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Official reprint from UpToDate


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ECG tutorial: Basic principles of ECG analysis

Author: Jordan M Prutkin, MD, MHS, FHRS


Section Editor: Ary L Goldberger, MD
Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: Oct 29, 2015.

INTRODUCTION Even though there continues to be new technologies developed for the
diagnostic evaluation of patients with cardiovascular disease, the electrocardiogram (ECG) retains
its central role. The ECG is the most important test for interpretation of the cardiac rhythm,
conduction system abnormalities, and for the detection of myocardial ischemia. The ECG is also of
great value in the evaluation of other types of cardiac abnormalities including valvular heart
disease, cardiomyopathy, pericarditis, and hypertensive disease. Finally, the ECG can be used to
monitor drug treatment (specifically antiarrhythmic therapy) and to detect metabolic disturbances.

A systematic approach to interpretation of the ECG is important in order to avoid overlooking


important abnormalities. Pattern recognition can be useful, but only after certain salient features
have been determined. This topic review provides the framework for a systematic analysis of the
ECG.

ECG GRID The electrocardiogram (ECG) is a plot of voltage on the vertical axis against time on
the horizontal axis. The electrodes are connected to a galvanometer that records a potential
difference. The needle (or pen) of the ECG is deflected a given distance depending upon the
voltage measured.

The ECG waves are recorded on special graph paper that is divided into 1 mm2 grid-like boxes
(figure 1). The ECG paper speed is ordinarily 25 mm/sec. As a result, each 1 mm (small)
horizontal box corresponds to 0.04 second (40 ms), with heavier lines forming larger boxes that
include five small boxes and hence represent 0.20 sec (200 ms) intervals. On occasion, the paper
speed is increased to 50 mm/sec to better define waveforms. In this situation, there are only six
leads per sheet of paper. Each large box is therefore only 0.10 sec and each small box is only
0.02 sec. In addition, the heart rate appears to be one-half of what is recorded at 25 mm/sec paper
speed, and all of the ECG intervals are twice as long as normal.

Vertically, the ECG graph measures the height (amplitude) of a given wave or deflection, as 10
mm (10 small boxes) equals 1 mV with standard calibration. On occasion, particularly when the
waveforms are small, double standard is used (20 mm equals 1 mv). When the wave forms are
very large, half standard may be used (5 mm equals 1 mv). Paper speed and voltage are usually
printed on the bottom of the ECG.

COMPLEXES AND INTERVALS The normal electrocardiogram (ECG) is composed of several


different waveforms that represent electrical events during each cardiac cycle in various parts of
the heart (figure 2). ECG waves are labeled alphabetically starting with the P wave, followed by the

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QRS complex and the ST-T-U complex (ST segment, T wave, and U wave). The J point is the
junction between the end of the QRS and the beginning of the ST segment (waveform 1).

P wave The P wave represents atrial depolarization. The normal sinus P wave demonstrates
right followed by left atrial depolarization and is an initial low amplitude positive deflection
preceding the QRS complex. The duration is generally <0.12 sec (three small boxes) and the
amplitude <0.25 mv (2.5 small boxes). Since right atrial depolarization precedes that of the left
atrium (as the sinus node is in the high right atrium), the P wave is often notched in the limb leads
and usually biphasic in lead V1. The initial positive deflection in V1 is due to right atrial
depolarization that is directed anteriorly, while the second negative deflection represents left atrial
depolarization that is directed posteriorly.

The atrial repolarization sequence (atrial ST and T wave phases) occurs just before,
simultaneously, and just after depolarization of the ventricular myocardium. The atrial "T wave"
itself is usually hidden by the QRS complex and not observed on the routine ECG. In addition, the
amplitude of the atrial T wave is often too small to be observed at standard gain. When the heart
rate is increased (eg, with sinus tachycardia) and there is enhanced sympathetic tone, the PR
interval is shortened; atrial repolarization (the atrial T wave) may sometimes then be observed at
the very end of the QRS complex, altering the J point, and resulting in J point depression with
rapidly upsloping ST segments, particularly during the first 80 msec after the QRS complex. This
finding is physiologic but may be confused with true ST depression, generating a false positive
reading. Clinically, atrial repolarization (the atrial ST phase) is most evident during acute
pericarditis, in which one often sees PR segment elevation in lead aVR and PR segment
depression in the infero-lateral leads, reflecting an atrial current of injury. The low amplitude atrial
T wave may also be unmasked in certain cases of high degree AV block, especially when the atria
are enlarged. Finally, alterations in the atrial ST segment and T wave may occur with other
pathologies, such as atrial infarction or atrial tumor invasion.

PR interval The PR interval includes the P wave as well as the PR segment. It is measured
from the beginning of the P wave to the first part of the QRS complex (which may be a Q wave or
R wave). It includes time for atrial depolarization (the P wave) and conduction through the AV node
and the His-Purkinje system (which constitute the PR segment). The length of the PR interval
changes with heart rate, but is normally 0.12 to 0.20 sec (three to five small boxes). The PR
interval is shorter at faster heart rates due to sympathetically mediated enhancement of
atrioventricular (AV) nodal conduction; it is longer when the rate is slowed as a consequence of
slower AV nodal conduction resulting from withdrawal of sympathetic tone or an increase in vagal
inputs.

QRS complex The QRS complex represents the time for ventricular depolarization.

If the initial deflection is negative, it is termed a Q wave. Small Q waves are often seen in
leads I, aVL, and V4-V6 as a result of initial septal depolarization and are considered normal.

The first positive deflection of the QRS complex is called the R wave. It represents
depolarization of the left ventricular myocardium. Right ventricular depolarization is obscured
because the left ventricular myocardial mass is much greater than that of the right ventricle.
The small R wave in lead V1 represents initial septal depolarization.

The negative deflection following the R wave is the S wave, which represents terminal
depolarization of the high lateral wall.

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If there is a second positive deflection, it is known as an R'.

Lower case letters (q, r, or s) are used for relatively small amplitude waves of less than 0.5
mV (less than 5 mm with standard calibration).

An entirely negative QRS complex is called a QS wave.

The entire QRS duration normally lasts for 0.06 to 0.10 seconds (1 to 2 small boxes) and is not
influenced by heart rate.

The R wave should progress in size across the precordial leads V1-V6. Normally there is a small R
wave in lead V1 with a deep S wave. The R wave amplitude should increase in size until V4-V6,
due to more left ventricular forces being seen, while the S wave becomes less deep. This is
termed R wave progression across the precordium.

ST segment The ST segment occurs after ventricular depolarization has ended and before
repolarization has begun. It is a time of electrocardiographic silence. The initial part of the ST
segment (the intersection of the end of the QRS complex and the beginning of the ST segment) is
termed the J point (waveform 1).

The ST segment is usually isoelectric (ie, zero potential as identified by the T-P segment) and has
a slight upward concavity. However, it may have other configurations depending upon associated
disease states (eg, ischemia, acute myocardial infarction, or pericarditis). In these situations, the
ST segment may be flattened, depressed (below the isoelectric line) with an upsloping, horizontal,
or downsloping morphology, or elevated in a concave or convex direction (above the isoelectric
line). (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "ECG
tutorial: ST and T wave changes" and "Clinical presentation and diagnostic evaluation of acute
pericarditis", section on 'Electrocardiogram'.)

In some normal cases (as with sinus tachycardia) the J point is depressed and the ST segment is
rapidly upsloping, becoming isoelectric within 0.08 seconds after the end of the QRS complex.

T wave The T wave represents the period of ventricular repolarization. Since the rate of
repolarization is slower than depolarization, the T wave is broad, has a slow upstroke, and rapidly
returns to the isoelectric line following its peak (ie, slow upstroke, rapid downstroke). Thus, the T
wave is asymmetric and the amplitude is variable. In addition, the T wave is usually smooth up and
down. If there is any irregularity on the T wave (bump, notch, rippled, nipple, etc) a superimposed
P wave should be considered.

Since depolarization begins at the endocardial surface and spreads to the epicardium, while
repolarization begins at the epicardial surface and spreads to the endocardium, the direction of
ventricular depolarization is opposite to that of ventricular repolarization. Thus, the T wave vector
on the ECG normally is in the same direction as the major deflection of the QRS. Another way of
saying this is that the QRS and T wave axes are generally concordant. Various disease states can
lead to T wave discordance. (See "ECG tutorial: ST and T wave changes".)

QT interval The QT interval consists of the QRS complex, the ST segment, and T wave. Thus,
the QT interval is primarily a measure of ventricular repolarization. The JT interval, which does not
include the QRS complex, is a more accurate measure of ventricular repolarization since it does
not include ventricular depolarization, but in most clinical situations, the QT interval is used. If the
QRS complex duration is increased, this will lead to an increase in QT interval but does not reflect

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a change in ventricular repolarization. A widened QRS, therefore, must be considered if a


prolonged QT interval is being evaluated.

The time for ventricular repolarization and therefore the QT (or JT) interval is dependent upon the
heart rate; it is shorter at faster heart rates and longer when the rate is slower. Thus, a QT interval
that is corrected for heart rate (QTc) is often calculated as follows (based on Bazett's formula):

QTc = QT interval square root of the RR interval (in sec)

Although this approach is simple, it is inaccurate at heart rate extremes and results in
overcorrecting at high rates and under correcting at low ones [1].

Another approach corrects the QT interval to the cubed root of the RR interval [1,2]. Linear and
logarithmic regression formulas have been used to predict the effect of heart rate on QT interval
[3,4]. However, because of substantial variability of the QT-RR relationship among individuals, no
formula for heart rate correction can be accurate for everyone [5,6].

The normal value for the QTc in men is 0.44 sec and in women is 0.45 to 0.46 sec. QTc values,
however, are on a bell curve and normal patients may have longer QTc values, while those with
Long QT syndrome may have shorter QT values. (See "Diagnosis of congenital long QT
syndrome".)

Since the QRS widens in the setting of a bundle branch block, the QT interval will widen. This
increase in QT interval does not reflect an abnormality of ventricular repolarization, since the
increase is due to an abnormality of depolarization. There have not been many descriptions on
how to measure QT interval in the setting of QRS widening. One study showed that the QT
increased 48.5 percent of the width of the QRS due to a left bundle branch block, and proposed a
rough formula of QTmodified = QTmeasured (QRSmeasured) to calculate the QT interval [7]. This must
be still be corrected for heart rate. Another option is to measure the JT interval, corrected for rate:
QTc QRS = JTc [8]. This equation has some limitations, as it is dependent on heart rate and as
normal values have not been derived.

U wave A U wave may be seen in some leads, especially the precordial leads V2 to V4. The
exact cause of this wave is uncertain, although it has been suggested that it represents
repolarization of the His-Purkinje system. Alternatively, some data suggest it may be from late
repolarization of the mid-myocardial M cells, due to a longer action potential duration compared
with the endocardium or epicardium, especially at slow heart rates [9].

The amplitude of the U wave is typically less than 0.2 mV and is clearly separate from the T wave.
It is more evident in some circumstances such as hypokalemia and bradycardia. The U wave may
merge with the T wave when the QT interval is prolonged (a QT-U wave), or may become very
obvious when the QT or JT interval is shortened (eg, with digoxin or hypercalcemia).

HEART RATE If the cardiac rhythm is regular, the interval between successive QRS complexes
determined from the electrocardiogram (ECG) grid can be used to determine heart rate.

The division of 300 by the number of large boxes calculates the heart rate. If the interval
between two successive complexes is one large box, then the rate is 300 beats/min (300 1
= 300 beats/min). If the interval is two large boxes, the rate is 150 (300 2 = 150 beats/min).
This calculation may be carried on down the line for each additional large box, to 100
beats/min, 75 beats/min, 60 beats/min, 50 beats/min, etc.

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Alternatively, the time between QRS complexes can be measured in seconds. This number
can be divided into 60 to derive the heart rate. For instance, if the time between two QRS
complexes is 0.75 seconds, the heart rate is 80 beats/min (60 seconds/minute 0.75
seconds/beat = 80 beats/min).

If the rhythm is irregular, the simplest way to determine the rate is by counting the number of
complexes on the ECG and multiplying by six, since the standard ECG displays 10 seconds of
time.

A rate of 60 to 100 is considered normal. A rate less than 60 is bradycardia, while a rate over 100
is tachycardia (algorithm 1A-B).

AXIS The electrical signal recorded on the electrocardiogram (ECG) contains information
relative to direction and magnitude of the various complexes. The average direction of any of the
complexes can be determined.

The normal QRS electrical axis, as established in the frontal plane, is between -30 and 90
(directed downward or inferior and to the left) in adults [10]. An axis between -30 and -90
(directed superior and to the left) is termed left axis deviation. If the axis is between 90 and 180
(directed inferior and to the right), then right axis deviation is present. An axis between -90 and
-180 (directed superior and to the right) is referred to as extreme right or left axis. If the QRS is
equiphasic in all leads with no dominant QRS deflection, it is indeterminate axis. The QRS axis
moves leftward throughout childhood and adolescence, from a normal value of 30 to 190 at birth
to 0 to 120 during ages 8 to 16 years. There is some disagreement among authors on the
definitions (in degrees) of a normal, right, and left axis. (See "Left anterior fascicular block" and
"Left posterior fascicular block".)

