ECG - A Pictorial Primer

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ECG – A Pictorial Primer: 1/44
ECG – A Pictorial Primer
Author:
David C Chung MD, FRCPC
Art work:
Nelson HM Ip
Affiliation:
The Chinese University of Hong Kong
Forward
Modern-day ECG machines can make accurate measurements and analysis. So why
bother to learn how to read an electrocardiogram? The answer is simple: A robotic
machine can follow algorithms but it takes a human mind to read beyond and
between the waveforms to make interpretation and collate it with clinical findings.
Electrocardiography can be the topic of a lifelong study. This Primer is only meant to
introduce the subject to medical students, interns, novice residents, and general
physicians in community practice. It is hoped the liberal use of diagrams and pictures
can help to improve understanding.
DC Chung
January 2008
Imagination is more important than knowledge.
Albert Einstein
Introduction
Origin of the Heart Beat and Electrocardiogram
Under physiological conditions, the sinoatrial (SA) node generates pacemaker
impulses that spread to the right and left atria, converge on the atrioventricular (AV)
node, and continue down the His bundle and
bundle branches (right bundle branch or RBB
and left bundle branch or LBB) to activate the
ventricles. Depolarization is followed by
repolarization and the sequence of
depolarization>activation-and-contraction>repo
larization repeats itself to generate rhythmical
heart beats. Under abnormal conditions, ectopic
foci in the atria, the AV junction, and the
ventricles can usurp pacing dominance from this
node and generate ectopic beats.
The wave of depolarization and repolarization
described above can be mapped on the body surface
by sensing electrodes placed on the extremities and
the chest wall. The resultant waveform traced on graph
paper is called the electrocardiogram (ECG).
The ECG Graph Paper
Horizontal axis of the ECG graph paper
represents time in milliseconds (ms) while the
vertical axis represents amplitude or voltage in
millivolts (mV). Each 1-mm-division on the
horizontal axis is 40 ms; each 5-mm-division is
200 ms. Two 5-mm-divisions on the vertical
axis are calibrated to represent 1 mV. Despite
the latter, ECG waves are commonly described
by their height in mm rather than by their
strength in mV.
The ECG Leads
The heart occupies a position in the center of the thorax and a 12-lead ECG is simply
a recording of the current flux of cardiac depolarization and repolarization obtained
from 12 different sites on the body surface.
There are six limb leads:
Lead I records from the left at a
coordinate of 0o.
Lead II records from the foot at a
coordinate of 60o.
Lead III records from the foot at
a coordinate of 120o.
Lead aVR records from the right
shoulder at a coordinate of
-150o.
Lead aVL records from the left
shoulder at a coordinate of -30o.
Lead aVF records directly from
the feet below at a coordinate of 90o.
There are also six chest leads with sensing electrodes positioned horizontally around
the left anterior hemi-thorax between the 4th and 5th interspaces:
Leads V1 and V2 record the current flux
over the right ventricle directly.
Leads V3 and V4 record directly the
electrical activities of the ventricular
septum and the anterior wall of the left
ventricle.
Leads V5 and V6 record the current flow
generated by the left ventricle directly.
Irrespective of whether it is a limb lead or chest lead, a current surging directly in the
direction of the recording electrode will cause a positive deflection on the ECG; a
current flowing in the direction but not directly toward the recording electrode will be
registered as a positive deflection of lower amplitude; a current running at right angle
to the direction of the recording electrode will cause no deflection or a biphasic
deflection; a current flowing away in a direction opposite to that of the recording
electrode will be registered as a negative deflection; and a current flowing away but
not directly will cause a negative deflection of smaller amplitude.
Waves and Intervals on the ECG
Atrial and ventricular depolarization and repolarization are
represented on the ECG as a series of waves: the P wave
followed by the QRS complex and the T wave.
The P Wave
The first deflection is the P wave associated with right and left atrial depolarization.
Wave of atrial repolarization is invisible because of low amplitude.
Normal P wave is no more than 2.5 mm (two-and-a
half 1-mm-divisions) tall and less than 120 ms
(three 1-mm-divisions) in width in any lead.
In sinus rhythm when the SA node is the pacemaker, the mean direction of atrial
depolarization (the P wave axis) points downward and to the left, in the general
direction of lead II within a coordinate between 15o and 75o and away from lead aVR.
On this count the P wave is always positive in lead II and always negative in lead aVR
during sinus rhythm. Conversely, a P wave that is positive in lead II and negative in
lead aVR indicates normal P wave axis and sinus rhythm.
