Morphine + OMI is a bad combination

This is written by Magnus Nossen, with some edits by Smith

This ECG diagnosis will be obvious to the majority of the readers of this blog. It is not obvious for the majority of doctors or even cardiologists. 

A 50 something male was seen in the emergency room due to typical chest pain. The pain had started the same day about two hours prior to medical contact. Previous medical hx notable for type II DM. The first ECG is shown below. The medical care providers ascribed the patient's chest pain to new onset atrial fibrillation with rapid ventricular response after having viewed the ECG. Do you agree?

The presentation ECG does show atrial fibrillation. I think for medical providers not familiar with OMI ECG findings, this ECG can appear quite "normal". If you are familiar with the OMI/NOMI paradigm the diagnosis is obvious to you and is made without any delay. I showed this to some of my colleagues and they were not able to confidently say that this is an acute coronary occlusion. 

Back to the case. Initial troponin I returned elevated at 84 ng/L (ref value <34 ng/L). Fluids and morphine had been given and the patient had spontaneously converted to sinus rhythm. Then when in sinus rhythm (right after morphine) the patient denied chest pain. The following ECG was recorded.

Guidelines say that if a patient has ACS but refractory pain, the patient should go emergently to the cath lab.  This patient's pain did indeed resolve.  But it only resolved with morphine!  Morphine will resolve any pain even if the pathology is ongoing.  Do not give morphine until you are committed to the cath lab.

Just as important, the ECG shows ongoing clear inferoposterior OMI in progression with hyperacute T-waves leads II, III, and aVF. Already forming Q-waves inferiorly. Reciprocal change in lead I and aVL with ST-depression and T wave inversion. The OMI was still not appreciated. The patient was admitted with telemetry. No further episodes of atrial fibrillation occurred during monitoring. Due to chest discomfort morphine was repeated during the night. Next day troponin I returned 48,131 ng/L. A very large myocardial infarction.

The next day the ECG not unexpectedly shows a completed transmural inferior and posterior wall infarction. There are now well formed Q waves inferiorly. Hyperacuity of the T waves is gone signifying very little salvageable myocardium. There is early R/S transition occurring by V2 (analogous to posterior Q waves). The patient, albeit very delayed was referred for angiography where a 99% stenosed pRCA was stented. 

Post PCI ECG shown below with reperfusion T waves inferior leads and posterior reperfusion T waves (affecting the size and shape of the T waves anteriorly especially noticeable in lead V2).

Formal echocardiography revealed a moderately depressed LVEF of 40%. WMA inferior and posteriorly. This patient overall clinically (at least in the short run) did well despite the delay in treatment. Others are not that fortunate. The delayed activation of the cath lab would have been avoided had the treating physicians been trained in recognizing occlusion myocardial infarction. The Queen of Hearts AI model (QoH) as well would have done the trick.

Below you can see the interpretation by the  AI algorithm. Also pay attention to the score number top left. It gives a value of 0,9979. The AI model puts out a number between 0 and 1. The closer to 1, the more sure the algorithm is of the OMI diagnosis. Here one can see the the number is very, very close to 1. Thus the AI algorithm is very sure there is a complete coronary occlusion despite there being any significant ST elevation. 

The PMCardio Queen of Hearts AI OMI ECG system now has explainability.  

Lack of explainability is one of the primary criticisms of AI -- but the Queen has it.

You can see that each lead is given a label of OMI or Not OMI with the associated confidence.  

Then, within each lead, blue highlighting is used to show the part of the complex in each lead that is most consistent with OMI.  Leads III and aVF have a lot of dark blue, and that dark blue is concentrated over the R-wave, the ST segment, and the T-wave (all 3, because this is an obvious OMI0. aVL has a lot of dark blue also, as does lead I.  V2, which shows posterior OMI, has a lot of dark blue as well.  

Notice that much of the dark blue is concentrated on the QRS (R-wave); the QRS is totally ignored in the STEMI paradigm!!

The neural network produces a numerical result ranging from 0 to 1, where 1 represents a perfect OMI score, and 0 represents a perfect not-OMI score. Through analysis of the tuning dataset, an optimal OMI threshold of 0.1106 was determined. Any scores above this threshold are considered OMI positive, while scores below the threshold are considered OMI negative (not-OMI).

