Shahbudin H.
Rahimtoola, MD, Section Coordinator
Abnormal ECG in
THE ECG is a record of the changing
potential of an electrical field gener-
ated by the heart and may not always
reflect accurately the electrical activ-
ity of the heart per se. The clinical
diagnosis extracted from the ECG is
based on studies correlating clinical,
anatomical, pathological, and experi-
mental findings coupled with careful,
frequently purely deductive, analysis
of numerous records. In reality,
therefore, the ECG reflects largely an
empirical body of information that
can be used, within limits, to identify
anatomical, metabolic, ionic, and he-
modynamic changes.
Despite this basic limitation, the
ECG is an extremely useful clinical
tool. It is the only practical method of
recording the electrical behavior of
the heart. It is often an independent
marker of myocardial disease and,
occasionally, the only indication of a
pathological process. Since the ECG
reflects an electrical phenomenon, it
is not surprising that it may be
normal in the presence of cardiac
abnormality and abnormal in the
This article is one of a series sponsored by the
American Heart Association.
From the Krannert Institute of Cardiology, Depart-
ment of Medicine, Indiana University School of
Medicine, and the Veterans Administration Medical
Center, Indianapolis.
Reprint requests to Department of Medicine,
Indiana University School of Medicine, Indianapolis,
IN 46202 (Dr Fisch).
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Clinically Normal Individuals
absence of cardiac disorder.
This discussion deals largely with
the abnormal ECG in the absence of
cardiac disease or extracardiac dis¬
turbance known to affect the heart
and the ECG.
The Normal ECG
Ranges of normalcy for ECG com¬
ponents should be based on an analy¬
sis of randomly selected, preferably
consecutive, routine ECGs recorded in
young persons without cardiovascular
disease. It is reasonable that only
unequivocal ECG changes should be
considered. Consideration of minor
changes such as, for example, QRS or
T-wave amplitude is often nonproduc¬
tive. Admittedly, a statistical differ¬
ence may exist between groups, but
for any one individual, the impor¬
tance of an absolute amplitude or of a
minor change from tracing to tracing
may be difficult to assess. This is true
because such variability often reflects
a normal curve of distribution and
because there is a lack of agreement
as to when a given value becomes
abnormal.
The prevalence of abnormal ECGs
was extremely low in a study of 776
consecutive patients 18 to 25 years of
age without cardiovascular disease.
The patients were admitted because
of acute psychiatric disorders. Left-
axis deviation in excess of —30 °C,
right-axis deviation greater than
Charles Fisch, MD
+120°, first-degree atrioventricular
block, right bundle-branch block, non¬
specific intraventricular conduction
defect, left ventricular hypertrophy,
atrial premature complexes and ven¬
tricular premature complexes greater
than six complexes per minute, and
Wolff-Parkinson-White syndrome
was noted in 1.4%, 2.1%, 0.3%, 0.3%,
0.1%, 0.1%, 0.7%, 0.8%, and 0.3%,
respectively.' These findings are in
agreement with observations made in
a group of 5,000 male members of the
Canadian Air Force.2 In neither series
were abnormalities of the ST seg¬
ment, left bundle-branch block, or
atrial fibrillation encountered.
An abnormal ECG in the absence of
heart disease may be the result of
faulty technique of recording, extra-
cardiac artifacts, or an abnormality
of the ECG per se.
Errors of Technique and Artifacts
Errors of Technique.—These include
application of electrode paste over the
precordium without ensuring discrete,
isolated contact for each of the pre¬
cordial electrodes, errors of lead
placement, failure to shift the switch
for aV„ to precordial V position,
improper standardization, excessive
paper speed, and incorrect mounting.
Poorly applied electrode paste
"joins" the precordial electrode sites
and may result in an abnormal record
reflecting the net or "average" of a
number of otherwise normal precor¬
dial complexes. Two common errors
of electrode placement include rever¬
sal of the left- and right-arm connec¬
tions and placement of the precordial
electrodes at the level of the second or
third rather than the appropriate
fourth interspace. The reversal of
limb leads simulates mirror-image
dextrocardia. This error can be easily
recognized because the precordial
complexes remain normal. Mirror
dextrocardia, on the other hand,
shows a gradual loss of precordial R
amplitude from right to left, simulat¬
ing clockwise rotation or, rarely, myo-
cardial infarction. When all precor¬
dial complexes are identical to the
aV„ the lead switch was not moved
from the aVF to the precordial V
position.