The QRS Complex
The second wave is the QRS complex. Typically this complex has a series of 3
deflections that reflect the current associated with right and left ventricular
depolarization. By convention the first deflection in the complex, if it is negative, is
called a Q wave. The first positive deflection in the complex is called an R wave. A
negative deflection after an R wave is called an S wave. A second positive deflection
after the S wave, if there is one, is called the R’ wave. Some QRS complexes do not
have all three deflections. But irrespective of the number of waves present, they are
all QRS complexes:
A QRS complex with QRS deflections:
A QRS complex with QR deflections:
A QRS complex with RS deflections:
A QRS complex with only an R wave:
A QRS complex with RSR’ deflections:
A QRS complex with a QS wave:
(NB: The first wave of the last complex is a negative deflection. Therefore, it qualifies
to be called a Q wave. Since all QRS complexes have an R wave, there must be one
in this example as well, although it may be so small that it is not visible. A negative
deflection following an R wave is an S wave. Hence this single negative deflection
deserves to be called a QS wave.)
QRS duration is the width of that complex from beginning to end, irrespective of the
number of deflections present. Normally it lasts no more than 120 ms (three
1-mm-divisions).
The normal QRS axis, like the P wave axis,
points downward and to the left within a
coordinate between -30o and +90o. This
axis is said to be deviated to the left (left
axis deviation or LAD) if it lies between -30o
and -90o; and deviated to the right (right
axis deviation or RAD) if it lies between
+90o and 180o. It is either far right or far left
axis deviation if it lies between 180o and
-90o. The method of determining QRS axis
will be explained in a later section.
The ST Segment
Following the QRS complex is the ST
segment, extending from where the QRS
ends (irrespective of what the last wave
in the complex is) to where the T wave
begins. The junction between the end of
the QRS and the beginning of the ST
segment is called the J point.
ST segment reflects the current flow associated
with phase 2 of ventricular repolarization. Since
there is no current flow during this plateau phase
of repolarization, the ST segment is normally
isoelectric with the baseline.
The T Wave
The T wave represents the current of rapid phase 3 ventricular repolarization (see
diagram above). The polarity of this wave normally follows
that of the main QRS deflection in any lead. The ventricles
are electrically unstable during that period of repolarization
extending from the peak of the T wave to its initial
downslope. A stimulus (e.g. a run away heart beat called a
premature beat) falling on this vulnerable period has the potential to precipitate
ventricular fibrillation: the so call R-on-T phenomenon.
The PR Interval
The PR interval extends from the
beginning of the P wave to the beginning
of the QRS, whatever the first wave of
this complex may be. This interval
measures the time from the initial
depolarization of the atria to the initial depolarization of the ventricles and reflects a
physiological delay in AV conduction imposed by the AV node. Normal range is 120 –
200 ms (3 to 5 1-mm-divisions) and no longer.
The QT Interval
The QT interval is measured from the beginning of the QRS to the end of the T wave.
It represents the time in which the ventricles depolarize and repolarize and is a
measure of ventricular action potential (AP) duration. This interval should be
determined in the ECG lead where it is longest. Normal intervals are < 460 ms for
women and < 450 ms for men. But QT values are heart-rate dependent and can vary
from 270 ms at a heart rate of 150
beats/min to 500 ms at a heart
rate of 40 beats/min. Corrected
QT interval (QTc), obtained by
dividing the measured QT interval
by the square root of the RR
interval, can be used in place of
raw QT interval. Normal QTc is
440 ms or less.
Interpretation of the Electrocardiogram
A systematic approach to reading the 12-lead ECG should be practised so as to
avoid missing data and making mistakes. The following or similar approach is
advised:

Check these data (patient’s name, birthday, and identification number; date and
time of tracing) on the ECG to make sure:
It belongs to the patient you are reviewing.
It was obtained on the day and time you requested the examination.
Review the patient’s medical history, physical and laboratory findings, diagnosis,
and indication of the ECG examination. These pieces of information help to
focus your attention when reviewing the tracing. However, to focus attention
does not mean developing tunnel vision. You still should review all aspects of the
ECG before drawing your conclusion.
Make old tracings available for comparison. In medical practice, changes in
findings over time are as important as the presence or absence of findings at any
discrete moment in time.
Check heart rate.
Check rhythm:
Primary rhythm: supraventricular (sinus, atrial, junctional) or ventricular in
origin.
Superimposed abnormalities (escape or premature beats).
Check heart blocks.
Check QRS axis.
Check signs of clinical abnormalities:
Right and left atrial abnormalities.
Right and left ventricular hypertrophy.
Right and left bundle branch block.
Acute myocardial infarction.
Electrolyte abnormalities.
Drug effects.
Pulmonary embolism.
Correlate the ECG findings with the patient’s clinical presentation. Treat the
patient; not the waveforms.
Heart Rate
Heart rate of a normal adult patient at rest is between 60 and 100 beats/min. A heart
rate slower than 60 beats/min is called bradycardia; a heart rate faster than 100
beats/min is called tachycardia. To determine the heart rate from a recording made
by modern ECG machines is relatively simple. These machines make a 12-lead ECG
tracing over a 10-second period. One row starts with lead I, switches to aVR to be
followed by V1, and ends with V4. A second row starts with lead II and records aVL,
V2, and V5 in sequence while a third row records lead III, aVF, V3, and V6 in
sequence. Nearly all machines offer continuous recording of lead II in a fourth row
and some others offer even more. Despite lead-switching in mid-course, recording is
continuous without interruption over the 10-second period. Therefore heart rate per
minute can be determined by counting the number of beats on any one row and
multiplying this number by 6.
