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ECG tutorial: Myocardial ischemia and infarction

ECG tutorial: Myocardial ischemia and infarction
Literature review current through: Jan 2024.
This topic last updated: Dec 08, 2022.

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 "Diagnosis of acute myocardial infarction", section on 'Definitions'.)

ELECTROPHYSIOLOGIC BASIS OF ST-SEGMENT DEVIATION — Under normal conditions, the ST segment is relatively isoelectric (ie, flat along the baseline), because healthy myocardial cells throughout the ventricles 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 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 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 MI in all patients but not all patients with myocardial ischemia develop MI. The 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 'Postischemic 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. Conversely, at the very onset of acute MI, the ST elevations may be more subtle, accounting for the importance of frequent serial ECGs in patients with ambiguous presentations.

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 (STEMI) 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, however, 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".)

As useful guidelines, the leads affected in STEMI 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 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, classically 180 degrees apart in the frontal (limb lead) or horizontal (chest lead) planes.

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 posterior or postero-lateral 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 or postero-lateral 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 (waveform 9 and waveform 10). 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 (NSTEMI) are different from those that occur with STEMI. The joint European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation (ESC/ACCF/AHA/WHF) committee for the Fourth Universal definition of MI recommended the following ECG criteria for the diagnosis of NSTEMI [5]: new horizontal or downsloping ST-depression ≥0.5 mm in two contiguous leads and/or T inversion >1 mm in two contiguous leads with prominent R wave or R/S ratio >1 [5]. As noted above, clinicians should be aware that any threshold-based criteria for ECG diagnoses have inherent limitations and that the ECG in the context of acute ischemia may rapidly evolve.

Postischemic T wave inversions — After an episode of anterior ischemia with ST elevation, some patients develop T wave inversions >0.5 mV in leads V1 to V4, and occasionally to V5. T wave inversions in I and aVL are also common in this context. 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 "postischemic 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; the differential diagnosis includes intracranial hemorrhage and some cardiomyopathies.

ST changes in the setting of conduction abnormalities — In the setting of left bundle branch block, there are baseline ST-T abnormalities that can influence the ability to assess for ischemia (see "ECG tutorial: Intraventricular block"). T wave inversions may also appear after intermittent pacing. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Abnormal T waves'.)

PRIOR Q WAVE MYOCARDIAL INFARCTION — A prior 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 11). 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 12). 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 13). 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 (>-30º 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 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 14). 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 – Acute ST-elevation myocardial infarction (STEMI) is characterized by the following evolutionary changes (waveform 8) (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.

Acute non-ST-elevation myocardial infarction – The electrocardiographic changes that occur in patients who sustain a non-ST-elevation MI (NSTEMI) 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. (See 'Non-ST-elevation MI' above.)

Remote myocardial infarction – 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) (waveform 11 and waveform 12 and waveform 13 and waveform 14). 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.)

Topic 2125 Version 23.0

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