Three prehospital ECGs in patients with chest pain

Written by Magnus Nossen with Edits by Grauer and Smith

The ECGs in today’s case are from 3 different patients all presenting with new-onset CP (Chest Pain). All ECGs were recorded by EMS, and transferred to a PCI capable center for evaluation. For 2 of the 3 patients — the cath lab was activated based on the ECG. One of the patients was lucky to have expert ECG interpretation by the Queen Of Hearts AI model.

The PMCardio Queen of Hearts AI model got all of these difficult ECGs correct.

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How would you assess the ECGs in today’s case?

ECG #1: The patient is a 70-something woman with acute CP and dyspnea. What do you think?

Smith: There is LBBB with a concordant STD in II and aVF (but not lead III) and in V2-V4 with excessively discordant STD in V5 and V6 (ST/R ratio > 30% is VERY specific in our studies of LBBB and paced rhythm!).  The abscence of STD in lead III is suspicious for Aslanger's pattern in LBBB.  In any case, the ECG is diagnostic of severe ischemia and probably OMI.

Smith Modified Sgarbossa Criteria for LBBB and Ventricular Paced Rhythm:

1.   Concordant STE of 1 mm in just one lead or

2a. LBBB: Concordant STD of 1 mm in just one of leads V1-V3

2b  Ventricular Paced Rhythm: Concordant STD of 1 mm in just one of leads V1-V6

3.   Excessively discordant ST elevation in just one lead with an ST/S ratio of 20-25%

Also: if there is one lead with excessively discordant STD of > 30%, that is 98% specific, but only 64% sensitive.

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ECG #2: The patient is a 45-year old man with new-onset retrosternal chest pressure. What do you think? 

Smith: Lead aVL is the critical lead: it has a hint of ST segment elevation and with very specific coving (convexity) and reciprocal STD in lead III.   There is some STE in lead I.  There is also some ST depression in V3.

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ECG #3: The patient is a 35-year old man with a history of tobacco smoking. He presented with new CP of 3 hours duration. What do you think? 

Smith: There is STE in lead III and reciprocal STD in aVL. This is OMI until proven otherwise. Arguing against OMI is the flat STE and the absence of large T-waves.  These latter findings are typical of pericarditis, but pericarditis never has reciprocal ST depression.  On the other hand, myocarditis does have reciprocal ST depression.  So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis.

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Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Also, the presence of ischemia on the ECG does not mean the cath lab should automatically be activated. For instance, most patients with Type-2 MI will benefit more from stabilizing measures than from an angiogram. 

• In short — it is not always clear whether or not to activate the cath lab from a single ECG, especially if the history is limited.

Patient #1 in today's post did not get expert ECG interpretation. Despite active CP — cath lab activation was deferred and this patient was transported to a local hospital without PCI capability. 

• Elevated troponins prompted an echocardiogram — which revealed an apical wall motion abnormality (WMA). It was at that time, with several hours delay — that the patient was finally transferred to a PCI-capable center. 
• Angiography showed a 90-99% instent thrombotic subtotal occlusion of the LAD.

Below you can see the QOH (QOH) interpretation. The overall read is OMI with HIGH confidence. 

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Below is the ECG of Patient #2 — as interpreted by the QOH. The ECG is diagnostic of occlusion myocardial infarction (OMI).

• To the uninitiated — this ECG may appear normal. It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. 
• The ECG shows ST depression in lead V3.  There may be hyperacute T waves from V2-V5, as well as in leads I and II. 
• Lead aVL is the critical lead: it has a hint of ST segment elevation and with very specific coving (convexity) and reciprocal STD in lead III. Compared to the QRS amplitude, the ST change in aVL is very abnormal. 
• In a word — Patient #2 was lucky to have his ECG interpreted by the Queen Of Hearts. This led to immediate cath lab activation — which revealed total occlusion of a large 1st diagonal branch that was stented.

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Below is the ECG of Patient #3 — recorded from a 35-year old man with sudden, new-onset CP.

• The ECG shows slight ST Elevation in an inferolateral distribution. That said — T-waves are not hyperacute, and do not have a typical ischemic appearance. 
• As a result of these ECG findings, this patient was rushed to the cath lab. All coronary arteries were patent without atherosclerotic change. 
• Troponin T at presentation 170ng/L later peaking at 291ng/L. 
• Notice how QOH is not fooled by this ST-Elevation. The overall interpretation is NOT OMI mid confidence.

