Depression of the ST segment of the heart. Ischemic ST elevation on ECG

Depression of the ST segment , in turn, manifests itself in the form of elevation of the ST segment, since electrocardiographic recorders in clinical practice use AC amplifiers that automatically compensate for any negative shift of the TQ segment. As a result of this electronic compensation, the ST segment will be proportionally raised. Therefore, according to the theory of diastolic damage current, the ST segment elevation is an imaginary displacement.

The true bias, which can be observed only in the presence of a direct current ECG amplifier , is that the TQ isoline is below normal, taking a negative value. 

This hypothesis suggests that the ischemic elevation of ST (and strongly pointed T waves ) is also associated with systolic damage current. Three factors can change the extracellular charge of myocardial cells in acute ischemia, relatively positive (compared to normal cells) during electrical systole (QT interval): (1) pathologically early repolarization (shortened duration of PD); (2) the slowed down speed of the ascending knee PD; (3) reduced amplitude of PD. The presence of one or more of these factors creates a voltage gradient between the normal and ischemic zones during the QT interval. Thus, the damage current vector will be directed to the ischemic zone.

The mechanism of this systolic damage current will result in an initial ST elevation, sometimes with high positive (sharp) T waves. 

When acute ischemia is transmural (due to diastolic and / or systolic damage current), the common ST vector is usually mixed in the direction of the outer (epicardial) layers, and ST elevation and sometimes high positive (sharp) T waves form above the ischemic zone. reciprocal ST depression in leads recording signals from the contralateral surface of the heart.

Sometimes, recirculating changes may be more pronounced than primary ST elevation. When ischemia is initially limited by the subendocardium, the general ST vector is usually biased towards the inner ventricular layer and the ventricular cavity, therefore the leads located above them (for example, the anterior chest) depress ST segment with ST elevation in the aVR lead.

Such a picture of subendocardial ischemia is typical during spontaneous episodes of angina pectoris, symptomatic or asymptomatic (painless) ischemia, provoked by stress or pharmacological stress studies.

The amplitude of ST changes in acute ischemia can be influenced by multiple factors. Severe (explicit) elevation or depression of ST in many leads usually indicates very severe ischemia. Conversely, the rapid elimination of ST elevation in thrombolytic therapy or percutaneous coronary intervention is a specific marker of successful reperfusion.

These relationships, however, are not universal because severe ischemia or MI may be accompanied by minor ST-T changes, or may not be accompanied by them. Moreover, the relative increase in the amplitude of the T wave (giant T wave) can be combined or precede the ST rise due to the damage current caused by myocardial ischemia with or without MI.

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