The patient: 79-year-old man complaining of severe “burning” chest pain, radiating to his neck. Walking exacerbates his discomfort. He has had nausea and vomiting for 24 hours. Past medical Hx includes high cholesterol and atrial fibrillation. Medications not known.
The ECGs: These ECGs could be called “classic”. There is a 100% occlusion of the right coronary artery (RCA), which was successfully repaired in the cath lab. About 80% of inferior wall M.I.s are due to occlusion of the right coronary artery. Depending on how proximal the occlusion is, we can expect a pattern on the ECG representing injury to all areas supplied by the RCA. This “package deal” can include:
· Inferior wall ST elevation.
· Posterior wall extension.
· Right ventricular M.I.
· Right atrial ischemia, including damage to the SA and AV nodes.
· Occasionally, low lateral wall ST elevation, when that area is solely perfused by the RCA.
ECG No. 1,obtained at 5:34 am, shows the following:
· Atrial fibrillation with a slow ventricular response. (AV node may be ischemic).
· ST elevation in Leads II, III, aVF, V4, V5, and V6. (Transmural injury in the inferior and low lateral wall).
· Reciprocal ST depression in I and aVL. (Leads reciprocal to inferior wall).
· Reciprocal ST depression in V1, V2, and V3. (Leads reciprocal to posterior wall).
· Hyperacute T waves in leads with STE (often a sign that precedes the STE).
· STE in Lead III is greater than STE in Lead II. STD in V1 minimal, compared to V2. (These are reliable signs that there is right ventricular M.I.)
From this list of ECG signs, we can say that there is INFERIOR WALL ST ELEVATION M.I., plus likely RIGHT VENTRICULAR M.I. and POSTERIOR WALL EXTENSION OF IWMI.
ECG No. 2, obtained at 5:37 a.m., has an additional lead: V4 Right. V4R shows ST elevation, with a flat ST segment and T wave inversion. The right ventricular M.I. has been confirmed. (Note: Posterior wall M.I. could be confirmed with posterior leads, V7, V8, V9. We do not have those here.)
Inferior wall M.I. has a relatively low mortality rate, usually less than 10%. However, the presence of RVMI increases the chance of hypotensive episodes and in-hospital mortality by up to half. RVMI does not change mortality rates after hospital discharge. In addition, the posterior wall extension indicates that this M.I. is a large one, from a proximal occlusion of the RCA.
Summary: Being able to quickly recognize this pattern will help you spot IWMI even before the ST elevations are large. When there is only very subtle ST elevation, the presence of the pattern of STE in the inferior leads and reciprocal STD in aVL make it easy to recognize. Reciprocal STD often shows up before STE, and is more dramatic and easier to spot. When there is also bradycardia, posterior wall M.I., and RVMI, it becomes even easier to diagnose right coronary artery occlusion.
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