Saturday, August 6, 2022

ECG Blog #324 — Only 1 Lead ...

The patient whose ECG is shown in Figure-1 — is an elderly woman, who was admitted for acute abdominal pain. CT scan revealed splenic infarction. She also complained of an atypical type of chest pain.
  • How would YOU interpret her ECG in Figure-1?
  • Should you activate the cath lab?

Figure-1: The initial ECG in today's case.

MY Thoughts on the ECG in Figure-1:
Although there is no long lead rhythm strip — it should be apparent that the rhythm is irregularly irregular — and that there are no P waves. The rhythm is AFib with an overall controlled ventricular response. There is 1 PVC (seen in simultaneously-recorded leads V4,5,6). Continuing with my Systematic Approach (as per ECG Blog #205):
  • The QRS is narrow. The QTc is at most no more than minimally prolonged. The frontal plane axis is slightly leftward — but not enough to qualify as LAHB (ie, the QRS in lead II is not predominantly negative).
  • Assuming normal standardization — there is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Other than the Qr complex in lead V1 (which by itself, is not significant) — there are no Q waves.
  • R Wave Progression is normal (with progressive increase in R wave amplitude — leading to normal transition between leads V3-to-V4).

The KEY findings relate to the ST-T Waves:
  • 1 mm of coved ST elevation is present in high-lateral lead aVL. Given modest height of the R wave in this lead — this finding is significant! There appears to be subtle-but-real beginning T wave inversion in this lead.
  • Otherwise — there is significant ST depression no less than 8/12 leads (ie, in leads II,III,aVF; and in V2-thru-V6).
  • There is ST elevation in lead aVR.

Putting It All Together:
Today's case presented a challenging clinical picture. On the one hand — this elderly woman presented with acute abdominal pain, and was found to have a splenic infarction. On the other hand — she did have chest pain, although this did not seem to be her primary complaint.
  • This patient's ECG showed AFib (which presumably was not new) — and suggested the following considerations: i) Diffuse Subendocardial Ischemia (with ST depression in 8/12 leads + ST elevation in lead aVR); ii) Acute MI (with isolated ST elevation in lead aVL); and/or, iii) A combination of i) and ii).

PEARL #1: As emphasized in ECG Blog #271 — Recognition of the above ECG pattern, in which there is diffuse ST segment depression (usually present in at least 7-8 leads+ ST elevation in lead aVR (and sometimes also in lead V1) — should immediately suggest the following Differential Diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock/profound hypotension; GI bleeding; anemia; "sick" patient, etc.).
To EMPHASIZE: The pattern of diffuse Subendocardial Ischemia by itself does not suggest acute coronary occlusion (ie, it is not the pattern of an acute MI) — but rather ischemia due to the above differential diagnosis!

PEARL #2: Complicating our differential diagnosis of the likely cause of the ECG findings in Figure-1 — is the isolated ST elevation in lead aVL. By way of review — I've reproduced in Figure-2, the Table published in ECG Blog #320 — in which I summarize optimal use of lead aVL for predicting the "culprit" artery.
  • According to Figure-2 — the finding of isolated ST elevation in lead aVL (without ST elevation in any other chest leads) — suggests LCx occlusion (especially of the 1st Obtuse Marginal Branch of the LCx).

Figure-2: Optimal use of lead aVL for predicting the "culprit" artery in acute OMI.

PEARL #3: As helpful as the general rules reviewed in ECG Blog #193 are for predicting the "culprit" artery in acute OMI ( = Occlusion-based MI) — these rules are not perfect. Potential confounding factors include anatomic variations — unusual patterns of collateralization (especially after prior infarction) — multi-vessel disease — and/or — other factors that may affect ST-T wave appearances (ie, drugs, electrolyte disorders, chamber enlargement, conduction defects — among others).
  • KEY Point: Much more important in Figure-1 than precise identification of the "culprit" artery — is recognition that in a patient with chest pain, prompt cath is indicated to clarify the anatomy.


