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.
Transmural and Subendocardial Ischemia
A simplified cross-sectional diagram of the left ventricle is presented in Figure 8-1. Notice that the left ventricle consists of an outer layer (epicardium or subepicardium) and an inner layer (subendocardium). This distinction is important because myocardial ischemia may be limited to just the inner layer, or it may affect virtually the entire thickness of the ventricular wall (transmural ischemia).
Myocardial Blood Supply
The cardiac blood supply is delivered by the three main coronary arteries and their branches (Fig. 8-2). The right coronary artery supplies both the inferior (diaphragmatic) portion of the heart and the right ventricle. The left main coronary artery is short and divides into the left anterior descending coronary artery, which generally supplies the ventricular septum and a large part of the left ventricular free wall, and the left circumflex coronary artery, which supplies the lateral wall of the left ventricle. This circulation pattern may be variable. Sometimes, for example, the circumflex artery also supplies the inferoposterior portion of the left ventricle. MIs tend to be localized to the region (e.g., anterior or inferior) of the left ventricle supplied by one of these arteries or their branches.
The serial, typical effects involving STEMI and Q wave MI on the ECG are examined in this chapter. Chapter 9 discusses the diversity of ECG patterns associated with non–ST segment elevation ischemia and non–Q wave infarctions.
ST Segment Elevation, Transmural Ischemia, and Acute Myocardial Infarction
The earliest ECG changes seen with an acute transmural ischemia/infarction typically occur in the ST-T complex in sequential phases:
1. The acute phase is marked by the appearance of ST segment elevations and sometimes tall positive (hyperacute) T waves in multiple (usually two or more) leads. The term “STEMI” refers to this phase.
2. The evolving phase occurs hours or days later and is characterized by deep T wave inversions in the leads that previously showed ST elevations.
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).
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.)
Key Clinical Correlates
Of major importance is the finding that acute reperfusion therapies with percutaneous coronary interventions (angioplasty procedures) or intravenous thrombolytic medications have been shown consistently to improve mortality rate only for acute STEMI.
Furthermore, the earlier such therapy is given after the onset of the acute STEMI the more likely it is to reduce the size of the infarct and the risk of major complications, including heart failure and death.
Successful reperfusion therapy for STEMI is generally associated with a prompt decrease in the amplitude of the ischemic ST elevations.