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Chapter 11: THE RESTING ELECTROCARDIOGRAM ABNORMAL ST-SEGMENT CHANGES

In orthodox ECG language, injury implies abnormal ST-segment changes, necrosis implies abnormalQ waves, and ischemia implies symmetricT-wave inversion (or elevation).5-7,9-13,16 Following conventional ECG theory, several authors consider that ECG "injury" occurs because the affected cells are unable to maintain their normal polarization during diastole.5-7,12,16,21 Various hypotheses have been postulated to explain how this diastolic hypopolarization or generalized diastolic depolarization is manifested as abnormal ST-segment shifts in the surface ECG21-24 (BhB; Fig. 11-3). One hypothesis is based on the existence of a diastolic current of "injury." During the control (diastolic) period, both membrane resting potential and surface ECG baseline are at their normal level. At the onset of injury, the resting intracellular potential decreases (e.g., from 90 to 70 mV), and the ECG baseline shifts below its preinjury level. Because the injured cells leak negative ions, their exterior becomes relatively negative (or less positive) than that of the normal cells. Thus a "current of injury" flows between the negative ("injured") zone and the positive ("normal") region.!0 This produces a negative displacement of the surface ECG baseline in the leads facing the injured region. In the surface ECG, depolarization (by virtue of the electrical negativization of the nonaffected area) practically reduces the potential difference between noninjured and injured regions. Therefore, the ST segment remains at the preinjury level, which is relatively elevated in reference to the injury baseline.21-24 Consequently, the ST segment appears to be abnormally displaced above the latter. Note that the apparent presence of a systolic current of injury actually reflects disappearance of the diastolic current of injury. Finally, after the end of repolarization, the current of injury between injured and noninjured regions is reestablished, and the ECG baseline is again depressed (as it was immediately before depolarization). Since the precise moment at which injury starts is not recorded in the usual alternating-current (ac) electrocardiographic recordings, the baseline that is almost invariably recorded is the postinjury baseline.10 It also has been shown that the abnormal ST-segment elevation in leads facing the affected zone does not merely represent the (passive) return of the baseline to its preinjury level but reflects a true, active, positive displacement.10,21-24 Thus, when depolarization of both normal and injured regions has occurred, the surface of the normal cells will (on account of their greater initial polarization) be able to accumulate more negative ions. Hence the normal regions become more negative than the injured regions, which are relatively more positive. In consequence, the ST segment becomes actively elevated above and beyond the preinjury baseline because of the relative potential difference existing at the end of depolarization. Most likely, injury reflects both disappearance of diastolic baseline shifts and active ST-segment elevation.10,24

According to the current-of-injury theory, this process results in ST-segment elevation when the injured muscle is located between normal muscle and the corresponding unipolar electrode. On the other hand, ST-segment depression occurs when normal muscle is located between the injured tissue and the corresponding electrode10'12 (see Fig. 11-3). The mechanism of abnormal ST-segment elevation in anatomically defined ventricular aneurysms has not been fully established. Some authors consider that it results from the earlier repolarization of a ring of persistently viable (but nevertheless affected) tissue surrounding the aneurysm.810 For other investigators, chronic ST-segment elevation reflects functional (echocardiographic) dyskinesia, thus not necessarily being due to a pathologic ventricular aneurysm.8,25-27 Coronary artery disease is the most frequent cause of abnormal ST-segment elevation. The latter, when generalized, also can be due to epicardial injury due to pericarditis. Both should be differentiated from the benign "early repolarization" pattern, a normal variant.28,29 In its classic form, there is J-point elevation (of no more than 3 mm) with an upwardly concave ST segment. R waves may be tall and at times have a distinct notch and slur on the downstroke (Fig. 11-4). ST-segment elevation is more frequent in chest leads but can occur in leads I and II. These dynamic ECG changes may be affected by exercise and hyperventilation. Isoproterenol reduces and propranolol increases ST-segment elevation.30,31 Although the mechanism of early repolarization has not been fully elucidated, it has been related to enhanced activity of the right sympathetic nerves.30

Figure 11-4: Early repolarization. This normal variant is characterized by narrow QRS complexes with J-point and ST-segment elevation in the chest leads. Left chest leads often show tall R waves with a distinct notch or slur in their downstroke (arrow in V5), while the right chest leads may display ST segments having a "saddleback" or "humpback" shape (arrow in V3).

Figure 11-4: Early repolarization. This normal variant is characterized by narrow QRS complexes with J-point and ST-segment elevation in the chest leads. Left chest leads often show tall R waves with a distinct notch or slur in their downstroke (arrow in V5), while the right chest leads may display ST segments having a "saddleback" or "humpback" shape (arrow in V3).

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