Serial ECGs for chest pain: at what point would you activate the cath lab?

Written by Jesse McLaren

 

A healthy 75 year old developed 7/10 chest pain associated with diaphoresis and nausea, which began on exertion but persisted. Below is the first ECG recorded by paramedics after 2 hours of chest pain, interpreted by the machine as “possible inferior ischemia”. What do you think?

 

 

There’s competing sinus bradycardia and junctional rhythm, with otherwise normal conduction, borderline right axis, normal R wave progression and voltages. The inferior STD/TWI which the machine sees is reciprocal to subtle high lateral hyperacute T waves, which are associated with hyperacute T waves V3-4, STE in V4 and convex ST segment in V5. While STEMI negative, the ECG is diagnostic of proximal LAD occlusion.

 

The patient had ongoing chest pain, so the paramedics recorded another ECG 10 minutes later:

 

There’s dynamic change, with loss of R wave, new STE and larger T wave in V3, smaller T wave in V4 and now STD in V5-6. The machine indicated STEMI (but it barely meets STEMI criteria, if at all) and the patient was brought to the ED:

 

On arrival 20 minutes later the pain had reduced to 1/10 after aspirin, and the patient had repeat ECG at triage:

 

 

 

Now the ST segments and T waves have normalized, and the only abnormality is sinus bradycardia and loss of R waves. In isolation this ECG does not show OMI, but following the paramedic ECGs this indicates spontaneous LAD reperfusion. It’s unclear if the paramedic ECGs were seen or missed in the ED. “Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky.

 

The emergency physician asked for serial ECGs every 15 minutes:

There’s sinus rhythm with PVCs in bigeminy, along with reocclusion of the proximal LAD. In the sinus conducted beats we can see STE in aVL with reciprocal inferior STD, and STE in V2 and V4-V5 (which meet STEMI criteria but were missed by the computer). We can also see OMI in the PVCs, including the subtle concordant STE in V2 and the obvious excessive discordant STE in V4-5 (both STE>25% of the preceding S wave).

 

This was missed and another ECG was done 15 minutes later:

The PVCs are gone and the ST/T waves have improved, along with terminal T wave inversion in V4 – indicating spontaneous reperfusion again.

 

Five minutes later the patient developed a wide complex rhythm:

Regular wide complex rhythm at normal rate with AV dissociation, indicating AIVR, which in the context of resolved chest pain is another indication of spontaneous reperfusion.

 

At this point the emergency physician asked for a stat cardiology consult. In the consult note there was no mention of lack of STEMI criteria or the presence of any of the subtle ECG signs of OMI, but the underlying pathology was identified: “75 year old presenting with an episode of significant chest pain, new reperfusion rhythm suggestive of Occlusion MI.”

 

Cath lab was activated, and found a 95% proximal LAD occlusion which was stented. First troponin I was 18ng/L which is in the normal range, which is common with only 2 hours of chest pain. Despite a door-to-cath time of less than 2 hours, the peak troponin was greater than 50,000 ng/L, and on echo there was anterior hypokinesis

Next day ECG showed anterolateral reperfusion TWI:

Paradigm shift

 

The patient was fortunate that they spontaneously reperfused twice, but still had a large infarct. Despite many ECG signs of OMI being missed the door-to-cath time was still fast, because all the healthcare providers were focused on the pathology of acute coronary occlusion and not were distracted by the lack of STEMI criteria. But the care of this and other patients could have been improved with earlier detection of OMI.

 

This case is an example of the steps we can all take in daily practice as the paradigm shifts from STEMI to OMI. As Smith and Meyers explained in a 2020 article in EM News:

“What should we do in the meantime while we are still stuck in the STEMI paradigm in daily practice? First, start using the terminology that allows our understanding to progress. Start using the terms acute coronary occlusion and occlusion MI. Second, consider learning more about ECG in OMI, especially about features other than ST elevation that help to diagnose OMI.

Learn the full progression of ECG findings of occlusion and reperfusion that have been hidden from your education due to the STEMI paradigm. Follow up your patient's cath results to learn which were false-positives or missed occlusions. Most importantly, while waiting for the paradigm to evolve, maintain focus on our true goal for our patients with ACS: to identify and reperfuse patients with acute occlusion MI.”

 

This paradigm shift can be accelerated by by expert-trained AI. Here are the ECGs as interpreted by the Queen of Hearts:

 

Both paramedic ECG: OMI high confidence, so the patient could have been taken directly the cath – saving 2 hours of reperfusion time:

First ECG not OMI high confidence – but in the context of the previous ECGs this indicates spontaneous reperfusion at risk of reocclusion.