The QRS axis can be determined by examining all of the limb leads, but the easiest method
involves looking at leads I, II, and aVF only (figure 3).

If the QRS complex is positive (upright) in both leads I and II, then the axis falls between -30
and 90, and the axis is normal.

If the QRS complex is positive in lead I but negative in lead II, then the axis is leftward (-30 to
-90).

If the complexes are negative in lead I and positive in aVF, then the axis is rightward (90 to
180).

If the complexes are negative in both I and aVF, then the axis is extreme (180 to -90).

Another method of axis determination is to find the lead in which the complex is most isoelectric;
the axis is directed perpendicular to this lead. As an example, if the QRS is isoelectric in lead 3
which is directed at 120, then the electrical axis is either 30 or -150.

A third method is to determine the frontal lead in which the QRS is of the greatest positive
amplitude. The axis is parallel to this lead.

By combining the quadrant determined by analysis of leads I, II, and aVF with the isoelectric lead
information, one can accurately and rapidly determine the electrical axis.

The causes of right axis deviation include:

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Normal variation (vertical heart with an axis of 90)


Mechanical shifts, such as inspiration and emphysema
Right ventricular hypertrophy
Right bundle branch block
Left posterior fascicular block
Dextrocardia
Ventricular ectopic rhythms
Pre-excitation syndrome (Wolff-Parkinson-White)
Lateral wall myocardial infarction
Secundum atrial septal defect

Causes for left axis deviation include:

Normal variation (physiologic, often with age)


Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, abdominal tumor)
Left ventricular hypertrophy
Left bundle branch block
Left anterior fascicular block
Congenital heart disease (primum atrial septal defect, endocardial cushion defect)
Emphysema
Hyperkalemia
Ventricular ectopic rhythms
Pre-excitation syndromes (Wolff-Parkinson-White)
Inferior wall myocardial infarction.

The heart also has an axis in the horizontal plane, which is determined by imagining the heart as
viewed from under the diaphragm. If the axis is rotated in a clockwise direction, left ventricular
forces are directed more posteriorly and occur later in the precordial leads. This is termed poor R
wave progression and late transition. If there is counterclockwise rotation, left ventricular forces
occur earlier in the right precordial leads and this is termed early transition in which there is a tall R
wave in lead V2.

There is no agreement on how to estimate the QRS axis in patients with bundle branch block
(BBB). As the prolonged terminal part of the QRS in right bundle branch block reflects delays in
right ventricular activation, and axis determination is of importance in diagnosing fascicular
blocks, one reasonable approach is to estimate the frontal plane QRS axis based on just the first
80 to 100 ms of the QRS deflection (primarily reflecting activation of the left ventricle). For left
bundle branch block and other intraventricular conduction delays, the entire QRS can be used or
just the initial 80 to 100 ms.

APPROACH TO ECG INTERPRETATION A systematic approach to interpreting an


electrocardiogram (ECG) is essential for correct diagnosis.

Step 1: Rate Is the rate between 60 and 100? Rates less than 60 are bradycardic and greater
than 100 are tachycardic.

Step 2: Rhythm Are P waves present? Is there a P wave before every QRS complex and a
QRS complex after every P wave? Are the P waves and QRS complexes regular? Is the PR
interval constant? (See 'Rhythm analysis' below.)

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Step 3: Axis Is there left or right axis deviation? (See 'Axis' above.)

Step 4: Intervals What is the PR interval? Short PR intervals are suggestive of Wolff-
Parkinson-White syndrome. Long PR intervals are usually seen in first degree AV block, but there
may be other causes. What is the QRS interval? Long QRS intervals represent a bundle branch
block, ventricular pre-excitation, ventricular pacing, or ventricular tachycardia. What is the QT
interval? Short and long QT intervals may be present.

Step 5: P wave What is the shape and axis of the P wave? The P wave morphology should be
examined to determine if the rhythm is sinus or from another atrial location. (See 'P wave' above.)
Amplitude and duration should also be analyzed to determine left and right atrial enlargement.
(See "Normal sinus rhythm and sinus arrhythmia".)

Step 6: QRS complex Is the QRS wide? If so, examination of the morphology can determine if
there is left or right bundle branch block or pre-excitation present. In addition, increased voltage
may indicate left or right ventricular hypertrophy. Are Q waves present, suggestive of infarction?

Step 7: ST segment-T wave Is there ST elevation or depression compared to the TP


segment? The TP segment, between the T wave of one beat and the P wave of the next beat,
should be used as the baseline. Are the T waves inverted? (See "ECG tutorial: ST and T wave
changes".) Abnormalities of the ST segment or T wave may represent myocardial ischemia or
infarction, among other causes.

Step 8: Overall interpretation Only after the prior steps have been completed should an
overall interpretation and possible diagnoses be determined. This ensures assimilation of all
information in the ECG and that no detail will be overlooked.

RHYTHM ANALYSIS Interpreting the rhythm of the electrocardiogram (ECG) is sometimes


difficult. However, as for ECG interpretation in general, a systematic approach along with a
knowledge of arrhythmias often leads to a correct diagnosis. Calipers are extremely helpful for
rhythm analysis.

Step 1: Locate the P wave The most important and first step in rhythm interpretation is the
identification of P waves and an analysis of their morphology. There are several questions that
should be addressed:

Are P waves visible? Each lead needs to be examined for P waves, as they may not be
obvious in some leads. On occasion, P waves may be located on or at the end of T waves
and not obvious. They will therefore cause the T wave upslope or downstroke to no longer be
smooth. It is also important to look for P waves during any pause in the rhythm. Absence of P
waves may occur secondary to atrial fibrillation. Alternatively, P waves may be present but not
visible if they are simultaneous with and buried within the QRS complex as in a junctional
rhythm or atrioventricular (AV) nodal re-entrant tachycardia. In addition, they may be located
within the ST segment as with an AV reciprocating tachycardia or ventricular tachycardia. If a
P wave is halfway between two QRS complexes, a second P wave is often buried within the
QRS complex.

What is the rate of the P waves (ie, the PP interval)? If the rate is less than 60, then a
bradycardia is present. If the atrial or P wave rate is over 100, then a tachycardia is present. In
general, sinus tachycardia occurs at rates of 100 to 180; atrial tachycardia, AV nodal re-
entrant tachycardia, or AV reciprocating tachycardia occur at rates of 140 to 220; atrial rates
of 260 to 320 are seen with atrial flutter.

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What is the morphology and axis of the P waves? The normal sinus P wave is generally
upright in leads I, II, aVF, and V4-V6. It is negative in lead aVR. It may be negative or biphasic
in leads III and V1. A negative P wave in the inferior leads or lead I suggests an ectopic
rhythm (low atrial or left atrial respectively). Similarly, a completely positive P wave in V1
suggests a left atrial location.

Step 2: Establish the relationship between P waves and the QRS complex The next step is
to determine the relationship between the P waves and the QRS complexes, addressing the
following questions:

Are the P waves associated with QRS complexes in a 1:1 fashion? If not, are there more or
less P waves than QRS complexes and what are the atrial and ventricular rates? If there are
more P waves than QRS complexes, then some form of AV block is present, which may be
physiologic if there is a concomitant atrial tachycardia or flutter. If there are more QRS
complexes than P waves, then the rhythm is an accelerated ventricular or junctional rhythm.

Do the P waves precede each QRS complex as is the case with most normal rhythms? What
is the PR interval, and is this interval fixed?

Do P waves occur after each QRS complex (ie, retrograde P waves) as occurs in junctional or
ventricular rhythms with retrograde VA conduction, or in AV nodal reentrant or AV
reciprocating tachycardias? The RP interval should be noted and it should be established if it
is fixed or variable.

Often, establishing the relationship between the P wave and the QRS complex is the most
important diagnostic step in rhythm interpretation. (See 'Overall approach to rhythm analysis'
below and "Approach to the diagnosis of wide QRS complex tachycardias".)

Step 3: Analyze the QRS morphology If the QRS complexes are of normal duration (<0.12
sec) and morphology, then the rhythm is supraventricular. It is essential to analyze the QRS in all
12 leads to be sure that it is normal.

If the QRS is wide (ie, >0.12 sec), then the rhythm is either supraventricular with aberrant
conduction, pre-excitation, or ventricular pacing, or it is of ventricular origin. It may be possible to
differentiate them by careful inspection of the QRS morphology, especially if the QRS morphology
appears similar to the baseline QRS. (See "Approach to the diagnosis of wide QRS complex
tachycardias" and "Basic approach to delayed intraventricular conduction".)

Step 4: Search for other clues Often the diagnosis of a rhythm disturbance can be made by
clues provided by breaks in the rhythm or other irregularities in an otherwise regular rhythm. As an
example, an increase in the degree of AV block as occurs with carotid sinus massage may
unmask the flutter waves of atrial flutter.

Capture beats and fusion beats may be the clues that help establish the diagnosis of ventricular
tachycardia.

The regularity of the QRS complexes should be established by asking the following questions:

Do the QRS complexes occur with regular intervals or are they irregular?

If the complexes are irregular, is there a pattern to the irregularity? Is the rhythm regularly
irregular (ie, there is a repeating pattern of irregularity) or is the rhythm irregularly irregular
without any pattern of irregularity? At least five supraventricular rhythms are irregularly

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irregular: sinus arrhythmia (in which there is only one P wave morphology and a stable PR
interval); sinus rhythm with premature atrial contractions; sinus or other rhythm with variable
AV block; multifocal atrial rhythm (wandering atrial pacemaker) when the rate is <100 or
multifocal atrial tachycardia with a rate >100 (in which there are 3 different P wave
morphologies and PR intervals); or atrial fibrillation (in which there is no organized electrical
activity).

Step 5: Interpret the rhythm in the clinical setting Often, the clinical history, including drugs
being taken, can be helpful in establishing a diagnosis. As an example, a regular wide complex
rhythm in an older patient with a history of ischemic cardiomyopathy is most likely ventricular
tachycardia. (See "Approach to the diagnosis of wide QRS complex tachycardias".) Similarly, a
narrow complex tachycardia of sudden onset in a young person with no medical history is likely AV
nodal re-entrant or AV reciprocating tachycardia. (See "Clinical manifestations, diagnosis, and
evaluation of narrow QRS complex tachycardias".)

However, the clinical presentation and associated hemodynamic findings do not necessarily
correlate with the etiology of an abnormal rhythm. The presence of hemodynamic stability during a
tachycardia, for example, does not imply a supraventricular etiology, nor does instability mean that
the diagnosis is ventricular tachycardia. Hemodynamic changes are related to the rate of the
arrhythmia and the presence and extent of underlying heart disease.

OVERALL APPROACH TO RHYTHM ANALYSIS Approaching each new rhythm with a


methodical standard, as shown in the following algorithms, permit the correct diagnosis to be
established in most circumstances. An approach to the diagnosis of tachycardia and bradycardia
is shown (algorithm 2A-B and algorithm 1A-B). This issue is discussed in other electrocardiogram
(ECG) tutorials. (See "ECG tutorial: Ventricular arrhythmias" and "ECG tutorial: Atrial and
atrioventricular nodal (supraventricular) arrhythmias" and "ECG tutorial: Rhythms and arrhythmias
of the sinus node".)

SUMMARY The electrocardiogram (ECG) is a graphical representation (time versus amplitude


of electrical vector projection) of the electrical activity of the heart. While imperfect as a diagnostic
or prognostic tool, it contains a wealth of information necessary for the proper care of the patient
with potential cardiovascular disease.

The electrical activity of each normal cardiac cycle is represented in sequence by the P wave, the
PR interval, the QRS complex, the ST segment, the T wave, and (sometimes) the U wave. The
following pieces of information should be evaluated for each of these.

A systematic approach to interpretation of the ECG is critically important. (See 'Approach to ECG
interpretation' above.)

Rate Is the rate between 60 and 100? (See 'Step 1: Rate' above.)

Rhythm Is it normal sinus or other? (See 'Step 2: Rhythm' above.)

Axis Is there axis deviation? (See 'Step 3: Axis' above.)

Intervals Are all intervals normal? (See 'Step 4: Intervals' above.)

P wave What is its height, width, and axis? (See 'Step 5: P wave' above.)

QRS complex Are there pathologic Q waves, bundle branch block, or chamber hypertrophy?
(See 'Step 6: QRS complex' above.)

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ST-T waves Is it isoelectric, elevated, or depressed relative to the TP segment? (See 'Step
7: ST segment-T wave' above.)

Overall interpretation What is the diagnosis? (See 'Step 8: Overall interpretation' above.)