A second method of determining heart rate is shown below:

The heart rate is 300 beats/min when 2 consecutive QRS complexes are one
5-mm-division (200 ms) apart.
By the same token, the heart rates are 150, 100, 75, 60, and 50 beats/min when
2 consecutive QRS complexes are two, three, four, five, and six 5-mm-divisions
(400, 600, 800, 1000, 1200 ms) apart respectively.
If the distance between 2 consecutive QRS complexes does not equal to a
whole number of 5-mm-divisions, a rough estimate of the heart rate will have to
be made as shown in the tracing.
This method is particularly useful in determining heart rates at different times in a
tracing in which the rhythm is irregular:
A third method applies to single-lead rhythm strips printed from ECG monitors in
critical care areas:
These rhythm strips have 3-second marks and heart rate is a matter of multiplying the
number of QRS complexes in a 6-second period by 10. For very slow heart rates in
which there are few QRS complexes in a 6-second interval, accuracy can be
improved by multiplying the number of QRS complexes in a 12-second period by 5.
Rhythm
Normal cardiac rhythm arises from the SA node (sinus rhythm) but pacemaker
impulses can come from ectopic foci in the atria, the AV junction, and the ventricles
under abnormal conditions. When an ectopic impulse occurs singly, it generates a
beat; when the beat repeats itself, it becomes a rhythm. In addition, ectopic impulses
can arise through an escape mechanism or through prematurely. Each of these
terms is explained in the sections that follow.
Sinus Rhythm
Sinus rhythm implies that the SA node is
the pacemaker and normal sinus rhythm
(NSR) is simply sinus rhythm with heart
rate in the normal range of 60 – 100
beats/min. The P waves in sinus rhythm
have normal axis and are positive in lead
II and negative in lead aVR. The QRS
width in sinus rhythm is normal because
the ventricles are activated rapidly by
impulses conducted down the His bundle and bundle branches.
Sinus rhythm is regular with the exception of a phenomenon called sinus arrhythmia
during which there is a minimal increase in heart rate during inspiration and a minimal
decrease in heart rate during expiration. Although arrhythmia means abnormal
cardiac rhythm, sinus arrhythmia is truthfully not an abnormal rhythm.
Sinus Pause or Arrest
In disease (e.g. sick sinus syndrome) the SA node can fail in its pacing function. If
failure is brief and recovery is prompt, the result is only a missed beat (sinus pause).
If recovery is delayed and no other focus assumes pacing function, cardiac arrest
follows.
Escape rhythms
An escape beat is a heart beat arising from an ectopic focus in the atria, the AV
junction, or the ventricles when the sinus node fails in its role as a pacemaker or
when the sinus impulse fails to be conducted to the ventricles as in complete heart
block (see section on “Heart Blocks” below”). The ectopic impulse in this instance is
always late, appearing only after the next anticipated sinus beat fails to materialize. If
the sinus node failure or heart block is only brief, the ectopic focus may generate only
a single escape beat; if the sinus node failure or heart block is prolonged, the ectopic
focus produces a rhythm of escape beats to assume full pacing function. This escape
mechanism offers protection against total cardiac standstill in the event of sinus node
failure or complete heart block.
Atrial Escape
Atria escape, either in escape beat or escape rhythm, produces a P wave
that has abnormal axis and looks different from the P wave produced by
the sinus beat. However, depolarization spreads to the ventricles normally
down the AV junction, the His bundle, and bundle branches. Therefore the
QRS complex of the atrial escape beats looks exactly like the QRS
complex of the sinus beat. The inherent rate of atrial escape rhythm is
between 60 and 80 beats/min.
Junctional Escape
In junctional (AV junctional) beat or rhythm the atrial depolarization current
points cephalad and to the right, away from lead II and toward lead aVR.
Therefore the P wave, if seen, would be
negative in lead II and positive in lead aVR.
However this P wave is usually buried by
the QRS complex and not visible. On less
common occasions when the P wave is
visible, it may be either immediately before
or immediately after the QRS complex.
Since the impulse is conducted to the
ventricles via the His bundle and bundle
branches, the QRS complex of junctional beats is narrow and looks exactly
like the QRS complex of the sinus beat. The inherent rate of junctional
escape rhythm is 40 – 60 beats/min.
Conceptually the visibility and position of the P wave in junctional beat or
rhythm can be explained as follows:

If the ectopic junctional focus is in the center of the node, the
depolarization impulse has to
travel an equal distance up and
down the node to depolarize the
atria and the ventricles. Hence
activation of atria and ventricles is
simultaneous (conduction down
the His bundle and bundle branch
is very fast) and the P wave is
buried within the QRS complex.

If the ectopic focus is low down in
the AV node, ventricular activation
precedes atrial activation and the
P wave follows the QRS complex.