 

 

 

Serial ED ECGs OMI high confidence – both during reocclusion and spontaneous reperfusion:

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Take home

 

1. OMI is a dynamic process that can fluctuate between spontaneous reperfusion and spontaneous reocclusion

2. serial ECGs (including reviewing paramedic ECGs) are crucial

3. 'transient STEMI' is at high risk for reocclusion

4. Use the terminology of Occlusion MI, and focus on the reperfusion of acute coronary occlusion

5. Learn OMI signs commonly missed by STEMI criteria - including acute loss of R waves, convex ST segments, hyperacute T wave, reciprocal change, and PVCs with concordance or excess discordance

6. Queen of Hearts can save myocardium

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MY Comment, by KEN GRAUER, MD (8/11/2024):

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Outstanding case study discussion by Dr. McLaren — that concisely reviews state-of-the-art assessment of serial ECG changes in this patient with acute LAD occlusion that spontaneously reperfuses and then reoccludes more than once.

• The door-to-cath time was less than 2 hours — which is fast compared many of the cases sent our way, because (as per Dr. McLaren) — "Health care providers were focused on the pathology of acute coronary occlusion, and were not distracted by the lack of STEMI critieria".
• The challenge that remains entails the difficult task of retrospective review on those details that can (and optimally should) enable even more streamlined OMI recognition and treatment.

As Dr. McLaren has expertly dissected today's case — I focus brief commentary on the first 2 EMS ECGs from the viewpoint of assessing the cardiac rhythm (Figure-1).

• As with many prehospital ECG recordings — a long lead rhythm strip is lacking. While not preventing overall assessment of this case (acute LAD OMI is clearly evident) — the lack of a long lead rhythm strip especially complicates rhythm interpretation in cases like today's, in which we only have 6 or 7 beats, with changing QRS morphology and uncertain P wave presence.
• In EMS ECG #1 — We know sinus rhythm is at least intermittently present, because despite the different QRS morphology of beats #4 and 5 in lead V3 — both of these beats are preceded by seemingly normal sinus P waves with constant (and no more than slightly prolonged) upright P waves (RED arrows seen before these 2 beats in both V3 and simultaneously-recorded lead V1).
• Although I suspect the tiny, upright deflection that precedes beat #6 in lead V6 represents another sinus P wave with the same PR interval — I don't see any other reliable indication of sinus P waves on the rest of the tracing.
• Significant bradycardia (rate in the 40s/minute) — is present throughout. Since no sign of atrial activity is evident in lead II (which is the best lead for detecting atrial activity if sinus rhythm is present) — we can quickly conclude (as did Dr. McLaren) that no "set" rhythm is present.
• Whether some form of 2nd-degree AV block might be present (ie, the question I raised about the tiny upright deflection seen between beats #4 and 5) — or whether this is simply "competing sinus bradycardia and junctional rhythm" (as described by Dr. McLaren) — is unimportant compared to recognizing that this significant bradycardia is yet one more indication of the ongoing acute OMI.
• Low-dose atropine may have been considered.

10 minutes later with EMS ECG #2 — there is even less indication of atrial activity.

• While "critieria" for 2nd- or 3rd-degree AV block are not satisfied (since no reliable atrial rhythm is seen) — the clinically important message is simply the presence of profound, persistent bradycardia as a manifestation of the ongoing acute OMI.

Figure-1: I've put together the 2 pre-hospital ECGs in today's case — which focus on the initial rhythm. (To improve visualization — I've digitized the original ECG using PMcardio).

Rapid Recognition:

As per Dr. McLaren — Given the history of new-onset CP in today's patient, the 2 EMS ECGs were instantly diagnostic of acute LAD OMI, meriting immediate cath lab activation at that time. For clarity in Figure-2 — I highlight the "path of my eyes" in these first 2 EMS ECGs. 

• On recognition of the profound, persistent bradycardia in ECG #1 — the acute-looking, ST segment straightening with elevation in lead V2 — followed by clearly "hypervoluminous" T waves in leads V3 and V4 make the diagnosis of proximal LAD occlusion within seconds.
• This ECG diagnosis is supported by the markedly disproportionate hyperacute T wave in lead aVL.
• Any doubt is erased by the inferior lead reciprocal depression.
• 
  
• Side-by-side comparison with the repeat EMS ECG #2, done 10 minutes later — makes the "dynamic" ST-T wave changes described by Dr. McLaren obvious.

In Summary: Real progress is marked in today's case by uniform recognition of health care providers of the OMI paradigm. The goal to attain is now implementing cath lab activation within the 10 minutes, which is all that it took for these 2 prehospital ECGs to be recorded.

Figure-2: Another look at side-by-side comparison of the 2 EMS ECGs.