The Expert Witness re-visits a chest pain Malpractice case using the Queen of Hearts

This case was posted by Eric Funk (https://twitter.com/medmalreviewer), editor of the Expert Witness Newsletter, on his site.

Here is the case on his site.   He has graciously allowed me to repost it here. It is a case he presented several years ago, but then want to re-visit in light of the Queen of Hearts AI system.

Don't miss his analysis and assessment of the Queen of Hearts AI OMI ECG bot 

       -- that assessment is at the very bottom of the post.

Click here to sign up for Queen of Hearts Access

Case

A 58-year-old woman presented to the ED with burning chest pain that started 2-3 hours earlier while sitting on a porch swing.

Her first set of vitals were documented:

• BP 116/57

• Pulse 94bpm

• Respiratory rate 24/min

• O2 sat 90% on room air

• Temp 97F

She had been cleaning a Jeep in the sun, and was sunburned.

Past medical history included Crohn’s disease, hyperlipidemia, hypothyroidism, and she smoked 1ppd.

Here is her ED EKG:

What do you think?

Since it is in the Expert Witness Newsletter, there must be something that was missed, right?

I would have very high suspicion for OMI on this ECG.  But which artery?  There is STE and a large T-wave in V1, with reciprocal ST depression in V5 and V6.  This is typical of LAD occlusion proximal to the first septal perforator, an ECG for which we have coined the term "Swirl".  

However, the pattern is also seen in inferior OMI with right ventricular OMI. (V1 sits over both the RV and the septum, so transmural ischemia of either one with give OMI pattern in V1 and reciprocal STD in V5 and V6.  

See this post: 

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6.  (Also seen in inferior + RV OMI.)

There appear to be hyperacute T-waves in inferior leads.  There is also STD in V2.  This suggests inferior-posterior OMI and makes me lean to a proximal RCA occlusion.  But there is also perhaps some STD in inferior leads -- this would support LAD.

In any case, it is diagnostic of OMI in a chest pain patient.

The Queen of Hearts agrees:

It is interesting to see what the Queen of Hearts highlights on this explainability map: ST depression in V5 is the most important finding for her.

Case progression:

The automated EKG interpretation was “sinus rhythm with sinus arrhythmia, right atrial enlargement, rightward axis, possible anterior infarct, age undetermined, abnormal ECG”.

The physician documented “normal sinus rhythm”.

The patient was given 0.4mg nitroglycerin SL, which did not change her pain.

She was given 500mL of normal saline and IV Toradol 30mg.

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CBC and CMP were unremarkable.

A troponin was normal at 0.06 (normal range 0.00 - 0.10).

CK MB was 1.9 (normal range 0.0 - 3.6).

A chest x-ray was unremarkable.

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The physician documented that she was “improved” and the patient was discharged.

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The following morning, the patient collapsed in the kitchen in front of her family.

EMS arrived to a pulseless patient in V fib.

She was successfully defibrillated and taken back to the ED.

After being transferred to an academic center, she was taken to the cath lab:

Proximal RCA occlusion (causing inferior and RV OMI)

Unfortunately, she continued to decline despite aggressive measures.

The family elected to switch to comfort care and she died.

The family filed a lawsuit against the physician and the hospital.

They sued the the county-operated EMS service for allegedly not dispatching the call fast enough.

They also sued both EMTs for allegedly not starting chest compressions and defibrillating quickly enough.

The family sued.  

You can read the defense EM expert report on Dr. Funk's site: 

https://expertwitness.substack.com/p/occlusion-myocardial-infarction-queen

Case Outcome

The EMTs were found to have personal immunity as part of their employment with the local government. They were dismissed.

The 911 call center and EMS service were also dismissed.

The hospital and doctor reached confidential settlements.

MedMalReviewer Analysis:

After originally working on this case several years ago, I became interested in re-analyzing it in light of The OMI Manifesto. In short, the OMI paradigm offers an improved method of EKG interpretation that seeks to replace the STEMI/NSTEMI dichotomy that currently dictates emergency cath lab activation (but is rife with false positives and false negatives). While initially promising, I grew frustrated with the OMI model due to the extreme nuance it mandates in EKG interpretation, and my own inability to identify findings that the OMI experts claimed were obvious. I remain skeptical that the average physician should be expected to unilaterally interpret EKGs to the level of the OMI experts.

However, my frustration quickly reversed with the release of the Queen of Hearts algorithm, which was trained by Dr. Stephen Smith using AI to detect occlusion myocardial infarction that is often missed using standard STEMI criteria. It allows users to take a picture of an EKG, which is digitized and then analyzed for OMI.

Naturally, I ran the EKG from this case through the Queen of Hearts algorithm. Sure enough, it detected OMI with high probability:

I was initially skeptical that the algorithm was just flagging everything as OMI. I repeatedly tested the algorithm with multiple other EKGs, and my anecdotal report is that I found it to be highly reliable.