If the ectopic focus is high
up in the AV node, the
depolarization wave
reaches the atria before
the ventricles and atrial
activation precedes
ventricular activation. As
a result, the P wave is in
front of the QRS complex.
Ventricular Escape
In ventricular escape beat or rhythm, the depolarization wave spreads
slowly via abnormal pathway in the ventricular myocardium and not via the
His bundle and bundle branches. Therefore, the QRS complex is wide
(>120 ms) and has a shape different from that of the sinus beat.
If the ventricular escape rhythm is the result of sinus node failure, no P
wave of atrial contraction is seen as in the tracing above. If the ventricular
escape rhythm is the result of 3rd degree (complete) heart block, the sinus
node paces the atria independently and regular P waves unrelated to the
ventricular escape beats can be seen. The inherent rate of ventricular
escape rhythm is between 20 and 40 beats/min.
Premature Beats
A premature beat also arises from an ectopic pacemaker: in the atria, the AV junction,
or the ventricles. The non-sinus impulse is early, initiating a heart beat before the
next anticipated sinus beat as its name implies. The reason the ectopic focus
discharges a pacing impulse early in this instance is because the ectopic focus is
irritable and competes with the sinus node.
Atrial Premature Beat
Atrial premature beat (APB) arises from an irritable focus in one of the atria.
It depolarizes the atria prematurely (premature to the next timely sinus beat)
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
(abnormal P wave axis). Since the premature atrial impulse is conducted in
a normal fashion via the AV node, the His bundle, and the bundle branches
to depolarize the ventricles, the QRS complex associated with an APB has
normal QRS duration and the same morphology as that of the sinus beat.
Junctional Premature Beat
Junctional premature beat (JPB) arises from an irritable focus at the AV
junction. The P wave associated with atrial depolarization in this instance is
usually buried inside the QRS complex and not visible (see “Junctional
Escape” above).
However, the P wave may appear on occasions either immediately before
or immediately after the
QRS complex. When it
is visible, the P wave is
negative in lead II and
positive in lead aVR
because of retrograde
atrial depolarization.
Since the premature junctional impulse is conducted in a normal fashion
down the His bundle and bundle branches to depolarize the ventricles, the
QRS associated with JPB has normal duration and the same morphology
as that of the sinus-node generated beat.
Ventricular Premature Beat
Ventricular premature beat arises from an irritable focus in the ventricles.
Ventricular premature impulse is not transmitted to the rest of the ventricles
along the His bundle and bundle branches. It is conducted along abnormal
pathway in the ventricular myocardium. This slow process produces an
abnormally wide QRS and bizarre looking T wave. Being a
ventricle-generated beat, there is no P wave activity before the QRS
complex.
Tachycardias
If an ectopic focus discharges a premature impulse only occasionally, the result is
premature beats superimposed on the basic rhythm; if the irritable focus generates 3
premature beat repeatedly in a continuous sequence, the result is ectopic
tachycardia. The run is called non-sustained if it lasts up to 30 seconds and sustained
if longer than 30 seconds.
Tachycardias, other than sinus tachycardia, can be classified into supraventricular
tachycardia (SVT) or ventricular tachycardia (VT), depending on their site of origin.
Supraventricular Tachycardia
Tachycardias arising from an ectopic focus in the atria or AV junction are
called supraventricular tachycardias (SVT). Heart rate is faster than 150
per minute and commonly around 180 per minute. At this very fast heart
rate, the P waves of atrial contraction are buried within the waves of the
beats before irrespective of whether the tachycardia is of atrial or junctional
origin. Differentiation of the two is not possible on the surface ECG and
they are simply called paroxysmal supraventricular tachycardia (PSVT)
because of their paroxysmal (sudden) onset. Since PSVT impulses
depolarize the ventricles by passing down the His bundle and bundle
branches, the accompanying QRS complexes are of normal width and
have the same morphology as that of sinus beats.
Atrial Flutter
In atrial flutter an atrial focus activates the atria at a rate of around 300
times per minute. The baseline of the ECG becomes all P waves, giving it a
“saw tooth” appearance in one or more leads. Since it is unusual for the AV
node to conduct impulses at a rate faster than 200 per minute, AV block
occurs: commonly at a 2 to 1, 3 to 1, or 4 to 1 ratio, yielding a ventricular
response rate of 150, 100, or 75 per minute respectively. (NB: When the
ratio of P waves to QRS complex is 2:1, 3:1, or 4:1 it would be more correct
to use the term 2:1, 3:1, or 4:1 conduction rather than block. To avoid
confusion, some authors simply use the term 2:1, 3:1, or 4:1 flutter.) Since
the atrial flutter impulses depolarize the ventricles by passing down the His
bundle and bundle branches, the accompanying QRS complexes are
normal in width and have the same morphology as that of sinus beats.
