Sunday, March 3, 2019

ECG Blog #162 (STEMI – Coronary Circulation – Culprit – BBB)

The ECG in Figure-1 was obtained from an older woman who called EMS because of new-onset chest pain.
  • How would you interpret this tracing?
  • Which coronary vessel is likely to be acutely involved?
Figure-1: Initial ECG obtained from an older woman with new-onset chest pain. NOTE — Enlarge by clicking on the Figure.
Interpretation: There is baseline artifact, especially in the inferior leads — as this ECG was obtained in the ambulance in route to the hospital. That said — the tracing is still interpretable. The rhythm is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement. Regarding Q-R-S-T Changes:
  • There are no Q waves.
  • R wave progression is normal — with transition (where the R becomes taller than the S wave is deep) occurring between lead V3-to-V4, which is normal.
  • There is 1-2 mm of J-point ST elevation in leads V4-thru-V6. Although marred by artifact — the T waves in each of the inferior leads (II, III, aVF) appear to be larger, wider at their base, and more-peaked-than-expected — consistent with hyperacute T wave changes. There is subtle-but-real ST-T wave depression in leads aVL, V1 and V2.
IMPRESSION: In a patient with new-onset chest pain — the ECG in Figure-1 is strongly suggestive of an acute lateral STEMI (ST Elevation Myocardial Infarction). In addition, there is most probably posterior and inferior wall involvement.
  • Although the vast majority (~80-90%) of acute inferior Mis are the result of acute RCA (Right Coronary Arteryocclusion — the culprit” artery in this case is much more likely to be the LCx (Left Circumflex Artery). This is because the most prominent area of ST elevation is in the lateral chest leads (V4,V5,V6— rather than in the inferior leads.
  • When the LCx is a dominant vessel — it supplies the lateral, posterior and inferior walls of the left ventricle. These are precisely the areas of the heart that appear to be affected in this initial ECG.
  • Because of the anatomic location of the RCA  acute occlusion of this vessel typically results in: iST elevation in lead III > lead II; iimarked reciprocal ST depression in lead aVL, that is characteristically the “mirror-image” of the ST elevation seen in lead III; iiiECG evidence suggesting acute RV involvement (ie, much less ST depression in right-sided lead V1 compared to lead V2 — or sometimes even ST elevation in V2); and, ivless ST elevation in lead V6 than is seen in lead III. None of these features is seen in this case.
Comment: Although relatively modest in amount — it is the composite of ST-T wave changes in virtually all leads in this patient with new-onset chest pain that makes the diagnosis of an acute STEMI.
  • Lack of any J-point notching — and, the shape of the ST elevation in lateral chest leads V4-thru-V6 that looks hyperacute — is what suggests acute lateral infarction.
  • In support that these findings are real (and not the result of early repolarization) — is the subtle-but-real ST-T wave depression in leads V1, V2 that suggests associated posterior infarction. Reasons why the amount of anterior ST depression is modest might include either multivessel disease, and/or attenuation of ST depression by the ST elevation in other chest leads.
  • In the setting of acute postero-lateral MI — we look extra close at the inferior leads. As noted earlier — the ST-T waves in each of the inferior leads appear to be hyperacute — with reciprocal ST depression in lead aVL.
  • Finally, the ST segment in lead V3 appears to be straighter-than-expected — consistent with what one might anticipate for a “transition lead” between ST depression in V1,V2 and ST elevation in V4-6.
  • Putting This Together — While none of these changes are marked, a “story” is clearly being told in this patient with new chest pain, in which 10 out of the 12 leads in this ECG are consistent with acutely evolving infero-postero-lateral STEMI. Another ECG should be obtained shortly in an attempt to clarify the picture.
A 2nd ECG was obtained 12-minutes later, as the ambulance arrived at the hospital. 
  • What does this 2nd ECG show (Figure-2)?
  • What has happened since the 1st ECG?
  • Why might this change in QRS appearance have occurred?
  • If you had not seen the 1st ECG in Figure-1 — Would you be able to make a definite diagnosis of acute STEMI from this 2nd ECG alone?
  • How does knowing what the 1st ECG looked like, help interpreting this 2nd ECG?
Figure-2: The 2nd ECG on this patient — obtained just 12-minutes after the initial ECG that was shown in Figure-1.