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MY Comment, by KEN GRAUER, MD (6/13/2024):

===================================

Interpretation of the subtle ECG changes seen in a significant percentage of acute OMIs can be difficult. This task is made even more challenging when technical issues such as erroneous lead placement or excessive artifact — call into question our ability to accurately interpret a number of leads on the tracing in front of us. 

• To illustrate this point — I've labeled the initial ECG in today's case.

 

QUESTIONS:

Before looking at my labeled Figure-1 — Take Another LOOK at the unlabeled initial tracing shown above at the beginning of today’s case.

• Is there ST depression in the inferior leads in Figure-1?
• Is there ST elevation in lead aVL?
• Are there any leads with definite abnormal findings?
  

MY Thoughts on Today’s Initial ECG:

The history in today’s case is concerning (ie, = a 58-year old woman with longterm tobacco use, who presented with new-onset CP [Chest Pain]).

• As we frequently emphasize — this type of history automatically places today’s patient in a higher-prevalence group at risk of an ongoing cardiac event. As a result — our threshold for interpreting ECG changes as “abnormal” should be lowered. Given this history — the onus falls on us is to rule out ACS (Acute Coronary Syndrome) — rather than ruling it in.
• 
  
• That said — technical issues with today’s initial ECG (in the form of an extremely wavy baseline in 4 of the limb leads) — make it difficult to know IF we truly are seeing ST depression in the inferior leads? — and, if there is truly ST elevation in lead aVL?
• KEY Point: I think it important to appreciate how we are handicapped in our interpretation of today’s initial ECG by the technical issue of a wavy baseline that calls into question the ECG information conveyed from 4 of the 12 leads. While I thought it likely that there is inferior lead ST depression — and Q waves with subtle-but-real ST elevation in lead aVL — I was less than certain about this given the excessively wavy baseline in these 4 limb leads.

       Figure-1: I've labeled the initial ECG in today's case. 

 

My Continuing Assessment of ECG #1:

Despite uncertainty about the ECG information provided by leads II,III,avF and aVL — there are other leads in this initial tracing that are definitely abnormal.

• In a patient such as the woman in today’s case (ie, who presents with new CP) — there is no way the ST-T wave appearance of the 2 leads within the RED rectangle in Figure-1 can be normal.
• In lead V1 — The ST segment straightening, with slight-but-real J-point ST elevation and hyperacute T wave appearance are never “normal” findings in this lead.
• Lead V1’s appearance is in sharp contrast to what we see in lead V2 — in which the usual slight, gently upsloping ST elevation that is normally seen in this lead — has been replaced by an isoelectric, straightened ST segment (RED arrow). In a patient with new CP — this suggests posterior OMI until proven otherwise.
• Additional definitely abnormal ST-T waves are seen in the 2 leads within the BLUE rectangle. In leads V5 and V6 — BLUE arrows highlight “ledge-like” and significant ST depression.
• BLUE arrows in lead I add support to the validity of the finding that there clearly is abnormal, straightened ST depression in the lateral leads.

IMPRESSION:

In a patient with new CP — today’s initial ECG has to be interpreted as clearly abnormal until proven otherwise.

• As enthusiastic as I am about the amazing (and ever increasing) accuracy of the QOH AI application — I believe that optimal clinical management must also depend on capable provider assessment of emergency ECGs. Optimal use of QOH can best be achieved by joint effort (ie, Pre-hospital and hospital providers seeing the ECG first — and then supplementing their interpretation by what they learn from QOH input).
• Therefore — an important benefit of QOH — is that providers can (and should) learn from this application — so that with time, the interpretations of all providers (pre-hospital, emergency clinicians and cardiologists) will improve regarding faster and more accurate recognition of acute OMI.
• 
  
• Regarding specifics of today's case — I fully acknowledge that I found myself unable to predict the “culprit” artery based solely on the initial ECG. That said — I nevertheless was able to strongly suspect acute OMI based on the history of new CP and the initial ECG. I believe recognition of the ST-T wave abnormalities I highlight in Figure-1 should be within the skill set of experienced prehospital providers, emergency physicians, and those cardiologists called on to perform acute cath lab activation.
• At the least — if technical issues (such as the overly wavy baseline in the limb leads from today’s case) prevent valid interpretation — then the ECG should be promptly repeated. The decision of whether or not to activate the cath lab hangs in the balance.
• And, if after assessment of a technically adequate tracing there is still uncertainty about whether this higher risk patient with new CP is having an acute OMI — then serial ECGs should be repeated frequently (ie, within every 10-30 minutes, or so) — until such time that joint decision-making between clinician with QOH input can comfortably rule in or rule out acute OMI. 

1.