Atrial Fibrillation
Atrial fibrillation is one of the most common arrhythmias in which multiple
foci in the atria depolarize rapidly and erratically at a combined rate of 400
times/min or more. Instead of generating well recognized P waves, the
atria just quiver and produce fine f waves on the ECG baseline seen in one
or more leads. The AV node is constantly bombarded by depolarization
impulses but only some of these impulses manage to get through. The
ventricular response is totally irregular without discernible pattern
(irregularly irregular) generally at a rate between 110 and 180 beats/min.
Since impulses that manage to pass through the AV node are conducted
down the His Bundle and bundle branches, the ventricles are activated
normally and their QRS complexes are normal in width and have the same
morphology as that of sinus beats.
Monomorphic Ventricular Tachycardia
Ventricular tachycardia (VT) arises from an irritable ventricular focus that
discharges premature impulses for 3 or more beats without interruption.
The rate of depolarization is 150/min or faster. Since these impulses are
conducted to the rest of the ventricles via abnormal pathway in the
ventricular myocardium and not via the His Bundle and bundle branches,
the QRS complexes are broader than normal and without distinguishable T
waves. In monomorphic VT, consecutive QRS complexes have the same
appearance.
Polymorphic Ventricular Tachycardia
In polymorphic ventricular tachycardia, there is beat-to-beat variation in the
QRS morphology. A common example is Torsades de Pointes (twisting of
the points) shown below:
Ventricular Fibrillation
Ventricular fibrillation occurs when multiple ventricular foci discharge
rapidly and chaotically. The ventricles twitch asynchronously and are not
effective as pumps. No organized QRS complexes are seen—just
disorganized oscillatory waves which can be coarse (as shown) or fine in
appearance.
Heart Blocks
Heart block refers to a pathological delay in AV conduction, either at the AV node or
beyond. Signs of heart block lie in the PR interval and P to QRS relationship.
First Degree Heart Block
In first degree heart block the cardiac rhythm is sinus in origin but the time from the
initial depolarization of the atria to the initial depolarization of the ventricles is
abnormally delayed. This pathologic delay is reflected in a PR interval longer than its
upper limit of 200 ms. Nevertheless, each P wave of atrial contraction is followed by a
QRS complex of ventricular contraction.
Second Degree Heart Block
When transmission of the depolarizing impulse from the sinus node through the AV
conduction system of the heart is interrupted intermittently, P wave of atrial
contraction is no longer followed by a QRS complex of ventricular contraction in the
interrupted beat. This is second degree heart block.
There are 2 types of second degree heart block: Mobitz type I & Mobitz type II. In
Mobitz type I block there is progressive prolongation of the PR interval, indicating
increasing delay in AV conduction, before it fails altogether. When failure in AV
conduction occurs, the P wave of atrial contraction is not followed by a QRS complex.
After this missed ventricular beat, the PR interval returns to its shorter duration and
the cycle of progressive PR prolongation and missed ventricular beat repeats itself.
In Mobitz Type II block, a non-conducted P wave not followed by a QRS complex
occurs suddenly without progressive prolongation of the PR interval. That is, the PR
interval, which can be normal or prolonged, is constant before the non-conducted
beat materializes. Mobitz type II second degree heart block indicates more serious
disease of the conduction system in regions below the AV node and can progress to
total failure of AV conduction (third degree heart block) without warning.
Third Degree Heart Block
In third degree (complete) heart block, all the SA node impulses are blocked and not
conducted to the ventricles. In the absence of an alternative pacemaker, ventricular
contraction comes to a standstill and the patient dies. But most probably an ectopic
pacemaker below the block takes over ventricular pacing and the patient survives.
Since the SA node and the ectopic pacemaker pace the atria and ventricles
independently, the P waves bear no relationship to the QRS complexes.
Two types of QRS complexes can be seen in third degree heart block:

If the block is high in the AV node and the ventricular pacemaker is located lower
in the AV junction, the QRS complex is normal in width because ventricular
activation is via the bundle branches.

If the block is low in the AV junction, the ventricles are paced by an
idioventricular pacemaker and the QRS complexes will be wider than normal
because the ventricles are no longer activated via the bundle branches.
Bundle Branch Block
This topic is covered in a later section.
QRS Axis
There are many ways to determine QRS axis. The one described below combines
simplicity and efficiency.
The limits of normal and abnormal QRS axis are
summarized in the diagram to the right.
QRS axis is the direction in which the mean QRS current
flows. The normal axis points mostly downward and to the left
because the more muscular left ventricle generates a
stronger depolarizing current that overwhelms that generated
by the less bulky right. Although both right axis deviation
(RAD) and left axis deviation (LAD) are not necessarily
associated with organic heart disease, they are seen in a
number of settings and their presence can provide added evidence to support a
clinical diagnosis.
RAD is seen in right ventricular (RV)
hypertrophy and in infarction
involving the left ventricle (LV). Right
ventricular muscle bulk is relatively
larger than that of the left in both
conditions and generates a stronger
depolarizing current in its direction.
LAD is seen, but not always, in
patients with left ventricular
hypertrophy. More commonly the
QRS axis is horizontal in this
condition.
