Monday, October 22, 2018

A man in his 80s with chest pain

Written by Pendell Meyers

A male in his 80s with history of colon cancer, HTN, and CAD with a newly placed LAD stent approximately 1 month ago, presenting with acute shortness of breath and chest pain. No prior ECG.

Here is his ECG at 07:08:
There is STE in V2, I and aVL, but it does not meet STEMI criteria because there are no two contiguous leads with STE meeting criteria. There is also STD in V3-V6, as well as II, III, and aVF. There is likely lead misplacement involving V2 explaining the R-wave progression. These findings and their associated morphology are definite evidence of transmural ischemia of the anterior and lateral walls, most commonly due to OMI. This distribution would sometimes be seen with a large first diagonal, however we have prior knowledge that the patient just had a proximal LAD stent placed, making this site very likely and also consistent with the pattern above. 

The cath lab was activated.

By the time the cardiologist arrived, the patient started to deteriorate rapidly. He was in acute, profound cardiogenic shock. He never had VF/VT, but instead became bradycardic and hypotensive quickly before suffering PEA arrest.

Here is his last available ECG prior to arrest at 07:29:
There is new RBBB and LAFB (the prior ECG shows similar frontal plane axis, but is now wider qualifying for LAFB). This is a very bad prognostic sign of LAD occlusion. This ECG may be barely positive for STEMI criteria with 1mm STE in lead I. Lead V2 is still clearly misplaced, likely too high on the chest wall.

CPR and ACLS were initiated without response.

Due to his age and baseline conditions he was not an ECMO candidate, and the clinical decision was made not to pursue cath during compressions. Lytics were considered but not given and are not the focus of this post. He never got cardiac catheterization and could not be resuscitated.

It is overwhelmingly likely (but not proven) that this patient died of acute LAD occlusion.

Learning Points:

Rapidly deadly OMI may present without STEMI criteria. Despite the fact that the clinicians activated the cath lab immediately on the first ECG, they were unable to save him. His chances would have been even worse had the clinicians waited for STEMI  criteria to be present.

New RBBB and LAFB is a very bad prognostic sign of LAD occlusion.

Comment by KEN GRAUER, MD (10/22/2018):
Unfortunate case presented by Dr. Meyers, regarding rapid demise of an 80yo man with new-onset chest pain, whose condition quickly deteriorated despite appropriate recognition and management. I limit my comments to a few points about his 2 ECG tracings (Figure-1).