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Dr. Nossen Discussion: The ECGs in today's post are challenging. Sometimes OMI findings are obvious and anyone can make the diagnosis. Other times, OMI findings on an ECG can be extremely subtle and difficult to identify — leading to delayed diagnosis and an increase in morbidity and even mortality.

• It is our job as health care providers to identify patients in need of urgent revascularization.
• QOH can provide assistance to even the most experienced clinician when it comes to ischemia diagnosis. 

Patient #1 — did not get expert ECG interpretation. Only after troponin returned elevated was an Echo was done, revealing a definite wall motion abnormality. Formal Echo showed an apical WMA, with an ejection fraction of 30%. Baseline Echo done 12 months earlier showed an EF of 45%.

Patient #2 — was lucky to have QOH assisting with ECG interpretation. As a result, this 45-year old man did not experince any delay in treatment — and a large diagonal branch of the LAD was stented with good outcome.

Patient #3 — turned out to have myocarditis. Myocarditis can be very difficult to separate from OMI on ECG, and often some form of coronary artery imaging will need to be done to rule out OMI. Usually with pericarditis and myocarditis — hyperacute T waves (HATW) are not present. It is of course acceptable to have a false positive cath lab activation with this type ECG. I would have favored emergent coronary CT angiogram had I cared for this patient.

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Learning points:  

• Diagnosis of occlusion myocardial infarction (OMI) can be extremely difficult and takes time and effort to learn well.

• The Queen Of Hearts app is an excellent tool to assist in expediting cardiac cath and emergent revascularization in the cath lab! 

• Myocarditis can be difficult to distinguish from OMI.

• If you do not have any false positive cath lab activations — then you probably aren't doing enough coronary angiographies (and you are probably missing a number of OMIs).

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MY Comment, by KEN GRAUER, MD (8/6/2024): 

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I viewed today’s excellent case by Dr. Nossen as illustrating the important concept of how to quickly decide whether or not to activate the cath lab.

• I focus my thoughts on a qualitative approach to these 3 pre-hospital ECGs — all obtained from patients presenting with acute CP (Chest Pain).

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ECG #1 — from a 70-ish year old Woman with acute CP and Dyspnea

• The rhythm is sinus tachycardia at a surprisingly rapid rate of ~115/minute.
• The QRS complex is wide — consistent with LBBB (Left Bundle Branch Block), in that there is a monophasic, all-upright R wave in high-lateral leads I and aVL — with a predominantly negative QRS in the first 4 chest leads. (The terminal S wave in lateral leads V5,V6 is consistent with LBBB — as an all-positive R wave is often not seen with LBBB until more posteriorly directed leads V7,V8 — especially when there is LVH, as is suggested here by the deep anterior S waves).

COMMENT:

In the absence of a prior ECG for comparison — we have no way of knowing if the LBBB in Figure-1 is a new finding.

• NOTE #1: Sinus tachycardia is not usually seen in an uncomplicated acute MI. As a result — the heart rate of ~115/minute in ECG #1 is a worrisome finding. It suggests a more extensive MI, potentially with resultant heart failure.
• NOTE #2: The findings of tachycardia — LBBB — and LVH — all make the assessment of ST-T wave appearance for acute ischemia more difficult, since each of these conditions may be associated with ST-T wave changes of their own that can either mask or simulate ischemia.
• The above said — My “eye” was immediately drawn to leads V5 and V6 (within the RED rectangle in Figure-1) — as there is no way the shape of the ledge-like J-point depression in these leads can be attributed solely to tachycardia, LBBB or LVH (RED arrows in these leads). Instead — regardless of whether you assess the ST-T wave appearance in these lateral chest leads by modified-Smith-Sgarbossa Criteria — or by the qualitative approach that I favor — this disproportionate discordance suggests an acute OMI until proven otherwise.
• 
  
• NOTE #3: The more leads that show abnormal findings — the greater the support in favor of an acute OMI. I thought the disproportionate ST segment discordance in lead II of Figure-1 was more subtle and more difficult to recognize as abnormal than the more obvious ledge-like depression in leads V5,V6. That said, in the context of how convincing the V5,V6 ST-T wave changes are — the J-point ST depression within the BLUE rectangle is also clearly abnormal. And although as isolated findings, I would not have been convinced by the J-point ST depression in lead I or in lead V4 — in the context of definite ST-T wave abnormalities in leads II,V5,V6 — I interpreted the BLUE arrow J-point depression in leads I and V4 as further evidence of acute ischemia.