It is only necessary to examine the QRS complexes in leads I and II to determine
whether the QRS axis in normal or deviated to the left or the right; a precise
calculation of the QRS axis is not required in clinical interpretation of the ECG.
It has been explained in a previous section that a current flowing in the direction of a
recording electrode (an ECG lead) registers a positive deflection and a current
flowing away registers a
negative deflection.
Therefore, the QRS in
lead I would be positive if
the QRS current flows in
the direction of lead I and
negative if away.
Similarly the QRS in lead
II would be positive if the QRS axis points in the direction of lead II and negative if
away.
By overlapping the two circles representing
leads I and II, it can be seen that the QRS
axis is between +90o and -30o and normal if
the QRS is positive both in lead I and lead II.
QRS axis is between -30o and -90o or
deviated to the left (left axis deviation or LAD)
if the QRS is positive in lead I but negative in
lead II.
QRS axis is between +90o and +150o or
deviated to the right (right axis deviation or
RAD) if the QRS is negative in lead I but
positive in lead II.
On occasions the QRS complexes in all 6 limb leads are biphasic, neither positive nor
negative. In these instances the QRS axis is said to be indeterminate.
In summary:
Normal QRS axis.
Left axis deviation
Right axis deviation
Right and Left Atrial Abnormalities
(NB: “Atrial abnormality” is a term being used increasingly in place of “atrial
enlargement”, “atrial dilatation” or “atrial hypertrophy”.)
Look for signs of atrial abnormalities in leads in which the P wave is most prominent:
usually lead II, but also leads III, aVF, and V1.
In sinus rhythm the right atrial
depolarization wave (brown) precedes that
of the left atrium (blue) and the combined
depolarization waves, the P wave, is less
than 120 ms wide and less than 2.5 mm
high.
In right atrial abnormality, right atrial depolarization lasts longer than normal and its
wave extends to the end of left atrial
depolarization. Although the amplitude of
the right atrial depolarization current
remains unchanged, its peak now falls on
top of that of the left atrial depolarization
wave. As a result, the combined waves of
right and left atrial depolarization, the P
wave, is taller than normal (taller than 2.5
mm) but its width remains within 120 ms.
In left atrial abnormality left atrial
depolarization lasts longer than normal but
its amplitude remains unchanged.
Therefore, the height of the resultant P
wave remains within normal limits but its
duration is longer than120 ms. A notch
(broken line) near its peak may or may not
be present.
A biphasic P wave in V1 is another sign suggesting atrial
abnormality. In right atrial abnormality, the initial positive
portion of the biphasic P wave is larger than the terminal
negative portion.
A biphasic P wave in V1, with its terminal negative deflection
more than 40 ms wide and more than 1 mm deep is another
ECG sign of left atrial abnormality.
Right and Left Ventricular Hypertrophy
Look for signs of right and left ventricular hypertrophy in the right chest leads (V1 and
V2) and left chest leads (V5 and V6).
When the ventricles are normal, the QRS complexes across the chest leads of an
ECG have these configurations:
In right chest leads V1 and V2, the QRS complexes are predominantly negative
with small R waves and relatively deep
S waves because the more muscular
left ventricle produces depolarization
current flowing away from these leads.
In left chest leads V5 and V6, the QRS
complexes are predominantly positive
with tall R waves because the more
muscular left ventricle produces net
current flowing towards these leads.
The QRS complexes in V3 and V4
reflect a transition between the right
and left chest leads. The normal
transition zone, where the R wave and
S wave are equal, is between V3 and V4. Early transition may appear in V2 while
late transition may not appear until V5 or V6.
In right ventricular hypertrophy (RVH), the configurations of the QRS complexes
across the chest leads are changed:
In V1 the QRS are positive with tall
R waves. This is because
increased right ventricular muscle
mass causes the net ventricular
depolarization current to move
towards this right chest lead. R
waves that are taller than S waves
are deep in V1 are highly
suggestive of RVH.
The S waves are unusually deep in V6 and may be even deeper than the R wave
is tall.
Other ECG signs of RVH include:
Right axis deviation due to the overpowering current generated by a
hypertrophied right ventricle.
Ventricular repolarization changes manifest as downward sloping of the ST
segment and T wave inversion, the so called ventricular strain pattern, may or
may not be present in the right chest leads. (See V1 in above ECG.)
P wave > 2.5 mm tall in lead II, III, aVF or biphasic P wave in V1 suggesting
the presence of right atrial enlargement. (Right atrial abnormality results from
the right atrium having to pump blood into a thick-wall non-compliant
hypertrophied right ventricle.)
In left ventricular hypertrophy (LVH), the configurations of the QRS complexes across
the chest leads are also changed and consist of:
Unusually tall R wave in left chest leads V5 and V6 and unusually prominent S
wave in right chest leads V1 and
V2. These are exaggerations of
the normal configurations due to
increase in left ventricular
muscle mass.
The sum of the S wave in V1
and the R wave in V5 or V6 is >
35 mm. (Tall R waves in chest
leads is common among young
and slender individuals. This
finding alone should not be
used as the only criteria of LVH.)