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patients with left bundle branch block. Heart Rhythm 2014; 11:2273.
8. Rautaharju PM, Zhang ZM, Prineas R, Heiss G. Assessment of prolonged QT and JT
intervals in ventricular conduction defects. Am J Cardiol 2004; 93:1017.
9. Hopenfeld B, Ashikaga H. Origin of the electrocardiographic U wave: effects of M cells and
dynamic gap junction coupling. Ann Biomed Eng 2010; 38:1060.
10. Surawicz B, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part III: intraventricular
conduction disturbances: a scientific statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the
International Society for Computerized Electrocardiology. J Am Coll Cardiol 2009; 53:976.

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GRAPHICS

Grid lines and standardization of the ECG

The electrocardiogam is recorded on paper that has large boxes (heavy lines) of
0.5 cm sides. On the horizontal axis, each large box, which represents 0.2
seconds at a typical paper speed of 25mm/sec, is divided into five smaller
boxes, each one representing 0.04 seconds. On the vertical axis, the large box
also has five subdivisions, each 1 mm in height; 10 mm equals 1 mV with
standard calibration.

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ECG complexes and intervals

ECG waves are labeled alphabetically starting with the P wave, followed by the
QRS complex, and the ST-T complex (ST segment and T wave). The J point is
the junction between the end of the QRS and the beginning of the ST segment.
The PR interval is measured from the beginning of the P wave to the first part of
the QRS complex. The QT interval consists of the QRS complex which represents
only a brief part of the interval, and the ST segment and T wave which are of
longer duration.

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J point

The J point is the junction between the end of the QRS and the beginning of the ST
segment.

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Approach to bradycardia

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Approach to tachycardia

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Calculation of frontal plane axis

If the QRS complex is positive in leads I and II, it falls between -30 and 90 and is normal, as
indicated by the yellow area. If the QRS complex is negative in I and positive in aVF, there is
right axis deviation. If the QRS complex is positive in I and negative in II, there is left axis
deviation. If the QRS complex is negative in I and aVF, there is extreme axis deviation.

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P wave before each QRS complex with constant PR relationship

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P wave in front of each QRS complex: P wave and QRS related

* P wave morphology and PR interval variable.

Graphic 52259 Version 2.0

Contributor Disclosures
Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: Boston Scientific; St.
Jude Medical [Cardiac electrophysiology (Pacemakers and ICDs)]. Ary L Goldberger,
MD Nothing to disclose Gordon M Saperia, MD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of
all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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Official reprint from UpToDate


www.uptodate.com 2017 UpToDate

ECG tutorial: Electrical components of the ECG

Author: Jordan M Prutkin, MD, MHS, FHRS


Section Editor: Ary L Goldberger, MD
Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: Jan 28, 2016.

INTRODUCTION The electrocardiogram (ECG) provides a graphic record of the electrical


activity of the heart. (See "Basic principles of electrocardiographic interpretation".) Each cardiac
cell generates an action potential as it becomes depolarized and then repolarized during a normal
cycle (movie 1). (See "Myocardial action potential and action of antiarrhythmic drugs".)

Depolarization of cardiac cells proceeds in an orderly fashion in the normal situation beginning in
the sinus node, and then spreading sequentially through the atria, atrioventricular (AV) node, and
ventricles. (See "ECG tutorial: Physiology of the conduction system".) The electrical signal spreads
through the heart as a wavefront(s) of depolarization. This wavefront(s) results in a minute
electrical field that can be detected at the body's surface as an ECG. (See "Left bundle branch
block" and "Right bundle branch block" and "ECG tutorial: Intraventricular block".) In particular, the
surface ECG records the activation and recovery signals of working myocardial cells, not of the
pacemaker cells of the SA and AV nodes, or of the specialized conduction system.

ELECTRICAL FIELDS All electrical fields have two important associated parameters:
magnitude and direction. The standard electrocardiogram (ECG) is simply a graphical
representation of the direction and magnitude of the electrical field of the heart as it changes with
time; each lead looks at this electrical field from a different angle.

One can imagine, for example, a strip of cardiac muscle that is being stimulated by an external
source. Initially, the inside of the cell is negative while the outside is relatively positive. When the
muscle is stimulated and sodium ions flow into the cell, the outside becomes negative with
reference to the inside of the cell (which is now positive). However, the section of the myocardial
membrane that has not yet become depolarized (or is in a resting state) remains positive. Thus,
this sequence establishes a dipole that has direction and magnitude (figure 1).

The direction of the dipole is simply the net direction of the positive charge relative to the negative
charge; this corresponds to the direction of the wavefront of depolarization for the muscle strip.
The magnitude of the dipole is determined by the amount of positive sodium ions that flow into the
cell (eg, how positive the inside of the cell becomes). Since the heart is a complex three-
dimensional structure consisting of millions of cells, the direction of the dipole changes with time
and is the result of a summation of all the instantaneous dipoles. At any point in time, the mean
dipole can be determined. This changing direction of the electrical impulse is the basis of
vectorcardiography.

The mean direction of the electrical field during the entire cardiac cycle is called the electrical axis.
The magnitude of the electrical field as measured by two leads is proportional to the distance

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between the electrodes and the dipole, the orientation of the electrodes to the dipole, and to the
size of the dipole. On the surface ECG, the distance between the electrodes and dipole may be
influenced by chest wall shape, presence of thoracic obesity, subcutaneous edema, pulmonary
emphysema, pericardial effusion, or other factors. The size of the dipole is predominantly related
to the mass of tissue being depolarized.

Three pairs of electrodes placed along the muscle strip will record different electric:

The first pair of electrodes are located at the site of origin of depolarization. The electrical
signal moves away from the origin at the start of depolarization; thus, a strong negative
charge is recorded. The electrode continually sees a negative charge throughout
depolarization of the strip since the dipole is constantly moving away from it until
depolarization of the muscle strip is completed, there is no further movement of an electrical
charge, and an isoelectric baseline is restored.

The second pair of electrodes records a dipole as seen from the middle of the muscle strip.
During the first half of depolarization, there is a positive electrical signal moving toward it;
thus, a continually growing upward deflection is recorded. When the dipole passes the
electrode, however, there is a sudden change from a positive to a negative deflection since
the electric charge is now moving away from the electrode. This deflection is at its most
negative magnitude immediately after the dipole passes beneath it; the magnitude of the
negative deflection subsequently decreases, returning to an isoelectric baseline at the end of
depolarization.

The third pair of electrodes, located at the end of the muscle strip, sees the electrical signal
continuously moving towards it. Thus, it records a positive deflection that increases in
magnitude as the dipole approaches it until the very end of depolarization when the potential
returns to an isoelectric baseline.

These depolarization waves, with associated positive and negative signal projections, are
recorded on the surface ECG; P waves are generated within the atrial myocardium, while QRS
complexes are generated within the ventricular myocardium. The dipole moves in the opposite
direction during repolarization, and, therefore, the deflection generated on the surface ECG is in
the opposite direction. This corresponds to the T wave, and when recorded directly from the
muscle strip its direction is opposite to that of the QRS complex. On the surface ECG, however,
the T wave is oriented in relatively the same direction (QRS-T concordance) as the QRS complex
since depolarization in the intact heart begins at the endocardium and moves towards the
epicardium, while repolarization begins at the epicardium and moves towards the endocardium.

Thus, information about the direction of the moving dipole and its magnitude (dependent upon its
proximity to the electrodes) are derived from the deflections recorded on the surface ECG. The
theoretic basis of ECG depends upon the assumptions that the heart is a single dipole generator,
the body is a homogeneous conductor, and all electrodes are equidistant from the dipole
generator. While none of the assumptions are entirely correct, they serve as the construct upon
which the science of ECG is based.

CARDIAC DEPOLARIZATION The sinus node spontaneously depolarizes, thereby initiating


the electrical cycle of the heart. (See "ECG tutorial: Physiology of the conduction system".) The
impulse spreads through the atria via specialized conduction pathways and the interatrial bundle of
Bachmann; this creates the P wave, which represents right and left atrial activation or
depolarization, and results in contraction of the atria. As the electrical signal reaches the

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atrioventricular (AV) node, the impulse is delayed (the PR segment on the electrocardiogram
[ECG]), thereby allowing the ventricles to fill via atrial contraction. The wavefront of depolarization
finally spreads via the His-Purkinje system to the ventricles, resulting in uniform ventricular
activation and contraction. QRS deflections on the ECG correspond to depolarization of the
ventricles. (See "Left bundle branch block" and "Right bundle branch block".)

At the beginning of ventricular activation, the septum is the first structure to depolarize, resulting in
a negative deflection (q wave) in leads that look from a left to right direction on the ECG (ie, Leads
I, aVL, and V5-V6). The mass of the ventricles subsequently depolarizes; a large positive
deflection (R wave) results because of the larger mass of the left ventricle compared to that of the
right ventricle. Repolarization occurs after a delay (the ST segment on the ECG), and results in the
T wave.

ECG LEADS The electrocardiogram (ECG) records the electrical field over time as it is
generated by all the cells of the heart. Instead of electrodes placed next to the muscle strip, there
are standard lead systems that record the potential generated by the heart at the body surface.
The most widely used system was developed by Willem Einthoven, the father of modern
electrocardiography, although it was modified in subsequent years. Einthoven described a system
of three bipolar leads located at the right arm, left arm, and left leg (the right leg is a ground) to
form a triangle (Einthoven's triangle). In addition to the original three bipolar leads, the standard
12-lead ECG now records three augmented limb leads and six precordial (chest) leads.

Limb leads Limb lead electrodes are placed on the arms and legs distal to the shoulders and
hips. In Einthoven's triangle, lead I records the difference between the right arm and the left arm
(impulses directed toward the left generate a positive waveform), lead II between the right arm and
left leg (impulses directed toward the leg or downward generate a positive waveform), and lead III
between the left arm and left leg (impulses directed toward the leg or downward generate a
positive waveform) (figure 2).

A "reference electrode," also called the Wilsons central terminal, is created for the augmented
leads by connecting the three limb electrodes (right arm [R], the left arm [L], and the left leg [F])
which, when summated, give zero potential (figure 3). The electrical signals for the augmented
leads are created by disconnecting the exploring electrode from the reference electrode. Put
another way, the augmented leads use a limb electrode for one electrode and the average of the
other two limb electrodes as the other electrode (ie, aVF is the difference between the left leg and
the average of right arm and left arm electrodes). The three augmented leads are designated aVR,
aVL, and aVF. Impulses directed toward the augmented lead generate a positive waveform, while
a negative waveform is generated if the impulse moves away from the lead.

The three bipolar limb leads and the three augmented limb leads can be assembled into a hexaxial
reference system:

Lead I, directed horizontally right to left, is the 0 line.


Lead II is 60
Lead III is 120
Lead aVF is 90
Lead aVL is -30
Lead aVR is -150.

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Thus, these six leads divide the heart into 30 degree sectors and view the electrical field in a
frontal plane (eg, right, left, superior, and inferior).

Precordial leads The precordial leads use the same reference electrode as the augmented
limb leads (eg, the Wilson central terminal) (figure 4). The exploring electrodes are connected to
the chest wall as follows:

V1 Fourth intercostal space to the right of the sternum


V2 Fourth intercostal space to the left of the sternum
V3 Midway between V2 and V4
V4 Fifth intercostal space at the midclavicular line
V5 Anterior axillary line at the level of V4, or halfway between V4 and V6 if the anterior
axillary line is unclear.
V6 Midaxillary line at the level of V4

Thus, these electrodes measure the electrical field in a horizontal plane (eg, right to left, anterior to
posterior).

Additional leads can be used in certain situations. As an example, right sided precordial leads
(RV1-RV6) are helpful for establishing right ventricular infarction. (See "Right ventricular
myocardial infarction".) Leads V7 (left posterior axillary line), V8 (tip of the left scapula), and V9 (to
the left of the vertebra) are useful for diagnosing a true posterior wall infarction [1].

FILTERING An electrocardiogram (ECG) is obtained analog and, in current machines, is


converted into a digital signal, where it is filtered to block out some of the noise while keeping
relevant parts of the signal. Low frequency signals such as respiration are eliminated using a
high pass filter. High frequency signals such as noncardiac muscle potentials are attenuated using
a low pass filter. Specific notch filters that eliminate electromagnetic interference at 50 to 60 Hz
may also be used.

Digital ECG data may also be compressed when sent to a database to be retrieved for later use.
Therefore, there may be a small difference in appearance of an ECG printed at the bedside versus
one downloaded from an electronic medical record [2].

SUMMARY

The electrocardiogram (ECG) provides a graphic record of the electrical activity of the heart.
Each cardiac cell generates an action potential as it becomes depolarized and then
repolarized during a normal cycle. Depolarization of cardiac cells proceeds in an orderly
fashion in the normal situation beginning in the sinus node, and then spreading sequentially
through the atria, atrioventricular (AV) node, and ventricles. (See 'Introduction' above.)

