of ST segment depression: (A) ascendant, (B) horizontal, (C)
descendent. Only the last two types correspond to the electrocardiographic term of lesion.
The complete occlusion of a coronary artery causes an acute myocardial infarction. If left
untreated, myocardial infarction usually leads to the necrosis of myocardial cells affected
by the lack of oxygen. The electrocardiographic sign of necrosis is the pathological Q wave.
The pathological Q wave is defined as a Q wave with duration of at least 0.04 sec and
amplitude of at least 1/4 of the adjacent R wave. Usually, this is the only mark that can be
seen on the ECG of a patient that has had a myocardial infarction at a certain point in
his/her life.
In acute myocardial infarction the ECG depicts five distinct consecutive phases (Figure 21),
according to the moment of ECG recording following the occlusion of the coronary artery:
- in the first phase (during the first minutes after coronary artery occlusion) T waves
become hyperacute (i.e., sharp and tall)
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- then, the ECG will show ST segment elevation - ST-segment elevation generally
occurs with reciprocal ST depression in ECG leads in which the axis is opposite in
direction from those with ST elevation
- then pathological Q waves appear
- within hours to days, an evolving myocardial infarction will typically demonstrate Twave inversion
- finally, after a peak elevation approximately 1 hour after the onset of chest pain, the
ST segment reaches a plateau at about 12 hours, and then normalizes completely
(goes back to the isoelectric line) within 2 weeks, and the T wave return to normal
(becomes positive again).

Figure 21. Evolving phases of myocardial infarction.

The typical ECG evolution of an acute myocardial infarction can be strongly influenced by
revascularization strategies, which can stop the ECG progression in any of the five phases.
These signs of myocardial infarction appear only in the leads that view the affected
territory of the heart muscle. Since different leads view the heart from different angles, the
12 ECG leads can be used to distinguish the localization of the myocardial infarction:
- ECG abnormalities in leads V1 to V6 indicate an anterior myocardial infarction
(affecting the entire territory serviced by the anterior descending artery) due to an
occlusion affecting the proximal segment of the anterior descending artery
- ECG abnormalities in leads V1 to V4 indicate an anteroseptal myocardial infarction
(affecting the anterior wall of the left ventricle and of the interventricular septum)
due to an occlusion affecting the middle segment of the anterior descending artery
- ECG abnormalities in the lateral leads (I, aVL, V5, V6) indicate a lateral myocardial
infarction (affecting the lateral wall of the left ventricle) due to an occlusion affecting
a diagonal artery (branch of the anterior descending artery), the circumflex artery, or
a marginal artery (branch of the circumflex artery)
- ECG abnormalities in the inferior leads (II, III, aVF) indicate an inferior myocardial
infarction (affecting the inferior wall of the left ventricle) due to an occlusion usually
affecting the right coronary artery or occasionally the circumflex artery.
Since none of the leads views the posterior wall of the left ventricle, in case of a posterior
myocardial infarction only a mirror image appears in leads V1-V2. To confirm the presence
of a posterior myocardial infarction the posterior leads (V7, V8, and V9) should be used
beside the standard 12 ECG leads, by placing the electrodes on the posterior chest wall.

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8. Other electrocardiographic abnormalities

8.1. Pre-excitation syndromes
Pre-excitation syndromes define the situations in which the passage of electrical impulses
from the atria to the ventricles does not occur exclusively through the normal
atrioventricular conduction system, but also directly from the atrial to the ventricular
muscle via an abnormal route (e.g., the bundle of Kent) that bypasses the atrioventricular
junction. Thus, part of the ventricular muscle is activated before normal activation reaches
it via the normal conduction system. The resulting ECG (Figure 22) depends on the specific
location of this accessory pathway, but QRS complexes are usually wider than normal and
present an early upstroke called the delta wave, and the PQ (PR) interval is shorter than
normal (below the normal limit of 120 msec).

