Sometimes a patient is fortunate to have a cardiac arrest

Written by Pendell Meyers 

A man in his 60s presented with acute chest pain.

Here is his triage ECG:

What do you think?

There is sinus rhythm with clear LVH. Leads V5-6 are suspicious for upright, enlarged T waves that are possibly inappropriate for the QRS complex, especially V6. But without a baseline for comparison, it would be difficult for me to say that it is specific and diagnostic for OMI. The Queen of Hearts agrees, calling the ECG not specific for OMI.

Smith comment: V6 is very atypical for LVH and very suspicious for OMI.  There is a very high voltage R-wave without any S-wave (terminal QRS distortion) and with a concordant ST segment and T-wave, with convex ST segment.  It is essential to compare with old ECGs.  In the absence of old ECGs, one must record serial ECGs every 15 minutes.

He had several older ECGs on file, here are two examples:

6 days prior:

2 months prior:

In the context of ACS symptoms, and when able to compare the new vs. old ECG, the top ECG is DIAGNOSTIC of OMI until proven otherwise. 

Unfortunately, the ECG was interpreted as no significant change from prior, "no STEMI"!!

He was sent back to the waiting room, where he suffered a VF arrest. Defibrillation was performed, and ROSC was achieved. 

Approximately 5 minutes after ROSC, this ECG was obtained (about 45 minutes after arrival):

Obvious anterolateral OMI, and STEMI criteria positive for those who care or need it.

Smith comment: The patient was lucky to have a cardiac arrest.  Had he not had one, he would have sat in the waiting room until his entire myocardium at risk infarcted.  By undergoing an arrest, providers became aware of his OMI which had not been noticed on his diagnostic ECG, and he thus has a chance at some myocardial salvage.

Also: notice how the LAD Occlusion results in DECREASED S-wave amplitude, compared to the previous ECGs, in V2 and V3.  I have noticed that this nearly always happens, and is the reason that you rarely find an ECG that shows BOTH LVH with high right precordial amplitudes AND acute STEMI/OMI.

Total proximal LAD occlusion was found and stented at angiography soon after the ECG above. Here are some images:

Next morning ECG:

Reperfusion findings are clear..

There is some R-wave preservation, a good sign that some myocardium remains viable

Echocardiogram:

EF 15%

Severe global hypokinesis

Akinesis of basal-mid inferior and inferoseptal myocardium

Severe hypokinesis to akinesis of apical anteroseptal, anterior, and inferoseptal myocardium

An echo from 3 months ago showed an EF of 40% with global mild hypokinesis, without focal wall motion abnormalities.

Smith comment: the initial echo was so bad because even myocardium that was salvaged was "stunned" and it takes time to recover function.  Weeks later, the EF improved from 15% to 40%.  If this patient had not had ventricular fibrillation and thus not had a reasonably short door to balloon time, all of that stunned myocardium would instead be permanently infarcted, with permanent 15% EF.

Troponin I quickly exceeded the laboratory limit of reporting at 25,000 ng/L.

4 days later:

Continued reperfusion.

He was discharged home, but quickly bounced back 4 times within the next few months for worsening heart failure. Long term outcome is not available.

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MY Comment, by KEN GRAUER, MD (2/2/2025):

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We need to learn from cases like today's. Today's initial ECG is not an easy tracing to interpret. This is because (as per Dr. Meyers) — there is obvious LVH that complicates assessment for potential acute ST-T wave abnormalities.

• To Emphasize: Once again — the history is KEY. This patient is a man in his 60s who presented to the ED with new CP. As a result — without yet looking at the initial ECG, our "mindset" has-to-be awareness that this history alone places this patient in a higher risk category for having an acute cardiac event. 
• As a result — Our "mindset" has-to-be that we need to rule out an acute event, rather than the other way around. This means that if there is any uncertainty about the diagnosis (or about the initial ECG) — that we need to "dig further" until we arrive at more certainty in our diagnosis. Unfortunately, this was not done in today's case. I say this — because compared to an ECG done just 6 days earlier — there clearly has been significant ST-T wave change, that in this patient who presents to the ED with new CP — has-to-be recogized as an acute OMI until proven otherwise (See Figure-1 below — in which I place these first 2 tracings in today's case together).