The sequential movement of electrical current with each depolarization, from the sinus node to
the entire ventricular myocardium, creates specific phases of the ECG: P wave, PR segment,
QRS complex, ST segment, and T wave. (See 'Cardiac depolarization' above.)

The electrical activity of the heart is captured by recording electrodes or leads placed on
both arms and legs (called the limb leads), and six on the chest (called the precordial leads).
The 12-lead ECG is created by simultaneously comparing electrical activity from two of these
in the following manner:

Lead I Right arm to left arm (see 'Limb leads' above)

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Lead II Right arm to left leg

Lead III Left arm to left leg

Lead aVR The average of left arm and left leg electrodes to the right arm

Lead aVL The average of the right arm and left leg electrodes to the left arm

Lead aVF The average of the right arm and left arm electrodes to the left leg

The precordial leads, V1-V6, compare electrical activity with one place on the chest to the
reference electrode. (See 'Precordial leads' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Casas RE, Marriott HJ, Glancy DL. Value of leads V7-V9 in diagnosing posterior wall acute
myocardial infarction and other causes of tall R waves in V1-V2. Am J Cardiol 1997; 80:508.
2. Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the standardization and
interpretation of the electrocardiogram: part I: the electrocardiogram and its technology a
scientific statement from the American Heart Association Electrocardiography and
Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology
Foundation; and the Heart Rhythm Society endorsed by the International Society for
Computerized Electrocardiology. J Am Coll Cardiol 2007; 49:1109.

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GRAPHICS

Electrical dipole

A dipole is created when one part of the muscle strip becomes electrically
negative relative to the rest of the muscle strip. Movement of the dipole from
negative to positive (arrow) creates an electrical field.

Graphic 53973 Version 1.0

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Bipolar limb lead system

Einthoven described a system of three bipolar leads located at the right arm, left arm, and left
leg to form a triangle. Lead I represents the potential difference between the right and left
arm; an electrical impulse moving from right to left generates a positive ECG deflection in this
lead. Lead II is the potential difference between the right arm and leg; a positive ECG
deflection occurs when the impulse direction is toward the leg. Lead III is the potential
difference between the left arm and leg; there is a positive ECG deflection when the impulse
direction is toward the leg.

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Augmented limb leads

The potential difference between the reference electrode and an exploring electrode
constitutes the augmented lead. The three exploring electrodes are the right arm
(R), the left arm (L), and the left leg (F). The electrical signals for the unipolar leads
are "augmented" by disconnecting the exploring electrode from the reference
electrode. Since the reference electrode has zero potential, the augmented potential
represents only that measured by the three electrodes. The three augmented leads
are designated aVR, aVL, and aVF. An impulse directed toward a limb lead records a
positive or upright deflection in that lead.

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Precordial chest leads V1 to V6

Similar to the unipolar leads, the reference electrode is zero potential while the
exploring electrode is attached to various locations of the anterior chest. An impulse
directed toward the exploring electrode generates a positive or upright deflection.

Graphic 63119 Version 1.0

Contributor Disclosures
Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: Boston Scientific; St.
Jude Medical [Cardiac electrophysiology (Pacemakers and ICDs)]. Ary L Goldberger,
MD Nothing to disclose Gordon M Saperia, MD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of
all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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Official reprint from UpToDate


www.uptodate.com 2017 UpToDate

ECG tutorial: Chamber enlargement and hypertrophy

Author: Jordan M Prutkin, MD, MHS, FHRS


Section Editor: Ary L Goldberger, MD
Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: May 06, 2016.

LEFT ATRIAL ABNORMALITY/ENLARGEMENT Atrial activation follows discharge of the


sinus node. Normally, activation of the right atrium occurs first, followed by left atrial activation,
sometimes leading to slight physiologic notching of the P wave. Delay of left atrial activation
(interatrial block), as may result from left atrial distension, hypertrophy, scarring, or conduction
delay, causes the P wave on the surface electrocardiogram (ECG) to become broadened and
often substantially notched, with an interpeak interval >0.04 seconds (figure 1 and waveform 1).
The voltage of the terminal portion of the P wave is increased if there is left atrial enlargement (P
mitrale), reflecting left atrial depolarization.

These ECG changes are most apparent in the inferior leads. Leads V1 and V2 show a deeply
inverted or negative portion of the P wave (reflecting left atrial activation, which is directed
posteriorly) with an area that is greater than that of the initial upright portion of the P wave
(reflecting right atrial activation, which is directed anteriorly). The negative portion of the P wave in
V1 is >1 mm wide and >1 mm deep, with normal voltage and sweep speed settings. If the P wave
in V1 is completely negative, this usually reflects left atrial abnormality, but may be normal or
indicate an ectopic atrial focus or lead malposition. In lead II, the P wave is .12 seconds. The left
atrial vector may also increase toward the left (-30 to -90) if left atrial enlargement progresses
and becomes more pronounced, resulting in a negative terminal deflection of the P wave in leads
III and aVF.

As noted below, a narrow but prominent, entirely negative P wave in lead V1 may also,
paradoxically, occur in certain cases of right atrial abnormality, especially when the right atrium is
located below the level of the V1 electrode. In such cases, tall, peaked P waves are usually seen
in the inferior leads, more typical of right atrial abnormality (P pulmonale).

The following criteria suggest left atrial enlargement/abnormality when correlated with
echocardiographic data:

Negative phase of P in V1 >0.04 sec sensitivity 83 percent; specificity 80 percent


Negative phase of P in V1 >1 mm sensitivity 60 percent; specificity 93 percent
P-terminal force >0.04 mm/sec sensitivity 69 percent; specificity 93 percent
Notched P, interpeak interval >0.04 sec sensitivity 15 percent; specificity 100 percent
P wave duration >0.11 sec sensitivity 33 percent; specificity 88 percent
P wave/PR duration >1.6 sensitivity 31 percent; specificity 64 percent

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Interatrial block Interatrial block reflects delay of conduction to the left atrium, usually at the
level of the Bachmann bundle. Diagnosis of interatrial block versus left atrial abnormality can be
difficult or impossible from the surface ECG. First degree interatrial block is recognized by a P
wave .12 sec, which is usually bimodal in leads I, II, or III. This common finding in the elderly may
be seen in those with no evidence of left atrial enlargement on imaging. So-called third degree
interatrial block is much less frequently seen. There is absent conduction through the interatrial
septum and conduction to the left atrium occurs through the coronary sinus musculature. The ECG
criteria are a P wave 0.12 sec, with a bimodal P wave in lead I and aVL and biphasic P wave
(positive then negative) in leads II, III, and aVF, and frequently also in V1-V2. Second degree
interatrial block has been defined by a pattern of changing P wave morphology from normal to
interatrial block or from first degree to third degree interatrial block.

First degree interatrial block with a prolonged P wave duration, especially with a P wave >.123
sec, has been associated with an increase in all-cause and cardiovascular mortality [1]. Third
degree interatrial block has been associated with supraventricular arrhythmias [2].

RIGHT ATRIAL ABNORMALITY/ENLARGEMENT Delayed activation of the right atrium as a


result of dilatation, hypertrophy, scarring, or a conduction abnormality leads to simultaneous
activation of the right and left atria. This synchronous electrical activity has an additive effect upon
the surface electrocardiogram, resulting in a relatively narrow P wave that is of increased
amplitude (P pulmonale) (figure 2 and waveform 2). The most common finding is a P wave >2.5
mm in lead II. In addition, a P wave >1.5 mm in V1 or V2 or a P wave that has a rightward axis
may be seen. The amplitude of the P wave may become significantly increased in the presence of
right atrial hypertrophy/overload, and it becomes peaked due to the increase in amount of
depolarized tissue. If the right atrium becomes sufficiently large, it may extend toward the left,
causing P waves in V1 to be inverted and giving the illusion of left atrial enlargement. In contrast to
left atrial abnormality or interatrial block, the P wave duration is usually normal.

LEFT VENTRICULAR HYPERTROPHY Pathologic left ventricular hypertrophy (LVH) is present


when there is substantially increased LV muscle mass associated with concentric, eccentric, or
asymmetric patterns. LVH is usually the result of an increase in systolic pressure generated by the
LV in response to increased resistance to contraction; this type of pressure load most commonly
occurs with long-standing hypertension or aortic outflow obstruction, particularly aortic stenosis.
LVH can also be due to sustained mitral or aortic regurgitation (volume loads) or to dilated
cardiomyopathies. More rarely, LVH can also be associated with other diseases such as
hypertrophic cardiomyopathy and its variants.

It takes longer for an electrical impulse to traverse the hypertrophied ventricular muscle, and the
amplitude of the impulse is increased since there is a greater muscle mass. Thus, the QRS
complex has an increased amplitude and is often slightly widened, reflecting an intraventricular
conduction delay (waveform 3). (See "Electrocardiographic diagnosis of left ventricular
hypertrophy".) The widening is primarily observed as an initial slowing in the inscription of the QRS
complex to >0.04 seconds (the time to reach the peak of the R wave is delayed); this is known as
a delay in the intrinsicoid deflection. A similar pattern of tall QRS voltage may be seen in young
people who have thin chest walls; however, in these patients, the intrinsicoid deflection is normal
and there is no hypertrophy or delay in activation or conduction.

The changes of LVH are often associated with other electrocardiographic (ECG) abnormalities,
including:

Left atrial abnormality

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Left axis deviation due to the increased mass of left ventricular muscle
ST segment and T wave abnormalities (downsloping ST segment depression and T wave
inversion)

The ST-T wave abnormalities have often been termed a "strain pattern," though are now more
frequently described as LVH with associated ST-T wave abnormalities. They probably represent
either subendocardial ischemia, which results from a relative lack of blood and oxygen supply to
the hypertrophied muscle as demand is greater than supply, or repolarization abnormalities of the
hypertrophied cardiac muscle. The changes are most frequently seen in the left lateral leads (I,
aVL, V5-6); they may also occur in the inferior leads when a vertical heart is present.

ECG criteria There have been multiple ECG criteria proposed for diagnosing LVH. The most
popular include:

Sokolow and Lyon Amplitude of S wave in lead V1 + amplitude of R wave in V5 or V6


(whichever is the tallest) 35 mm.

Cornell Amplitude of R wave in aVL + amplitude of S wave in V3 >28 mm for men, or >20
mm for women.

Roberts QRS voltage in all leads >175 to 225 mm.

Scott

Limb leads:

R in I + S in 3 more than 25 mm
R in aVL more than 11 mm or >18 mm if left axis is present
R in aVF more than 20 mm
S in aVR more than 14 mm

Chest leads:

S in V1 or V2 + R in V5 or V6 more than 35 mm
R in V5 or V6 more than 26 mm
R + S in any V lead more than 45 mm

Romhilt-Estes scoring system This index gives different weights to specific findings (table
1). A score of 5 or more indicates "definite" LVH; a score of 4 indicates "probable" LVH.

Among the most specific (although not sensitive) criterion is the amplitude of the R wave in lead
aVL; LVH is present when this is greater than 11 mm (or 18 mm in the presence of left axis
deviation).

RIGHT VENTRICULAR HYPERTROPHY Right ventricular hypertrophy (RVH) is present when


there is a pathologic increase in muscle mass of the right ventricle. This may be seen with
pulmonary hypertension, pulmonic stenosis, or severe lung disease and cor pulmonale. There are
multiple criteria for the diagnosis of RVH that have been proposed [3]. However, no one set of
criteria has sufficiently high sensitivity and specificity to allow it to be used to screen for RVH [4].

The RV forces become predominant in patients with RVH (especially due to a pressure load as
with pulmonic outflow obstruction or severe pulmonary hypertension), producing tall R waves in
the right precordial leads (V1 and V2), and deep S waves in the left precordial leads (V5 and V6)

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(waveform 4). Because of the increase in the amplitude of the R wave and decrease in the depth
of the S wave, the R:S ratio in V1 >1 is suggestive of RVH. However, there are other causes of an
increased R:S ratio in adults that must be excluded before a diagnosis of RVH can be definitively
established (table 2):

Right bundle branch block


Posterior wall myocardial infarction
Wolff-Parkinson-White pattern (especially due to lateral or poster-lateral left ventricular pre-
excitation)
Hypertrophic cardiomyopathy (septal hypertrophy)
Early precordial transition (counterclockwise rotation)
Normal or positional variant

Obtaining an R:S ratio >1 from a right sided precordial lead (V3R or V4R) may be a more reliable
indicator of RVH.

Right axis deviation (axis >+90-100) is often present with RVH. There also may be associated
right atrial overload and ST segment and T wave abnormalities in the right precordial leads
(formerly called RV strain), reflecting subendocardial ischemia or repolarization abnormalities of
the right ventricular myocardium.