Availability of the standardization
signal is important for proper ECG
interpretation. Incorrect standardiza¬
tion may result in either abnormally
low or high voltage. Similarly, inspec¬
tion of the standard signal would
alert the reader to the presence of
excessive stylus inertia, which may
prove a source of serious errors of
interpretation. Stylus "drag" may
obscure low-amplitude waves such as
the Q waves, simulate intraventricu-
lar conduction delay or ST-segment
depression, and negate minor but
important ST-segment elevation. Ex¬
cessive (50 mm/s) paper speed may
lead to an erroneous diagnosis of
intra-atrial, atrioventricular, and in-
traventricular conduction delays and
QT prolongation. Recognition of inap¬
propriate paper speed should be sim¬
ple because of a uniform prolongation
of all the ECG components. Incorrect
mounting, particularly of the precor¬
dial leads, may result in an "abnor¬
mal" R-wave progression with an
erroneous diagnosis of myocardial
disease.
Artifacts.—As a rule, artifacts sim¬
ulate atrial arrhythmias. Muscle
tremor may suggest atrial fibrillation
or flutter; infusion pumps, atrial
tachycardia with block or atrial flut¬
ter. Hiccough has been mistaken for
atrial parasystole and intra-atrial
dissociation. The artifacts simulating
arrhythmias can be recognized by the
presence of a normal sinus rhythm in
some leads with an RR interval iden¬
tical to that in the leads with the
suspected artifacts.
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The Abnormal ECG
Central to any discussion of an
abnormal ECG in a normal heart is
acceptance of the fact that anatomi¬
cal and functional disorders are
excluded on the basis of clinical and
laboratory evaluation. It is probable,
however, that occasionally the ECG is
a more sensitive marker of myocar-
dial abnormality than either the clin¬
ical or laboratory evaluation. For
example, right bundle-branch block is
almost always an acquired lesion and
indicative of anatomical abnormality,
despite the fact that it is often
recorded in the absence of clinically
evident heart disease and is frequent¬
ly associated with a favorable long-
term prognosis. Despite the latter,
right bundle-branch block is rarely a
false-positive finding. The absence of
clinical evidence of organic heart dis¬
ease and a favorable prognosis are
not necessarily assurances of a nor¬
mal heart. Despite these reservations
regarding our ability to exclude heart
disease, abnormal tracings may be
recorded in patients with unequivo¬
cally normal hearts and in the
absence of extracardiac disorders ca¬
pable of affecting the heart.
The ECG abnormality in the pres¬
ence of a normal heart may be that of
the P wave, QRS complex, ST seg¬
ment, or T wave.
The P Wave.—The occasional high
amplitude of P waves in leads II, III,
and aVF, the so-called P pulmonale,
may be recorded in the absence of
cardiac abnormality.3 Abnormally tall
P waves may be seen during sinus
tachycardia or can be recorded in tall
asthénie individuals with a low dia¬
phragm and a vertical position of the
heart. Similarly, the specificity of an
abnormal left atrial P wave, "P
mitrale," for heart disease is relative¬
ly low. A falsely abnormal P wave
should be suspected in the absence of
other ECG changes indicative of
right- or left-sided heart involve¬
ment.
QRS Complex.—Abnormalities of
the QRS complex include abnormal Q
waves, usually in leads aV,, III, and
aV,; QS complex in leads V„ V2, and,
rarely, V3; tall R wave in leads V, and
V2; abnormal voltage in "left ventric¬
ular" leads I, aV,, V„, V5, and V6;
intraventricular conduction delays;
and an altered sequence of ventricu¬
lar activation.
The most common cause of an
abnormal Q wave is an unusual posi¬
tion of the heart in the thorax. An
"abnormal" Q wave in leads III and
aV, is frequently observed in obese
individuals with high diaphragms.
Similarly, a Q wave can be observed
in leads II, III, and aV, in association
with tall R waves, both the result of a
vertical position seen in asthénie indi¬
viduals with a low diaphragm. The QS
complex in leads V„ V2, and V3 can be
due to a low-lying diaphragm with a
relatively high position of the elec¬
trodes in relation to the heart, and
placement of electrodes one or two
interspaces lower will display an R
wave. Failure to register an R wave
suggests an organic cause for its
absence.
Presence of a tall R wave in V„
although suggestive of right ventricu¬
lar hypertrophy or posterior myocar-
dial infarction, may be seen in the
absence of heart disease and is most
likely positional in origin. The latter
is suggested by absence of other signs
of right ventricular hypertrophy or
myocardial infarction. Although ab¬
normally high voltage registered over
the left ventricle may indicate left
ventricular hypertrophy, the sensitiv¬
ity and specificity of voltage alone for
such a diagnosis are relatively low.
The criteria are not applicable, for
example, to individuals younger than
age 25 or to patients in other age
groups with thin chest walls.
Although the accepted upper limit
of QRS complex duration is 0.10 s,
QRS complex duration between 0.10
and 0.12 s may be seen in the absence
of heart disease, particularly in well-
developed athletic individuals.
The pattern of RR' can be recorded
in many young individuals from the
V, position and in most, if not all,
from positions to the right of V,. The
R' is a normal reflection of late
activation of the posterior septum. It
can be differentiated from incomplete
right bundle-branch block by the R'
amplitude being lower than that of
the R and especially if the R' is of
brief duration, the wave being simply
a "spike."