CASE Follow-Up:
Suspicion from the ECG in Figure-1 that an acute OMI was actively evolving — was confirmed by return of a markedly elevated troponin.
  • Echo revealed an ejection fraction of ~25% — and — wall motion abnormalities localized to the mid-inferoseptal and apical-septal areas.
  • Cardiac Cath was performed — and revealed that the "culprit" artery was a large 1st Diagonal Branch of the LAD (RED arrow in Figure-3). This was successfully reperfused. There was minimal disease in the LCx. The RCA was a hypoplastic vessel with ~80% narrowing that was not felt to be a "culprit" in this patient's ongoing infarction.

Figure-3: Cardiac Catheterization (Left coronary angiogram — RAO caudal view) — showing high-grade stenosis of a very large 1st Diagonal Branch off of the LAD (See text).

Final Concepts:
I recently reviewed the typical ECG picture for recognizing acute OMI in a 1st or 2nd Diagonal Branch of the LAD (See ECG Blog #320):
  • Look for the "South African Flag" Sign — in which the leads showing maximal ST-T wave deviation take the form of the horizontal "Y" of the South African Flag (Figure-4). 

  • Note in Figure-4 — that there is significant ST elevation in leads I, aVL and V2 — but not in other chest leads.
  • Completing the horizontal "Y" of the South African Flag — maximal ST depression is seen in lead III. 

Figure-4: The pattern of maximal ST-T wave deviation with acute occlusion of the 1st or 2nd Diagonal Branch of the LAD — corresponds to the the arrangement of GREEN coloring in the horizontal "Y" of the South African Flag (This ECG is taken from the case presented in ECG Blog #320).

PEARL #4: The unique aspects of today's case relate to the ECG finding in high-lateral lead aVL of isolated ST elevation limited to this single lead (with exception of lead aVR — that manifests ST elevation as a reciprocal change).
  • KEY Point: It is important to recognize that acute OMI may occasionally present with ST elevation only in lead aVL!

  • Whereas most of the time with acute occlusion of the 1st or 2nd Diagonal, there will be ST elevation in lead V2 (but not in other chest leads)No chest lead in today's case showed ST elevation.

  • Instead, despite ST elevation limited to lead aVL — the area of infarction in today's case corresponded to the distribution of the occluded large 1st Diagonal Branch. This corroborates the Advanced Point brought out in ECG Blog #320 — namely, that MRI anatomic correlations support the concept that lead aVL provides an electrical perspective of ongoing events in the mid-anterior wall more than from a "high-lateral" viewpoint.

  • Finally — the diffuse ST depression in 8/12 leads (with modest ST elevation in lead aVR) suggest a component of diffuse subendocardial ischemia — most probably reflective of severe 2-vessel disease (ie, the ~80% narrowing of the hypoplastic RCA) occurring in the setting of extensive myocardial injury (marked by greatly increased troponin) that resulted from acute occlusion of the very large 1st Diagonal Branch.

P.S.: It remains uncertain as to whether the patient's AFib exerted a causative or contributing role in the splenic infarction and/or acute occlusion of the 1st Diagonal. Coronary thromboembolism is a potential complication of AFib — but available evidence suggests this is not a common event (El-Shetry et al Br  Hosp Med, 2021).


Acknowledgment: My appreciation to Nelson Nersisyan (from Yerevan, Armenia) for the case and this tracing.


Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery.

  • ECG Blog #320 — Reviews the typical ECG picture for recognizing the 1st or 2nd Diagonal as the "culprit" artery (ie, the "South African Flag" Sign).

  • ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.

  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T-waves).

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.


  1. Doesn't the QRS appear wide here (particularly in II and III)?
    I would have mistaken this for LBBB and applied Scarbossa criteria

    1. Thanks for your comment. Your point is a GOOD one! Sometimes the QRS “looks wide” but isn’t. Here — I think the QRS is borderline (ie, up to between 0.10-0.11 second in duration). The reason I did not call this lbbb — is that although monophasic, the QRS just is not wide enough in the lateral leads (ie, in leads I, aVL, V5,V6). And I thought QRS morphology “looked supraventricular” — so I didn’t think that a conduction defect existed. But you are correct that QRS duration is at the least borderline prolonged.

    2. thanks a lot for taking the time to respond!