ST Elevation

ST elevation in AMI occurs in the presence of myocardium that is in the process of dying, and it is often called a current of injury. It typically appears in those infarctions that are transmural, meaning they involve the full

Figure 9.5. Inferior wall AMI producing ST elevation in leads II, III, and aVF. Note that while the force vectors of the current of injury are coming toward II, III, and aVF, they are going away from the reciprocal leads of I and aVL, and the precordial leads represented in the diagram by V3. The deviation of the ECG needle is therefore negative in the reciprocal leads, producing what is called reciprocal ST depression.

Figure 9.5. Inferior wall AMI producing ST elevation in leads II, III, and aVF. Note that while the force vectors of the current of injury are coming toward II, III, and aVF, they are going away from the reciprocal leads of I and aVL, and the precordial leads represented in the diagram by V3. The deviation of the ECG needle is therefore negative in the reciprocal leads, producing what is called reciprocal ST depression.

thickness of the ventricular wall as opposed to a partial thickness. Most STEMIs are therefore transmural.

Note in Figure 9.2 that the ST elevation of AMI is typically, but not always, upwardly convex, meaning that it bows upward. This produces an appearance that some have likened to that of a fireman's cap. However, ST elevation may also be upwardly concave.

Because ST elevation is an upward deflection of the ECG needle, it is clear that the current of injury in the infarcted wall of myocardium is producing force vectors similar to those of a T wave that are coming toward the lead in which we view the ST elevation. In other words, the current of injury is spreading from endocardium to epicardium.

In Figure 9.5, we see the force vectors of a current of injury in the inferior wall coming toward leads II, III, and aVF and producing ST elevation in those leads. By the same token, the force vectors are going away from the leads in the reciprocal or opposite leads I and aVL and the precordial leads of V2-V2, represented in the diagram by V3. This produces what is called reciprocal depression in the wall of the heart opposite the location of the infarction.

Thus, inferior wall STEMIs produce reciprocal depression in the anterior and high lateral walls (leads V2-V4 and I and aVL). Anterior STEMIs produce reciprocal depression in the inferior wall (leads II, III, and aVF), as shown in Figure 9.6.

However, classical reciprocal depression does not always appear with the ST elevation of AMI. Reciprocal depression is fleeting, and depending on the timing of the tracing, a substantial number of acute infarctions may not show it. When present, however, reciprocal depression greatly enhances the confidence of labeling an infarction as acute (as opposed to old).

I II III aVRaVLaVF V1 V2 V3 V4 V5 V6

Acute Inferior Myocardial Infarction
Figure 9.6. Acute anterior wall myocardial infarction. Note that, in addition to ST-segment elevation across the anterior precordial leads, there is reciprocal depression seen in leads III and aVF. Also note that, in this particular patient, the ST elevation is slightly upwardly concave,

When ST elevation alone is seen without other confirming evidence of AMI, most electrocardiographers require for diagnosis that at least 1 mm of elevation be seen in two or more contiguous limb leads for inferior infarctions and at least 2 mm in two or more contiguous precordial leads for anterior wall infarctions.

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