Additional ECG signs of LVH include:
R waves taller than 14 mm in lead I or taller than 11 mm in Lead aVL. However,
tall R waves in limb leads and chest leads do not always coexist.
Left axis deviation may or may not be present.
Repolarization abnormalities of ST segment depression and T wave inversion
suggesting ventricular strain may be present in the left chest leads with tall R
waves. (See leads V5 and V6 in above ECG.)
Signs of left atrial enlargement in leads II, III, aVF or V1 may be present. Left
atrial abnormality is the result of having to pump blood into a muscular
non-compliant left ventricle.
Bundle Branch Blocks
Look for signs of bundle branch block (BBB) in V1 and V6.
In the absence of BBB, passage of the
depolarizing impulse down the His
bundle and bundle branches is rapid and
activation of the right and left ventricles
is simultaneous and synchronous. The
individual QRS complexes of the right
and the left ventricles superimpose on
each other and produce a composite
QRS complex that is narrow in width (< 120 ms).
In BBB, irrespective of whether it is right or left, activation of the ventricles becomes
asynchronous: Depolarization of the
ventricle on the blocked side is delayed.
This delay causes the individual QRS
complex of the blocked ventricle to be
wider than normal and appear after the
individual QRS complex of the
not-blocked ventricle. As a result, the
composite QRS complex is > 120 ms
wide and has RSR’ waves: the R wave belongs to the individual QRS of the
not-blocked ventricle and the R’ wave to the individual QRS of the blocked ventricle.
The S wave between the R and R’
waves may be deep and falls below the
baseline; it may not be so deep and
causes a notch between the R and R’
waves only; or it may be hardly visible such that the QRS complex is simply a tall and
wide R wave.
In right bundle branch block (RBBB),
the widened RR’ complex is seen most
typically in V1. Secondary T wave
inversion can also be seen in this lead
because when depolarization is
abnormal repolarization can also be
expected to be abnormal. Since the
late right ventricular depolarization
current moves away from left chest
leads, it shows up as wide S waves in
V6. When there is an RR’ complex in
V1 but it is less than 120 ms wide, the condition is called incomplete right bundle
branch block.
In left bundle branch block (LBBB) the
widened RR’ complex is seen most
typically in V6. Secondary T wave
inversion is present in the left but not
right chest leads. Since the late left
ventricular depolarization current
moves away from the right chest leads,
it shows up as deep and broad S
waves in V1.
Bundle branch block or ventricular rhythm?
The QRS complexes are wider than normal in both BBB and ventricular
rhythm. But the rhythm in BBB is supraventricular in origin. There is a
one-to-one P wave to QRS relationship in BBB:
In sinus rhythm with 3rd degree heart block, there are regular P waves
that are totally asynchronous with the QRS complexes, which represent
escape rhythm from a ventricular focus.
In ventricular rhythm with sinus arrest, only wide QRS complexes are
seen and P waves are absent.
Acute Myocardial Infarction
Acute myocardial infarction (MI) affects both
ventricular depolarization (appearance of
pathological Q waves) and repolarization (ST-T
wave changes). Specific manifestations depend
on whether the lesion is subendocardial or
transmural in location.
The ECG sign of subendocardial ischemia is ST segment depression (A). Depression
is reversible if ischemia is only transient but
depression persists if ischemia is severe
enough to produce infarction. T wave
inversion with or without ST segment
depression (B) is sometimes seen but not ST
segment elevation or Q wave. That is why
subendocardial infarction is also called non-ST-elevation myocardial infarction
(NSTEMI) and less commonly non-Q wave myocardial infarction.
ST segment depression seen in subendocardial ischemia or infarction can take on
different patterns: The most typical being horizontal or down-sloping depression.
Up-sloping ST depression is less specific. In exercise stress tests, horizontal or
down-sloping depression of 1 mm or more (A, B, & C) or up-sloping depression of the
same magnitude 80 ms beyond the J point (D) is considered positive signs of
ischemia. Up-sloping depression of less than 1 mm at 80 ms beyond the J point (E) is
simply J point depression and not ST segment depression.
In transmural MI,
ischemia in the
subendocardium spreads
to the epicardium and
involves full thickness of
the myocardium. In the
acute phase, the ECG signs are ST segment elevation. The elevated ST segment
may slope upward or be horizontal or dome-shape.
Hyperacute (tall positive) T waves may
precede ST segment elevation (A) or seen
at the same time with ST elevation (B)
during this acute phase.
Hours to days later during the evolving phase, pathological Q
waves appear, the elevated ST segments return towards
baseline, and the T waves become inverted.
Q wave is normal if it is shallow and brief (A).
Q wave is pathological if it is wider than 40
ms or deeper than a third of the height of
the entire QRS complex (B & C).
Significant Q wave usually persists even
after recovery.
