Myocardial Infarction and Ischemia, I: ST Segment Elevation and Q Wave Syndromes

Chapter 8 Myocardial Infarction and Ischemia, I ST Segment Elevation and Q Wave Syndromes

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This chapter and the next (forming one unit) examine one of the most important topics in clinical electrocardiography and clinical medicine—the diagnosis of myocardial ischemia and infarction (ischemic heart disease), including ST segment elevation myocardial infarction (STEMI). Basic terms and concepts are briefly discussed first.

ST Segment Elevation, Transmural Ischemia, and Acute Myocardial Infarction

“Transmural” MI is characterized by ischemia and ultimately necrosis of a portion of the entire (or nearly the entire) thickness of the left ventricular wall. Most patients who present with acute MI have underlying atherosclerotic coronary artery disease. The pathophysiology of acute STEMI and subsequent evolving Q wave MI most often relates to occlusion of one of the coronary arteries by a ruptured atherosclerotic plaque, followed by the formation of a clot at this site. The clot in the “culprit artery” is composed of platelets and fibrin, blocking the blood flow downstream.

Other factors can cause or contribute to acute STEMI, including cocaine, coronary artery dissections (spontaneous or induced during interventional procedures), coronary emboli, and other factors.

Not surprisingly, large transmural MIs generally produce changes in both myocardial depolarization (QRS complex) and myocardial repolarization (ST-T complex).

The earliest ECG changes seen with an acute transmural ischemia/infarction typically occur in the ST-T complex in sequential phases:

Transmural MIs can also be described in terms of the location of the infarct. Anterior means that the infarct involves the anterior or lateral wall of the left ventricle, whereas inferior indicates involvement of the inferior (diaphragmatic) wall of the left ventricle (Fig. 8-3). The anatomic location of the infarct determines the leads in which the typical ECG patterns appear. For example, with an acute anterior wall MI, the ST segment elevations and tall hyperacute T waves appear in one or more of the anterior leads (chest leads V1 to V6 and extremity leads I and aVL) (Fig. 8-4). With an inferior wall MI the ST segment elevations and tall hyperacute T waves are seen in inferior leads II, III, and aVF (Fig. 8-5).

An important (but not always present) feature of the ST-T changes seen with STEMI is their reciprocity. The anterior and inferior leads tend to show inverse patterns. Thus in an anterior infarction with ST segment elevations in two or more of leads V1 to V6, I, and aVL, ST segment depression is often seen in leads II, III, and aVF. Conversely, with an acute inferior wall infarction, leads II, III, and aVF show ST segment elevation, with reciprocal ST depressions often seen in one or more of leads V1 to V3, I, and aVL. Reciprocal changes are illustrated in Figures 8-4 and 8-5.

The ST segment elevation seen with acute MI is called a current of injury and indicates that damage has occurred to the epicardial (outer) layer of the heart as a result of severe ischemia. The exact reasons that acute MI produces ST segment elevation are complex and not fully understood. Normally the ST segment is isoelectric (neither positive nor negative) because no net current flow is occurring at this time. MI alters the electrical charge on the myocardial cell membranes in a number of ways. As a result, current flow becomes abnormal (current of injury) and produces ST segment deviations.

The ST segment elevation seen with acute MI may have different shapes and appearances (Fig. 8-6). Notice that the ST segment may be plateau-shaped or dome-shaped. Sometimes it is obliquely elevated.

The ST segment elevations (and reciprocal ST depressions) are the earliest ECG signs of infarction, and are generally seen within minutes of blood flow occlusion. Tall, positive (hyperacute) T waves may also be seen at this time (Figs. 8-7 and 8-8). These T waves have the same significance as the ST elevations. In some cases, hyperacute T waves actually precede the ST elevations.

Guidelines for assessing whether ST segment (and usually J point) elevations are due to acute ischemia have been suggested. However, strict criteria are limited because of false-positives (due to normal variants, left ventricular hypertrophy, etc., as described in Chapter 9) and false-negatives (e.g., T wave positivity may precede ST elevations or the ST elevations may be less than 1-2 mm).

Clinicians should be aware that ST changes in acute ischemia may evolve with the patient under observation. If the initial ECG is not diagnostic of STEMI but the patient continues to have symptoms consistent with myocardial ischemia, serial ECGs at 5- to 10-minute intervals (or continuous 12-lead ST segment monitoring) should be performed.

After a variable time lag (usually hours to a few days) the elevated ST segments start to return to the baseline. At the same time the T waves become inverted in leads that previously showed ST segment elevations. This phase of T wave inversions is called the evolving phase of the infarction. Thus with an anterior wall infarction the T waves become inverted in one or more of the anterior leads (V1 to V6, I, aVL). With an inferior wall infarction the T waves become inverted in one or more of the inferior leads (II, III, aVF). (These T wave inversions are illustrated in Figs. 8-4 and 8-5.)

Jun 11, 2016 | Posted by in CARDIOLOGY | Comments Off on Myocardial Infarction and Ischemia, I: ST Segment Elevation and Q Wave Syndromes

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