To further classify the predictions, the OMI positive and OMI negative segments are divided equally into confidence tertiles. If the neural network's output is higher than the threshold, a higher score indicates greater confidence in it being an OMI. Conversely, if the score is lower than the threshold, there is a higher confidence in it being a negative ECG for OMI (not-OMI).

Example:

- A score of 0.6743 would be OMI Mid Confidence because it’s under the High confidence threshold (1-((1-0.1106)/3) = **0.70353**) and over the Low confidence threshold (**0.40706**)

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MY Comment, by KEN GRAUER, MD (9/24/2023):

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I found today's case by Dr. Nossen interesting for a number of reasons.

• I focus my comments on the initial ECG — that I have reproduced in Figure-1.

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

Thoughts about Today's CASE:

On occasion — a patient may present for acute care because of CP (Chest Pain) due solely to a tachyarrhythmia (including new AFib, a reentry SVT or VT). In my experience — tachyarrhythmic-related CP is a real but uncommon phenomenon, in which the patient notes immediate relief of symptoms virtually at the moment that the tachyarrhythmia resolves.

• IF CP does not promptly resolve within moments of the resumption of sinus rhythm — it becomes a tenuous assumption that the tachyarrhythmia was the direct cause of that patient's chest pain. This is especially true if duration of the tachyarrhythmia was significant — since increased demand from a new tachyarrhythmia of itself may result in myocardial injury.
• Missing from the history that we are told, is how soon after resumption of sinus rhythm it was until the patient's CP resolved. This historical detail is clinically relevant — since medical providers in today's case erroneously attributed this patient's CP to his new-onset AFib, which should not have been done if there was a lag time between resolution of CP and resumption of sinus rhythm.

There is often reservation about relieving a patient's chest pain by giving morphine — because of the delay this has been shown to cause in securing prompt cardiac cath in patients with acute OMI.

• In my opinion — the problem is not giving morphine, but rather the inability to recognize acute ECG changes when millimeter-based stemi criteria are not attained.
• As per Dr. Nossen — the QoH (Queen of Hearts) AI algorithm immediately recognized high-likelihood of acute OMI from ECG #1. But as helpful as increasingly widespread use of QoH in general practice will be — We need to do better!
• In a patient with new-onset CP — the ST-T wave abnormalities in 5/6 limb leads in ECG #1 need to be recognized. Each of the inferior leads manifests disproportionate (Taller and "fatter"-at-their-peak, as well as wider-at-their-base than they should be) hyperacute T waves. Given these inferior lead T waves — there is no way the ST-T wave depression in high-lateral leads I and aVL does not represent reciprocal change that confirms acute inferior OMI. Further support is provided by the small-but-real Q waves in each of the inferior leads.
• Routine assessment for posterior OMI needs to be undertaken whenever there is suspicion of acute inferior OMI. Normally — there should be slight, upward-sloping ST elevation in anterior leads V2 and V3. The flat (if not downsloping) ST segment in lead V2 is therefore diagnostic of acute posterior OMI in this context. Further support of posterior OMI is suggested by the relatively early chest lead transition (Much taller than expected R wave already in lead V2).

NOTE: I'll finish with mention of the following points:

• It's important to be aware that the same 9 beats are shown in both the limb leads and the chest leads. This type of monitoring system results in a shorter rhythm strip (Only 6 seconds in duration) — but provides the advantage of showing us what each beat looks like in all 12 leads.
• 
  
• Changes in heart rate sometimes result in changes of the amount of ST-T wave deviation. For example — I've seen fast AFib be associated with significant ST elevation and depression that resolves after heart rate slows, and which was not a result of ischemia. For this reason — I often reserve judgment about the clinical significance of ST-T wave changes until heart rate slows and/or there has been conversion to sinus rhythm. In today's case — the disproportionate (hyperacute) limb lead ST-T wave changes described above largely persisted after conversion to sinus rhythm, confirming an acute event and the need for prompt cath.
• 
  
• Finally — Did YOU notice that the first ST-T wave in each of the 3 groupings clearly shows more pronounced changes than are seen in other beats (ie, BLUE arrows highlighting the ST-T wave changes of beats #1, 3 and 7 — which are clearly more marked than is seen for the ST-T waves of other beats). I fully acknowledge that I'm not sure why the slight pause before beats #3 and 7 produces these accentuated ST-T wave changes — but there is no denying that this occurrence is real.