Thus, reported clues to the diagnosis of right ventricular hypertrophy include:

Right axis deviation (>+90)


R in V1 >6 mm
R in V1 + S in V5 or V6 >10.5 mm
R/S ratio in V1 >1
S/R ratio in V6 >1
Late intrinsicoid deflection in V1 (>0.035 sec)
Incomplete right bundle branch block
ST-T wave abnormalities ("strain") in inferior leads
Right atrial hypertrophy/overload (P pulmonale)
S>R in leads I, II, III, particularly in children (S1S2S3 pattern)

Clinicians should also be aware that apparent limitations in the accuracy of RVH criteria, and
conflicting results in the literature, may reflect the fact that different pathophysiologic substrates
give rise to very different ECG findings. Tall (normal duration) right precordial R waves (as part of
R, RS, or qR morphologies) with right axis deviation, as noted above, are most likely to be
associated with severe RV pressure overloads due to pulmonic stenosis (and its variants) or
pulmonary hypertension from causes other than chronic obstructive pulmonary disease (COPD)
(eg, primary pulmonary hypertension or recurrent pulmonary emboli). Pulmonary hypertension due
to severe COPD (emphysema) may be associated with very slow R wave progression, delayed
precordial transition zone, and right axis deviation. In contrast, RVH due to a classic volume load
state (eg, ostium secundum atrial septal defect) may be associated with RV conduction delay and
right axis deviation.

BIVENTRICULAR HYPERTROPHY Biventricular hypertrophy is suggested on the


electrocardiogram if there are voltage criteria for left ventricular hypertrophy, combined with right
axis deviation, prominent R wave in V1-V2, prominent S wave in V5-6, tall biphasic R/S

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complexes, and/or right atrial abnormality (waveform 5). In some cases, there will be evidence of
left atrial enlargement or tall R wave and deep S waves in V2-V4 (>60mm combined) combined
with criteria diagnostic of right ventricular hypertrophy, including R/S ratio >1 in V1-V2 or S/R ratio
>1 in V5-V6, a deep S wave in V5-V6, or right axis deviation. The latter may also be seen with
mitral stenosis.

SUMMARY

There is no single best electrocardiographic (ECG) criterion for diagnosis of hypertrophy of


any of the cardiac chambers. Several different sets of criteria have been used with various
sensitivities and specificities.

Left atrial abnormality/enlargement is characterized by P waves that are broad and often
notched, with an interpeak interval >0.04 seconds (figure 1 and waveform 1). The voltage of
the terminal portion of the P wave may be increased, especially if there is left atrial
enlargement (classical P mitrale), reflecting left atrial depolarization. These ECG changes
are most apparent in the inferior leads and V1. (See 'Left atrial abnormality/enlargement'
above.)

Right atrial abnormality/enlargement is characterized by P waves that are relatively narrow but
of increased amplitude (classic P pulmonale) (figure 2 and waveform 2). (See 'Right atrial
abnormality/enlargement' above.)

Left ventricular hypertrophy is characterized by the QRS complex having increased amplitude
and usually slight widening, reflecting an intraventricular conduction delay (waveform 3).
There are often associated ST segment and T wave abnormalities. Evidence of left atrial
abnormality and left axis deviation is commonly seen. (See 'Left ventricular hypertrophy'
above.)

Right ventricular hypertrophy, especially due to right ventricular pressure loads from pulmonic
stenosis or pulmonary hypertension not due to chronic obstructive pulmonary disease, may be
characterized by an increase in the amplitude of the R wave and a decrease in the depth of
the S wave in the right precordial leads, causing an increase in the R:S ratio (waveform 4)
usually with a vertical or frankly rightward QRS axis. Evidence of right atrial abnormality may
be present. (See 'Right ventricular hypertrophy' above.)

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REFERENCES

1. Bays de Luna A, Platonov P, Cosio FG, et al. Interatrial blocks. A separate entity from left
atrial enlargement: a consensus report. J Electrocardiol 2012; 45:445.
2. Magnani JW, Gorodeski EZ, Johnson VM, et al. P wave duration is associated with
cardiovascular and all-cause mortality outcomes: the National Health and Nutrition
Examination Survey. Heart Rhythm 2011; 8:93.
3. Hancock EW, Deal BJ, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part V: electrocardiogram
changes associated with cardiac chamber hypertrophy: a scientific statement from the
American Heart Association Electrocardiography and Arrhythmias Committee, Council on

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Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm
Society: endorsed by the International Society for Computerized Electrocardiology.
Circulation 2009; 119:e251.
4. Whitman IR, Patel VV, Soliman EZ, et al. Validity of the surface electrocardiogram criteria for
right ventricular hypertrophy: the MESA-RV Study (Multi-Ethnic Study of Atherosclerosis-
Right Ventricle). J Am Coll Cardiol 2014; 63:672.

Topic 2123 Version 11.0

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GRAPHICS

Left atrial enlargement

The left panel shows the normal pattern of atrial activation as it would appear on
lead II of the electrocardiogram; activation of the right atrium (RA) occurs first,
followed by left atrial (LA) activation. The right panel shows the pattern in a
patient with left atrial enlargement. Delay of left atrial activation causes notching
and a prolonged duration of the P wave, and the presence of left atrial
hypertrophy results in increased P wave amplitude.

Graphic 79437 Version 1.0

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Left atrial enlargement

The P wave in lead II is broad and substantially notched, while V1 reveals a


deeply inverted (negative) P wave.

Graphic 52162 Version 2.0

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Right atrial enlargement

The left panel shows the normal pattern of atrial activation as it would appear on lead
II of the electrocardiogram: activation of the right atrium (RA) occurs first, followed by
left atrial (LA) activation. The right panel shows the pattern in a patient with right
atrial enlargement: delayed activation of the right atrium, due to dilatation,
hypertrophy, scarring, or a conduction abnormality, results in simultaneous activation
of the right and left atria. The synchronous electrical activity has an additive effect
upon the surface ECG, resulting in a relatively narrow P wave which is of increased
amplitude (P pulmonale). The amplitude of the P wave may become significantly
increased in the presence of right atrial hypertrophy; it also becomes peaked due to
the increase in amount of depolarized tissue.

Graphic 63181 Version 1.0

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Electrocardigram showing right atrial enlargement

Delayed activation of an enlarged right atrium leads to simultaneous activation


of the right and left atria; this results in a relatively narrow P wave which is of
increased amplitude.

Graphic 78126 Version 3.0

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Left ventricular hypertrophy

The electrocardiogram demonstrates a number of features of left ventricular hypertrophy


(LVH). The QRS complex is slightly widened (about 0.11 sec), the frontal plane axis is
leftward, tall R waves are present in multiple leads, and ST-T changes (formerly called a
"strain" pattern) are present. The somewhat prominent P waves also raise consideration of left
atrial abnormality. Slow R wave progression (V1-V3) is non-specific and may be seen with
LVH, or with multiple other factors. Underlying anteroseptal MI is not excluded.

Graphic 69040 Version 4.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Romhilt-Estes point score system for ECG diagnosis of LVH

Criterion Points

Any limb R wave or S wave 2.0 mV (20 mm) 3

OR S in V1 or S in V2 3.0 mV (30 mm)

OR R in V5 or R in V6 3.0 mV (30 mm)

ST-T wave changes typical of LVH

Taking digitalis 1

Not taking digitalis 3

Left atrial abnormality

P terminal force in V1 is 1 mm or more in depth with a duration 40 ms (0.04 sec) 3

Left axis deviation 30 2

QRS duration 90 ms 1

Intrinsicoid deflection in V5 or V6 50 ms (0.05 sec)* 1

A score of 5 or more indicates "definite" LVH; a score of 4 indicates "probable" LVH.

* Intrinsicoid deflection is defined as interval between beginning of QRS interval and the peak of the R wave.

Graphic 51012 Version 3.0

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Right ventricular hypertrophy

The right ventricular forces become predominant in patients with right ventricular
hypertrophy (RVH), producing tall R waves in the right precordial leads (V1 and V2), and
deep S waves in the left precordial leads (V5 and V6); a R:S ratio >1 in V1 and V2 is
suggestive of RVH. Other features in this case include right axis deviation and RV1 >7 mm.

Graphic 63763 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Causes and diagnosis of tall R waves in V1

Diagnosis Confirmatory clues

True posterior infarct ST , T in V1-V2; Q waves and ST V7-V9

Right ventricular hypertrophy RAD; RAE; secondary ST-Ts; V7-V9 normal

Ventricular septal Associated Q waves; LVH; V7-V9 normal or deep narrow Q waves
hypertrophy

Right bundle branch block Wide QRS; broad S in V1, V6; R peaks late in V1; V7-V9 normal or
broad S waves

Wolff-Parkinson-White Short PR; delta wave; V7-V9 normal or delta wave


syndrome

Normal variant No other abnormalities

LVH: left ventricular hypertrophy; RAD: right-axis deviation; RAE: right atrial enlargement.

Graphic 72039 Version 2.0

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Combined ventricular hypertrophy

This ECG satisfies voltage criteria for left ventricular hypertrophy (S in V2 + R in V5 >35
mm), combined with a prominent R wave in V1 and right axis deviation (suggestive of
right ventricular hypertrophy).

Graphic 75570 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

Contributor Disclosures
Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: Boston Scientific; St.
Jude Medical [Cardiac electrophysiology (Pacemakers and ICDs)]. Ary L Goldberger,
MD Nothing to disclose Gordon M Saperia, MD, FACC Nothing to disclose

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Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of
all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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Official reprint from UpToDate


www.uptodate.com 2017 UpToDate

ECG tutorial: Myocardial ischemia and infarction

Author: Jordan M Prutkin, MD, MHS, FHRS


Section Editor: Ary L Goldberger, MD
Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: Mar 08, 2016.

INTRODUCTION The electrocardiogram (ECG) is an important test used in the clinical


evaluation of patients with suspected or known myocardial ischemia or myocardial infarction (MI).
In order to recognize abnormalities that suggest ischemia or infarction, it is important to
understand the components of a normal ECG. (See "ECG tutorial: Basic principles of ECG
analysis".)

In patients with myocardial ischemia or infarction, findings on the ECG are influenced by multiple
factors, including the following:

Duration Hyperacute/acute versus evolving/chronic


Size Amount of myocardium affected
Anatomic location Anterior, lateral, or inferior-posterior
Baseline (prior) electrocardiographic abnormalities

For the purpose of this topic, ECG evidence of ischemia refers to abnormalities (which are
sometimes referred to as changes) that are reversible once ischemia of the myocardium is no
longer present. ECG evidence of infarction refers to abnormalities that are likely permanent and
represent myocardial tissue that has been infarcted. This topic will present the classic ECG
abnormalities seen with acute myocardial ischemia and infarction. It needs to be kept in mind that
not all patients with ischemia or infarction will manifest all of the possible abnormalities and some
patients may have none.

It should also be emphasized that the ECG can only suggest an acute or evolving MI. The
accepted definition requires the detection of a rise and/or fall of cardiac biomarker values. (See
"Criteria for the diagnosis of acute myocardial infarction", section on 'Third universal definition of
MI'.)

ELECTROPHYSIOLOGIC BASIS OF ST-SEGMENT DEVIATION Under normal conditions, the


ST-segment is relatively isoelectric (ie, flat along the baseline), because healthy myocardial cells
attain about the same potential during the plateau phase of repolarization, that is, during phase 2
of the cardiac action potential. Ischemia has complex time-dependent effects on the electrical
properties of the affected myocardial cells [1,2]. Severe, acute ischemia lowers the resting
membrane potential (that is, makes it less negative, inside relative to outside charge), shortens the
duration of the action potential, and changes the shape of the plateau (phase 2) of the action
potential in the ischemic area. These changes create a voltage gradient between normal and
ischemic zones, leading to current flow between these regions during both systolic (due to

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changes in the shape of the action potential) and diastolic (due to changes in the resting
membrane potential) portions of the cardiac cycle. These electrophysiologic fluxes, referred to as
currents of injury, are represented on the surface electrocardiogram (ECG) by deviations of the
ST segment from the isoelectric (TP) baseline. The polarity and magnitude of these changes
depend upon the location and the severity of the ischemic insult.

Although ST segment deviation in acute myocardial infarction (MI) is often referred to as a "current
of injury," we will use the terms "ischemia" and "infarction" in this discussion and do not define
"injury" as a separate category of ECG changes.

When acute ischemia is severe (usually transmural), the ST vector is shifted in the direction of the
outer (epicardial and subepicardial) layers, producing ST elevations and sometimes tall positive (or
hyperacute) T waves over the ischemic zone. The shift in the ST vector is due, at least in part, to
ischemia-induced shortening of the action potential duration. This pathologic early (accelerated)
repolarization causes the outside surface of ischemic cells to become positively charged relative to
nonischemic cells, which are still in a depolarized state (negative charge outside). The ECG is
configured such that the ST vector always points away from electronegative and toward positive
zones. In the setting described here, the ST vector will be directed toward the epicardium to
produce ST segment elevation.