Figure-1: I've consolidated and labeled ECG #1 — obtained from a woman in her 70s who presented with CP and dyspnea. (Digitized using PMcardio to improve visualization).

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ECG #2 — from a 45-year old Man with acute CP

• The rhythm is sinus at ~60/minute. All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.
• There are small, narrow q waves in multiple leads of unknown (if any) significance.
• There is early transition (with the R wave already taller than the S wave is deep by lead V2).
• 
  
• NOTE #4: The KEY lead in this 2nd tracing is lead aVL (within the RED rectangle). Although assessment is made more difficult by the tiny size of the QRS in lead aVL — there is no way that the ST segment coving with slight-but-real ST elevation and terminal T wave inversion in this lead is “normal”. Given the history of new CP — the abnormal ST-T wave appearance in lead aVL says, "acute OMI" — until proven otherwise.

COMMENT:

The point to emphasize about this 2nd case, is that were it not for lead aVL — I would have a difficult time recognizing an acute cardiac event. Supportive findings are seen in a number of leads — but are extremely subtle.

• The ST segment is elevated in lead I, which is the other high-lateral lead (BLUE arrow). Given the upward concavity of the ST segment ("smiley"-configuration) in this lead — I would have interpreted the appearance in lead I as a repolarization variant had it not been for the history of new CP and the clearly abnormal ST-T wave in lead aVL.
• The ST segment in inferior leads III and aVF is straightened. This is a subtle, nonspecific finding that I find helpful only in the context of the clear abnormality in neighboring lead aVL.

NOTE #5: I found the chest lead picture in ECG #2 confusing — primarily because of the surprisingly early transition, in which we see a qRs complex with predominant positivity already by lead V2.

• As per Dr. Nossen — the T wave in lead V2 looks disproportionately tall (upright BLUE arrow in this lead). Neighboring lead V3 shows clearly abnormal ST depression (that I do not see in V4,V5,V6) — and those T waves ...
• 
  
• BOTTOM Line for ECG #2: Given the history of sudden new CP — I would have suspected acute LCx OMI (with reperfusion T waves in leads aVL and V2,3,4) — but I would have probably wanted a repeat ECG within the next few minutes, as well as gathering more information before activating the cath lab. Sometimes — You have to be there ...
• P.S.: I would not have predicted the acute 1st Diagonal occlusion that was found on cath from this single ECG (See My Comment in the November 21, 2020 post for expected 1st Diagonal ECG findings — as well as the April 8, 2022 post which regards the S. African Flag Sign that is not quite fulfilled here). That said — What counts is the strong suspicion of acute OMI from ECG #2 — and the obvious need to very quickly find out more — so it is good that prompt cath with PCI was accomplished!

Figure-2: I've consolidated and labeled ECG #2 — obtained from a 45-year old man who presented with acute CP. (Digitized using PMcardio to improve visualization).

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ECG #3 — from a 35-year old Man with 3 Hours of CP

I especially liked this 3rd case — which illustrates the diagnostic challenge of distinguishing between acute myocarditis vs OMI in a younger adult with new CP. We have addresssed this issue on a number of occasions (See My Comment in the April 25, 2023 — July 21, 2019 — December 10, 2019 — and January 10, 2020 posts). 

As to the findings in ECG #3:

• The rhythm is sinus — intervals and axis are normal — and there is no chamber enlargement.
• There is ST segment straightening and elevation in each of the inferior leads (within the RED rectangles) — with reciprocal ST depression in lead aVL (within the BLUE rectangle).
• The anterior lead ST depression of posterior involvement is absent. Instead — lateral leads I, V5,V6 all show ST straightening and elevation.
• 
  
• BOTTOM Line: The differential diagnosis is between acute myocarditis (given younger age of this patient) vs acute OMI. As illustrated in the above links to similar cases with the same differential diagnosis — cardiac cath may sometimes be needed to make the distinction.

Figure-3: I've consolidated and labeled ECG #3 — obtained from a 35-year old man who presented with 3 hours of CP. (Digitized using PMcardio to improve visualization).