Sent by anonymous, edited by Pendell Meyers
A man in his 50s with history only of hypertension presented with acute chest pain that started 45 minutes prior to presentation while doing yard work. It radiated to both shoulders and both upper extremities, and there was shortness of breath and diaphoresis as well. He reported a normal stress test a few years ago.
Triage ECG (no prior for comparison):
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| Computer algorithm read: "Sinus rhythm, low voltage QRS, inferior myocardial infarction, probably old." |
Meyers: There is STE in V2-V4, which cannot be called normal because there is a Q wave in V3, R wave regression from V2 to V3, and likely hyperacute T waves in V2-V4. Inferior T waves also likely abnormal, but not diagnostic to me without a prior for comparison.
I texted this ECG with no information to Dr. Smith, who immediately said:
"If CP, then anterior OMI until proven otherwise."
I then sent it to the Queen of Hearts AI bot for diagnosis of acute OMI (A deep convolutional neural network created by Powerful Medical, also known as PMCardio, and trained by Smith and Meyers)
Here is the QOH interpretation:
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| You can see many examples of use of the PM Cardio Queen of Hearts AI Bot from PMCardio HERE; you can sign up to get it HERE. |
Below you can see some new functionality of the AI that we are developing: lead-by-lead breakdown of the likelihood of OMI for each lead, and time-specific highlighting of the features that the AI judged to be most important for the diagnosis it made:
As far as I can tell, no action was taken based on the ECG.
Initial high sensitivity troponin I = less than 6 ng/L.
Second trop 19 ng/L.
Repeat ECG:
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| New developing Q waves in V2 and V3, further confirming evolving OMI. |
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| Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Terminal T wave inversion could me some reperfusion, or just part of untreated completing MI. Smith: the profound persistent STE suggests either persistent occlusion or "no reflow" with persistent downstream ischemia. |
FINAL DIAGNOSIS: "NSTEMI"
In the first year since discharge, he has been hospitalized 3 times with CHF.
Use of Morphine in Non-STE-ACS is independently associated with mortality, at odds ratio of 1.4
http://prdupl02.ynet.co.il/ForumFiles_2/14835373.pdf
STUDY OBJECTIVES:
Worldwide guidelines recommend emergent catheterization for any ACS patient (regardless of ECG findings) whose ischemic symptoms are not resolved with maximal medical therapy. Despite not being considered in this category, opioid medications are sometimes given for ACS. Prior evidence has shown association between opioids and increased mortality in ACS; however, the mechanism(s) of potential harm remain unelucidated. We hypothesize that opioids mask the ongoing symptoms of otherwise unrecognized Occlusion MI (OMI), without improving downstream ischemia, thus preventing the recognition of “ongoing ischemia despite maximal medical therapy” and causing delays to the cath lab for patients with STEMI(-) OMI who would benefit from emergent reperfusion. Our aim was to explore the association between opioid pain medication, delays to cath lab activation for suspected ACS, and outcomes.
METHODS:
Study design – retrospective, observational. Setting – large, academic, suburban ED. Patients – We performed a case-control study by combining patients from 1) a consecutive cohort of ED patients with suspected ACS over a 4-month period who were admitted and/or underwent catheterization, and 2) an additional group of occlusion myocardial infarction cases from our catheterization lab activation database. Patients were identified by whether they had received opioid pain medications prior to cath, post cath, or not at all. Main Outcomes – Door-to-balloon times and peak troponin elevations between those that received opioids versus those that did not. Data analysis – Descriptive statistics were used to summarize findings.
RESULTS:
During the study period 271 patients underwent cardiac catheterization. 31.7% were female, average age was 65 years, 85.2% were Caucasian, and 6.6% were Hispanic.
All Patients
We analyzed 271 patients who underwent cardiac catheterization during the study period. Of those, 228 (84.1%) did not receive opioids prior to cardiac catheterization. The 43 (15.8%) patients that received opioids had an average door-to-balloon time of 2123 minutes compared to 1643 minutes in those without pre-cath opioids. Patients without pre-cath opioids had a median peak Troponin T of 0.55 ng/mL, vs. 1.35 ng/mL in patients with pre-cath opioids. Of the 228 without pre-cath opioids, 45 (19.7%) were found to have STEMI(-) OMI, while 20 (46.5%) of the 43 that did receive pre-cath opioids were found to have STEMI(-) OMI.
STEMI(-) OMI Patients
65 (23.9%) patients were found to have STEMI(-) occlusion myocardial infarction (OMI) at the time of cardiac catheterization. The 45 patients with STEMI(-) OMI without pre-cath opioids had a door-to-balloon time of 75 minutes, vs. 684 minutes for the 25 STEMI(-) OMI with pre-cath opioids.
DISCUSSION:
The administration of opioid analgesia prior to cath in patients with concern for ACS is associated with longer door-to-balloon times, and greater peak troponin levels. The rate of Occlusion MI in those who received pre-cath opioids was double the rate of those without pre-cath opioids, and STEMI(-) OMI patients who received pre-cath opioids waited 10 hours on average longer to get cath than those who did not received opioids. These results add support to our hypothesis that a major mechanism of harm caused by opioid medications in ACS patients involves delays to the cath lab for patients with STEMI(-) OMI.