Abnormal left axis or axis in excess
of —30°, also referred to as left ante¬
rior divisional block or left anterior
fascicular block, is found in 1.4% of
individuals younger than 25 years
without heart disease and in a signifi-
cantly higher proportion of individu¬
als older than 70 years.14 Whether in
the young without heart disease or in
the aged reflecting an acquired ana¬
tomical disorder, abnormal left axis is
frequently registered in the absence
of clinically evident heart disease and
is often associated with a good long-
term prognosis. In essence, the prog¬
nosis of abnormal left-axis deviation
is that of the underlying heart dis¬
ease.
Atrioventricular Conduction.—The ac¬
cepted upper limit of 0.22 s for the
PR interval may be exceeded in the
absence of heart disease. Occasion¬
ally, especially in the asthénie or
athletic vagotonic individual with a
slow resting heart rate, second-degree
atrioventricular block or Wencke-
bach's type 1 block may be present.
The block usually disappears with
exercise or after administration of
atropine.
ST Segment and T Wave.—A com¬
monly encountered deviation of the
ST segment in the absence of heart
involvement is an elevation, so-called
early repolarization.56 The elevated
ST segment is usually concave, most
often present in leads II, III, and aV„
less commonly in lateral leads V4, V5,
and V6, and least commonly in leads
V„ V2, and V3. Elevation in right
1. Fisch C: The electrocardiogram in the
Cardiovasc Clin 1981;12:65-74.
2. Manning GW: Electrocardiography in selec-
tion of Royal Canadian Air Force crew. Circula-
tion 1954;10:401-412.
3. Chou T-C, Helm RA: The pseudo P pulmo-
nale. Circulation 1965;32:96-105.
Downloaded from jama.ama-assn.org by guest on April 24, 2011
ventricular leads is frequently associ¬
ated with an RR' pattern in the same
leads. The diagnosis of "early repolar-
ization" is fairly secure in the young
and especially when accompanied by
slow heart rates. In the presence of
symptoms or in older age groups,
serial tracings and clinical correla¬
tion may be essential to rule out an
organic cause for the ST-segment
elevation.
Of all the ECG abnormalities, fail¬
ure to appreciate the fact that the
T-wave inversion is not necessarily a
marker of disease is the most com¬
mon and most serious form of iatro-
genic ECG form of "heart disease."
Normal juvenile, symmetrically in¬
verted T waves in leads V„ V2, V3, and
occasionally V„ may persist into the
teens and occasionally into the 20s
and rarely into the 30s.' On the basis
of morphologic conditions alone, such
T waves cannot be differentiated from
T-wave inversion due to organic heart
disease. A correlation with available
laboratory and clinical findings may
be essential to establish the benign
nature of such T-wave changes.
In the young, usually younger than
20 years, one can record an elevated
ST segment probably due to "early
repolarization" with a terminal T-
wave inversion. The combination may
References
aged. 4. Fisch C: Theelectrocardiogram in the aged:
An independent marker of heart disease? Am J
Med 1981;70:4-6.
5. Parisi AF, Beckman CH, Lancaster MC:
The spectrum of ST-segment elevation in the
electrocardiograms of healthy adult men. J
Electrocardiol 1971;4:137-144.
give the appearance of a saddle. It is
most often recorded in leads V«, V5,
and V6 and less commonly in leads I
and aV,.
Occasionally, an isolated precordial
T-wave negativity may be a normal
variant. It may manifest, for exam¬
ple, by upright T waves in leads V,, V2,
V5, and V„ and inverted T waves in
leads V3 and V4.7
Frequently, abnormal T waves are
registered in leads V,, V2, and V, in
middle-aged women in the absence of
heart disease. The genesis of such
T-wave inversion is obscure. The T
wave is usually "shallow" and its
limbs asymetrical, in contrast to the
symetrical inversion of the T wave
when caused by ischémie heart dis¬
ease.
Conclusion
These ECG abnormalities may be
recorded in the presence of a clini¬
cally normal heart. Since the preva¬
lence of such abnormalities is rela¬
tively rare, it is prudent that these
should be viewed with suspicion and
correlated with the available clinical
and other laboratory data.
This investigation was supported in part by
the Herman C. Krannert Fund, grants HL-06308
and HL-07182 from the National Heart, Lung,
and Blood Institute, and the American Heart
Association, Indiana Affiliate, Inc.
6. Spodick DH: Differential characteristics of
the electrocardiogram in early repolarization
and acute pericarditis. N Engl J Med 1976;
295:523-526.
7. Grant RP: Clinical Electrocardiography:
The Spatial Vector Approach. New York,
McGraw-Hill Book Co, 1957, p 47.