A so-called "diastolic current of injury" due to a lower (ie, more positive) myocardial membrane
resting potential may also contribute to the appearance of ST elevation on the ECG. The ECG
vector created by this voltage gradient will be directed away from the epicardium to produce the
equivalent of TP segment depression. Because the clinical ECG is recorded with capacitor
coupled (AC) amplifiers and the TP segment is used as the isoelectric baseline for measuring the
other portions of the ECG waveform, this TP segment depression is not actually observed. Rather,
lowering the baseline creates the appearance of greater ST-segment elevation. Thus, the
observed ST elevation is due to both real ST elevation due to systolic currents of injury and
apparent elevation of the ST segment due to TP diastolic injury currents.

When ischemia is confined primarily to the subendocardium (as during a positive exercise stress
test in patients with coronary artery disease), the systolic ST vector typically shifts toward the inner
ventricular layer and the ventricular cavity, while the diastolic injury vector points toward the
epicardium, that is, the opposite of the directions observed with transmural (epicardial) ischemia.
Thus, the overlying (eg, anterior precordial) leads show ST segment depression with ST elevation
in lead aVR (attributed to potentials that would be recorded in the ventricular cavity) (waveform 1).

Clinicians should also be aware that severe ischemia due to left main stenosis or occlusion may
cause the ST vector to deviate toward the base of the ventricles, causing ST elevations in lead
aVR and V1, in concert with ST depressions in multiple other leads. This set of findings also
illustrates an important limitation in the clinical parlance that associates pathologic ST elevations or
ST depressions with pure transmural or subendocardial ischemia, respectively. (See "ECG tutorial:
ST and T wave changes".)

ACUTE MYOCARDIAL ISCHEMIA AND INFARCTION Myocardial ischemia precedes acute


myocardial infarction (MI) in all patients but not all patients with myocardial ischemia develop MI.
The electrocardiogram (ECG), which is capable of detecting ischemia and infarction, evolves
through sequential abnormalities (changes) in the transition from ischemia to infarction. ECG
evidence of myocardial ischemia includes new ST-segment elevation or depression or the
development of hyperacute T waves or T wave inversion (in leads in which they were previously
upright). ST and T (ST-T) wave abnormalities suggestive of myocardial ischemia may be present

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in many leads; more commonly, they are localized, although they do not always correlate with the
involved region of the myocardium. (See "Electrocardiogram in the diagnosis of myocardial
ischemia and infarction".)

T wave changes Isolated T wave changes in the absence of ST changes are less frequently
seen with acute ischemia, except for the presence of symmetrically-inverted T waves after an
episode of clinical ischemia (Wellens sign), which suggests proximal left anterior descending
stenosis. (See 'Post-ischemic T wave inversions' below.) T wave inversions are defined as 0.1
mV in two contiguous leads.

ST-segment depression ST depression is defined by a horizontal or down-sloping ST-


segment that is depressed 0.05 mV below the baseline, measured at 0.08 seconds after the J
point, in two contiguous leads (waveform 2). The TP segment should be used as the baseline, and
the PR interval used only if there is no obvious TP-segment. The strongest correlation with
ischemia is with a downsloping or horizontal ST-segment depression. Upsloping ST-segment
depression has a weaker correlation, as this type of ST-segment depression may be seen as a
normal change with sinus tachycardia.

ST-segment elevation To be considered pathologic, the ST elevation, measured at the J point,


must be 0.1 mV, except for leads V2 to V3, where it needs to be 0.2 mV in men 40 years,
0.25 mV in men <40 years, and 0.15 mV in women [3]. ST-segment elevation can be caused by
states other than myocardial ischemia however. (See "ECG tutorial: ST and T wave changes".)
Furthermore, not all ischemic events cause ST deviations exceeding these thresholds.

ST-segment elevation, associated with epicardial coronary vasospasm or actual occlusion, is a


relatively specific sign of acute transmural ischemia. ST-T wave abnormalities that are suggestive
of acute myocardial ischemia in the earliest phase of ST elevation MI are usually localized to those
leads that reflect the involved regions of the myocardium:

V1-V2 Anteroseptal
V3-V4 Anteroapical
V5-V6 Anterolateral
I, aVL Lateral
II, III, aVF Inferior

Location of ECG changes It should be emphasized that these are ECG terms that do not
necessarily correspond to exact anatomic location of the infarction as determined by imaging
studies or postmortem examination. (See "Electrocardiogram in the diagnosis of myocardial
ischemia and infarction".)

The leads affected in ST elevation MI depend upon the location of the infarction:

An acute anterior wall MI presents with the changes in some or all of the precordial chest
leads V1 to V6 (waveform 3). Reciprocal ECG changes occasionally are observed during the
initial period of the acute infarction, presenting most often as depressions of the ST segments
in the inferior leads (II, III, and aVF). Reciprocal changes are actually the same ST segment
shifts as seen from a different angle or direction.

An acute anteroseptal MI presents with the changes in leads V1 to V2 (waveform 4).


Reciprocal ECG changes occasionally are observed during the initial period of the acute

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infarction, presenting as depressions of the ST segments in the inferior (II, II, aVF) or lateral
leads (I, aVL, V5, and V6).

An acute anteroapical MI presents with the changes in leads V3 and V4 (waveform 5).
Reciprocal ECG changes occasionally are observed during the initial period of the acute
infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF).

An acute anterolateral MI presents with the changes in leads V5 and V6, often in association
with changes in leads I and aVL (waveform 6). Reciprocal ECG changes occasionally are
observed during the initial period of the acute infarction, presenting as depressions of the ST
segment in the inferior leads (II, III, aVF), and in some cases in leads V1 and V2.

An acute lateral MI presents with the changes confined to leads I and aVL (waveform 7).
Reciprocal ECG changes occasionally are observed during the initial period of the acute
infarction, presenting as ST segment depressions in the inferior leads (II, III, and aVF) or
leads V1 and V2.

An acute inferior wall MI presents with the changes in leads II, III, and aVF (figure 1).
Reciprocal ECG changes occasionally are observed during the initial period of the acute
infarction, presenting with ST segment depressions in leads I and aVL. The ST segment
depression in the precordial leads V1 to V2 may be reciprocal, but more likely represents true
posterior wall involvement (which may be diagnosed by ST elevation in leads V7 to V9) [4]. In
addition, there may be the presence of ST elevation in the precordial chest leads V1 to V2.
Involvement of the right ventricle may occur with an inferior wall MI and is confirmed by the
presence of ST segment elevation in V3R and V4R. (See "Right ventricular myocardial
infarction".) The amount of time when ST elevation occurs in the right precordial leads may be
shorter compared with the inferior leads, and, therefore, a right-sided ECG should be obtained
as soon as possible after inferior wall ST elevation is noted.

An acute posterior wall transmural MI reflecting left circumflex coronary artery involvement
may be missed on a typical ECG. Posterior lead ECG (leads V7 to V9) should be completed if
there is a high degree of suspicion or if ST depression is present in V1 to V3. The criteria for
ST elevation in leads V7 to V9 are 0.05 mV in men over 40 years and women and ST
elevation of 0.1 mV for men <40 years.

ST-elevation MI evolution The classic (but not invariable) sequence of ECG changes in
patients with STEMI is as follows:

The first change may be a hyperacute T wave. It is tall, peaked, and symmetric (the normal T
wave is asymmetric with an upstroke that is slower than the downstroke) in at least two
contiguous leads.

Initially, there is elevation of the J point and the ST segment retains its concave configuration
but may become convex or rounded upward (waveform 8).

Over time, the ST-segment elevation becomes more pronounced and the ST segment
changes its morphology, becoming more convex or rounded upward.

The ST segment eventually merges with the T wave and the ST-segment and T wave become
indistinguishable. The QRS-T complex can actually resemble a monophasic action potential.
This is a current of injury or so-called tombstone pattern. Reciprocal ST-segment
depressions are usually observed in other leads.

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The ST-segment returns to baseline, an initial Q wave develops, and there is a loss of R wave
amplitude. When the ST segment elevation persists for greater than three weeks after the
event, a ventricular aneurysm in the area may be suspected.

The T wave becomes inverted and it may remain inverted or return to upright.

Over time, there is continued evolution of ECG changes. The R wave amplitude becomes
markedly reduced, the Q wave deepens, and the T wave remains inverted or becomes
positive. These changes generally occur within the first two weeks after the event; however, in
some patients, they occur within a few hours of presentation.

Non-ST elevation MI ECG changes that occur in patients who sustain a non-ST elevation MI
are different from those that occur with ST elevation MI. T wave flattening or inversion typically
precedes ST-segment depression. Q waves are typically absent but can occur, and the duration of
the ST and T wave changes are variable. The ST-segment is horizontal or down-sloping, 0.05
mV in two contiguous leads, and frequently associated with T wave inversion 0.1 mV in two
contiguous leads and prominent R waves or R/S ratio >1 [3].

Post-ischemic T wave inversions After an episode of clinical ischemia, some patients develop
T wave inversions >0.5 mV in leads V1 to V4, and occasionally to V5. The T waves are frequently
deep and symmetric, with QT prolongation. This ECG pattern is seen after the chest pain has
subsided and there is a post-ischemic state with no features of ST elevation or depression. This
is also known as Wellens sign. It is associated with proximal left anterior descending stenosis and
impending acute anterior wall infarct, though it is also seen in those with intracranial hemorrhage
and some cardiomyopathies.

ST changes in the setting of conduction abnormalities In the setting of left bundle branch
block (LBBB), there are baseline ST-T abnormalities that can influence the ability to assess for
ischemia. Three criteria have been developed to assess for ischemia in the setting of LBBB: ST
elevation 0.1 mV in leads with a positive QRS complex, ST depression 0.1mm in leads V1 to
V3, and ST elevation 5 mm with a negative QRS complex. In the setting of right bundle branch
block or fascicular blocks, ST segment changes can still be interpreted normally. (See "ECG
tutorial: Intraventricular block".)

PRIOR Q WAVE MYOCARDIAL INFARCTION A prior myocardial infarction (MI) is


characterized by initial Q waves that are deep (>1 mm) and broad (>0.03 to 0.04 seconds). The Q
waves are more likely to be diagnostic of a prior MI if there is also an inverted T wave in the same
lead. The location of these changes is dependent upon the location of the MI. (See "Pathogenesis
and diagnosis of Q waves on the electrocardiogram".)

An abnormal Q wave is defined by [3]:

Any Q wave in leads V2 to V3 20 msec or QS complex in lead V2 to V3

In two contiguous leads, Q wave 30 msec and 0.1 mV deep, or QS complex in leads I, II,
aVL, aVF, or V4 to V6.

R wave 40 msec in V1 to V2 and R/S1, with a concordant positive T wave (in the absence
of conduction abnormalities).

Anterior wall MI An old anterior wall infarction is characterized by the presence of initial deep
and broad Q waves in any of the precordial leads (waveform 9). In some cases, there are no Q

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waves, but rather poor R wave progression across the precordium (the R wave amplitude does not
increase progressively from leads V1 to V3, to V4, V5, or V6). This situation must be distinguished
from other causes of poor R wave progression, including late transition (previously referred to as a
clockwise rotation pattern) or a normal variant (often seen in women). (See "ECG tutorial:
Miscellaneous diagnoses".)

Infrequently, there may be reverse R wave progression where the R wave amplitude becomes
progressively smaller from lead V2 or V3 to lead V6. Similar to the electrocardiogram of an acute
infarction, the location of the Q waves establishes the area of infarcted myocardium, septum (V1 to
V2), apex (V3 to V4), or anterolateral wall (V5 to V6).

The ST segment typically is isoelectric. However, an aneurysm is suspected if it remains elevated


greater than three weeks after the acute event.

Anterolateral wall MI An old anterolateral wall infarction typically is diagnosed by the presence
of Q waves that are deep and broad in the anterolateral precordial leads V4 to V6. However, the Q
waves may extend across the entire precordium and are usually associated with inverted T waves.
In addition, there may be Q waves and T wave inversions in leads I and aVL.

Lateral wall MI An old lateral wall infarction is diagnosed by the presence of initial Q waves that
are deep and broad in leads I and aVL (waveform 10). If the Q waves are very deep (or complex),
the axis appears to be rightward. This has been termed a peri-infarction block. However, if the R
wave in these leads is small (ie, an rS complex), the rightward axis (>+90) is due to a left
posterior fascicular block. (See "ECG tutorial: Basic principles of ECG analysis", section on 'Axis'.)
There is also an inverted T wave in these leads.

Inferior wall MI An old inferior wall MI is diagnosed by the presence of initial Q waves that are
deep and broad in the inferior leads II, III, and aVF (waveform 11). There are usually inverted T
waves associated with the Q waves. If the R wave amplitude is reduced, the QRS complex (Qr)
may appear to have a leftward axis (>-30 the left axis is actually the result of the infarction and not
a conduction abnormality; it is known as a peri-infarction block). If the axis is very leftward (>-30
as a result of a small r and deep S wave [rS complex] in leads II and aVF), then this is a
conduction abnormality due to a left anterior fascicular block. (See "ECG tutorial: Basic principles
of ECG analysis", section on 'Axis'.)