Figure 22. Pre-excitation syndrome. Note the short PR interval (80 msec) and the presence
of the delta wave (arrow).
8.2. Cardiac pacing
Whenever the intrinsic electrical system of the heart is unable to maintain an adequate
heart rate, either because the sinus node is to slow or unable to deliver electrical impulses,
or there is a block in the heart's electrical conduction system, an artificial pacemaker can
be used to restore the normal heart rate.
Pacemakers are small electronic devices consisting of a small pulse generator, usually
implanted below the subcutaneous fat of the chest wall, above the muscles and bones of
the chest, and one or several leads that carry the electrical signals from the pulse generator
to the heart, implanted within the heart by transvenous way.
These implantable pacemakers monitor the heart's native electrical rhythm. When the
pacemaker does not detect a heartbeat within a normal beat-to-beat time period, it will
stimulate the heart with a short low-voltage pulse. These sensing and stimulating activities
continue on a beat by beat basis.
When the cardiac rhythm is stimulated by the artificial pacemaker, this can usually be
recognized on the ECG trace, due to the presence of stimulation spikes sharp, vertical
signals that represent the electrical activity of the pacemaker. The location of pacemaker
spikes in relationship with the ECG elements depicting atrial and ventricular depolarization
(P waves and QRS complexes, respectively) depends on the site of stimulation when the
pacemaker stimulates electrically the atria there will be a stimulation spike in front of the P
wave; when the pacemaker stimulates the ventricles there will be a stimulation spike in
front of the QRS complex (Figure 23); when both the atria and the ventricles are stimulated
both the P waves and the QRS complexes will be preceded by stimulation spikes.

52

Figure 23. Ventricular stimulation by an artificial pacemaker. Note the stimulation spike
preceding the broad, deformed QRS complex.
8.3. Electrolyte disorders
In case of hyperkalemia, narrow and tall T waves appear on the ECG trace (Figure 24).
Normally, it is unusual for T waves to be taller than 5 mm in the limb leads and taller than 10
mm in the chest leads. As serum potassium concentration continues to rise, PQ intervals
become longer, P waves loose amplitude and may disappear, and QRS complexes widen. If
the rise in serum potassium continues, the heart arrests in systole.

Figure 24. Electrocardiographic changes in hyperkalemia (lead V4). Note the tall (16 mm),
sharp T wave and the P wave with low amplitude (1 mm).
In case of hypokalemia the T waves flatten and may even become inverted, the ST
segment may be depressed, the QT interval widens, and prominent U waves become
visible on the ECG trace. Unlike in hyperkalemia, these additional changes are not related
to the degree of hypokalemia. If the drop in serum potassium is not corrected, severe
ventricular arrhythmias can occur.

As a general rule, whenever one has to interpret an ECG trace he/she has to correlate the
ECG findings with the patients clinical presentation. If there is a previous ECG in the
patient's file, the current ECG should be compared with it to see if any significant changes
have occurred. These changes may have important implications for clinical management
decisions.

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TEST YOUR KNOWLEDGE

1.

The pathological Q wave:

a. represents the ECG sign of necrosis
b. has an amplitude higher than 0.3 mV
c. has a duration longer than 0.04 sec
d. appears within the QRS complex after the R wave
e. may be seen in the natural evolution of myocardial infarction, if left untreated

2.

Which of the following ECG abnormalities are usually seen in a patient with left
ventricular hypertrophy?
a. duration of the QRS complex longer than 120 msec
b. amplitude of the P wave higher than 0.3 mV
c. RV1 + SV5 > 35 mm
d. left axial deviation
e. pathological Q wave

3.

Which of the following ECG abnormalities are usually seen in a patient with left atrial
abnormality?
a. irregularly spaced QRS complexes
b. PQ intervals longer than 210 msec
c. notched P waves in leads II, III, and aVF
d. P wave amplitude higher than 3 mm
e. absent P waves

4.

Which of the following statements are true regarding second-degree atrioventricular

block type Mobitz II?
a. the cardiac rhythm originates in the sinus node
b. all P waves are followed by a QRS complex
c. there is progressive prolongation of the PQ interval
d. the PQ interval is shorter than 120 msec
e. none of the above

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