What Are the Oversights?

In my experience — many (if not most) clinicians do not compare serial ECGs by placing both ECGs that they are looking at side-by-side.

• I fully acknowledge that I miss important findings when I do not do this. I know this was not done in today's case — because if side-by-side comparison had been done — then the difference in ST-T wave appearance between leads V4,V5,V6 in ECG #1 and ECG #2 would not have gone unnoticed. 
• We have often remarked on the challenge that LVH may pose for recognizing acute ischemic changes. This is because LV "strain" often manifests straightened and elevated ST segments in anterior leads with deep S waves from marked LVH. For example, as an isolated finding — I would not necessarily interpret the ST segment straightening and elevation that we see in leads V2,V3 of ECG #1 (outlined in RED and light BLUE) as abnormal in a patient with marked LVH.
• The other challenge posed by the ECG of a patient with marked LVH with "strain" — is distinguishing between the ST-T wave inversion in one or more lateral leads due solely to LVH — vs that due to acute ischemia or infarction. This distinction is further complicated because marked LVH may at times mask the ST-T wave changes of acute ischemia. That said — the asymmetric ST-T wave depression in lead V6 of ECG #2 is classic for the ECG appearance of LV "stain". But 6 days later (ie, when ECG #1 was recorded) — there is not even a hint of ST flattening or depression in leads V4,V5,V6. This means that the ST-T wave appearance in ECG #1 clearly represents an acute change (compared to ECG #2) that would not be missed if there had been lead-to-lead comparison between these 2 tracings.

Figure-1: Comparison between today's initial ECG — with a prior ECG done just 6 days earlier.

How to Remember ECG Findings of LVH and LV "Strain"?

There are over 50 criteria in the literature for the ECG diagnosis of LVH. And — the ST-T wave appearance of LV "Strain" and "Strain Equivalents" is subjective, and can be confusing.

• To facilitate recall of these concepts — We've conveniently added a link in the menu at the top of every page in Dr. Smith's ECG Blog that takes you to My Comment in the June 20, 2020 post, in which I review a user-friendly approach to ECG recognition of LVH and "Strain" (See Figure-2).

Figure-2: Handy link to LVH Criteria (conveniently placed in the menu at the top of every page in Dr. Smith's ECG Blog).

WHY then is Today's Initial ECG So Difficult to Interpret?

The above said — I still found today's ECG incredibly difficult to interpret for the simple reason that there is marked overlap of QRS complexes in virtually all of the chest leads.

• Confession: I spent over half an hour staring at the QRS complexes in each of the chest leads, trying to distinguish between the limit of R waves from overlapping S waves. I am still not certain that my color-coding in Figure-1 is completely correct.
• KEY Point: Whereas the ST segment straightening and elevation that we see in leads V2 and V3 of ECG #1 does not necessarily look abnormal (because as noted earlier — LV "strain" from marked LVH may show this ST-T wave appearance in anterior leads) — the same is not true for leads V4,V5,V6.
• Lead V4 in ECG #1 (outlined in dark BLUE) — manifests an S wave that is only 13 mm deep. Doesn't the coved and elevated ST segment in this lead look disproportionate and abnormal?
• As noted earlier — LV "Strain" manifests as ST-T wave depression in lateral leads (or at least as ST-T wave flattening). LV "strain" does not manifest as ST segment coving and elevation, as we see in lead V5 and especially in lead V6 of ECG #1.

What Could Have Been Done to Facilitate Interpretation? 

• Rather than normal standardization — I would have immediately repeated today's initial ECG at half-standard voltage. Doing so would have minimized overlap — and facilitated appreciation of disproportionality by clarifying relative size of QRS complexes and ST-T waves.