It is not uncommon to see a Q wave in lead III only in patients who have not had an MI. The depth
of this Q wave usually varies with respiration (respiratory Q wave). It represents a nonspecific
normal finding. A diagnosis of inferior MI can only be made if there are also Q waves in either of
the other inferior leads.

Q waves may resolve within one year after an inferior wall MI in up to 30 percent of cases. The
only remaining abnormalities in these instances are flattened or inverted T waves and ST segment
changes.

Posterior wall MI An old posterior wall MI is diagnosed when there is a tall R wave in V1 to V2
(R/S >1.0) (waveform 12). Frequently, there is also evidence of an inferior wall infarction. Other
causes for a tall R wave in these leads, including right ventricular hypertrophy, dextrocardia,
Duchennes muscular dystrophy, Wolff-Parkinson-White pattern, hypertrophic cardiomyopathy,
lead malposition, or early transition (counterclockwise rotation), must be considered in these
patients. (See "ECG tutorial: Miscellaneous diagnoses".) The finding of Q waves and ST segment
changes in leads V7 to V9 is helpful in diagnosing a true posterior MI (table 1) [4].

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Septal Q waves Septal Q waves are physiologic Q waves <30 msec and <25 percent the
height of the associated R wave amplitude, seen in leads I, aVL, aVF, and V4 to V6. They
demonstrate the normal pattern of initial depolarization of the ventricular myocardium from the left
to the right of the septum and do not represent a prior MI. (See "ECG tutorial: Physiology of the
conduction system", section on 'Ventricular activation'.)

SUMMARY

Acute ST-elevation myocardial infarction (MI) is characterized by the following evolutionary


changes (see 'Acute myocardial ischemia and infarction' above):

Hyperacute T waves, which are tall, peaked, and symmetric.

Elevation of the ST segment in contiguous leads, depending upon the location of the MI.
The ST elevation is at first concave and then becomes convex, merging with the T wave
(current of injury).

Often, but not always, the development of Q waves and T wave inversions as the ST
segments return to baseline.

The electrocardiographic changes that occur in patients who sustain a non-ST elevation MI
are different. T wave flattening or inversion typically precedes ST segment depression. Q
waves are typically absent but can occur, and the duration of the ST and T wave changes is
variable.

A chronic Q wave MI (or Q wave infarction of indeterminate age) is characterized by initial Q


waves that are deep (>1 mm) and broad (>0.03 to 0.04 seconds). The Q waves may be
associated with an inverted T wave. The location of these changes is dependent upon the
location of the MI. (See 'Prior Q wave myocardial infarction' above.)

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REFERENCES

1. Mirvis D, Goldberger AL. Electrocardiography. In: Braunwald's Heart Disease: A Textbook of


Cardiovascular Medicine, 10th ed, Mann DL. (Ed), Elsevier/Saunders, Philadelphia 2014.
2. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction:
a scientific statement from the American Heart Association Electrocardiography and
Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology
Foundation; and the Heart Rhythm Society. Endorsed by the International Society for
Computerized Electrocardiology. J Am Coll Cardiol 2009; 53:1003.
3. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction.
Circulation 2012; 126:2020.
4. Casas RE, Marriott HJ, Glancy DL. Value of leads V7-V9 in diagnosing posterior wall acute
myocardial infarction and other causes of tall R waves in V1-V2. Am J Cardiol 1997; 80:508.

Topic 2125 Version 13.0

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GRAPHICS

ECG diffuse subendocardial ischemia

Diffuse subendocardial ischemia manifested by prominent ST depressions in leads I, II, aVL, aVF,
and V2 to V6, with ST elevation in aVR. A prolonged PR interval (0.28 sec) is also present. The
findings also raise the possiblitity of severe multivessel or left main coronary artery disease.

Courtesy of Ary Goldberger, MD.

Graphic 65963 Version 3.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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J point

The J point is the junction between the end of the QRS and the beginning of the ST
segment.

Graphic 82922 Version 2.0

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Acute transmural anterior wall myocardial infarction

ST elevation in some or all of the precordial leads is characteristic of an acute anterior wall
infarct.

Graphic 78453 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Acute anteroseptal myocardial infarction

ST segment elevation in V1 and V2 is characteristic of an acute anteroseptal infarct. There is


also reciprocal ST segment depression in V5 and V6.

Graphic 75683 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Acute anteroapical transmural myocardial infarction

ST elevation is present in V3 and V4 in patients with an anteroapical infarct.

Graphic 52433 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Acute anterolateral transmural myocardial infarction

ST elevation is prominent in leads I, aVL, V5, and V6 in patients with an acute anterolateral
infarct.

Graphic 64952 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Acute lateral transmural myocardial infarction

ST elevation in leads I and aVL is characteristic of an acute lateral wall infarct. Reciprocal ST
depression is evident in this case in the inferior leads (II, III, and aVF) and in V1.

Graphic 82413 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Acute inferior transmural myocardial infarction

ST segment elevation in leads II, III, and aVF is characteristic of an acute inferior infarct.
Reciprocal ST segment depression is present in this case in leads V1 to V4, and aVL.

Graphic 57189 Version 1.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Myocardial infarction

J point and ST segment elevation are the hallmarks of acute myocardial


infarction. The ST segment eventually becomes indistinguishable from the T
wave.

Graphic 82020 Version 3.0

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Chronic anterior wall myocardial infarction

A chronic anterior wall infarction is diagnosed by the presence of initial deep and broad Q
waves in any of the precordial leads; in this case they are present in leads V1 to V4.

Graphic 66472 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Chronic lateral wall myocardial infarction

A chronic lateral wall infarction is characterized by the presence of initial Q waves which are
deep and broad in leads 1 and aVL.

Graphic 55529 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Chronic inferior wall myocardial infarction

A chronic inferior wall infarct is characterized by the presence of initial Q waves which are
deep and broad in the inferior leads 2, 3, aVF.

Graphic 81282 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Chronic posterior wall myocardial infarction

A chronic posterior wall infarct is characterized by a tall R wave in V1 (R/S >1.0). There is
also a rightward axis.

Graphic 68277 Version 2.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Causes and diagnosis of tall R waves in V1

Diagnosis Confirmatory clues

True posterior infarct ST , T in V1-V2; Q waves and ST V7-V9

Right ventricular hypertrophy RAD; RAE; secondary ST-Ts; V7-V9 normal

Ventricular septal Associated Q waves; LVH; V7-V9 normal or deep narrow Q waves
hypertrophy

Right bundle branch block Wide QRS; broad S in V1, V6; R peaks late in V1; V7-V9 normal or
broad S waves

Wolff-Parkinson-White Short PR; delta wave; V7-V9 normal or delta wave


syndrome

Normal variant No other abnormalities

LVH: left ventricular hypertrophy; RAD: right-axis deviation; RAE: right atrial enlargement.

Graphic 72039 Version 2.0

Contributor Disclosures
Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: Boston Scientific; St.
Jude Medical [Cardiac electrophysiology (Pacemakers and ICDs)]. Ary L Goldberger,
MD Nothing to disclose Gordon M Saperia, MD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of
all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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Official reprint from UpToDate


www.uptodate.com 2017 UpToDate

ECG tutorial: ST and T wave changes

Author: Jordan M Prutkin, MD, MHS, FHRS


Section Editor: Ary L Goldberger, MD
Deputy Editor: Gordon M Saperia, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: Aug 18, 2016.

INTRODUCTION ST and T wave changes may represent cardiac pathology or be a normal


variant. Interpretation of the findings, therefore, depends on the clinical context and presence of
similar findings on prior electrocardiograms.

NONSPECIFIC ST-T WAVE CHANGES Nonspecific ST-T wave changes are very common
and may be seen in any lead of the electrocardiogram. The changes may be seen in all or most of
the leads (diffuse changes), or they may be present contiguous leads, such as the inferior, lateral,
or anterior leads.

The types of abnormalities are varied and include subtle straightening of the ST segment, actual
ST segment depression or elevation, flattening of the T wave, biphasic T waves, or T wave
inversion (waveform 1). In the absence of a clinical history or symptoms, T wave abnormalities and
flattened and depressed ST segment changes are nonspecific. Causes of these changes include:

Functional and physiologic variants (eg, post-prandial)


Electrolyte abnormalities
Post-cardiac surgical state
Anemia
Fever
Acidosis or alkalosis
Endogenous catecholamines
Drugs, such as digoxin
Acute abdominal process
Endocrine abnormalities
Metabolic changes
pH changes
Cerebrovascular accidents
Diseases such as myocarditis, pericarditis, cardiomyopathy, pulmonary emboli, infections,
amyloidosis, systemic diseases, lung diseases.
Myocardial ischemia

Flat T waves and small ST segment changes may also be seen in healthy individuals, including
well-trained athletes, leading to mistaken diagnosis of heart disease. T wave inversions, however,
are more concerning for cardiomyopathy or other cardiac syndrome, depending on the clinical
context.

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Persistent juvenile T wave pattern The T wave vector may be directed posteriorly in children,
resulting in an inverted T wave in the right precordial leads V1 to V3. The vector usually becomes
anterior with age, resulting in upright T waves in these leads; however, the T waves may remain
inverted in V1 to V3 in a minority of adults, a finding known as a persistent juvenile pattern
(waveform 2).

Right precordial T-wave inversion in adults may also represent myocardial disease such as
ischemia, the Brugada syndrome (especially with coved-type ST elevations), or arrhythmogenic
right ventricular cardiomyopathy. (See "Brugada syndrome: Epidemiology and pathogenesis",
section on 'Brugada pattern versus Brugada syndrome' and "Arrhythmogenic right ventricular
cardiomyopathy: Diagnostic evaluation and diagnosis", section on '12-lead ECG'.) Lead
misplacement, especially when the right-mid precordial leads are located above their usual
positions, may also account for this pattern.

The prevalence and prognostic significance of right precordial T-wave inversion were evaluated in
a study of over 10,000 middle-aged (mean age of 44 years) Finnish citizens followed for an
average of 30 years [1]. T-wave inversion in leads V1 to V3 was present in 0.5 percent (more
commonly in women) but this pattern did not predict increased mortality compared to individuals
without this pattern. In contrast, those with T wave inversions in leads other than V1 to V3 had an
increased mortality compared to no T wave inversions.

Black/African athlete T wave variant In up to 13 percent of Black/African athletes, a pattern of


dome-shaped ST elevation with T wave inversions, sometimes with biphasic T waves, may be
seen in leads V1 to V4 [2]. This is considered a normal pattern in the asymptomatic athlete unless
there is a positive family history or abnormal physical exam. ST changes or T wave inversions in
other leads are considered abnormal. T wave inversions in the inferior and lateral leads may also
be normal in Black/African athletes, but this variant needs further study [3].

ST-T WAVE CHANGES ASSOCIATED WITH SPECIFIC DISEASE STATES Specific patterns
of ST-T wave changes may be seen in association with various pathophysiologic states.

Myocardial ischemia, injury, and infarction The electrocardiographic abnormalities seen with
myocardial ischemia, injury, and infarction are presented separately. (See "ECG tutorial:
Myocardial ischemia and infarction", section on 'Acute myocardial ischemia and infarction'.)

Pericarditis ST-T wave changes that are suggestive of pericarditis are usually seen diffusely in
most or all limb and precordial leads, although in some cases, the changes may be isolated to only
a few leads. (See "Clinical presentation and diagnostic evaluation of acute pericarditis", section on
'Electrocardiogram'.)

There is J point elevation and ST segment elevation, which has a concave morphology (waveform
3). The ST segment elevation continues to have a normal concave morphology, regardless of how
high the ST segment elevates. There are no reciprocal changes present and the T waves maintain
a normal morphology, ie, it is asymmetric. Often, there is associated depression of the PR
segment, although this does not have to be present to diagnose pericarditis. The PR and ST
segment return to the isoelectric baseline. Some patients may later develop T wave inversions
after the ST segment has normalized, which frequently returns to normal over time.

Left ventricular hypertrophy The ST-T wave abnormalities secondary to left ventricular
hypertrophy (formerly termed "strain") are most often seen in the anterolateral leads (eg, I, aVL, V4
to V6); changes may also be seen in other leads when the hypertrophy is very severe (waveform

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4). (See "Electrocardiographic diagnosis of left ventricular hypertrophy".) Typical abnormalities


include a horizontal or downsloping ST segment and T wave inversions. In some cases, there is
concavity to the ST segment, which has a final downward turn that blends into an inverted T wave.
Although most often there will be voltage criteria for left ventricular hypertrophy and often left atrial
enlargement or left axis deviation, in some cases, only the ST-T wave changes are observed.

