Official reprint from UpToDate®

www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

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: Sep 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 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 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 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.

● 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/S≥1, 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 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 (>+90º) 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
(>-30º 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 º 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, Duchenne’s 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].

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.)

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

Topic 2125 Version 13.0

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Nothing to disclose 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