Localization of myocardial infarction
By way of their position, the 12 ECG leads can be used to distinguish
myocardial infarction occurring in different regions of the heart. The chest
leads cluster around the heart in the horizontal plane and look in from the
front (V1 to V4) and from the left (V5 and V6); leads I and aVL also look
in from the left while leads II, III, and aVF look in at the under surface.
Signs of anterior MI (grey area),
territory supplied by the left anterior
descending coronary artery (LAD),
are seen in V1 to V4.
Signs of lateral MI (grey
area), territory supplied by
the left circumflex coronary
artery (LC), are seen in
leads I, aVL, V5 and V6.
Signs of inferior MI (grey area),
territory supplied by the right
coronary artery (RCA), are seen in
leads II, III, and aVF.
Signs of posterior MI on a 12-lead ECG are not the characteristic ST
elevation and Q waves, which would be the case if there is a lead
recording from the patient’s back. Since V1 and V2 are attached to
the patient’s front, they will record changes reciprocal to changes
seen from the back, which are ST depression and tall R waves.
These uncharacteristic signs make the diagnosis of posterior MI
difficult without heightened vigilance. Suffice it to say, pure posterior
wall infarctions are rare. Most extend to involve the inferior wall or
lateral wall and leads II, III, and aVF should be examined for
characteristic signs of this extension in the former and leads I, aVL,
V5 and V6 in the latter.
MI in the presence of LBBB
The presence of LBBB complicates the ECG diagnosis of acute MI. This
is because LBBB alone can produce signs that may be confused with
those of infarction: deep QS waves in the right chest leads and ST
depression and T wave inversion in the left chest leads. Furthermore, the
Q wave of left ventricular MI may be buried within the widened QRS
complex. Therefore, the diagnosis of acute myocardial infarction should
be made circumspectively in the presence of pre-existing LBBB. On the
other hand, the appearance of new LBBB should be regarded as sign of
acute MI until proven otherwise.
Electrolyte Abnormalities
Hyperkalemia and Hypokalemia
Serum potassium is the major intracellular ion that participates in the
depolarization and repolarization of myocardial cells. Hence its serum
concentration has a profound effect on the QRS and ST-T complex.
Narrow and tall peaked T wave (A) is an early sign of hyperkalemia. It is
unusual for T waves to be taller than 5 mm in limb leads and taller than
10 mm in chest leads. Hyperkalemia
should be suspect if these limits are
exceeded in more than one lead. As
serum potassium concentration
continues to rise, the PR interval becomes longer, the P wave loses its
amplitude and may disappear, and the QRS complex widens (B). When
hyperkalemia is very severe, the widened QRS complexes merge with
their corresponding T waves and the resultant ECG looks like a series of
sine waves (C). If the rise in serum
potassium continues unabated, the heart
arrests in asystole. (NB: The narrow and tall
peaked T wave of hyperkalemia may be
confused with the hyper-acute T wave
occasionally seen in transmural myocardial infarction. The patient’s
presenting history and physical findings would help to differentiate the
two.)
With hypokalemia, the T wave becomes flattened
together with appearance of a prominent U wave. The
ST segment may become depressed and the T wave
inverted. Unlike hyperkalemia, these additional changes
are not related to the degree of hypokalemia.
Hypercalcemia and Hypocalcemia
ECG signs of hypercalcemia and hypocalcemia may not be obvious even
in patients who have deranged plasma
calcium concentrations that are clinically
significant. If they are present,
hypercalcemia is associated with short QT
interval (A) and hypocalcemia with long
QT interval (B). Interval shortening or lengthening is mainly in the ST
segment.
Drug Effects
Digoxin
Digoxin is a potent pro-arrhythmic drug. At therapeutic plasma level, it
causes nonspecific ST segment depression that has a scooping
appearance (A) or looks like a reversed
“9” (B). (See Case 067: Abnormal ECG at
http://www.medicine-on-line.com.) At toxic
levels, digoxin can cause virtually all kinds
of arrhythmia but particularly sinus
bradycardia, SA and AV blocks, atrial and junctional tachycardias, and
VPB and ventricular tachycardia.
Anti-arrhythmic Drugs
Quinidine, procainamide, and disopyramide (Class IA agents) prolong
the QRS duration and the QT interval with or without the appearance of
U wave and have the propensity to cause polymorphic ventricular
tachycardia (torsade de pointes).
Sotalol and amiodarone (Class III agents) can increase PR, QRS, and
QT intervals, leading to similar risks of torsade de pointes. They also
have significant beta-blocking properties, causing bradyarrhythmias.
Pulmonary Embolism
The classical ECG signs of acute pulmonary embolism are SIQIIITIII, which are
mnemonics representing deep S wave in lead I, pathological Q wave in lead III, and
inverted T wave in lead III:
Other nonspecific signs include (see ECG above):

Sinus tachycardia and atrial and ventricular ectopic beats.
Right axis deviation.
Right ventricular strain pattern with inverted T waves in right chest leads.
Incomplete or complete right bundle branch block pattern.
Slow R wave progression in chest leads
But all these ECG signs may not be present even in frank pulmonary embolism.