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MY Comment, by KEN GRAUER, MD (9/10/2023):
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Today's case illustrates a series of instructive teaching points. I focus my comments on Points of Interest that I'll add to Dr. Meyers' excellent discussion.
- NOTE: We are told that the patient in today's case is man in his 50s who presented with new CP (Chest Pain) — but whose prior medical history was remarkable only for hypertension — with mention of a "normal stress test" a few years earlier.
- Extra Credit: How does this patient's report of a "normal stress test" a few years earlier help us in our evaluation of this case?
- As you take another LOOK at ECG #1 — What is the relevance of the findings that I've labeled in Figure-1?
-USE.png) |
| Figure-1: The initial ECG in today's case. |
- Prior to QOH (Queen Of Hearts) — all computerized ECG interpretation programs that I have encountered over recent decades have proved themselves useless for recognition of hyperacute T waves. As happened in today's initial tracing — the computer algorithm completely overlooked the hyperacute T waves that are present in no less than 8/12 leads.
- In this patient with new CP — I thought T waves are hyperacute in leads II,III,aVF; and in leads V2-thru-V6. I find it easiest to start by identifying those T waves that are definitely "hypervoluminous" (ie, Taller and "Fatter"-at-their-peak as well as Wider-at-their-base than they should be, given R wave amplitude in the lead you are looking at). For example — there should be no doubt that the T waves in leads II, aVF and V4 are "too big", as T wave amplitude in these leads equals or exceeds R wave amplitude. Similarly, judging from the predominantly negative QRS complexes in leads V2 and V3 — the T waves in those leads are "too bulky". By extension — T waves are probably also hyperacute in neighboring leads III, V5 and V6.
- While "localization" of these hyperacute T waves in 8/12 leads is generalized (ie, covering infero-antero-lateral anatomic areas) — regardless of what the "culprit" artery turns out to be (ie, extensive LAD occlusion and/or associated multivessel disease) — the findings in today's case of new CP, in association with hyperacute T waves in multiple leads is already indication for prompt cath.
- In this age of sophisticated internet transmission — it should not take long to gain access for review of a prior ECG (from whatever institution the patient went to for the stress test).
- However, even without access to a prior ECG — the fact that this patient was never told that he may have had a previous "event" (infarction) — tells us that the loss of r wave after leads V1,V2 in ECG #1 — with development of a frank QS complex in lead V3 — are new findings (at least "new" since that prior stress test was done). There simply should be no way that this QS complex in lead V3 should have been missed IF it was previously present on a baseline ECG done at the time of this patient's prior stress test. This strongly suggests that loss of anterior r wave and the QS complex in lead V3 are part of the picture "painted" in today's initial tracing, in which there are hyperacute T waves in 8/12 leads of this ECG from a patient with new CP.
- If you look at the 3 beats in lead II of the 12-lead ECG in Figure-1 — the ST-T wave in the 1st beat is uninterpretable because of baseline wander and the artifactual steep (unphysiologic) rise of the ascending limb of the T wave. Artifactual undulations in the baseline account for variation and uncertainty in ST-T wave morphology in the remaining 2 beats in lead II of the 12-lead ECG. We often forget to look at the long lead II rhythm strip at the bottom of the tracing — which is an oversight, because instead of just 3 beats, there are 11 beats in this long lead II — which will clearly give us a much better idea of true ST-T wave morphology in this lead. Apart from the baseline wander and artifactual steep ascending T wave rise seen in the 1st beat of this long lead II rhythm strip — the remaining 10 beats confirm that the T wave in lead II is truly hyperacute (ie, truly hypervoluminous — and virtually as tall as the R wave in this lead).
- There is marked fragmentation in leads III and aVF of ECG #1 (ie, The blue-pink arrows pointing to obvious notching of the S wave in lead III — with a multiphasic rSr's'r'' complex in lead aVF). In association with a wider-than-it-should-be Q wave in lead II — this excessive fragmentation in leads III and aVF clearly indicates "scar", most likely from significant coronary disease and/or infarction at some point in time.
- Note that I added the vertical blue-pink line in simultaneously-recorded leads V1,V2,V3 — to highlight that the QRS complex in lead V2 actually begins with a slight negative deflection. This means that the QRS complex in lead V2 is also "fragmented" — with the finding of a small q — followed by a small-amplitude r wave — followed by a deep S wave — in which this fragmentation is indicative of anterior infarction at some point in time (presumably "new" given the QS complex seen in lead V3).
- Finally — it should be noted that the Q waves in lateral chest leads V4,V5,V6 are indicative of infarction at some point in time. While small "normal septal q waves" may be commonly seen in lateral leads (such as leads V5,V6) — the Q wave in lead V4 (RED arrow) should never normally be larger than "normal" septal q waves that may sometimes be seen in leads V5,V6 — but the PINK arrows highlighting the q waves in leads V5,V6 confirm that the larger Q wave in lead V4 is an "infarction" Q wave.
- P.S.: As per Dr. Meyers — Excessive delay in today's case until cardiac cath was finally performed on the grounds that the diagnosis was a "NSTEMI" — defies logic. One has to wonder how longterm outcome might have been improved had today's lessons been learned.
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