ANSWERS: The rhythm for the 2nd ECG that is shown in Figure-2 is again sinus. However, since the 1st ECG was done — the heart rate has increased slightly (up to ~85/minute — compared to ~70/minute for the ECG in Figure-1).
  • The QRS complex has widened. QRS morphology is now fully consistent with complete LBBB (Left Bundle Branch Block— in that there is a monophasic R wave in left-sided leads I and V6 — and a predominantly negative QRS complex in right-sided lead V1.
  • Although diagnosis of acute MI is often more difficult in the setting of complete LBBB — definitive diagnosis of an acute STEMI is possible in Figure-2because there is clearly abnormal coved ST elevation that should not be there in lateral chest leads V5 and V6!
  • There are 2 reasons why this patient may have developed complete LBBB since the 1st ECG was done: iThis may be a rate-related BBB — since the heart rate is now faster (~85/minute) than it was at the time the 1st ECG was done (~70/minute); and/oriiAcute ischemia from ongoing acute infarction, with compromised perfusion to the bundle branch system. Regardless of which cause(s) is operative — development of new LBBB implies a more significant lesion.
COMMENT: From a teaching perspective — Comparison of the 2 ECGs in this case is a “golden opportunity” to appreciate how to recognize some of the some of the subtleties of acute ischemia/infarction in association with complete LBBB. For clarity — We put both tracings together in Figure-3:
Figure-3: Comparison of the 2 ECGs in this case (See text). 
What WSee in Figure-3: As mentioned — the presence of clearly abnormal ST elevation (in leads V5 and V6) in association with LBBB in this patient with new chest pain is diagnostic of an acute STEMI.
  • The ST-T wave in lead V4 of the LBBB tracing is also clearly abnormal, and represents a hyperacute ST-T wave. Note how unexpectedly tall, wide-at-its-base, and fat-at-its-peak this T wave in lead V4 is.
  • Similarly, the T wave in lead V3 of the LBBB tracing is unexpectedly tall with an inappropriately wide base. This also reflects a hyperacute change. We know these findings in leads V3 and V4 of the LBBB tracing are real — because we saw ST-T wave abnormalities in these same leads in the initial ECG when the QRS complex was narrow.
  • PEARL: Keep looking at neighboring leads when assessing to see if subtle changes are likely to be abnormal. We did this in Figure-1 — when we looked at lead V3. The ST segment flattening in V3 was extremely subtle, and recognized as abnormal primarily because it occurred as a “transition lead” between the ST depression we saw in neighboring lead V2 — and the hyperacute ST-T wave we saw in lead V4. Similarly, the flat “shelf” for the ST segment in lead V2 of the LBBB tracing can be recognized as abnormal, given its proximity to clearly abnormal leads V3-thru-V6.
  • Finally, the ST-T waves in each of the inferior leads in the LBBB tracing are hyperacute. In addition to their appearance in the LBBB tracing (wider-than-expected base + fat-at-their-peak) — we know that these inferior lead changes are real — because we saw similar hyperacute changes in these same leads in the initial ECG when the QRS was narrow.
  • Note that although there is ST-T wave depression in both leads I and aVL in the LBBB tracing — even in retrospect, it’s difficult to know if this finding is marked enough to qualify as "abnormal" in the setting of LBBB. But even without counting what we see in leads I and aVL — we see clearly abnormal ST-T wave findings in 8 of the 12 leads in the LBBB tracing!
BOTTOM Line: This patient is in process of a large acute infero-postero-lateral STEMI — with development of new LBBB just 12 minutes after the initial ECG.
  • The patient was taken to the cath lab soon after arrival at the hospital. The “culprit” artery was the Obtuse Marginal Branch of the LCx.
Acknowledgment: My thanks to Rory Prevett from Dublin, Ireland for his permission allowing me to use this tracing and clinical case.
NOTE: For more on how to determine the Culprit Artery” — Please CLICK HERE.
For quick review on ECG Basics of BBB — Please CLICK HERE.
  • NOTE: If you click onSHOW MORE just below the video on the YouTube page — You’ll see a linked Contents of everything in this 17-minute video.
For written review on ECG Basics of BBB — Please CLICK HERE.
  • NOTE: For more on how to diagnose acute ischemia/infarction in association with underlying BBB — See Sections 05.24-thru-05.29 in the above pdf.
  • For more on Rate-Related BBB — Please CLICK HERE.

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