The ST-T changes associated with left ventricular hypertrophy are termed strain but are thought
to be either subendocardial ischemia or primary repolarization abnormalities. Subendocardial
ischemia results from a relative lack of blood and oxygen supply to the hypertrophied muscle, as
demand is greater than supply. Alternatively, the ST-T changes may be due to primary
repolarization abnormalities of the hypertrophied cardiac muscle.

Right ventricular hypertrophy Similar to the situation with left ventricular hypertrophy, ST-T
wave changes may be seen with right ventricular hypertrophy, likely representing subendocardial
ischemia or primary repolarization abnormalities of the thickened right ventricle. These changes
are seen in the right precordial leads V1 to V3.

Intraventricular conduction delays ST-T wave abnormalities secondary to intraventricular


conduction disturbances, primarily left or right bundle branch block, are commonly seen and look
similar to those that occur during ischemia (waveform 5). (See "Basic approach to delayed
intraventricular conduction".)

The ST segments may be depressed or elevated. When there is an ST segment shift present, it is
most often in a direction opposite to the polarity of the QRS complex. Similarly, the T wave also
has a polarity opposite to the direction of the QRS complex. Thus, there are typically ST segment
depressions and T wave inversions in leads V1 to V3 with a right bundle branch block, reflecting
repolarization abnormalities of the right ventricular myocardium. In contrast, repolarization changes
in the left ventricular myocardium due to a left bundle branch block result in downsloping ST
depression and T wave inversion in leads I, aVL, and V5 to V6, while the ST segment is elevated
and the T wave is upright in leads V1 to V4.

Persistent ST elevation compatible with an aneurysm Persistent ST segment elevation


compatible with an aneurysm may be seen in any leads showing changes of a previous myocardial
infarction. There is usually coexistent evidence of a chronic myocardial infarction, such as a Q
wave, an inverted T wave, and even reciprocal ST depressions (waveform 6). Elevation of the J
point and ST segment elevation, which is convex upward, is typically present, similar to what is
seen with an evolving acute myocardial infarction pattern. The suspicion of an aneurysm is based
upon the duration of this pattern, greater than three weeks after the acute infarction. The
aneurysm is in the anterior wall when these persistent abnormalities are seen in the precordial
leads V1 to V6, in the lateral wall when seen in leads I and aVL, and in the inferior wall when they
are in the inferior leads II, III, and aVF. As the ST segment elevation is similar to what is seen with
an acute myocardial infarction, the clinical history and time course of the acute infarction is
important to establish the cause. Patients may have an aneurysm without ST elevation. It is
thought that in some patients, persistent ST elevation may be more consistent with a dyskinetic
wall rather than true aneurysm, due to abnormal stretch on the ventricular wall.

Prolonged Q-T interval The QT interval is primarily a measure of membrane repolarization.


The QT interval is measured from the beginning of the QRS complex (either a Q or R wave) to
where a tangent line drawn on the downslope of the T wave intersects with the baseline. This is
usually easiest to complete in leads II or V5. Any U wave, following the T wave, is not considered
as part of the QT interval.

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The time for ventricular repolarization and therefore the QT interval is dependent upon the heart
rate; it is shorter at faster heart rates and longer when the rate is slower. Thus, a QT interval that is
corrected for heart rate (QTc) is often calculated based on Bazetts formula as follows:

QTc = QT interval square root of the RR interval (in sec)

Although this approach is simple, it is inaccurate at heart rate extremes and results in over-
correcting at high rates and under-correcting at low ones

A prolonged QT interval is present when the corrected QT interval is >0.44 in men and >0.45 sec
in women (waveform 7). QT prolongation may be associated with either a prolonged ST segment
or broad duration T wave. This may be due to genetic causes (congenital long QT syndrome) or
acquired, due to drugs (class 1A or 3 antiarrhythmic agents, phenothiazines, tricyclic
antidepressants), hypothermia, cerebrovascular diseases, or ischemic heart disease. A long QT
(either acquired or congenital) is associated with a form of polymorphic ventricular tachycardia
known as torsades des pointes. (See "Clinical features of congenital long QT syndrome" and
"Prognosis and management of congenital long QT syndrome" and "Acquired long QT syndrome".)

Since the QRS widens in the setting of a bundle branch block, the QT interval will lengthen. This
increase in QT interval does not reflect an abnormality of ventricular repolarization, since the
increase is due to an abnormality of depolarization. There have not been many descriptions on
how to measure QT interval in the setting of QRS widening. In the setting of left bundle branch
block, in one study, the QT interval prolonged by about half the QRS duration [4]. Therefore, a
modified QT interval could be calculated as QT 48.5 percent (QRS duration). This value must
still be corrected for heart rate using Bazetts or another formula. Another option is to measure the
JT interval, corrected for rate: QTc QRS = JTc. This equation has some limitations, as it is
dependent on heart rate and normal values have not been derived. (See "ECG tutorial: Basic
principles of ECG analysis", section on 'QT interval'.)

Short QT interval A short QT interval, indicative of acceleration of ventricular repolarization, is


present when the QTc is <0.36 sec (waveform 8). A short QT interval is seen with hypercalcemia,
hyperkalemia, or digitalis use. A hereditary short QT syndrome has also been described as
associated with increased risk of sudden cardiac arrest due to ventricular tachyarrhythmias [5].
(See "Short QT syndrome".)

Tall T waves Tall T waves may be seen in a variety of settings. Classical peaked or tented
narrow-based T waves are usually the result of hyperkalemia, which may be systemic or localized
(waveform 9). While no frequently-used criteria have been validated, they may be generally >10
mm in height as measured in the precordial leads, and >5 mm in height in the limb leads, or only
relatively tall compared with baseline. This appearance is in contrast to the normal T wave, which
is asymmetric (the initial upstroke is slow while the end or downstroke is rapid) regardless of its
amplitude. Tall T waves may be seen with left ventricular hypertrophy or even in normal subjects
who have tall QRS complex amplitude.

In addition to hyperkalemia, prominent (so-called hyperacute) T waves may be seen in the early
phases of an acute myocardial infarction or with myocardial ischemia (possibly related in part to
localized extracellular hyperkalemia). (See "Electrocardiogram in the diagnosis of myocardial
ischemia and infarction".) Tall T waves may also be seen in the presence of left ventricular
hypertrophy or left bundle branch block, in which the amplitude of the QRS complex is increased,
or may even be a normal variant; in these cases, the T waves are not peaked and still have an
asymmetric morphology, often as part of the benign early repolarization variant.

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Prominent U waves U waves are positive deflections that are generally seen in leads V2 to V4.
They are usually low voltage (<0.2 mV) and have the same polarity as the T wave. U waves may
be seen in normal individuals, primarily in the right precordial leads. Their origin is not certain, but
they may represent late repolarization of the His Purkinje system or of the mid-myocardial M cells.
Abnormalities of the U wave may be seen in the following circumstances:

A prominent U wave may be indicative of hypokalemia (figure 1). Other conditions that may
increase the amplitude of the U wave include bradycardia, class 1A and 3 antiarrhythmic
drugs (as well as multiple others), intracranial hemorrhage, and certain forms of the congenital
long QT syndrome. In this situation, the U wave is not after the T wave, but is superimposed
on the T wave, interrupting it. (See "Clinical features of congenital long QT syndrome".)

The polarity of the U wave may reverse (eg, become negative in mid-lateral precordial leads)
in the presence of myocardial ischemia or left ventricular overload. Negative U waves during
exercise testing have been reported to correlate with significant stenosis of the left main or left
anterior descending coronary artery.

SUMMARY

Nonspecific ST-T wave abnormalities are very common and may be seen in any limb or
precordial leads of the electrocardiogram. (See 'Nonspecific ST-T wave changes' above.)

More specific patterns of ST-T wave changes, which may be seen in association with various
disease states, include:

Acute ischemia: Typically, there are ST segment changes (eg, depression or elevation)
associated with T wave flattening or inversion. Inverted T waves are often symmetric.

Myocardial injury: ST segment elevation (above baseline, ie, T-P segment) and T wave
abnormalities that are indicative of transmural myocardial ischemia or injury or a
myocardial infarction. They are usually localized to those leads that reflect the involved
regions of the myocardium. Reciprocal changes (ST depression in other leads) and
hyperacute T waves (tall, peaked, and symmetric) are usually present.

Pericarditis: ST-T wave changes that are suggestive of pericarditis are usually diffusely
seen in most or all limb and precordial leads, although in some cases, the changes may
be isolated to only a few leads. Reciprocal changes and hyperacute T waves are not
seen.

Intraventricular conduction delays: ST-T wave abnormalities secondary to intraventricular


conduction disturbances (eg, left or right bundle branch block) are commonly seen and
look similar to those that occur during ischemia.

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REFERENCES

1. Aro AL, Anttonen O, Tikkanen JT, et al. Prevalence and prognostic significance of T-wave
inversions in right precordial leads of a 12-lead electrocardiogram in the middle-aged
subjects. Circulation 2012; 125:2572.

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2. Papadakis M, Carre F, Kervio G, et al. The prevalence, distribution, and clinical outcomes of
electrocardiographic repolarization patterns in male athletes of African/Afro-Caribbean origin.
Eur Heart J 2011; 32:2304.
3. Sheikh N, Papadakis M, Ghani S, et al. Comparison of electrocardiographic criteria for the
detection of cardiac abnormalities in elite black and white athletes. Circulation 2014;
129:1637.
4. Bogossian H, Frommeyer G, Ninios I, et al. New formula for evaluation of the QT interval in
patients with left bundle branch block. Heart Rhythm 2014; 11:2273.
5. Antzelevitch C, Pollevick GD, Cordeiro JM, et al. Loss-of-function mutations in the cardiac
calcium channel underlie a new clinical entity characterized by ST-segment elevation, short
QT intervals, and sudden cardiac death. Circulation 2007; 115:442.

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GRAPHICS

Nonspecific ST and T wave changes

The types of abnormalities include ST segment depression or elevation (leads I, aVL, V4-
V6), flattening of the T wave (leads I, aVR, aVL, V5, V6), or T wave inversion (I, V2-V4).

Graphic 60478 Version 2.0

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Persistent juvenile pattern

T wave inversion in V1 to V3 in an adult is consistent with a persistent juvenile pattern.

Graphic 64032 Version 2.0

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Pericarditis

J point and concave ST segment elevation seen diffusely in most of the precordial and limb
leads are the hallmarks of pericarditis. There are no reciprocal ST changes. PR depression is
evident in some leads.

Graphic 57517 Version 2.0

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Left ventricular hypertrophy (LVH) with strain pattern

The ST-T wave abnormalities secondary to LVH (often termed "strain") are most often seen in
the anterolateral leads (eg, I, aVL, V4-V6). Typical abnormalitites include a horizontal or
downsloping ST segment and T wave inversions. In some cases there is concavity to the ST
segment which has a final downward turn that blends into an inverted T wave.

Graphic 76497 Version 5.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Intraventricular conduction delay

ST-T wave abnormalities secondary to intraventricular conduction disturbances (eg, left or


right bundle branch block) look similar to those that occur during ischemia. The ST segments
may be depressed or elevated; when there is an ST segment shift present, it is most often in
a direction opposite to the polarity of the QRS complex. The T wave also has a polarity
opposite to the direction of the QRS complex. Thus, there are typically ST segment
depressions and T wave inversions in leads V1 to V3 with a right bundle branch block (RBBB),
reflecting repolarization abnormalities of the right ventricular myocardium. Repolarization
changes in the left ventricular myocardium due to a left bundle branch block (LBBB) result in
downsloping ST depression and T wave inversion in leads V4 or V5 to V6.

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Persistent ST segment elevation post-MI

The presence of an anterior wall aneurysm following an acute myocardial infarction is


suspected because of persistent ST elevation in leads V2 to V4. Inverted T waves are
evidence of the old infarct.

Graphic 74283 Version 5.0

Normal ECG

Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of


0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 3.0

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Single-lead electrocardiogram (ECG) showing a


prolonged QT interval

The corrected QT interval (QTc) is calculated by dividing the QT interval (0.60


seconds) by the square root of the preceding RR interval (0.92 seconds). In this
case, the QTc is 0.625 seconds.

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Short QT interval

The QT interval (not corrected) in this case is approximately 0.24 seconds.

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Hyperacute (peaked) T waves

Hyperacute T waves are >5 mm in the limb leads, and usually >10 mm in the precordial
leads. They have a peaked, symmetric morphology.

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Prominent U waves

A prominent U wave (>0.2 mV) is usually suggestive of hypokalemia, although it


may be seen in other circumstances.

Graphic 57086 Version 1.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS
duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

Contributor Disclosures
Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: Boston Scientific; St.
Jude Medical [Cardiac electrophysiology (Pacemakers and ICDs)]. Ary L Goldberger,
MD Nothing to disclose Gordon M Saperia, MD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of
all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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