Figure-1: Comparison of the 2 ECGs shown in this case (See text).
It is cases like these that we’d love to learn from. The patient had an LAD stent placed just 1 month earlier — but his prior ECG was not available: 
  • If we could obtain access to that prior ECG — we would be in much better position to answer questions about lead placement issues and prior ECG abnormalities that he may have had after his stent placement a month earlier.  
  • And, since this patient died before cardiac catheterization — we’ll never know for certain the anatomic cause of his demise.
Thoughts about ECG #1:
  • The rhythm is sinus tachycardia, at a rate just over 100/minute. There is diffuse ST depression — with the exception of leads I, aVL, aVR and V2 that show ST segment elevation.
  • I interpret the mean frontal plane axis at -30 degrees, if not a little less. That’s because if one “averages” the net QRS deflection for the 4 beats in lead II of ECG #1 — the axis is virtually isoelectric (equal parts positive and negative). For there to be LAHB, the frontal plane axis should be clearly more negative than -30 degrees — which is easy to recognize by simply noting if the net QRS deflection in lead II is clearly negative. The frontal plane axis is ~90 degrees away from a frontal plane lead that is isoelectric. So if the net QRS deflection in lead II (at +60 degrees) is more negative than positive — then the frontal plane axis is more than 90 degrees away (or more negative than -30 degrees). This point is relevant in this case — because there is no doubt that the net QRS deflection in lead II of ECG #2 now is more negative than positive. NOTE: It is estimated that the presence of a hemiblock (lahb or lphb) adds no more than 0.01-to-0.02 second to QRS duration. As a result — the QRS complex does not necessarily have to be wide for there to be LAHB (although most of the time there is at least slight QRS widening).
  • As per Dr. Meyers — QRS morphology does not make sense in lead V2 of ECG #1. While true that acute occlusion of the 1st or 2nd diagonal branch of the LAD may produce an ECG picture of ST elevation limited to lead V2 (or limited to lead V2 + lead aVL) — I’m at a loss to explain the qR pattern in V2, that occurs here in association with contiguous rS complexes in neighboring leads V1 and V3 — unless there was significant lead placement error. This is relevant — because key ECG information about OMI may be missing due to precordial lead misplacement errors. Whether the “culprit” artery in this case is the 1st diagonal, the proximal LAD — or perhaps there is severe multivessel disease, possibly without acute occlusion — I think is open to question.
  • KEY POINT — None of our discussion about the potential “culprit” matters nearly as much as the fact that the treating clinicians in this case promptly recognized that regardless of whether or not STEMI criteria were formally met — this was a patient who needed immediate activation of the cath lab!
Thoughts about ECG #2:
  • In ECG #2 — The rhythm has changed! The upright P wave with normal PR interval that was clearly seen in lead II of ECG #1 is no longer present! Except for a single late-cycle (end-diastolic) PVC — the rhythm looks regular at a slightly slower rate (80-85/minute) — and, the rhythm in ECG #2 looks to be coming from the conduction system because of virtually identical initial deflections in virtually all leads as was seen in ECG #1. Although difficult to be certain because of baseline artifact and the low amplitude of atrial activity — there appear to be small upright P waves with a very short PR interval in leads I and aVL. Atrial activity is uncertain in other leads. This suggests a low atrial rhythm.
  • As per Dr. Meyers — the QRS complex of the supraventricular rhythm has widened compared to what was seen in ECG #1. RBBB is suggested by what looks to be an rsR’ in lead V1 (or perhaps it is a qR in V1?) — with new development in ECG #2 of a terminal S wave that admittedly is narrow in lead I, but which now is also much wider than it had been in lead V6. New LAHB is diagnosed by now predominant negative activity of the QRS complex in lead II — compared to the essentially isoelectric QRS complex in lead II that was seen in ECG #1.
  • Perhaps more than anything, it is the combination of rapidly deteriorating clinical condition + new RBBB/LAHB + ST elevation in at least one anterior lead that suggests the “culprit” may be proximal LAD occlusion. That said, as emphasized above — the KEY point in this case is that regardless of which vessel might be the "culprit" artery, this patient needs immediate cath for diagnosis of the acute problem, as well as for probable reperfusion.


  1. There's also an evident high-lateral STEMI meeting the criteria, and ST depression in D2, D3, aVF mirroring the STE.

  2. Very sad case with excellent comments by Dr. Grauer. I suspect V2 is actually V6 And V3 is actually V2 with the remaining leads shifted to the left in order. It would certainly match with Lead I more realistically.

    1. Thanks for your comment Jerry! I agree completely with your thought, which certainly would make for a much more reasonable chest lead progression sequence! — :)

  3. Great article, I just am a little confused and only a year experience of ekg interpretation.

    That first EKG you stated had no two consecutive leads of ST elevation, but you stated there is significant STE in 1 and aVL, which are both lateral facing leads. With the reciprical depression in i, ii, and aVF, shouldn't this automatically alert a stemi considering presentation?

    Although I and aVL both are lateral views, have I been mistaken in assuming they are consecutive?

    1. I and aVL are consecutive leads, but they don't both have 1 mm of STE (thus, don't meet criteria).

  4. very unfortunate case., excellent discussions. shows how time is sometimes critical in the ED. as Pendell mentioned, thrombolytics was not the point of the discussion.
    just wondering if i might have given it a try, either TNK, or 50-100 mg of tPA, before ending the resuscitation.

    thank you, Pendell.

    1. Tom, My own opinion is that would be futile.
      Couldn't hurt, except for the $10,000 price tag.

  5. I saw this and immediately thought about great post:
    It seems to confirm high lateral STEMI and justifies V2 morphology in this case.

    1. @ Anonymous — The "12 Leads of Christmas" series (that you link to) was written up in EMS 12-Lead by our good friend & colleague Vince DiGiulio. Vince is a MASTER at breaking down the heart's depolarization forces into vectors, and visualizing them in 3 dimensions. That said, I don't think Vince's article justifies the QRS appearance of lead V2 in the 1st tracing in this case, in which both V1 and V3 were predominantly negative. I think ( = my opinion) that Jerry Jones' comment above (2nd Comment above) is a more plausible explanation. Thanks again for your input! — :)


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